Publications by category
Books
Zeman A, Kapur N, Jones-Gotman M (2012).
Epilepsy and Memory - a comprehensive multi-author review of the interactions between epilepsy and memory. , Oxford University Press.
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Epilepsy and Memory - a comprehensive multi-author review of the interactions between epilepsy and memory.
Abstract.
Zeman A (2008). A Portrait of the Brain. London, Yale University Press.
Zeman A (2002). Consciousness: a User's Guide. Yale, Yale University Press.
Journal articles
Zeman A (In Press). Blind Mind's Eye.
American Scientist MagazineAbstract:
Blind Mind's Eye
(sorry unsure where to put this), this is the published version, I have permission from the publisher that this can be downloaded to ORE
Abstract.
Savage SA, Baker J, Milton F, Butler CR, Zeman A (In Press). Clinical outcomes in Transient Epileptic Amnesia: a 10-year follow-up cohort study of 47 cases. Epilepsia
MacKisack M, Zeman A, Winlove C, Onians J, Macpherson F, Aldworth S (In Press). Extended Imagining: the case of the aphantasic artist.
Abstract:
Extended Imagining: the case of the aphantasic artist
Can visual imagining ever be other than a brain-bound, organismically internal process? the practices of artists with aphantasia - the congenital or acquired incapacity to generate visual mental imagery - suggests that it can. Here we report on a qualitative study of ‘aphantasic’ artists and find that imagery lack coincides with a dependence on external, environmental, structures to generate artwork. Indeed, physical manipulations of external media seem to take place in lieu of the ability to generate and manipulate internal, mental images. Cognitive functions that could, for the non-aphantasic, be carried out by mental imagery - such as bringing non-conscious visio-spatial relationships to awareness - can only be carried out for the aphantasic by manipulating their environment. Thus aphantasic art-making constitutes extended visual imagining. As such, it undermines the universality of the ‘hylomorphic’ model of art-making, in which the work is mentally preconceived before being realised in the material world, with the fact of neurocognitive diversity.
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Knight K, Milton F, Zeman A (In Press). Memory without Imagery: No Evidence of Visual Working Memory Impairment in People with Aphantasia. Proceedings of the Cognitive Science Society
Zeman A, MacKisack M, Aldworth S, MacPherson F, Onians J, Winlove C (In Press). plural imagination: diversity in mind and making. Art Journal
Monzel M, Mitchell D, Macpherson F, Pearson J, Zeman A (2022). Aphantasia, dysikonesia, anauralia: call for a single term for the lack of mental imagery-Commentary on Dance et al. (2021) and Hinwar and Lambert (2021).
Cortex,
150, 149-152.
Abstract:
Aphantasia, dysikonesia, anauralia: call for a single term for the lack of mental imagery-Commentary on Dance et al. (2021) and Hinwar and Lambert (2021).
Recently, the term 'aphantasia' has become current in scientific and public discourse to denote the absence of mental imagery. However, new terms for aphantasia or its subgroups have recently been proposed, e.g. 'dysikonesia' or 'anauralia', which complicates the literature, research communication and understanding for the general public. Before further terms emerge, we advocate the consistent use of the term 'aphantasia' as it can be used flexibly and precisely, and is already widely known in the scientific community and among the general public.
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Monzel M, Mitchell D, Macpherson F, Pearson J, Zeman A (2022). Proposal for a consistent definition of aphantasia and hyperphantasia: a response to Lambert and Sibley (2022) and Simner and Dance (2022).
Cortex,
152, 74-76.
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Zhao B, Della Sala S, Zeman A, Gherri E (2022). Spatial transformation in mental rotation tasks in aphantasia.
Psychonomic Bulletin and Review,
29(6), 2096-2107.
Abstract:
Spatial transformation in mental rotation tasks in aphantasia
Aphantasia refers to the inability to summon images to one’s own mind’s eye, resulting in selective deficits of voluntary object imagery. In the present study, we investigated whether M. X. a case of acquired aphantasia, can still retain some form of spatial transformation processes even though he is unable to subjectively experience voluntary object imagery. M. X. and a group of control participants were asked to complete a letter mental rotation task (MRT), typically used to assess the nature of the spatial transformation, while behavioural and electrophysiological responses were recorded. M. X. was able to complete the MRTs as accurately as controls, showing the pattern of increasing RTs as a function of rotation angle typical of MRTs. However, event-related potential (ERP) results showed systematic differences between M. X. and controls. On canonical letter trials, the rotation-related negativity (RRN), an ERP component considered as the psychophysiological correlate of the spatial transformation of mental rotation (MR), was present in both M. X. and controls and similarly modulated by rotation angle. However, no such modulation was observed for M. X. on mirror-reversed letter trials. These findings suggest that, at least under specific experimental conditions, the inability to create a depictive representation of the stimuli does not prevent the engagement of spatial transformation in aphantasia. However, the ability to apply spatial transformation varies with tasks and might be accounted for by the specific type of mental representation that can be accessed.
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Keogh R, Pearson J, Zeman A (2021). Aphantasia: the science of visual imagery extremes.
Handb Clin Neurol,
178, 277-296.
Abstract:
Aphantasia: the science of visual imagery extremes.
Visual imagery allows us to revisit the appearance of things in their absence and to test out virtual combinations of sensory experience. Visual imagery has been linked to many cognitive processes, such as autobiographical and visual working memory. Imagery also plays symptomatic and mechanistic roles in neurologic and mental disorders and is utilized in treatment. A large network of brain activity spanning frontal, parietal, temporal, and visual cortex is involved in generating and maintain images in mind. The ability to visualize has extreme variations, ranging from completely absent (aphantasia) to photo-like (hyperphantasia). The anatomy and functionality of visual cortex, including primary visual cortex, have been associated with individual differences in visual imagery ability, pointing to a potential correlate for both aphantasia and hyperphantasia. Preliminary evidence suggests that lifelong aphantasia is associated with prosopagnosia and reduction in autobiographical memory; hyperphantasia is associated with synesthesia. Aphantasic individuals can also be highly imaginative and are able to complete many tasks that were previously thought to rely on visual imagery, demonstrating that visualization is only one of many ways of representing things in their absence. The study of extreme imagination reminds us how easily invisible differences can escape detection.
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Milton F, Fulford J, Dance C, Gaddum J, Heuerman-Williamson B, Jones K, Knight KF, Mackisack M, Winlove C, Zeman A, et al (2021). Behavioral and Neural Signatures of Visual Imagery Vividness Extremes: Aphantasia vs Hyperphantasia. Cerebral Cortex Communications, 2, 1-15.
Lomas M, Rickard V, Milton F, Savage S, Weir A, Zeman A (2021). Electroconvulsive Therapy related Autobiographical Amnesia: ‘Somatoform’ or ‘Organic’? - a review and case report. Cognitive Neuropsychiatry, 26, 107-121.
Patel D, Ibrahim H, Rankin J, Hilton D, Barria MA, Ritchie DL, Smith C, Zeman A (2021). Fatal insomnia: the elusive prion disease.
BMJ Case Rep,
14(6).
Abstract:
Fatal insomnia: the elusive prion disease.
A previously well 54- year-old woman presented with a short history of diplopia, cognitive decline, hallucinations and hypersomnolence. The patient had progressive deterioration in short-term memory, ocular convergence spasm, tremor, myoclonus, gait apraxia, central fever, dream enactment and seizures. Results of investigations were normal including MRI brain, electroencephalogram, cerebrospinal fluid (CSF, including CSF prion protein markers) and brain biopsy. The patient died from pneumonia and pulmonary embolus. Brain postmortem analysis revealed neuropathological changes in keeping with Fatal familial insomnia (FFI); the diagnosis was confirmed on genetic testing. FFI is caused by an autosomal dominant and highly penetrant pathogenic Prion Protein gene PRNP Although usually familial, fatal insomnia (FI) also occurs in a rare sporadic form. FI is a rare human prion disease with prominent sleep disturbance, autonomic, motor, cognitive and behavioural involvement. Patient management is with best supportive care and early suspected diagnosis allows for timely palliation.
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Baker J, Savage S, Milton F, Butler C, Kapur N, Hodges J, Zeman A (2021). The Syndrome of Transient Epileptic Amnesia: a combined series of 115 cases and literature review. Brain Communications, 3
Dance CJ, Jaquiery M, Eagleman DM, Porteous D, Zeman A, Simner J (2021). What is the relationship between Aphantasia, Synaesthesia and Autism?.
Conscious Cogn,
89Abstract:
What is the relationship between Aphantasia, Synaesthesia and Autism?
For people with aphantasia, visual imagery is absent or markedly impaired. Here, we investigated the relationship between aphantasia and two other neurodevelopmental conditions also linked to imagery differences: synaesthesia, and autism. In Experiment 1a and 1b, we asked whether aphantasia and synaesthesia can co-occur, an important question given that synaesthesia is linked to strong imagery. Taking grapheme-colour synaesthesia as a test case, we found that synaesthesia can be objectively diagnosed in aphantasics, suggesting visual imagery is not necessary for synaesthesia to occur. However, aphantasia influenced the type of synaesthesia experienced (favouring 'associator' over 'projector' synaesthesia - a distinction tied to the phenomenology of the synaesthetic experience). In Experiment 2, we asked whether aphantasics have traits associated with autism, an important question given that autism - like aphantasia - is linked to weak imagery. We found that aphantasics reported more autistic traits than controls, with weaknesses in imagination and social skills.
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Romiszewski S, May FEK, Homan EJ, Norris B, Miller MA, Zeman A (2020). Medical student education in sleep and its disorders is still meagre 20 years on: a cross-sectional survey of UK undergraduate medical education.
J Sleep Res,
29(6).
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Medical student education in sleep and its disorders is still meagre 20 years on: a cross-sectional survey of UK undergraduate medical education.
Sleep is a pillar of health, alongside adequate nutrition and exercise. Problems with sleep are common and often treatable. Twenty years ago, UK medical school education on sleep disorders had a median teaching time of 15 min; we investigate whether education on sleep disorders has improved. This is a cross-sectional survey, including time spent on teaching sleep medicine, subtopics covered and forms of assessment. Thirty-four medical degree courses in the UK were investigated via a questionnaire. We excluded responses not concerned with general undergraduate education (i.e. optional modules). Twenty-five (74%) medical schools responded. Time spent teaching undergraduates sleep medicine was: median, 1.5 hr; mode,
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Argyropoulos GPD, Moore L, Loane C, Roca-Fernandez A, Lage-Martinez C, Gurau O, Irani SR, Zeman A, Butler CR (2020). Pathologic tearfulness after limbic encephalitis. Neurology, 10.1212/WNL.0000000000008-10.1212/WNL.0000000000008.
Zeman AZJ, Milton F, Della Sala S, Dewar M, Frayling T, Gaddum J, Hattersley A, Heuerman-Williamson B, Jones K, Mackisack M, et al (2020). Phantasia - the psychological significance of lifelong visual imagery vividness extremes. Cortex, 130, 426-440.
Baker J, Libretto T, Henley W, Zeman A (2019). A Longitudinal Study of Epileptic Seizures in Alzheimer's Disease.
Front Neurol,
10Abstract:
A Longitudinal Study of Epileptic Seizures in Alzheimer's Disease.
The prevalence of epileptic seizures is increased in patients in the clinical stages of Alzheimer's disease (AD) when compared to age-matched cognitively normal populations. In previously reported work from the Presentation of Epileptic Seizures in Dementia (PrESIDe) study, we identified a clinical suspicion of epilepsy in between 12.75 and 28.43% of patients with AD recruited from a memory clinic. EEGs were not performed in this study. Patients with epilepsy performed similarly to patients without epilepsy on cognitive testing at the time of recruitment but were more impaired on two measures of everyday functioning [Cambridge Behavioral Inventory-Revised and Clinical Dementia Rating (CBI-R and CDR)]. On repeated testing in this 12-month follow-up study, patients in whom a suspicion of epilepsy was identified performed significantly worse on cognitive function testing (p = 0.028) in addition to maintaining a difference on the informant questionnaires (CBI-R p < 0.001, CDR p = 0.020). These findings suggest that seizures in this population could be a marker of a more rapid decline and worse prognosis.
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Hoefeijzers S, Zeman A, Della Sala S, Dewar M (2019). Capturing real-life forgetting in transient epileptic amnesia via an incidental memory test.
Cortex,
110, 47-57.
Abstract:
Capturing real-life forgetting in transient epileptic amnesia via an incidental memory test
Transient epileptic amnesia (TEA) is an epileptic syndrome characterized by recurrent, brief episodes of amnesia. Patients with TEA often complain of interictal (between attacks) retention deficits, characterised by an ‘evaporation’ of memories for recent events over days to weeks. Clinical tests of anterograde memory often fail to corroborate these complaints as TEA patients commonly perform within the normal range after the standard 10–30-min delay period. Modified laboratory tests that include a 1–3 week delay period frequently reveal clear evidence of ‘accelerated long-term forgetting’ (ALF). However, they are not used routinely and lack ecological validity. In the present study we examined whether ‘real-life’ ALF can be captured via a controlled incidental memory test in TEA patients. To this end, the experimenter told 27 TEA patients and 32 controls a well-rehearsed amusing story, apparently as a way of making light conversation before starting a set of research experiments. Without prior warning, the experimenter subsequently probed the participants' memory of this story via tests of free recall and forced choice recognition after 30 min or 1 week. After 30 min retention was comparable in TEA patients and controls. After 1 week TEA patients retained significantly less story material than controls, and significant ALF was revealed in the TEA patients in the recognition test. Our data show that ALF in a ‘real-life’ situation can occur even when standard memory tests indicate normal memory function. Moreover, our data suggest that incidental memory tests can capture real-life ALF, and that forced-choice recognition tests might be more sensitive than free recall tests for the detection of real-life ALF.
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Bowman P, Day J, Torrens L, Shepherd MH, Knight BA, Ford TJ, Flanagan SE, Chakera A, Hattersley AT, Zeman A, et al (2019). Cognitive, Neurological, and Behavioral Features in Adults with KCNJ11 Neonatal Diabetes.
Diabetes Care,
42(2), 215-224.
Abstract:
Cognitive, Neurological, and Behavioral Features in Adults with KCNJ11 Neonatal Diabetes.
OBJECTIVE: Central nervous system (CNS) features in children with permanent neonatal diabetes (PNDM) due to KCNJ11 mutations have a major impact on affected families. Sulfonylurea therapy achieves outstanding metabolic control but only partial improvement in CNS features. The effects of KCNJ11 mutations on the adult brain and their functional impact are not well understood. We aimed to characterize the CNS features in adults with KCNJ11 PNDM compared with adults with INS PNDM. RESEARCH DESIGN AND METHODS: Adults with PNDM due to KCNJ11 mutations (n = 8) or INS mutations (n = 4) underwent a neurological examination and completed standardized neuropsychological tests/questionnaires about development/behavior. Four individuals in each group underwent a brain MRI scan. Test scores were converted to Z scores using normative data, and outcomes were compared between groups. RESULTS: in individuals with KCNJ11 mutations, neurological examination was abnormal in seven of eight; predominant features were subtle deficits in coordination/motor sequencing. All had delayed developmental milestones and/or required learning support/special schooling. Half had features and/or a clinical diagnosis of autism spectrum disorder. KCNJ11 mutations were also associated with impaired attention, working memory, and perceptual reasoning and reduced intelligence quotient (IQ) (median IQ KCNJ11 vs. INS mutations 76 vs. 111, respectively; P = 0.02). However, no structural brain abnormalities were noted on MRI. The severity of these features was related to the specific mutation, and they were absent in individuals with INS mutations. CONCLUSIONS: KCNJ11 PNDM is associated with specific CNS features that are not due to long-standing diabetes, persist into adulthood despite sulfonylurea therapy, and represent the major burden from KCNJ11 mutations.
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Helbig KL, Lauerer RJ, Bahr JC, Souza IA, Myers CT, Uysal B, Schwarz N, Gandini MA, Huang S, Keren B, et al (2019). De Novo Pathogenic Variants in CACNA1E Cause Developmental and Epileptic Encephalopathy with Contractures, Macrocephaly, and Dyskinesias.
Am J Hum Genet,
104(3).
Author URL.
Atherton KE, Filippini N, Zeman AZJ, Nobre AC, Butler CR (2019). Encoding-related brain activity and accelerated forgetting in transient epileptic amnesia.
Cortex,
110, 127-140.
Abstract:
Encoding-related brain activity and accelerated forgetting in transient epileptic amnesia.
The accelerated forgetting of newly learned information is common amongst patients with epilepsy and, in particular, in the syndrome of transient epileptic amnesia (TEA). However, the neural mechanisms underlying accelerated forgetting are poorly understood. It has been hypothesised that interictal epileptiform activity during longer retention intervals disrupts normally established memory traces. Here, we tested a distinct hypothesis-that accelerated forgetting relates to the abnormal encoding of memories. We studied a group of 15 patients with TEA together with matched, healthy control subjects. Despite normal performance on standard anterograde memory tasks, patients showed accelerated forgetting of a word list over one week. We used a subsequent memory paradigm to compare encoding-related brain activity in patients and controls. Participants studied a series of visually presented scenes whilst undergoing functional MRI scanning. Recognition memory for these scenes was then probed outside the scanner after delays of 45 min and of 4 days. Patients showed poorer memory for the scenes compared with controls. In the patients but not the controls, subsequently forgotten stimuli were associated with reduced hippocampal activation at encoding. Furthermore, patients demonstrated reduced deactivation of posteromedial cortex regions upon viewing subsequently remembered stimuli as compared to subsequently forgotten ones. These data suggest that abnormal encoding-related activity in key memory areas of the brain contributes to accelerated forgetting in TEA. We propose that abnormally encoded memory traces may be particularly vulnerable to interference from subsequently encountered material and hence be forgotten more rapidly. Our results shed light on the mechanisms underlying memory impairment in epilepsy, and offer support to the proposal that accelerated forgetting may be a useful marker of subtle dysfunction in memory-related brain systems.
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Berkovic SF, Oliver KL, Canafoglia L, Krieger P, Damiano JA, Hildebrand MS, Morbin M, Vears DF, Sofia V, Giuliano L, et al (2019). Kufs disease due to mutation of CLN6: clinical, pathological and molecular genetic features.
Brain,
142(1), 59-69.
Abstract:
Kufs disease due to mutation of CLN6: clinical, pathological and molecular genetic features.
Kufs disease is the major adult form of neuronal ceroid lipofuscinosis, but is rare and difficult to diagnose. Diagnosis was traditionally dependent on the demonstration of characteristic storage material, but distinction from normal age-related accumulation of lipofuscin can be challenging. Mutation of CLN6 has emerged as the most important cause of recessive Kufs disease but, remarkably, is also responsible for variant late infantile ceroid lipofuscinosis. Here we provide a detailed description of Kufs disease due to CLN6 pathogenic variants. We studied 20 cases of Kufs disease with CLN6 pathogenic variants from 13 unrelated families. Mean age of onset was 28 years (range 12-51) with bimodal peaks in teenage and early adult life. The typical presentation was of progressive myoclonus epilepsy with debilitating myoclonic seizures and relatively infrequent tonic-clonic seizures. Patients became wheelchair-bound with a mean 12 years post-onset. Ataxia was the most prominent motor feature. Dementia appeared to be an invariable accompaniment, although it could take a number of years to manifest and occasionally cognitive impairment preceded myoclonic seizures. Patients were usually highly photosensitive on EEG. MRI showed progressive cerebral and cerebellar atrophy. The median survival time was 26 years from disease onset. Ultrastructural examination of the pathology revealed fingerprint profiles as the characteristic inclusions, but they were not reliably seen in tissues other than brain. Curvilinear profiles, which are seen in the late infantile form, were not a feature. of the 13 unrelated families we observed homozygous CLN6 pathogenic variants in four and compound heterozygous variants in nine. Compared to the variant late infantile form, there was a lower proportion of variants that predicted protein truncation. Certain heterozygous missense variants in the same amino acid position were found in both variant late infantile and Kufs disease. There was a predominance of cases from Italy and surrounding regions; this was partially explained by the discovery of three founder pathogenic variants. Clinical distinction of type a (progressive myoclonus epilepsy) and type B (dementia with motor disturbance) Kufs disease was supported by molecular diagnoses. Type a is usually caused by recessive pathogenic variants in CLN6 or dominant variants in DNAJC5. Type B Kufs is usually associated with recessive CTSF pathogenic variants. The diagnosis of Kufs remains challenging but, with the availability of genetic diagnosis, this will largely supersede the use of diagnostic biopsies, particularly as biopsies of peripheral tissues has unsatisfactory sensitivity and specificity.
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Savage SA, Irani S, Leite MI, Zeman A (2019). NMDA receptor antibody encephalitis presenting as Transient Epileptic Amnesia. Journal of Neuroimmunology
Savage S, Hoefeijzers S, Milton FN, Streatfield C, Dewar M, Zeman A (2019). The evolution of accelerated long-term forgetting: Evidence from the TIME study. Cortex, 110, 16-36.
Baker J, Libretto T, Henley W, Zeman A (2019). The prevalence and clinical features of epileptic seizures in a memory clinic population. Seizure, 71, 83-92.
Weston PSJ, Nicholas JM, Henley SMD, Liang Y, Macpherson K, Donnachie E, Schott JM, Rossor MN, Crutch SJ, Butler CR, et al (2018). Accelerated long-term forgetting in presymptomatic autosomal dominant Alzheimer's disease: a cross-sectional study.
LANCET NEUROLOGY,
17(2), 123-132.
Author URL.
Helbig KL, Lauerer RJ, Bahr JC, Souza IA, Myers CT, Uysal B, Schwarz N, Gandini MA, Huang S, Keren B, et al (2018). De Novo Pathogenic Variants in CACNA1E Cause Developmental and Epileptic Encephalopathy with Contractures, Macrocephaly, and Dyskinesias.
Am J Hum Genet,
103(5), 666-678.
Abstract:
De Novo Pathogenic Variants in CACNA1E Cause Developmental and Epileptic Encephalopathy with Contractures, Macrocephaly, and Dyskinesias.
Developmental and epileptic encephalopathies (DEEs) are severe neurodevelopmental disorders often beginning in infancy or early childhood that are characterized by intractable seizures, abundant epileptiform activity on EEG, and developmental impairment or regression. CACNA1E is highly expressed in the central nervous system and encodes the α1-subunit of the voltage-gated CaV2.3 channel, which conducts high voltage-activated R-type calcium currents that initiate synaptic transmission. Using next-generation sequencing techniques, we identified de novo CACNA1E variants in 30 individuals with DEE, characterized by refractory infantile-onset seizures, severe hypotonia, and profound developmental impairment, often with congenital contractures, macrocephaly, hyperkinetic movement disorders, and early death. Most of the 14, partially recurring, variants cluster within the cytoplasmic ends of all four S6 segments, which form the presumed CaV2.3 channel activation gate. Functional analysis of several S6 variants revealed consistent gain-of-function effects comprising facilitated voltage-dependent activation and slowed inactivation. Another variant located in the domain II S4-S5 linker results in facilitated activation and increased current density. Five participants achieved seizure freedom on the anti-epileptic drug topiramate, which blocks R-type calcium channels. We establish pathogenic variants in CACNA1E as a cause of DEEs and suggest facilitated R-type calcium currents as a disease mechanism for human epilepsy and developmental disorders.
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Romiszewski S, Croft D, Veale J, Matthews L, Ryland H, May F, Zeman A (2018). Neurological sleep medicine: a case note audit from a specialist clinic.
Progress in Neurology and Psychiatry,
22(2), 9-17.
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Neurological sleep medicine: a case note audit from a specialist clinic
On average, humans sleep for a third of their lives, and sleep disorders are common and treatable. However, services for most sleep disorders are highly variable across the UK, and sleep medicine is neglected in the medical curriculum. We report the findings of an audit of patients with neurological sleep disorders seen in a combined cognitive neurology and sleep disorder clinics over a seven‐year period, 75 with hypersomnias, 67 with parasomnias and 39 with insomnia. Also, the results of a pilot of a cognitive behavioural therapy service for insomnia undertaken in the same population are analysed.
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Zeman A, MacKisack M, Onians J (2018). The Eye's mind – Visual imagination, neuroscience and the humanities. Cortex, 105, 1-3.
Fulford J, Milton F, Salas D, Smith A, Simler A, Winlove C, Zeman A (2018). The neural correlates of visual imagery vividness – an fMRI study and literature review.
Cortex,
105, 26-40.
Abstract:
The neural correlates of visual imagery vividness – an fMRI study and literature review
Using the Vividness of Visual Imagery Questionnaire we selected 14 high-scoring and 15 low-scoring healthy participants from an initial sample of 111 undergraduates. The two groups were matched on measures of age, IQ, memory and mood but differed significantly in imagery vividness. We used fMRI to examine brain activation while participants looked at, or later imagined, famous faces and famous buildings. Group comparison revealed that the low-vividness group activated a more widespread set of brain regions while visualising than the high-vividness group. Parametric analysis of brain activation in relation to imagery vividness across the entire group of participants revealed distinct patterns of positive and negative correlation. In particular, several posterior cortical regions show a positive correlation with imagery vividness: regions of the fusiform gyrus, posterior cingulate and parahippocampal gyri (BAs 19, 29, 31 and 36) displayed exclusively positive correlations. By contrast several frontal regions including parts of anterior cingulate cortex (BA 24) and inferior frontal gyrus (BAs 44 and 47), as well as the insula (BA 13), auditory cortex (BA 41) and early visual cortices (BAs 17 and 18) displayed exclusively negative correlations. We discuss these results in relation to a previous, functional imaging study of a clinical case of ‘blind imagination’ and to the existing literature on the functional imaging correlates of imagery vividness and related phenomena in visual and other domains.
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Winlove CIP, Milton F, Ranson J, Fulford J, MacKisack M, Macpherson F, Zeman A (2018). The neural correlates of visual imagery: a co-ordinate-based meta-analysis.
Cortex,
105, 4-25.
Abstract:
The neural correlates of visual imagery: a co-ordinate-based meta-analysis
Visual imagery is a form of sensory imagination, involving subjective experiences typically described as similar to perception, but which occur in the absence of corresponding external stimuli. We used the Activation Likelihood Estimation algorithm (ALE) to identify regions consistently activated by visual imagery across 40 neuroimaging studies, the first such meta-analysis. We also employed a recently developed multi-modal parcellation of the human brain to attribute stereotactic co-ordinates to one of 180 anatomical regions, the first time this approach has been combined with the ALE algorithm. We identified a total 634 foci, based on measurements from 464 participants. Our overall comparison identified activation in the superior parietal lobule, particularly in the left hemisphere, consistent with the proposed ‘top-down’ role for this brain region in imagery. Inferior premotor areas and the inferior frontal sulcus were reliably activated, a finding consistent with the prominent semantic demands made by many visual imagery tasks. We observed bilateral activation in several areas associated with the integration of eye movements and visual information, including the supplementary and cingulate eye fields (SCEFs) and the frontal eye fields (FEFs), suggesting that enactive processes are important in visual imagery. V1 was typically activated during visual imagery, even when participants have their eyes closed, consistent with influential depictive theories of visual imagery. Temporal lobe activation was restricted to area PH and regions of the fusiform gyrus, adjacent to the fusiform face complex (FFC). These results provide a secure foundation for future work to characterise in greater detail the functional contributions of specific areas to visual imagery.
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Zeman AZJ, Baker J (2017). Accelerated Long-Term Forgetting in Epilepsy - and Beyond. Cognitive Neuroscience of Memory Consolidation, Studies in Neuroscience, Psychology and Behavioural Economics, 401-417.
Vossel KA, Tartaglia MC, Nygaard HB, Zeman AZ, Miller BL (2017). Epileptic activity in Alzheimer's disease: causes and clinical relevance.
The Lancet Neurology,
16(4), 311-322.
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Epileptic activity in Alzheimer's disease: causes and clinical relevance
Epileptic activity is frequently associated with Alzheimer's disease; this association has therapeutic implications, because epileptic activity can occur at early disease stages and might contribute to pathogenesis. In clinical practice, seizures in patients with Alzheimer's disease can easily go unrecognised because they usually present as non-motor seizures, and can overlap with other symptoms of the disease. In patients with Alzheimer's disease, seizures can hasten cognitive decline, highlighting the clinical relevance of early recognition and treatment. Some evidence indicates that subclinical epileptiform activity in patients with Alzheimer's disease, detected by extended neurophysiological monitoring, can also lead to accelerated cognitive decline. Treatment of clinical seizures in patients with Alzheimer's disease with select antiepileptic drugs (AEDs), in low doses, is usually well tolerated and efficacious. Moreover, studies in mouse models of Alzheimer's disease suggest that certain classes of AEDs that reduce network hyperexcitability have disease-modifying properties. These AEDs target mechanisms of epileptogenesis involving amyloid β and tau. Clinical trials targeting network hyperexcitability in patients with Alzheimer's disease will identify whether AEDs or related strategies could improve their cognitive symptoms or slow decline.
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Day JO, Flanagan SE, Shepherd MH, Patrick AW, Abid N, Torrens L, Zeman AJ, Patel KA, Hattersley AT (2017). Hyperglycaemia-related complications at the time of diagnosis can cause permanent neurological disability in children with neonatal diabetes. Diabetic Medicine, 34(7), 1000-1004.
Zeman A (2017). Michael R. Trimble, the Intentional Brain (Baltimore, MD: John Hopkins University Press, 2016), pp. x, 308, $29.95, hardback, ISBN: 978-1-4214-1949-7.
Med Hist,
61(2), 329-330.
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Zeman AZJ, Byruck M, Tallis P, Vossel K, Tranel D (2017). NSY-D-17-00057R1 Touching the Void. Neuropsychologia
Savage SA, Butler CR, Milton F, Han Y, Zeman AZ (2017). On the nose: olfactory disturbances in transient epileptic amnesia. Epilepsy and Behavior, 66, 113-113.
Day JO, Zeman AJ (2016). Limbic encephalitis driven by a pleural mesothelioma: a paraneoplastic complication.
Middle East Journal of Cancer,
7(4), 221-223.
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Limbic encephalitis driven by a pleural mesothelioma: a paraneoplastic complication
Paraneoplastic neurological syndromes have only been described with pleural mesothelioma in five cases. We have described a 72-year-old man who developed anterograde amnesia 27 months after diagnosis of epithelioid pleural mesothelioma. Investigations revealed a limbic encephalitis with no alternative causes identified. Limbic encephalitis is a classical paraneoplastic syndrome and presentation within five years of a cancer with no other causes identified is sufficient to diagnose a paraneoplastic etiology. This is the first case of isolated paraneoplastic limbic encephalitis driven by a pleural mesothelioma.
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MacKisack M, Aldworth S, Macpherson F, Onians J, Winlove C, Zeman A (2016). On picturing a candle: the prehistory of imagery science.
Frontiers in Psychology,
7(APR), 515:1-16.
Abstract:
On picturing a candle: the prehistory of imagery science
© 2016 MacKisack, Aldworth, Macpherson, Onians, Winlove and Zeman.The past 25 years have seen a rapid growth of knowledge about brain mechanisms involved in visual mental imagery. These advances have largely been made independently of the long history of philosophical - and even psychological - reckoning with imagery and its parent concept 'imagination'. We suggest that the view from these empirical findings can be widened by an appreciation of imagination's intellectual history, and we seek to show how that history both created the conditions for - and presents challenges to - the scientific endeavor. We focus on the neuroscientific literature's most commonly used task - imagining a concrete object - and, after sketching what is known of the neurobiological mechanisms involved, we examine the same basic act of imagining from the perspective of several key positions in the history of philosophy and psychology. We present positions that, firstly, contextualize and inform the neuroscientific account, and secondly, pose conceptual and methodological challenges to the scientific analysis of imagery. We conclude by reflecting on the intellectual history of visualization in the light of contemporary science, and the extent to which such science may resolve long-standing theoretical debates.
Abstract.
Zeman A, Zaiwalla Z (2016). Prescribing sodium oxybate for narcolepsy.
BMJ,
353 Author URL.
Zeman A, Dewar M, Della Sala S (2016). Reflections on aphantasia.
Cortex,
74, 336-337.
Author URL.
Atherton KE, Nobre AC, Lazar AS, Wulff K, Whittaker RG, Dhawan V, Lazar ZI, Zeman AZ, Butler CR (2016). Slow wave sleep and accelerated forgetting.
Cortex,
84, 80-89.
Abstract:
Slow wave sleep and accelerated forgetting
We investigated whether the benefit of slow wave sleep (SWS) for memory consolidation typically observed in healthy individuals is disrupted in people with accelerated long-term forgetting (ALF) due to epilepsy. SWS is thought to play an active role in declarative memory in healthy individuals and, furthermore, electrographic epileptiform activity is often more prevalent during SWS than during wakefulness or other sleep stages. We studied the relationship between SWS and the benefit of sleep for memory retention using a word-pair associates task. In both the ALF and the healthy control groups, sleep conferred a memory benefit. However, the relationship between the amount of SWS and sleep-related memory benefits differed significantly between the groups. In healthy participants, the amount of SWS correlated positively with sleep-related memory benefits. In stark contrast, the more SWS, the smaller the sleep-related memory benefit in the ALF group. Therefore, contrary to its role in healthy people, SWS-associated brain activity appears to be deleterious for memory in patients with ALF.
Abstract.
Zeman A, Hoefeijzers S, Milton F, Dewar M, Carr M, Streatfield C (2016). The GABAB receptor agonist, baclofen, contributes to three distinct varieties of amnesia in the human brain - a detailed case report.
Cortex,
74, 9-19.
Abstract:
The GABAB receptor agonist, baclofen, contributes to three distinct varieties of amnesia in the human brain - a detailed case report.
We describe a patient in whom long-term, therapeutic infusion of the selective gamma-amino-butyric acid type B (GABAB) receptor agonist, baclofen, into the cerebrospinal fluid (CSF) gave rise to three distinct varieties of memory impairment: i) repeated, short periods of severe global amnesia, ii) accelerated long-term forgetting (ALF), evident over intervals of days and iii) a loss of established autobiographical memories. This pattern of impairment has been reported in patients with temporal lobe epilepsy (TLE), in particular the subtype of Transient Epileptic Amnesia (TEA). The amnesic episodes and accelerated forgetting remitted on withdrawal of baclofen, while the autobiographical amnesia (AbA) persisted. This exceptional case highlights the occurrence of 'non-standard' forms of human amnesia, reflecting the biological complexity of memory processes. It suggests a role for GABAB signalling in the modulation of human memory over multiple time-scales and hints at its involvement in 'epileptic amnesia'.
Abstract.
Author URL.
Dewer B, Rogers P, Ricketts J, Mukonoweshuro W, Zeman A (2016). The radiological diagnosis of frontotemporal dementia in everyday practice: an audit of reports, review of diagnostic criteria, and proposal for service improvement.
Clin Radiol,
71(1), 40-47.
Abstract:
The radiological diagnosis of frontotemporal dementia in everyday practice: an audit of reports, review of diagnostic criteria, and proposal for service improvement.
AIM: to investigate how commonly valuable diagnostic information regarding the frontotemporal dementias (FTDs) may be missed on routine radiological reporting. MATERIALS AND METHODS: the magnetic resonance imaging (MRI) examination results of a series of 39 consecutive patients in whom the diagnosis was initially thought to be a form of FTD were audited. Twenty-two patients satisfied formal diagnostic criteria for subtypes of FTD. The initial non-specialist radiological reports of the MRI examinations were compared with those of a radiologist who specifically examined the images for the possibility of atypical dementia. RESULTS: Six of the 22 original reports provided a full and accurate description of the radiological findings, while two provided a fully accurate interpretation. CONCLUSION: Valuable diagnostic information may be missed unless clinicians and radiologists jointly review and discuss brain imaging in cases of dementia. The use of standardised scales may enhance the reporting of MRI examinations for dementia.
Abstract.
Author URL.
Savage SA, Butler CR, Hodges JR, Zeman AZ (2016). Transient Epileptic Amnesia over twenty years: Long-term follow-up of a case series with three detailed reports. Seizure, 43, 48-55.
Hoefeijzers S, Dewar M, Della Sala S, Butler C, Zeman A (2015). Accelerated long-term forgetting can become apparent within 3-8 hours of wakefulness in patients with transient epileptic amnesia.
Neuropsychology,
29(1), 117-125.
Abstract:
Accelerated long-term forgetting can become apparent within 3-8 hours of wakefulness in patients with transient epileptic amnesia.
OBJECTIVE: Accelerated long-term forgetting (ALF) is typically defined as a memory disorder in which information that is learned and retained normally over standard intervals (∼30 min) is forgotten at an abnormally rapid rate thereafter. ALF has been reported, in particular, among patients with transient epileptic amnesia (TEA). Previous work in TEA has revealed ALF 24 hr - 1 week after initial memory acquisition. It is unclear, however, if ALF observed 24 hr after acquisition reflects (a) an impairment of sleep consolidation processes taking place during the first night's sleep, or (b) an impairment of daytime consolidation processes taking place during the day of acquisition. Here we focus on the daytime-forgetting hypothesis of ALF in TEA by tracking in detail the time course of ALF over the day of acquisition, as well as over 24 hr and 1 week. METHOD: Eleven TEA patients who showed ALF at 1 week and 16 matched controls learned 4 categorical word lists on the morning of the day of acquisition. We subsequently probed word-list retention 30 min, 3 hr, and 8 hr postacquisition (i.e. over the day of acquisition), as well as 24-hr and 1-week post acquisition. RESULTS: ALF became apparent in the TEA group over the course of the day of acquisition 3-8 hr after learning. No further forgetting was observed over the first night in either group. CONCLUSIONS: the results of this study show that ALF in TEA can result from a deficit in memory consolidation occurring within hours of learning without a requirement for intervening sleep.
Abstract.
Author URL.
Dewar M, Hoefeijzers S, Zeman A, Butler C, Della Sala S (2015). Impaired picture recognition in transient epileptic amnesia.
Epilepsy Behav,
42, 107-116.
Abstract:
Impaired picture recognition in transient epileptic amnesia.
Transient epileptic amnesia (TEA) is an epileptic syndrome characterized by recurrent, brief episodes of amnesia. Transient epileptic amnesia is often associated with the rapid decline in recall of new information over hours to days (accelerated long-term forgetting - 'ALF'). It remains unknown how recognition memory is affected in TEA over time. Here, we report a systematic study of picture recognition in patients with TEA over the course of one week. Sixteen patients with TEA and 16 matched controls were presented with 300 photos of everyday life scenes. Yes/no picture recognition was tested 5min, 2.5h, 7.5h, 24h, and 1week after picture presentation using a subset of target pictures as well as similar and different foils. Picture recognition was impaired in the patient group at all test times, including the 5-minute test, but it declined normally over the course of 1week. This impairment was associated predominantly with an increased false alarm rate, especially for similar foils. High performance on a control test indicates that this impairment was not associated with perceptual or discrimination deficits. Our findings suggest that, at least in some TEA patients with ALF in verbal recall, picture recognition does not decline more rapidly than in controls over 1week. However, our findings of an early picture recognition deficit suggest that new visual memories are impoverished after minutes in TEA. This could be the result of deficient encoding or impaired early consolidation. The early picture recognition deficit observed could reflect either the early stages of the process that leads to ALF or a separable deficit of anterograde memory in TEA. Lastly, our study suggests that at least some patients with TEA are prone to falsely recognizing new everyday visual information that they have not in fact seen previously. This deficit, alongside their ALF in free recall, likely affects everyday memory performance.
Abstract.
Author URL.
Zeman A, Dewar M, Della Sala S (2015). Lives without imagery - Congenital aphantasia.
Cortex,
73, 378-380.
Author URL.
Zeman A (2014). Brain imaging - what it can (and cannot) tell us about consciousness.
Neuropsychol Rehabil,
24(1), 144-146.
Author URL.
Bäumer D, East SZ, Tseu B, Zeman A, Hilton D, Talbot K, Ansorge O (2014). FTLD-ALS of TDP-43 type and SCA2 in a family with a full ataxin-2 polyglutamine expansion.
Acta Neuropathol,
128(4), 597-604.
Abstract:
FTLD-ALS of TDP-43 type and SCA2 in a family with a full ataxin-2 polyglutamine expansion.
Polyglutamine expansions in the ataxin-2 gene (ATXN2) cause autosomal dominant spinocerebellar ataxia type 2 (SCA2), but have recently also been associated with amyotrophic lateral sclerosis (ALS). We present clinical and pathological features of a family in which a pathological ATXN2 expansion led to frontotemporal lobar degeneration with ALS (FTLD-ALS) in the index case, but typical SCA2 in a son, and compare the neuropathology with a case of typical SCA2. The index case shares the molecular signature of SCA2 with prominent polyglutamine and p62-positive intranuclear neuronal inclusions mainly in the pontine nuclei, while harbouring more pronounced neocortical and spinal TDP-43 pathology. We conclude that ATXN2 mutations can cause not only ALS, but also a neuropathological overlap syndrome of SCA2 and FTLD presenting clinically as pure FTLD-ALS without ataxia. The cause of the phenotypic heterogeneity remains unexplained, but the presence of a CAA-interrupted CAG repeat in the FTLD case in this family suggests that one potential mechanism may be variation in repeat tract composition between members of the same family.
Abstract.
Author URL.
Zeman A, Rickards H, White P (2014). Integrating alienists.
LANCET PSYCHIATRY,
1(5), 333-333.
Author URL.
Warren-Gash C, Zeman A (2014). Is there anything distinctive about epileptic déjà vu?.
Journal of Neurology, Neurosurgery and Psychiatry,
85(2), 143-147.
Abstract:
Is there anything distinctive about epileptic déjà vu?
Background Déjà vu can occur as an aura of temporal lobe epilepsy and in some psychiatric conditions but is also common in the general population. It is unclear whether any clinical features distinguish pathological and physiological forms of déjà vu. Methods 50 epileptic patients with ictal déjà vu, 50 non-epileptic patients attending general neurology clinics and 50 medical students at Edinburgh University were recruited. Data were collected on demographic factors, the experience of déjà vu using a questionnaire based on Sno's Inventory for Déjà Vu Experiences Assessment, symptoms of anxiety and depression using the Hospital Anxiety and Depression Scale as well as seizure characteristics, anti-epileptic medications, handedness, EEG and neuroimaging findings for epileptic patients. Results 73.5% of neurology patients, 88% of students and (by definition) all epilepsy patients had experienced déjà vu. The experience of déjà vu itself was similar in the three groups. Epileptic déjà vu occurred more frequently and lasted somewhat longer than physiological déjà vu. Epilepsy patients were more likely to report prior fatigue and concentrated activity, associated derealisation, olfactory and gustatory hallucinations, physical symptoms such as headaches, abdominal sensations and fear. After controlling for study group, anxiety and depression scores were not associated with déjà vu frequency. Conclusions Déjà vu is common and qualitatively similar whether it occurs as an epileptic aura or normal phenomenon. However ictal déjà vu occurs more frequently and is accompanied by several distinctive features. It is distinguished primarily by 'the company it keeps'.
Abstract.
Zeman A (2014). Mirrors in the Brain.
AMERICAN JOURNAL OF PSYCHOLOGY,
127(2), 264-268.
Author URL.
Zeman A (2014). Neurology is psychiatry--and vice versa.
Pract Neurol,
14(3), 136-144.
Abstract:
Neurology is psychiatry--and vice versa.
This paper explores the relationship between neurology and psychiatry. It marshals evidence that disorders of the brain typically have neurological and psychological-cognitive, affective, behavioural-manifestations, while disorders of the psyche are based in the brain. Given the inseparability of neurological and psychiatric disorders, their disease classifications should eventually fuse, and joint initiatives in training, service and research should be strongly encouraged.
Abstract.
Author URL.
Wells CE, Moulin CJA, Ethridge P, Illman NA, Davies E, Zeman A (2014). Persistent psychogenic déjà vu: a case report.
J Med Case Rep,
8Abstract:
Persistent psychogenic déjà vu: a case report.
INTRODUCTION: Déjà vu is typically a transient mental state in which a novel experience feels highly familiar. Although extensively studied in relation to temporal lobe epilepsy as part of simple partial seizures, déjà vu has been less studied in other clinical populations. A recent review of temporal lobe epilepsy suggested a possible link between clinical levels of anxiety and debilitating déjà vu, indicating further research is required. Here, for the first time in the literature, we present a case study of a young man with anxiety and depersonalisation who reported experiencing persistent and debilitating déjà vu. This report therefore adds to the limited literature on the relationship between anxiety and déjà vu. CASE PRESENTATION: a 23-year-old White British man presented with a form of persistent déjà vu in 2010, approximately 3 years since symptom onset. He reported a history of anxiety and experiencing feelings of depersonalisation. Neurological assessment (electroencephalogram and magnetic resonance imaging) did not indicate any abnormalities. We assessed his recognition memory with a task used in patients with dementia who report similar experiences but lack awareness of their falseness. CONCLUSIONS: Our case's memory performance was more conservative than controls but did not indicate a memory deficit. Unlike other patients with chronic déjà vu (for example, in dementia), he is fully aware of the false nature of his déjà vu and this presumably leads to his intact recognition memory performance. We suggest that his persistent déjà vu is psychogenic and conclude that déjà vu should be further studied in psychiatric disorders.
Abstract.
Author URL.
Atherton KE, Nobre AC, Zeman AZ, Butler CR (2014). Sleep-dependent memory consolidation and accelerated forgetting.
Cortex,
54(1), 92-105.
Abstract:
Sleep-dependent memory consolidation and accelerated forgetting
Accelerated long-term forgetting (ALF) is a form of memory impairment in which learning and initial retention of information appear normal but subsequent forgetting is excessively rapid. ALF is most commonly associated with epilepsy and, in particular, a form of late-onset epilepsy called transient epileptic amnesia (TEA). ALF provides a novel opportunity to investigate post-encoding memory processes, such as consolidation. Sleep is implicated in the consolidation of memory in healthy people and a deficit in sleep-dependent memory consolidation has been proposed as an explanation for ALF. If this proposal were correct, then sleep would not benefit memory retention in people with ALF as much as in healthy people, and ALF might only be apparent when the retention interval contains sleep. To test this theory, we compared performance on a sleep-sensitive memory task over a night of sleep and a day of wakefulness. We found, contrary to the hypothesis, that sleep benefits memory retention in TEA patients with ALF and that this benefit is no smaller in magnitude than that seen in healthy controls. Indeed, the patients performed significantly more poorly than the controls only in the wake condition and not the sleep condition. Patients were matched to controls on learning rate, initial retention, and the effect of time of day on cognitive performance. These results indicate that ALF is not caused by a disruption of sleep-dependent memory consolidation. Instead, ALF may be due to an encoding abnormality that goes undetected on behavioural assessments of learning, or by a deficit in memory consolidation processes that are not sleep-dependent. © 2014 the Authors.
Abstract.
Baker S, Williams H, Sharp D, Gardner A, Harris A, Zeman A, Fulford J (2014). Sports-related concussion and diffusion tensor imaging findings in rugby players.
BRAIN INJURY,
28(5-6), 686-686.
Author URL.
Hoefeijzers S, Dewar M, Della Sala S, Zeman A, Butler C (2013). Accelerated long-term forgetting in transient epileptic amnesia: an acquisition or consolidation deficit?.
Neuropsychologia,
51(8), 1549-1555.
Abstract:
Accelerated long-term forgetting in transient epileptic amnesia: an acquisition or consolidation deficit?
Accelerated Long-term Forgetting (ALF) is the rapid loss of newly acquired memories over days to weeks despite normal retention at standard (~30 min) intervals. It has recently been described in association with epilepsy, particularly the syndrome of Transient Epileptic Amnesia (TEA). The cognitive mechanisms underlying ALF remain uncertain, but disruption either of memory acquisition or consolidation processes has been postulated. To arbitrate between these accounts, we reanalysed data from an existing word-list recall data set to investigate whether ALF can be observed for words learned under precisely matched conditions in TEA patients and controls. We reanalysed the data of 24 patients with TEA and 24 matched healthy controls who learnt a 15-item word list to a learning criterion of 90% with a minimum of five learning trials. Free recall of the words was probed at delays of 30 min and 1 week and 3 weeks after learning. In addition, a 'yes-no' recognition test was conducted after the 3-week free recall. Forgetting rates across the first 30 min delay and the subsequent 1 week and 3 week delay were compared between patients and controls. To ensure that learning conditions were closely matched between patients and control participants, we excluded exceptionally fast (N(TEA)=1, N(controls)=4) and slow (N(TEA)=6, N(controls)=2) learners. Furthermore, we analysed only words that were presented five or six times during learning and retrieved successfully on four or five occasions during learning. Recall performance on the last learning trial and 30 min after acquisition were indistinguishable between TEA patients and controls. Over the delay interval of 30 min to 1 week, however, accelerated forgetting of this newly learned verbal material was observed in TEA patients. This severe forgetting is also reflected in the three-week recognition test, where TEA patients performed significantly worse than controls. Moreover, whereas recall on the last learning trial correlated significantly with the 30 min delayed recall in both groups, recall on the last learning trial correlated significantly with 1 week and 3 week delayed recall only in the controls. In both groups, the three-week free recall performance correlated with the three-week recognition test. Patients with TEA demonstrate ALF even for verbal material that is learned under precisely matched conditions. These results are consistent with the hypothesis that ALF represents a disruption of memory consolidation rather than an acquisition deficit.
Abstract.
Author URL.
Charland-Verville V, Bruno MA, Bahri MA, Demertzi A, Desseilles M, Chatelle C, Vanhaudenhuyse A, Hustinx R, Bernard C, Tshibanda L, et al (2013). Brain dead yet mind alive: a positron emission tomography case study of brain metabolism in cotard's syndrome. Cortex, 49(7), 1997-1999.
Zeman AZJ, Milton FN, Smith A, Rylance R (2013). By heart. An fMRI study of brain activation by poetry and prose. Journal of Consciousness Studies, 20(9-10), 132-158.
Zeman AZJ, Beschin N, Dewar M, Della Sala S (2013). Imagining the present: Amnesia may impair descriptions of the present as well as of the future and the past.
Cortex,
49(3), 637-645.
Abstract:
Imagining the present: Amnesia may impair descriptions of the present as well as of the future and the past
Recent evidence suggests that in some patients with amnesia the capacity to imagine the future is impaired in parallel with the capacity to remember the past. This paper asks whether descriptions of the present may be similarly affected. We recruited 7 patients with amnesic syndromes of varying aetiologies who were matched for age, sex and education with 7 control participants. Patients showed no deficits on subjective measures of visual imagery. They were impaired by comparison with controls on measures of imagination and future thinking. However there was an even more marked impairment on tasks requiring them to give descriptions of their current experience. Potential explanations include effects of amnesia on narrative construction or on the texture of experience itself, and the confounding influence of cognitive impairments outside the memory domain. We conclude that tasks requiring descriptions of current experience provide a valuable control condition in studies examining the relationship between memory and imagination. © 2012 Elsevier Ltd.
Abstract.
Butler C, van Erp W, Bhaduri A, Hammers A, Heckemann R, Zeman A (2013). Magnetic resonance volumetry reveals focal brain atrophy in transient epileptic amnesia.
Epilepsy Behav,
28(3), 363-369.
Abstract:
Magnetic resonance volumetry reveals focal brain atrophy in transient epileptic amnesia.
Transient epileptic amnesia (TEA) is a recently described epilepsy syndrome characterized by recurrent episodes of isolated memory loss. It is associated with two unusual forms of interictal memory impairment: accelerated long-term forgetting (ALF) and autobiographical amnesia. We investigated the neural basis of TEA using manual volumetry and automated multi-atlas-based segmentation of whole-brain magnetic resonance imaging data from 40 patients with TEA and 20 healthy controls. Both methods confirmed the presence of subtle, bilateral hippocampal atrophy. Additional atrophy was revealed in perirhinal and orbitofrontal cortices. The volumes of these regions correlated with anterograde memory performance. No structural correlates were found for ALF or autobiographical amnesia. The results support the hypothesis that TEA is a focal medial temporal lobe epilepsy syndrome but reveal additional pathology in connected brain regions. The unusual interictal memory deficits of TEA remain unexplained by structural pathology and may reflect physiological disruption of memory networks by subclinical epileptiform activity.
Abstract.
Author URL.
Zeman A, Butler C, Muhlert N, Milton F (2013). Novel forms of forgetting in temporal lobe epilepsy.
Epilepsy and Behavior,
26(3), 335-342.
Abstract:
Novel forms of forgetting in temporal lobe epilepsy
Transient Epileptic Amnesia (TEA) is a recently defined subtype of temporal lobe epilepsy, principally affecting people in middle age with a male predominance. Its key manifestation is the occurrence of recurring episodes of transient amnesia, usually lasting less than an hour and often occurring on waking. One-third of patients have exclusively amnestic attacks, while in two-thirds, at least some attacks are accompanied by other manifestations of epilepsy, especially olfactory hallucinations. Several lines of evidence point to a seizure focus in the medial temporal lobes. Transient Epileptic Amnesia is accompanied by a striking loss of autobiographical memories in two-thirds of sufferers, accelerated loss of memories which had been acquired successfully in around one half, and topographical amnesia in around one-third. This paper reviews the findings of the TIME project (The Impairment of Memory in Epilepsy - http://sites.pcmd.ac.uk/time/tea.php) in relation to TEA, accelerated long-term forgetting, and remote memory impairment.This article is part of a Special Issue entitled "The Future of Translational Epilepsy Research". © 2012.
Abstract.
Sabah M, Zeman A (2013). Oculo-Dento-Digital Dysplasia (ODDD). Advances in Clinical Neuroscience and Rehabilitation, 13, 16-17.
Brázdil M, Zeman A (2013). The boundaries of epilepsy: Where is the limit? a reply to Labate and Gambardella. Cortex, 49(4), 1163-1164.
Zeman A, Coebergh JA (2013). The nature of consciousness.
Handb Clin Neurol,
118, 373-407.
Author URL.
Zeman A, Dewar B, Butler C (2013). Transient epileptic amnesia: the contribution of the british neurological surveillance unit.
J Neurol Neurosurg Psychiatry,
84(11).
Abstract:
Transient epileptic amnesia: the contribution of the british neurological surveillance unit.
Transient Epileptic Amnesia (TEA) is a subtype of temporal lobe epilepsy characterised by recurrent episodes of transient amnesia, usually in middle aged people, often occurring on waking, which prove to be due to epilepsy. Attacks are sometimes accompanied by other more familiar manifestations of epilepsy, especially olfactory hallucinations. The epilepsy typically responds very well to anticonvulsant treatment but interictal memory disturbance often persists despite abolition of the seizures, in particular an extensive autobiographical amnesia (AA), and a tendency for memories to fade more rapidly than usual over days to weeks (accelerated long-term forgetting, ALF). The TIME project (The Impairment of Memory in Epilepsy: see http://www.exeter.ac.uk/time/) was established in 2003 to study TEA and its associated interictal memory disturbance. It has since generated around 20 publications describing the clinical, neuropsychological and radiological features of TEA, AA and ALF.(1-4) the British Neurological Surveillance Unit (BNSU) contributed to patient recruitment in 2003-2005 and again recently (2011-present). In 2003-5, 32 patients were referred via the BNSU. 16 were included in the patient cohort described in our 2007 report,(1) nine were excluded as they did not satisfy our diagnostic criteria, seven were potentially suitable but study resources did not allow us to assess them fully. 22 cases have been referred recently. Details are awaited for 13, one refused consent, four have been assessed, three await assessment, one was excluded after assessment. The BNSU has made a major contribution to the success of the TIME project. The recruitment process would work more smoothly if participating neurologists i) asked patients for consent to pass on demographical and clinical details at the time of the clinic visit on which they are identified, ii) communicated these immediately to the researcher or iii) kept a note of patient details if i) and ii) are not feasible. The current system works well, and helps greatly in the recruitment of series of cases of moderately rare disorders, but its efficiency could be improved.
Abstract.
Author URL.
Milton F, Butler CR, Benattayallah A, Zeman A (2012). An fMRI study of autobiographical memory deficits in transient epileptic amnesia.
Journal of Neurology, Neurosurgery and Psychiatry,
83(10).
Abstract:
An fMRI study of autobiographical memory deficits in transient epileptic amnesia
Objective:
to identify the neural basis of autobiographical memory deficits in transient epileptic amnesia (TEA).
Method:
11 people (mean age: 65.91; SD=7.63) diagnosed with transient epileptic amnesia, all of whom complained of extensive autobiographical memory loss, and 17 age and IQ matched controls were recruited. Participants were matched on standard measures of anterograde memory. Participants recalled 32 previously identified autobiographical memories, specific in time and place, from four different time periods (childhood, young adult, middle aged and recent), during fMRI scanning. Activations were analysed using SPM8 software, effective connectivity using dynamic causal modelling (DCM). Post-scan ratings of the subjective vividness, level of detail, pleasantness, personal significance and frequency of retrieval of the memories were recorded.
Results:
Both patients and controls activated core regions of the autobiographical memory network. However, patients had reduced activation in the right posterior parahippocampal gyrus (pPHG), particularly for more recent memories, together with decreased engagement of the right temporoparietal junction and the right cerebellum. In addition, we found reduced effective connectivity in patients between the right pPHG and the right middle temporal gyrus. There were no differences in the subjective ratings of memories between patients and control participants.
Conclusion:
the reduction of activity in the right pPHG is consistent with other evidence that TEA is a disorder of the medial temporal lobes (MTL) and further implicates the pPHG as a key region for contextual information. These MTL differences were most marked for recent and mid-life periods suggesting that, at least at the neural level, remote memories are more robust than recent memories. We also found reduced effective connectivity in patients between the right pPHG and the right middle temporal gyrus. This may reflect persisting effects of the seizures, the continued presence of sub-clinical epileptiform activity or the sequelae of subtle structural changes in the MTL in our patient group.
Abstract.
White PD, Rickards H, Zeman AZJ (2012). Classifying mental and neurological conditions together: Authors' reply to letters. BMJ (Online), 345(7867).
Butler C, Kapur N, Zeman A, Weller R, Connelly A (2012). Epilepsy-related long-term amnesia: Anatomical perspectives.
Neuropsychologia,
50(13), 2973-2980.
Abstract:
Epilepsy-related long-term amnesia: Anatomical perspectives
There are few clues as to the neural basis of selective long-term amnesia. We report group and single-case data to shed light on this issue. In a group study of patients with transient epileptic amnesia, there were no significant correlations between volumetric measures of the hippocampus and indices of accelerated long-term forgetting or longer-term autobiographical memory loss. Post-mortem investigations in a patient with temporal lobe epilepsy who showed accelerated long-term forgetting, together with a degree of autobiographical memory loss, yielded evidence of neuronal loss and gliosis in regions of both the right and the left hippocampus. Neuronal loss and gliosis were more evident in anterior than posterior hippocampus. These results indicate that the unusual forms of long-term forgetting seen in some patients with temporal lobe epilepsy have no gross anatomical correlate. The findings leave open the possiblities that subtle structural damage or subtle functional disturbance, perhaps in the form of subclinical epileptiform activity, underly epilepsy-related long-term amnesia. © 2012 Elsevier Ltd.
Abstract.
Sabah M, Mulcahy J, Zeman A (2012). Herpes simplex encephalitis. Praxis, 101(22), 1437-1440.
Sabah M, Mulcahy J, Zeman A (2012). Herpes simplex encephalitis. BMJ, 344:e3166, 47-49.
White PD, Rickards H, Zeman AZ (2012). Mental and neurological illnesses should be classified together as conditions of the nervous system. British Medical Journal, 344:e3454, 26-28.
Muhlert N, Zeman A (2012). The enigma of long-term forgetting.
Seizure,
21(2), 77-78.
Author URL.
Ryland H, Williams WH, Zeman A, Murray J, Turner M (2012). The impact of neurological indicators of severity of concussion on neurocognitive performance in a sports population.
BRAIN INJURY,
26(4-5), 627-628.
Author URL.
Milton FN, Butler CR, Benattayallah A, Zeman, A.Z.J. (2012). The neural basis of autobiographical memory deficits in transient epileptic amnesia. Neuropsychologia, 50(14), 3528-3541.
Brázdil M, Mareček R, Urbánek T, Kašpárek T, Mikl M, Rektor I, Zeman A (2012). Unveiling the mystery of déjà vu: the structural anatomy of déjà vu.
Cortex,
48(9), 1240-1243.
Abstract:
Unveiling the mystery of déjà vu: the structural anatomy of déjà vu
Déjà vu (DV) is a widespread, fascinating and mysterious human experience. It occurs both in health and in disease, notably as an aura of temporal lobe epilepsy. This feeling of inappropriate familiarity has attracted interest from psychologists and neuroscientists for over a century, but still there is no widely agreed explanation for the phenomenon of non-pathological DV. Here we investigated differences in brain morphology between healthy subjects with and without DV using a novel multivariate neuroimaging technique, Source-Based Morphometry. The analysis revealed a set of cortical (predominantly mesiotemporal) and subcortical regions in which there was significantly less gray matter in subjects reporting DV. In these regions gray matter volume was inversely correlated with the frequency of DV. Our results demonstrate a structural correlate of DV in healthy individuals for the first time and support a neurological explanation for the phenomenon. We hypothesis that the observed local gray matter decrease in subjects experiencing DV reflects an alteration of hippocampal function and postnatal neurogenesis with resulting changes of volume in remote brain regions. © 2012 Elsevier Srl.
Abstract.
Pal S, Zeidler M, Ironside JW, Zeman A (2011). 31st Advanced Clinical Neurology Course, Edinburgh 2009: progressive cognitive impairment, behavioural change and upper motor neuron signs in a 57-year-old woman.
Pract Neurol,
11(2), 71-80.
Author URL.
Butler CR, Zeman A (2011). The causes and consequences of transient epileptic amnesia.
Behav Neurol,
24(4), 299-305.
Abstract:
The causes and consequences of transient epileptic amnesia.
Transient epileptic amnesia (TEA) is a recently recognised syndrome of epilepsy in which the principle manifestation of seizures is recurrent episodes of isolated memory loss. In this article, we describe the clinical and cognitive profile of this emerging syndrome, and present new data that provide at most weak support for its proposed relationship to cerebrovascular disease. TEA is often associated with two unusual forms of interictal memory impairment: accelerated long-term forgetting and remote memory impairment. We discuss the clinical and theoretical implications of these relatively novel cognitive deficits.
Abstract.
Author URL.
Milton F, Muhlert N, Butler C, Zeman A (2011). The neural correlates of everyday recognition memory at a six month delay. Memory, 19, 733-744.
Milton F, Muhlert N, Butler CR, Benattayallah A, Zeman AZJ (2011). The neural correlates of everyday recognition memory.
Brain and Cognition,
76(3), 369-381.
Abstract:
The neural correlates of everyday recognition memory.
We used a novel automatic camera, SenseCam, to create a recognition memory test for real-life events.
Adapting a ‘Remember/Know’ paradigm, we asked healthy undergraduates, who wore SenseCam for 2
days, in their everyday environments, to classify images as strongly or weakly remembered, strongly
or weakly familiar or novel, while brain activation was recorded with functional MRI. Overlapping, widely
distributed sets of brain regions were activated by recollected and familiar stimuli. Within the medial
temporal lobes, ‘Remember’ responses specifically elicited greater activity in the right anterior and posterior
parahippocampal gyrus than ‘Know’ responses. ‘New’ responses activated anterior parahippocampal
regions. A parametric analysis, across correctly recognised items, revealed increasing activation in the
right hippocampus and posterior parahippocampal gyrus (pPHG). This may reflect modulation of these
regions by the degree of recollection or, alternatively, by increasing memory strength. Strong recollection
elicited greater activity in the left posterior hippocampus/pPHG than weak recollection indicating that
this region is specifically modulated by the degree of recollection.
Abstract.
Milton F, Butler CR, Zeman AZJ (2011). Transient epileptic amnesia: déjà vu heralding recovery of lost memories. Journal of Neurology, Neurosurgery, & Psychiatry, 82, 1178-1179.
Muhlert N, Milton F, Butler CR, Kapur N, Zeman AZJ (2010). Accelerated forgetting of real life events in Transient Epileptic Amnesia. Neuropsychologia, 48, 3235-3244.
Zeman AZJ, Della Sala S, Torrens LA, Gountouna VE, McGonigle DJ, Logie RH (2010). Loss of imagery phenomenology with intact visuo-spatial task performance: a case of 'blind imagination'.
NEUROPSYCHOLOGIA,
48(1), 145-155.
Abstract:
Loss of imagery phenomenology with intact visuo-spatial task performance: a case of 'blind imagination'
The capacity for imagery, enabling us to visualise absent items and events, is a ubiquitous feature of our experience. This paper describes the case of a patient, MX, who abruptly lost the ability to generate visual images. He rated himself as experiencing almost no imagery on standard questionnaires, yet performed normally on standard tests of perception, visual imagery and visual memory. These unexpected findings were explored using functional MRI scanning (fMRI). Activation patterns while viewing famous faces were not significantly different between MX and controls, including expected activity in the fusiform gyrus. However, during attempted imagery, activation in MX's brain was significantly reduced in a network of posterior regions while activity in frontal regions was increased compared to controls. These findings are interpreted as suggesting that MX adopted a different cognitive strategy from controls when performing the imagery task. Evidence from experimental tasks thought to rely on mental imagery, such as the Brooks' matrices and mental rotation, support this interpretation. Taken together, these results indicate that successful performance in visual imagery and visual memory tasks can be dissociated from the phenomenal experience of visual imagery. (C) 2009 Elsevier Ltd. All rights reserved.
Abstract.
Shankar R, Jalihal V, Walker M, Zeman A (2010). Pseudocataplexy and transient functional paralysis: a spectrum of psychogenic motor disorder.
J Neuropsychiatry Clin Neurosci,
22(4), 445-450.
Abstract:
Pseudocataplexy and transient functional paralysis: a spectrum of psychogenic motor disorder.
The authors describe and discuss a syndrome of transient psychogenic weakness usually mistaken for cataplexy but which has a close association with a depressive mental state. Four patients were referred to the authors with suspected neurological causes of transient weakness, including cataplexy in three cases, for whom the eventual diagnosis was of a functional or psychogenic motor disorder, related in most cases to depression. This variety of transient functional weakness is related to conditions such as nonepileptic attack disorder, persistent functional weakness, catatonia, and depressive motor retardation. These cases point to the existence of a syndrome of transient motor weakness which resembles cataplexy and has features in common with other forms of mood induced psychogenic weakness such as psychomotor retardation and catatonia. Psychogenic "pseudocataplexy" is a diagnostic consideration in patients with atypical cataplexy, especially in the context of mood disturbance. Despite its close resemblance to cataplexy, pseudocataplexy has a different pathogenesis and requires a different approach to management.
Abstract.
Author URL.
Milton F, Muhlert N, Pindus D, Butler CR, Kapur N, Graham KS, Zeman AZJ (2010). Remote memory deficits in transient epileptic amnesia. Brain, 133, 1368-1379.
Smith A, Milton F, Rylance R, Zeman AZJ (2010). Rhyme and reason: the neural correlates of reading poetry and prose. Journal of Neurology, Neurosurgery, & Psychiatry, 81, e9-e9.
Zeman A, Butler C (2010). Transient epileptic amnesia.
Curr Opin Neurol,
23(6), 610-616.
Abstract:
Transient epileptic amnesia.
PURPOSE OF REVIEW: Case reports over the past 100 years have raised the possibility that epilepsy can manifest itself in episodes of amnesia. Recent research has established that this is indeed the case, and indicates that characteristic varieties of interictal memory disturbance co-occur with this form of epilepsy. RECENT FINDINGS: Transient epileptic amnesia is a distinctive syndrome of temporal lobe epilepsy principally affecting middle-aged people, giving rise to recurrent, brief attacks of amnesia, often occurring on waking. It is associated with novel forms of interictal memory disturbance: accelerated long-term forgetting, remote memory impairment, especially affecting autobiographical memory, and topographical memory impairment. The seizure focus lies in the medial temporal lobes. The seizures respond promptly to treatment, whereas the interictal impairments generally persist. Further work is required to establish whether the interictal memory impairment is due to physiological or structural disturbance. SUMMARY: Transient epileptic amnesia is an under-recognized but treatable cause of transient memory impairment. Accelerated long-term forgetting and autobiographical amnesia, which are invisible to standard memory tests, help to explain the discrepancy between normal test performance and prominent memory complaints among patients with epilepsy. Further investigation of these forms of memory impairment promises to shed light on processes of human memory.
Abstract.
Author URL.
Laureys S, Celesia GG, Cohadon F, Lavrijsen J, León-Carrión J, Sannita WG, Sazbon L, Schmutzhard E, von Wild KR, Zeman A, et al (2010). Unresponsive wakefulness syndrome: a new name for the vegetative state or apallic syndrome.
BMC Med,
8Abstract:
Unresponsive wakefulness syndrome: a new name for the vegetative state or apallic syndrome.
BACKGROUND: Some patients awaken from coma (that is, open the eyes) but remain unresponsive (that is, only showing reflex movements without response to command). This syndrome has been coined vegetative state. We here present a new name for this challenging neurological condition: unresponsive wakefulness syndrome (abbreviated UWS). DISCUSSION: Many clinicians feel uncomfortable when referring to patients as vegetative. Indeed, to most of the lay public and media vegetative state has a pejorative connotation and seems inappropriately to refer to these patients as being vegetable-like. Some political and religious groups have hence felt the need to emphasize these vulnerable patients' rights as human beings. Moreover, since its first description over 35 years ago, an increasing number of functional neuroimaging and cognitive evoked potential studies have shown that physicians should be cautious to make strong claims about awareness in some patients without behavioral responses to command. Given these concerns regarding the negative associations intrinsic to the term vegetative state as well as the diagnostic errors and their potential effect on the treatment and care for these patients (who sometimes never recover behavioral signs of consciousness but often recover to what was recently coined a minimally conscious state) we here propose to replace the name. CONCLUSION: Since after 35 years the medical community has been unsuccessful in changing the pejorative image associated with the words vegetative state, we think it would be better to change the term itself. We here offer physicians the possibility to refer to this condition as unresponsive wakefulness syndrome or UWS. As this neutral descriptive term indicates, it refers to patients showing a number of clinical signs (hence syndrome) of unresponsiveness (that is, without response to commands) in the presence of wakefulness (that is, eye opening).
Abstract.
Author URL.
Zeman AZJ (2009). Do you remember the TIME?. Transient Epileptic Amnesia: the TIME Project. Epilepsy Professional, 13, 10-14.
Demertzi A, Liew C, Ledoux D, Bruno M-A, Sharpe M, Laureys S, Zeman A (2009). Dualism persists in the science of mind.
Ann N Y Acad Sci,
1157, 1-9.
Abstract:
Dualism persists in the science of mind.
The relationship between mind and brain has philosophical, scientific, and practical implications. Two separate but related surveys from the University of Edinburgh (University students, n= 250) and the University of Liège (health-care workers, lay public, n= 1858) were performed to probe attitudes toward the mind-brain relationship and the variables that account for differences in views. Four statements were included, each relating to an aspect of the mind-brain relationship. The Edinburgh survey revealed a predominance of dualistic attitudes emphasizing the separateness of mind and brain. In the Liège survey, younger participants, women, and those with religious beliefs were more likely to agree that the mind and brain are separate, that some spiritual part of us survives death, that each of us has a soul that is separate from the body, and to deny the physicality of mind. Religious belief was found to be the best predictor for dualistic attitudes. Although the majority of health-care workers denied the distinction between consciousness and the soma, more than one-third of medical and paramedical professionals regarded mind and brain as separate entities. The findings of the study are in line with previous studies in developmental psychology and with surveys of scientists' attitudes toward the relationship between mind and brain. We suggest that the results are relevant to clinical practice, to the formulation of scientific questions about the nature of consciousness, and to the reception of scientific theories of consciousness by the general public.
Abstract.
Author URL.
Zeman A (2009). The problem of unreportable awareness.
Prog Brain Res,
177, 1-9.
Abstract:
The problem of unreportable awareness.
We tend to regard consciousness as a fundamentally subjective phenomenon, yet we can only study it scientifically if it has objective, publicly visible, manifestations. This creates a central, recurring, tension in consciousness science which remains unresolved. On one 'objectivist' view, consciousness is not merely revealed but endowed by the process of reporting which makes it publicly accessible. On a contrasting 'subjectivist' view, consciousness, per se, is independent of the possibility of report, and indeed will always remain beyond the reach of direct observation. I shall explore this tension with examples drawn from clinical neurology, cognitive neuroscience and philosophy. The underlying aim of the paper is to open up the simple but profoundly difficult question that lurks in the background of consciousness science: what is it that are studying?
Abstract.
Author URL.
Butler CR, Bhaduri A, Acosta-Cabronero J, Nestor PJ, Kapur N, Graham KS, Hodges JR, Zeman AZ (2009). Transient epileptic amnesia: regional brain atrophy and its relationship to memory deficits.
Brain,
132(Pt 2), 357-368.
Abstract:
Transient epileptic amnesia: regional brain atrophy and its relationship to memory deficits.
Transient epileptic amnesia (TEA) is a recently recognised form of epilepsy of which the principle manifestation is recurrent, transient episodes of isolated memory loss. In addition to the amnesic episodes, many patients describe significant interictal memory difficulties. Performance on standard neuropsychological tests is often normal. However, two unusual forms of memory deficit have recently been demonstrated in TEA: (i) accelerated long-term forgetting (ALF): the excessively rapid loss of newly acquired memories over a period of days or weeks and (ii) remote autobiographical memory loss: a loss of memories for salient, personally experienced events of the past few decades. The neuroanatomical bases of TEA and its associated memory deficits are unknown. In this study, we first assessed the relationship between subjective and objective memory performance in 41 patients with TEA. We then analysed MRI data from these patients and 20 matched healthy controls, using manual volumetry and voxel-based morphometry (VBM) to correlate regional brain volumes with clinical and neuropsychological data. Subjective memory estimates were unrelated to performance on standard neuropsychological tests but were partially predicted by mood, ALF and remote autobiographical memory. Manual volumetry identified subtle hippocampal volume loss in the patient group. Both manual volumetry and VBM revealed correlations between medial temporal lobe atrophy and standard anterograde memory scores, but no relation between atrophy and ALF or remote autobiographical memory. These results add weight to the hypothesis that TEA is a syndrome of mesial temporal lobe epilepsy. Furthermore, they suggest that although standard anterograde memory test performance is related to the degree of mesial temporal lobe damage, this is not true for ALF and autobiographical amnesia. It is possible that these unusual memory deficits have a more diffuse physiological basis rather than being a consequence of discrete structural damage.
Abstract.
Author URL.
Zeman A (2009). When a patient with epilepsy complains about poor memory.
Pract Neurol,
9(2), 85-89.
Abstract:
When a patient with epilepsy complains about poor memory.
Patients with epilepsy often complain of "poor memory". The first step in managing this complaint is a clinical evaluation to define and, if possible, quantify the problem. The memory difficulty may be entirely unconnected to the epilepsy. But if the two appear to be linked, establish whether the memory problem is due to the seizures themselves, the pathology that underlies the seizures, their treatment, or their psychological sequelae such as anxiety or depression. Further management depends on the cause, while practical advice on the amelioration of poor memory can be useful.
Abstract.
Author URL.
Butler CR, Zeman A (2008). A case of transient epileptic amnesia with radiological localization.
Nat Clin Pract Neurol,
4(9), 516-521.
Abstract:
A case of transient epileptic amnesia with radiological localization.
BACKGROUND: a 54-year-old man presented to a cognitive disorders clinic having experienced recurrent episodes of transient amnesia over a number of years. The attacks often occurred on waking, did not affect other cognitive abilities such as perception, language or judgment, and typically lasted about half an hour. The attacks were sometimes associated with olfactory hallucinations. Between amnestic episodes, the patient noticed a gradual deterioration in his recall of remote events, despite normal performance on standard memory tests. INVESTIGATIONS: Physical examination, laboratory tests, EEG, MRI brain scan, PET imaging, and neuropsychological assessment. DIAGNOSIS: Transient epileptic amnesia. MANAGEMENT: Anticonvulsant medication.
Abstract.
Author URL.
Zeman A (2008). Consciousness: concepts, neurobiology, terminology of impairments, theoretical models and philosophical background. Handb Clin Neurol, 90, 3-31.
Ambrose T, Butler C, Myles L, Zeman A (2008). Pitfalls in the diagnosis of hydrocephalus.
Br J Hosp Med (Lond),
69(4), 192-195.
Abstract:
Pitfalls in the diagnosis of hydrocephalus.
Hydrocephalus is a life-threatening condition presenting with a wide range of symptoms to a variety of specialties. Resulting delays in diagnosis can be hazardous. Doctors in all specialties should be familiar with the protean presentations of hydrocephalus.
Abstract.
Author URL.
Butler CR, Zeman AZ (2008). Recent insights into the impairment of memory in epilepsy: transient epileptic amnesia, accelerated long-term forgetting and remote memory impairment.
BRAIN,
131, 2243-2263.
Abstract:
Recent insights into the impairment of memory in epilepsy: transient epileptic amnesia, accelerated long-term forgetting and remote memory impairment
Complaints of memory difficulties are common among patients with epilepsy, particularly with temporal lobe epilepsy where memory-related brain structures are directly involved by seizure activity. However, the reason for these complaints is often unclear and patients frequently perform normally on standard neuropsychological tests of memory. In this article, we review the literature on three recently described and interrelated forms of memory impairment associated with epilepsy: (i) transient epileptic amnesia, in which the sole or main manifestation of seizures is recurrent episodes of amnesia; (ii) accelerated long-term forgetting, in which newly acquired memories fade over days to weeks and (iii) remote memory impairment, in which there is loss of memories for personal or public facts or events from the distant past. Accelerated long-term forgetting and remote memory impairment are common amongst patients with transient epileptic amnesia, but have been reported in other forms of epilepsy. Their presence goes undetected by standard memory tests and yet they can have a profound impact on patients lives. They pose challenges to current theoretical models of memory. We discuss the evidence for each of these phenomena, as well as their possible pathophysiological bases, methodological difficulties in their investigation and their theoretical implications.
Abstract.
Torrens L, Burns E, Stone J, Graham C, Wright H, Summers D, Sellar R, Porteous M, Warner J, Zeman A, et al (2008). Spinocerebellar ataxia type 8 in Scotland: frequency, neurological, neuropsychological and neuropsychiatric findings.
Acta Neurol Scand,
117(1), 41-48.
Abstract:
Spinocerebellar ataxia type 8 in Scotland: frequency, neurological, neuropsychological and neuropsychiatric findings.
OBJECTIVES: the objectives of this study were to: (i) establish whether the spinocerebellar ataxia type 8 (SCA 8) expansion is associated with ataxia in Scotland; (ii) test the hypothesis that SCA 8 is associated with neuropsychological impairment; and (iii) review neuroradiological findings in SCA 8. METHODS: the methods included: (i) measurement of SCA 8 expansion frequencies in ataxic patients and healthy controls; (ii) comprehensive neuropsychological assessment of patients with SCA 8 and matched controls, neuropsychiatric interview; and (iii) comparison of patient and matched control magnetic resonance imaging (MRI) scans. RESULTS: (i) 10/694 (1.4%) unrelated individuals with ataxia had combined CTA/CTG repeat expansions >100 compared to 1/1190 (0.08%) healthy controls (P < 0.0005); (ii) neuropsychological assessment revealed a dysexecutive syndrome among SCA 8 patients, not readily explained by motor or mood disturbance; neuropsychiatric symptoms occurred commonly; (iii) cerebellar atrophy was the only salient MRI abnormality in the patient group. CONCLUSIONS: the SCA 8 expansion is associated with ataxia in Scotland. The disorder is associated with a dysexecutive syndrome.
Abstract.
Author URL.
Butler C, Zeman A (2008). Transient epileptic amnesia: Old syndrome or new? Reply.
ANNALS OF NEUROLOGY,
63(3), 409-409.
Author URL.
Kalra S, Chancellor A, Zeman A (2007). Recurring déjà vu associated with 5-hydroxytryptophan.
Acta Neuropsychiatrica,
19(5), 311-313.
Abstract:
Recurring déjà vu associated with 5-hydroxytryptophan
Background: Déjà vu occurs both in normal experience and as a neuropsychiatric symptom. Its pathogenesis is partially understood. We describe an iatrogenic case with implications for the neuropharmacological basis of déjà vu. Case presentation: a 42-year-old woman received 5-hydroxytryptophan, in combination with carbidopa, as treatment for palatal tremor, on two occasions, separated by 1 week. On each occasion, she experienced intense, protracted déjà vu, lasting for several hours. We discuss her case in relation to the neuroanatomical and neuropharmacological basis of déjà vu. Conclusion: the serotonergic system is involved in the genesis of déjà vu. © 2007 Blackwell Munksgaard.
Abstract.
Zeman A (2007). Sherrington's philosophical writings--a 'zest for life'.
Brain,
130(Pt 8), 1984-1987.
Abstract:
Sherrington's philosophical writings--a 'zest for life'.
Sherrington's late writings are often described as dualistic, yet Sherrington was deeply uneasy with theories that radically separate mind and brain. His questioning, open-minded and historically-informed approach to their relationship eschews dogmatic solutions.
Abstract.
Author URL.
Butler CR, Graham KS, Hodges JR, Kapur N, Wardlaw JM, Zeman AZJ (2007). The syndrome of transient epileptic amnesia.
ANNALS OF NEUROLOGY,
61(6), 587-598.
Author URL.
Zeman A, Carson A, Rivers C, Nath U (2006). A case of evolving post-ictal language disturbance secondary to a left temporal arteriovenous malformation: jargon aphasia or formal thought disorder?.
Cogn Neuropsychiatry,
11(5), 465-479.
Abstract:
A case of evolving post-ictal language disturbance secondary to a left temporal arteriovenous malformation: jargon aphasia or formal thought disorder?
INTRODUCTION: Wernicke's dysphasia and formal thought disorder are regarded as distinct diagnostic entities although both are linked to pathology in the left superior temporal gyrus (STG). We describe a patient with focal pathology in the left STG, giving rise acutely to a fluent dysphasia, which gradually evolved into formal thought disorder. METHOD: Clinical, neuropsychological, neuropsychiatric, and neuroradiological assessment. RESULTS: a right-handed patient, AJ, presented acutely with a fluent dysphasia. His speech output gradually evolved from undifferentiated jargon, through neologistic jargon, to an intelligible but bizarre form of discourse. Comprehension was relatively well preserved. Radiology revealed an arteriovenous malformation in the left middle, and inferior temporal gyri, with reduced perfusion of the left STG. Six months later his overt dysphasia had recovered, but his speech retained some of its previous characteristics, in particular a tendency to a loose association of ideas which now suggested a disorder of thought. CONCLUSIONS: AJ's case illustrates that comprehension may be unexpectedly preserved in jargon aphasia, and that an overtly linguistic impairment can gradually evolve to an apparent disorder of thought. Indistinguishable formal thought disorders can result from "structural" and "functional" pathology in the dominant temporal lobe.
Abstract.
Author URL.
Wright H, Wardlaw J, Young AW, Zeman A (2006). Prosopagnosia following nonconvulsive status epilepticus associated with a left fusiform gyrus malformation.
Epilepsy Behav,
9(1), 197-203.
Abstract:
Prosopagnosia following nonconvulsive status epilepticus associated with a left fusiform gyrus malformation.
A 67-year-old, right-handed woman became unable to recognize familiar faces following a period of nonconvulsive status epilepticus. Neuropsychological assessment revealed a relatively selective impairment of familiar face recognition in the absence of low-level visual deficits or widespread cognitive impairment. MRI scanning demonstrated an isolated lesion, probably a venous angioma, involving the left fusiform gyrus, mirror-symmetrical to the site typically linked to prosopagnosia. Potential explanations for the patient's prosopagnosia include seizure-related damage to a left fusiform region required for fully competent face recognition and damage to the contralateral fusiform gyrus via interhemispheric connections. Focal neuropsychological deficits in patients with refractory partial epilepsy who develop nonconvulsive status epilepticus may be underdiagnosed.
Abstract.
Author URL.
Butler C, Zeman A (2006). Syndromes of transient amnesia. Advances in Clinical Neuroscience and Rehabilitation, 6, 13-14.
Zeman A (2006). What do we mean by "conscious" and "aware"?.
Neuropsychol Rehabil,
16(4), 356-376.
Abstract:
What do we mean by "conscious" and "aware"?
The concepts of consciousness and awareness are multifaceted, and steeped in cultural and intellectual history. This paper explores their complexities by way of a series of contrasts: (1) states of consciousness, such as wakefulness and sleep are contrasted with awareness, a term that picks out the contents of consciousness: these range across all our psychological capacities; the scientific background of the two concepts is briefly outlined; (2) consciousness is contrasted to self-consciousness, itself a complex term embracing self-detection, self-monitoring, self-recognition, theory of mind and self-knowledge; (3) "narrow" and "broad" senses of consciousness are contrasted, the former requiring mature human awareness capable of guiding action and self-report, the latter involving the much broader capacity to acquire and exploit knowledge; (4) an "inner" conception of consciousness, by which awareness is essentially private and beyond the reach of scientific scrutiny, is contrasted with an "outer" conception which allows that consciousness is intrinsically linked with capacities for intelligent behaviour; (5) finally "easy" and "hard" questions of consciousness are distinguished, the former involving the underlying neurobiology of wakefulness and awareness, the latter the allegedly more mysterious process by which biological processes generate experience: Whether this final distinction is valid is a focus of current debate. Varied interests converge on the study of consciousness from the sciences and the humanities, creating scope for interdisciplinary misunderstandings, but also for a fruitful dialogue. Health professionals treating disorders of consciousness should be aware both of its scientific complexities and of its broad cultural background, which influences the public understanding of these conditions.
Abstract.
Author URL.
Manes F, Graham KS, Zeman A, de Luján Calcagno M, Hodges JR (2005). Autobiographical amnesia and accelerated forgetting in transient epileptic amnesia.
J Neurol Neurosurg Psychiatry,
76(10), 1387-1391.
Abstract:
Autobiographical amnesia and accelerated forgetting in transient epileptic amnesia.
BACKGROUND: Recurrent brief isolated episodes of amnesia associated with epileptiform discharges on EEG recordings have been interpreted as a distinct entity termed transient epileptic amnesia (TEA). Patients with TEA often complain of autobiographical amnesia for recent and remote events, but show normal anterograde memory. OBJECTIVE: to investigate (a) accelerated long term forgetting and (b) autobiographical memory in a group of patients with TEA. METHODS: Seven patients with TEA and seven age matched controls were evaluated on a range of anterograde memory tasks in two sessions separated by 6 weeks and by the Galton-Crovitz test of cued autobiographical memory. RESULTS: Patients with TEA showed abnormal long term forgetting of verbal material, with virtually no recall after 6 weeks. In addition, there was impaired recall of autobiographical memories from the time periods 1985-89 and 1990-94 but not from 1995-1999. CONCLUSIONS: TEA is associated with accelerated loss of new information and impaired remote autobiographical memory. There are a number of possible explanations including ongoing subclinical ictal activity, medial temporal lobe damage as a result of seizure, or subtle ischaemic pathology. Future analyses should seek to clarify the relationship between aetiology, seizure frequency, and degree of memory impairment.
Abstract.
Author URL.
Zeidler M, Zeman A (2005). Can brain biopsy aid the diagnosis of dementia?.
NATURE CLINICAL PRACTICE NEUROLOGY,
1(2), 82-83.
Author URL.
Zeman A, Daniels G, Tilley L, Dunn M, Toplis L, Bullock T, Poole J, Blackwood D (2005). McLeod syndrome: life-long neuropsychiatric disorder due to a novel mutation of the XK gene.
Psychiatr Genet,
15(4), 291-293.
Abstract:
McLeod syndrome: life-long neuropsychiatric disorder due to a novel mutation of the XK gene.
A 50-year-old man presented with worsening, virtually lifelong, chorea and progressive behavioural disturbance, involving disinhibition and hoarding, over 10 years. Clinical assessment revealed chorea, dysarthria, areflexia, an inappropriately jovial, impulsive manner and neuropsychological evidence of frontosubcortical dysfunction. Investigation results included an elevated creatine kinase, caudate atrophy and hypoperfusion, acanthocytes in the peripheral blood and the McLeod phenotype. DNA studies demonstrated a single-base deletion at position 172 in exon 1 of the XK gene, giving rise to a premature stop codon at position 129 in exon 2.
Abstract.
Author URL.
Zeman A, Butler C (2005). Neurological syndromes which can be mistaken for psychiatric conditions. Journal of Neurology Neurosurgery & Psychiatry, 76(suppl_1), 31-38.
Zeman A (2005). Tales from the temporal lobes.
N Engl J Med,
352(2), 119-121.
Author URL.
Zeman A, Reading P (2005). The science of sleep.
Clin Med (Lond),
5(2), 97-101.
Author URL.
Zeman A (2004). Conference report - ASSC 8. Journal of Consciousness Studies, 11(9), 70-75.
Zeman A, Britton T, Douglas N, Hansen A, Hicks J, Howard R, Meredith A, Smith I, Stores G, Wilson S, et al (2004). Narcolepsy and excessive daytime sleepiness.
BMJ,
329(7468), 724-728.
Author URL.
Zeman A, Shenton G (2004). Neuroacanthocytosis. Practical Neurology, 4, 298-301.
Zeman A (2004). Soul made flesh - the discovery of the brain - and how it changed the world.
NEW YORK TIMES BOOK REVIEW, 16-16.
Author URL.
Zeman A, Burns E, Porteus M, Stone J (2004). Spinocerebellar ataxia type 8 in Scotland: genetic and clinical features in 7 unrelated cases and a review of the literature. Journal of Neurology Neurosurgery & Psychiatry, 75(3), 459-465.
Warren-Gash C, Zeman A (2003). Déjà vu. Practical Neurology, 3(2), 106-109.
Zeman A (2003). What is consciousness and what does it mean for the persistent vegetative state?. Advances in Clinical Neuroscience and Rehabilitation, 3, 12-14.
Al-Shahi R, Scolding NJ, Bell JE, Zeman AZ, Warlow CP (2002). A young man with a fatal encephalopathy. Practical Neurology, 2(1), 26-35.
Stone J, Zeman A, Sharpe M (2002). Functional weakness and sensory disturbance.
J Neurol Neurosurg Psychiatry,
73(3), 241-245.
Abstract:
Functional weakness and sensory disturbance.
In the diagnosis of functional weakness and sensory disturbance, positive physical signs are as important as absence of signs of disease. Motor signs, particularly Hoover's sign, are more reliable than sensory signs, but none should be used in isolation and must be interpreted in the overall context of the presentation. It should be borne in mind that a patient may have both a functional and an organic disorder.
Abstract.
Author URL.
Zeman A (2002). The persistent vegetative state: conscious of nothing?. Practical Neurology, 2, 214-217.
Zeman A (2001). Consciousness.
BRAIN,
124, 1263-1289.
Author URL.
Zeman A, Narcolepsy MGW (2001). Evidence based guidelines for the management of narcolepsy.
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY,
71(3), 424-424.
Author URL.
Manes, F. Hodges, J.R. Graham, K.S. (2001). Focal autobiographical amnesia in association with transient amnesia. Brain, 124(3), 499-509.
Stone J, Smith L, Watt K, Barron L, Zeman A (2001). Incoordinated thought and emotion in spinocerebellar ataxia type 8.
J Neurol,
248(3), 229-232.
Author URL.
Zeman A, Douglas N, Aylward R (2001). Narcolepsy mistaken for epilepsy. British Medical Journal, 322(7280), 216-217.
Zeman A, Stone J, Porteous M, Barron L, Warner J (2001). Study of the neurological, cognitive, and behavioural features of spinocerebellar ataxia type 8.
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY,
71(3), 420-420.
Author URL.
Zeidler M, Hughes T, Zeman A (2000). Confused by arteritis.
Lancet,
355(9201).
Author URL.
Graham NL, Zeman A, Young AW, Patterson K, Hodges JR (1999). Dyspraxia in a patient with corticobasal degeneration: the role of visual and tactile inputs to action.
J Neurol Neurosurg Psychiatry,
67(3), 334-344.
Abstract:
Dyspraxia in a patient with corticobasal degeneration: the role of visual and tactile inputs to action.
OBJECTIVES: to investigate the roles of visual and tactile information in a dyspraxic patient with corticobasal degeneration (CBD) who showed dramatic facilitation in miming the use of a tool or object when he was given a tool to manipulate; and to study the nature of the praxic and neuropsychological deficits in CBD. METHODS: the subject had clinically diagnosed CBD, and exhibited alien limb behaviour and striking ideomotor dyspraxia. General neuropsychological evaluation focused on constructional and visuospatial abilities, calculation, verbal fluency, episodic and semantic memory, plus spelling and writing because impairments in this domain were presenting complaints. Four experiments assessed the roles of visual and tactile information in the facilitation of motor performance by tools. Experiment 1 evaluated the patient's performance of six limb transitive actions under six conditions: (1) after he described the relevant tool from memory, (2) after he was shown a line drawing of the tool, (3) after he was shown a real exemplar of the tool, (4) after he watched the experimenter perform the action, (5) while he was holding the tool, and (6) immediately after he had performed the action with the tool but with the tool removed from his grasp. Experiment 2 evaluated the use of the same six tools when the patient had tactile but no visual information (while he was blindfolded). Experiments 3 and 4 assessed performance of actions appropriate to the same six tools when the patient had either neutral or inappropriate tactile feedback-that is, while he was holding a non-tool object or a different tool. RESULTS: Miming of tool use was not facilitated by visual input; moreover, lack of visual information in the blindfolded condition did not reduce performance. The principal positive finding was a dramatic facilitation of the patient's ability to demonstrate object use when he was holding either the appropriate tool or a neutral object. Tools inappropriate to the requested action produced involuntary performance of the stimulus relevant action. CONCLUSIONS: Tactile stimulation was paramount in the facilitation of motor performance in tool use by this patient with CBD. This outcome suggests that tactile information should be included in models which hypothesise modality specific inputs to the action production system. Significant impairments in spelling and letter production that have not previously been reported in CBD have also been documented.
Abstract.
Author URL.
Zeman AZ (1999). Episodic memory in transient global amnesia.
J Neurol Neurosurg Psychiatry,
66(2).
Author URL.
Halligan PW, Zeman A, Berger A (1999). Phantoms in the brain. British Medical Journal, 319(7210), 587-588.
Zeman A (1998). The consciousness of sight.
BMJ,
317(7174), 1696-1697.
Author URL.
Zeman AZ, Boniface SJ, Hodges JR (1998). Transient epileptic amnesia: a description of the clinical and neuropsychological features in 10 cases and a review of the literature.
J Neurol Neurosurg Psychiatry,
64(4), 435-443.
Abstract:
Transient epileptic amnesia: a description of the clinical and neuropsychological features in 10 cases and a review of the literature.
OBJECTIVES: to clarify the clinical and neuropsychological aspects of transient epileptic amnesia (TEA) based on 10 personally studied cases as well as review of 21 previously published cases; and to propose tentative diagnostic criteria for the diagnosis of TEA. METHODS: all 10 patients and informants underwent a standardised clinical interview. The radiological and neurophysiological (EEG) data were also reviewed in all cases. The diagnosis of transient epileptic amnesia was made on the basis of the following criteria: (1) there was a history of recurrent witnessed episodes of transient amnesia; (2) cognitive functions other than memory were judged to be intact during typical episodes by a reliable witness; (3) there was evidence for a diagnosis of epilepsy. This evidence was provided by either (a) wake or sleep EEG, or (b) the co-occurrence of other seizure types (if their roughly concurrent onset or close association with episodes of transient amnesia suggested a connection), or (c) a clear cut response to anticonvulsant therapy, or by a combination of these three factors. In addition all patients were administered a comprehensive neuropsychological test battery designed to assess verbal and non-verbal anterograde memory and retrograde memory for famous personalities and personal events. Their results were compared with those of 25 age and IQ matched normal controls. RESULTS: TEA usually begins in later life, with a mean age of 65 years in this series. Episodes are typically brief, lasting less than one hour, and recurrent, with a mean frequency of three a year. Attacks on waking are characteristic. Repetitive questioning occurs commonly during attacks. The anterograde amnesia during episodes is, however, often incomplete so that patients may later be able to "remember not being able to remember". The extent of the retrograde amnesia during attacks varies from days to years. Most patients experience other seizure types compatible with an origin in the temporal lobes, but transient amnesia is the only manifestation of epilepsy in about one third of patients. Epileptiform abnormalities arising from the temporal lobes are most often detected on interictal sleep EEG. Despite normal performance on tests of anterograde memory, many patients complain of persistent interictal disturbance of autobiographical memory, involving a significant but variable loss of recall for salient personal episodes. The epochs affected may predate the onset of epilepsy by many years. CONCLUSIONS: TEA is an identifiable syndrome and comprises episodic transient amnesia with an epileptic basis, without impairment of other aspects of cognitive function. Future studies should consider the question of whether TEA reflects ictal activity or a postictal state, and the mechanism of the persistent autobiographical amnesia. It is hypothesised that the latter may result in part from impairment of very long term memory consolidation as a result of epileptic activity in mesial temporal structures.
Abstract.
Author URL.
Zeman AZ, Grayling AC, Cowey A (1997). Contemporary theories of consciousness.
J Neurol Neurosurg Psychiatry,
62(6), 549-552.
Author URL.
Zeman A (1997). Persistent vegetative state.
Lancet,
350(9080), 795-799.
Author URL.
Zeman AZ, Hodges JR (1997). Transient global amnesia.
Br J Hosp Med,
58(6), 257-260.
Abstract:
Transient global amnesia.
Transient global amnesia is an alarming but benign disorder of middle age, which prevents both the formation of new memories, and the retrieval of recently formed ones, for some hours. Research over the last 10 years has shed light on the epidemiology, neuropsychology, functional anatomy and differential diagnosis of this distinctive condition, and clarified its management.
Abstract.
Author URL.
ZEMAN AZJ, KEIR G, LUXTON R, THOMPSON EJ, MILLER D, MCDONALD WI (1994). OLIGOCLONAL BANDS IN MULTIPLE-SCLEROSIS - RECENT FINDINGS, FUTURE USES.
ANNALS OF NEUROLOGY,
36(2), 325-325.
Author URL.
Zeman A, McLean B, Keir G, Luxton R, Sharief M, Thompson E (1993). The significance of serum oligoclonal bands in neurological diseases.
J Neurol Neurosurg Psychiatry,
56(1), 32-35.
Abstract:
The significance of serum oligoclonal bands in neurological diseases.
The presence of oligoclonal bands (OCBs) of immunoglobulin G (IgG) in CSF provides evidence for the occurrence of a humoral immune response, but it is not always appreciated that the oligoclonal IgG may have originated in the serum. To determine the diagnostic significance of serum OCBs 146 patients with serum OCBs were identified among 1874 patients with suspected neurological disorders (7.6%). Clear diagnoses had been made in 112 of these patients: in 56 identical CSF and serum bands were present, revealing a systemic immune response, while in 46 additional unique CSF bands indicated that intrathecal IgG synthesis was also occurring. In the first group neoplasia and peripheral neuropathies accounted for over 50% of the diagnoses, infections and systemic inflammatory disorders for 32%, and multiple sclerosis was diagnosed in only one case. These figures contrast considerably with those reported for patients with CSF OCBs alone. Diagnoses in the second group of patients, with unique CSF OCBs in addition to serum OCBs, resembled those among patients with CSF OCBs alone. Examining CSF and serum in parallel for OCBs of IgG provides more diagnostic information than examining CSF alone, and the latter is potentially misleading.
Abstract.
Author URL.
Chapters
Zeman A (2020). Aphantasia. Adam Zeman. Chapter in the Cambridge Handbook of the Imagination, ed Anna Abraham, Cambridge University Press, 2020. In Abraham A (Ed) The Cambridge Handbook of the Imagination, ed Anna Abraham, Cambridge University Press, 2020, Cambridge University Press, 692-710.
Zeman A, Baker J, Savage S (2019). Cognitive Assessment. https://doi.org/10.1017/9781108593946.003. In Butler R, Katona C (Eds.) Seminars in Old Age Psychiatry, ed. Rob Butler and Cornelius Katona, Cambridge University Press, December 20, 2019, 27-40.
Davis P, Corcoran R, Rylance R, Zeman A, Kidd D, de Bezenac C (2019). Reading: Brain, mind and body. In (Ed) Reading and Mental Health, 293-320.
Zeman AZJ (2017). Foreword to Aphantasia – experiences, perceptions and insights. Alan Kendle, Dark River, Bennion Kearny 2017. In (Ed) Aphantasia – experiences, perceptions and insights. Alan Kendle, Dark River, Bennion Kearny 2017.
Zeman A (2017). The syndrome of transient epileptic amnesia: Diagnose "psychogenic" causation carefully: Remember that "standard tests" can sometimes miss the point, and discuss difficult cases with colleagues when in doubt. In (Ed) Neuropsychiatry Case Studies, 121-125.
Butler C, Zeman A (2015). Syndromes of Transient Amnesia. In Laureys S, Tononi G (Eds.) The Neurology of Consciousness.
Zeman A (2015). The origins of subjectivity. In Jeeves M (Ed) In the Emergence of Personhood. Eerdmans.
Hoefeijzers S, Zeman A (2015). Transient Epileptic Amnesia. In (Ed)
International Encyclopedia of the Social & Behavioral Sciences: Second Edition, 554-561.
Abstract:
Transient Epileptic Amnesia
Abstract.
Hoefeijzers S, Zeman A (2015). Transient Epileptic Amnesia. In: James D Wright (editor-in-chief), International Encyclopedia of the Social & Behavioral Sciences. In (Ed) , 554-561.
Butler C, Zeman A (2014). Transient Epileptic Amnesia. In Aminoff MJ, Daroff RB (Eds.) Encyclopedia of the Neurological Sciences, Oxford: Academic Press, 485-488.
Butler C, Zeman A (2013). Transient global amnesia. In Reuber M, Schacter S (Eds.) In the Borderlands of Epilepsy, Oxford University Press.
Carson A, Stone J, Zeman A (2012). Neuropsychiatry for liaison psychiatrists. In Guthrie E, Rao S, Temple M (Eds.) Seminars in Liaison Psychiatry, RCPsych publications.
Butler C, Muhlert N, Zeman A (2010). Accelerated long-term forgetting. In (Ed) Forgetting, 211-234.
Zeman A, Torrens L (2010). Cognitive Assessment. In Puri B, Treasaden I (Eds.) Psychiatry: an Evidence-based Text, Hodder Arnold.
Zeman AZJ (2010). Mind and Brain: building bridges between neurology, psychiatry and psychology. In (Ed) Oxford Textbook of Medicine, Oxford University Press.
Zeman AZJ (2009). Epilepsy, Deja vu, Automatisms. In Wilken P, Bayne T, Cleeremans A (Eds.) The Oxford Companion to Consciousness, Oxford University Press.
Butler C, Zeman A (2009). Syndromes of transient amnesia. In (Ed) The Neurology of Consciousness, 339-351.
Zeman AZJ (2008). Does consciousness spring from the brain?. Dilemmas of awareness in practice and in theory. In Davies M, Weiskrantz L (Eds.) The Frontiers of Consciousness. Chichele Lectures, Oxford University Press.
Zeman AZJ (2008). Foreword. In Olins Alpert B (Ed) The Creative Ice Age Brain: cave art in the light of neuroscience, M.A.T. Foundation.
Zeman AZJ (2007). Conscience and Consciousness. In Walker G (Ed) The Science of Morality, Royal College of Physicians.
Zeman AZJ (2007). Diagnosis of brain death and persistent vegetative state. In (Ed) Reviews in Neurology, Continuing Medical Education Program of the Indian Academy of Neurology.
Carson A, Zeman A, Myles L, Sharpe M (2007). Neurological Disorders. In Guthrie E, Lloyd G (Eds.) The Handbook of Liaison Psychiatry, University Press, Cambridge.
Carson AJ, Zeman A, Myles L, Sharpe M (2007). Neurology and Neurosurgery. In Levenson J (Ed) Essentials of Psychosomatic Medicine, American Psychiatric Publishing Incorporated, Washington DC.
Zeman AZJ (2006). Consciousness. In Hallett M (Ed) Psychogenic Movement Disorders, Lipincott, Williams and Wilkins, Philadelphia.
Carson A, Zeman A, Myles L, Sharpe M (2005). Neurology and Nuerosurgery. In Levenson J (Ed) The American Psychiatric Textbook of Psychosomatic Medicine, Washington: American Psychiatric Press Incorporated.
Zeman A (2005). What in the world is consciousness?. In Laureys S (Ed) The Boundaries of Consciousness, Amsterdam: Elsevier.
Carson A, Zeman A, Brown TM, Sharpe M (2004). Organic Psychiatry. In Jonstone EC (Ed) Companion to Psychiatric Studies, Edinburgh: Churchill Livingstone.
Zeman A (2004). Theories of visual awareness. In (Ed) Progress in Brain Research, Elsevier, 321-329.
Zeman A (2004). Theories of visual awareness. In (Ed)
, 321-329.
Abstract:
Theories of visual awareness.
Abstract.
Author URL.
Zeman AZJ (2002). Consciousness. In Nadel L (Ed) Macmillan Encyclopaedia of Cognitive Science, Nature Publishing.
Stone J, Zeman A (2001). Conversion hysteria: the view from neurology. In Halligan P, Bass C, Marshall J (Eds.) Conversion Hysteria, Oxford: Oxford University Press.
Zeman AZJ, Emanuel L (2000). Ethical Dilemmas in Neurology. In (Ed) Major Problems in Neurology, W B Saunders, London.
Zeman A, Hodges J (2000). Transient global amnesia and transient eplieptic amnesia. In Berrios G, Hodges J (Eds.) Memory Disorders in Psychiatric Practice, Cambridge: Cambridge University Press.
Conferences
Knowles L, Jones K, Zeman A (2021). ACQUIRED APHANTASIA IN 88 CASES: a PRELIMINARY REPORT.
Author URL.
Baker J, Savage S, Zeman A (2020). DIFFERENTIATING TRANSIENT EPILEPTIC AMNESIA FROM EPILEPSY IN DEMENTIA AND MILD COGNITIVE IMPAIRMENT.
Author URL.
Zeman A (2020). THE EYE'S MIND: PERSPECTIVES ON VISUAL IMAGERY.
Author URL.
May F, Romiszewski S, Norris B, Miller M, Zeman A (2019). MEDICAL STUDENT EDUCATION IN SLEEP AND ITS DISORDERS: HAS IT IMPROVED OVER 20 YEARS?.
Author URL.
Cuttle G, Burn W, Zeman A (2017). INTEGRATING NEUROSCIENCE INTO PSYCHIATRIC TRAINING - AND VICE VERSA.
Author URL.
Savage SA, Butler CR, Baker J, Hodges JR, Zeman AZ (2017). LONG-TERM FOLLOW-UP IN TRANSIENT EPILEPTIC AMNESIA: PROGNOSIS OVER 10-20 YEARS.
Author URL.
Savage S, Baker J, Butler C, Hodges J, Zeman A (2017). Long-term prognosis of transient epileptic amnesia: Evidence from the time project.
Author URL.
Baker J, Savage S, Zeman A (2017). TIME 2: a REPLICATION STUDY OF TRANSIENT EPILEPTIC AMNESIA.
Author URL.
Day J, Torrens L, Bowman P, Shepherd M, Chakera A, Hattersley A, Zeman A (2016). KCNJ11 MUTATIONS CAUSE SEVERE NEUROPSYCHOLOGICAL DEFICITS.
Author URL.
Day JO, Torrens L, Bowman P, Shepherd M, Chakera A, Hattersley AT, Zeman AJ (2016). KCNJ11 mutations can result in severe cognitive and behavioural problems as well as neonatal diabetes: evaluation of seven adult patients.
Author URL.
Weston P, Liang Y, Henley S, Nicholas J, Ryan N, Schott J, Rossor M, Butler C, Zeman A, Fox N, et al (2016). LONG-TERM FORGETTING IN PRECLINICAL FAMILIAL ALZHEIMER'S DISEASE.
Author URL.
Dewer B, Rogers P, Ricketts J, Mukonoweshuro W, Zeman A (2015). DIAGNOSING FRONTOTEMPORAL DEMENTIA IN OUTPATIENTS: AN AUDIT OF RADIOLOGICAL REPORTS AND REVIEW OF DIAGNOSTIC CRITERIA.
Author URL.
Zeman A (2015). NEW THEORIES OF MEMORY SYSTEMS AND NETWORKS.
Author URL.
Dharia S, Zeman A, Devon R (2015). SLEEP-DEPRIVATION AMNESIA.
Author URL.
Atherton K, Lazar A, Wulff K, Nobre K, Zeman A, Butler C (2015). Slow wave sleep is detrimental for memory consolidation in transient epileptic amnesia.
Author URL.
Fred A, De Marsico M, Tabbone A (2014). Foreword.
Butler CR, van Erp W, Bhaduri A, Hammers A, Heckemann R, Zeman AZ (2012). Magnetic Resonance Volumetry Reveals Focal Brain Atrophy in Transient Epileptic Amnesia.
Author URL.
Jung HH, Geser F, Haybaeck J, Bader B, Danek A, Fuhr P, Neumann M, Reichard R, Udd B, Zeman A, et al (2012). Neuropathology of McLeod neuroacanthocytosis syndrome.
Author URL.
Zeman A, Butler CR (2012). The Syndrome of Transient Epileptic Amnesia (TEA).
Author URL.
Brazdil M, Marecek R, Urbanek T, Kasparek T, Mikl M, Rektor I, Zeman A (2012). UNVEILING THE MYSTERY OF DEJA VU.
Author URL.
Benattayallah A, Milton F, Muhlert N, Butler CR, Zeman AZJ (2010). The neural correlates of everyday recognition memory. 18th Proceedings of the International Society for Magnetic Resonance in Medicine. 1st May 2020 - 7th May 2010.
Muhlert N, Milton FN, Butler CR, Zeman A (2009). ACCELERATED LONG TERM FORGETTING OF REAL LIFE EVENTS IN PATIENTS WITH TRANSIENT EPILEPTIC AMNESIA.
Author URL.
Butler CR, Zeman AZJ (2009). TRANSIENT EPILEPTIC AMNESIA: a CASE REPORT WITH RADIOLOGICAL LOCALISATION.
Author URL.
Butler CR, Bhaduri A, Acosta-Cabronero J, Nestor PJ, Zeman A (2009). TRANSIENT EPILEPTIC AMNESIA: REGIONAL BRAIN ATROPHY AND ITS RELATION TO MEMORY DEFICITS.
Author URL.
Shankar R, Jalihal V, Zeman A (2008). Pseudo-cataplexy.
Author URL.
Zeman A, McGonigle D, Gountouna E, Torrens L, Della Sala S, Logie R (2007). "Blind imagination'': Brain activation after loss of the mind's eye.
Author URL.
Stone J, Zeman A, Simonotto E, Meyer M, Azuma R, Flett S, Sharpe M (2007). FMRI in patients with motor conversion symptoms and controls with simulated weakness.
Abstract:
FMRI in patients with motor conversion symptoms and controls with simulated weakness.
Abstract.
Author URL.
Zeman A, Torrens L, Sala SD, Logie R (2005). A case of blind imagination?.
Author URL.
Butler CR, Zeman AZJ (2005). Time - a study of epileptic amnesia.
Author URL.
Zeman A (2004). The concept of consciousness.
Author URL.
Warren-Gash C, Zeman A (2003). A study of deja vu in patients with temporal lobe epilepsy, students, and neurology outpatients.
Author URL.
Louis-Auguste J, Zeman A (2003). A study of impaired awareness due to stroke.
Author URL.
Reports
. (2003). The Vegetative State. Guidance on diagnosis and management. Report of a working party of the Royal College of Physicians, RCP.
Zeman AZJ (2002). Guidelines for the Management of Narcolepsy in Children and Adults. Report of an interdisciplinary working party. Taylor Patten Communications.
Publications by year
In Press
Zeman A (In Press). Blind Mind's Eye.
American Scientist MagazineAbstract:
Blind Mind's Eye
(sorry unsure where to put this), this is the published version, I have permission from the publisher that this can be downloaded to ORE
Abstract.
Savage SA, Baker J, Milton F, Butler CR, Zeman A (In Press). Clinical outcomes in Transient Epileptic Amnesia: a 10-year follow-up cohort study of 47 cases. Epilepsia
MacKisack M, Zeman A, Winlove C, Onians J, Macpherson F, Aldworth S (In Press). Extended Imagining: the case of the aphantasic artist.
Abstract:
Extended Imagining: the case of the aphantasic artist
Can visual imagining ever be other than a brain-bound, organismically internal process? the practices of artists with aphantasia - the congenital or acquired incapacity to generate visual mental imagery - suggests that it can. Here we report on a qualitative study of ‘aphantasic’ artists and find that imagery lack coincides with a dependence on external, environmental, structures to generate artwork. Indeed, physical manipulations of external media seem to take place in lieu of the ability to generate and manipulate internal, mental images. Cognitive functions that could, for the non-aphantasic, be carried out by mental imagery - such as bringing non-conscious visio-spatial relationships to awareness - can only be carried out for the aphantasic by manipulating their environment. Thus aphantasic art-making constitutes extended visual imagining. As such, it undermines the universality of the ‘hylomorphic’ model of art-making, in which the work is mentally preconceived before being realised in the material world, with the fact of neurocognitive diversity.
Abstract.
Knight K, Milton F, Zeman A (In Press). Memory without Imagery: No Evidence of Visual Working Memory Impairment in People with Aphantasia. Proceedings of the Cognitive Science Society
Zeman A, MacKisack M, Aldworth S, MacPherson F, Onians J, Winlove C (In Press). plural imagination: diversity in mind and making. Art Journal
2022
Monzel M, Mitchell D, Macpherson F, Pearson J, Zeman A (2022). Aphantasia, dysikonesia, anauralia: call for a single term for the lack of mental imagery-Commentary on Dance et al. (2021) and Hinwar and Lambert (2021).
Cortex,
150, 149-152.
Abstract:
Aphantasia, dysikonesia, anauralia: call for a single term for the lack of mental imagery-Commentary on Dance et al. (2021) and Hinwar and Lambert (2021).
Recently, the term 'aphantasia' has become current in scientific and public discourse to denote the absence of mental imagery. However, new terms for aphantasia or its subgroups have recently been proposed, e.g. 'dysikonesia' or 'anauralia', which complicates the literature, research communication and understanding for the general public. Before further terms emerge, we advocate the consistent use of the term 'aphantasia' as it can be used flexibly and precisely, and is already widely known in the scientific community and among the general public.
Abstract.
Author URL.
Monzel M, Mitchell D, Macpherson F, Pearson J, Zeman A (2022). Proposal for a consistent definition of aphantasia and hyperphantasia: a response to Lambert and Sibley (2022) and Simner and Dance (2022).
Cortex,
152, 74-76.
Author URL.
Zhao B, Della Sala S, Zeman A, Gherri E (2022). Spatial transformation in mental rotation tasks in aphantasia.
Psychonomic Bulletin and Review,
29(6), 2096-2107.
Abstract:
Spatial transformation in mental rotation tasks in aphantasia
Aphantasia refers to the inability to summon images to one’s own mind’s eye, resulting in selective deficits of voluntary object imagery. In the present study, we investigated whether M. X. a case of acquired aphantasia, can still retain some form of spatial transformation processes even though he is unable to subjectively experience voluntary object imagery. M. X. and a group of control participants were asked to complete a letter mental rotation task (MRT), typically used to assess the nature of the spatial transformation, while behavioural and electrophysiological responses were recorded. M. X. was able to complete the MRTs as accurately as controls, showing the pattern of increasing RTs as a function of rotation angle typical of MRTs. However, event-related potential (ERP) results showed systematic differences between M. X. and controls. On canonical letter trials, the rotation-related negativity (RRN), an ERP component considered as the psychophysiological correlate of the spatial transformation of mental rotation (MR), was present in both M. X. and controls and similarly modulated by rotation angle. However, no such modulation was observed for M. X. on mirror-reversed letter trials. These findings suggest that, at least under specific experimental conditions, the inability to create a depictive representation of the stimuli does not prevent the engagement of spatial transformation in aphantasia. However, the ability to apply spatial transformation varies with tasks and might be accounted for by the specific type of mental representation that can be accessed.
Abstract.
2021
Knowles L, Jones K, Zeman A (2021). ACQUIRED APHANTASIA IN 88 CASES: a PRELIMINARY REPORT.
Author URL.
Keogh R, Pearson J, Zeman A (2021). Aphantasia: the science of visual imagery extremes.
Handb Clin Neurol,
178, 277-296.
Abstract:
Aphantasia: the science of visual imagery extremes.
Visual imagery allows us to revisit the appearance of things in their absence and to test out virtual combinations of sensory experience. Visual imagery has been linked to many cognitive processes, such as autobiographical and visual working memory. Imagery also plays symptomatic and mechanistic roles in neurologic and mental disorders and is utilized in treatment. A large network of brain activity spanning frontal, parietal, temporal, and visual cortex is involved in generating and maintain images in mind. The ability to visualize has extreme variations, ranging from completely absent (aphantasia) to photo-like (hyperphantasia). The anatomy and functionality of visual cortex, including primary visual cortex, have been associated with individual differences in visual imagery ability, pointing to a potential correlate for both aphantasia and hyperphantasia. Preliminary evidence suggests that lifelong aphantasia is associated with prosopagnosia and reduction in autobiographical memory; hyperphantasia is associated with synesthesia. Aphantasic individuals can also be highly imaginative and are able to complete many tasks that were previously thought to rely on visual imagery, demonstrating that visualization is only one of many ways of representing things in their absence. The study of extreme imagination reminds us how easily invisible differences can escape detection.
Abstract.
Author URL.
Milton F, Fulford J, Dance C, Gaddum J, Heuerman-Williamson B, Jones K, Knight KF, Mackisack M, Winlove C, Zeman A, et al (2021). Behavioral and Neural Signatures of Visual Imagery Vividness Extremes: Aphantasia vs Hyperphantasia. Cerebral Cortex Communications, 2, 1-15.
Lomas M, Rickard V, Milton F, Savage S, Weir A, Zeman A (2021). Electroconvulsive Therapy related Autobiographical Amnesia: ‘Somatoform’ or ‘Organic’? - a review and case report. Cognitive Neuropsychiatry, 26, 107-121.
Patel D, Ibrahim H, Rankin J, Hilton D, Barria MA, Ritchie DL, Smith C, Zeman A (2021). Fatal insomnia: the elusive prion disease.
BMJ Case Rep,
14(6).
Abstract:
Fatal insomnia: the elusive prion disease.
A previously well 54- year-old woman presented with a short history of diplopia, cognitive decline, hallucinations and hypersomnolence. The patient had progressive deterioration in short-term memory, ocular convergence spasm, tremor, myoclonus, gait apraxia, central fever, dream enactment and seizures. Results of investigations were normal including MRI brain, electroencephalogram, cerebrospinal fluid (CSF, including CSF prion protein markers) and brain biopsy. The patient died from pneumonia and pulmonary embolus. Brain postmortem analysis revealed neuropathological changes in keeping with Fatal familial insomnia (FFI); the diagnosis was confirmed on genetic testing. FFI is caused by an autosomal dominant and highly penetrant pathogenic Prion Protein gene PRNP Although usually familial, fatal insomnia (FI) also occurs in a rare sporadic form. FI is a rare human prion disease with prominent sleep disturbance, autonomic, motor, cognitive and behavioural involvement. Patient management is with best supportive care and early suspected diagnosis allows for timely palliation.
Abstract.
Author URL.
Baker J, Savage S, Milton F, Butler C, Kapur N, Hodges J, Zeman A (2021). The Syndrome of Transient Epileptic Amnesia: a combined series of 115 cases and literature review. Brain Communications, 3
Dance CJ, Jaquiery M, Eagleman DM, Porteous D, Zeman A, Simner J (2021). What is the relationship between Aphantasia, Synaesthesia and Autism?.
Conscious Cogn,
89Abstract:
What is the relationship between Aphantasia, Synaesthesia and Autism?
For people with aphantasia, visual imagery is absent or markedly impaired. Here, we investigated the relationship between aphantasia and two other neurodevelopmental conditions also linked to imagery differences: synaesthesia, and autism. In Experiment 1a and 1b, we asked whether aphantasia and synaesthesia can co-occur, an important question given that synaesthesia is linked to strong imagery. Taking grapheme-colour synaesthesia as a test case, we found that synaesthesia can be objectively diagnosed in aphantasics, suggesting visual imagery is not necessary for synaesthesia to occur. However, aphantasia influenced the type of synaesthesia experienced (favouring 'associator' over 'projector' synaesthesia - a distinction tied to the phenomenology of the synaesthetic experience). In Experiment 2, we asked whether aphantasics have traits associated with autism, an important question given that autism - like aphantasia - is linked to weak imagery. We found that aphantasics reported more autistic traits than controls, with weaknesses in imagination and social skills.
Abstract.
Author URL.
2020
Baker J (2020). A Study of Interactions Between Memory Disorders and Epilepsy: Epileptic Seizures in Dementia, Contrasted with Transient Epileptic Amnesia.
Abstract:
A Study of Interactions Between Memory Disorders and Epilepsy: Epileptic Seizures in Dementia, Contrasted with Transient Epileptic Amnesia
The term dementia refers to a group of progressive neurodegenerative diseases in which patients experience a range of cognitive symptoms, with memory impairment the most common. These patients are also at risk of experiencing epileptic seizures. Transient Epileptic Amnesia (TEA) is a syndrome of temporal lobe epilepsy in which the principal manifestation of a seizure is a brief episode of amnesia during which other mental functions are predominantly or entirely preserved. Patients with TEA describe persistent memory impairments which are distinct from their seizures. In this thesis two studies are described which look in detail at each of these conditions separately. The demographic features, seizure presentations and cognitive profiles of these two groups are then compared in order to improve our understanding of these under-recognised conditions, and to assist clinicians tasked with their diagnosis.
It has been known for over a century that patients with Alzheimer’s disease (AD) can experience epileptic seizures. However, the degree to which the risk of epilepsy is increased in these patients remains unclear. Seizures were long thought of as a feature of advanced disease in these patients, only occurring several years after the onset of symptoms. However, more recent evidence has suggested that seizures can occur at an early stage of the disease, maybe even prior to the onset of memory symptoms. This suggests that seizures in this population may be a cause of decline, rather than purely a marker of severe disease. The aim of the work reported in this thesis is to investigate a cohort of patients with dementia and Mild Cognitive Impairment (MCI), recruited from a regional memory clinic in order to determine the prevalence, clinical features and prognosis of epileptic seizures in patients with MCI and all forms of dementia. A UK-based, prospective study of this nature has not been conducted before
144 patients with MCI and dementia were recruited from the Exeter memory clinic. Diagnoses were confirmed using established diagnostic criteria, together with a group of 80 age- and gender- matched healthy control subjects. Participants underwent a clinical interview and cognitive testing, in the company of a reliable informant, who also completed further questionnaires. Cognitive testing and informant questionnaires were repeated following a 12-month interval.
A prevalence of epilepsy of between 12.5 and 25.7% is identified in this population. Patients in whom a clinical suspicion of epilepsy was suspected were no different to those in whom there was no clinical evidence of epilepsy in terms of age of onset or cognitive performance at their initial study assessment. However epilepsy patients scored higher on the informant questionnaires, suggesting a greater impairment and increased care requirements. At the time of their 12-month assessment, the patients in whom epilepsy had been identified performed significantly worse on cognitive testing, suggesting that the presence of seizures was associated with a more rapid decline in this group.
The concept of TEA has been established for over 25 years. These patients describe amnesic episodes which are brief and frequently occur upon waking. Seizures may be associated with olfactory hallucinations. Studies have shown that they respond well to anti-epileptic medications. An initial cohort of 50 patients with TEA was described in 2007. In this thesis a further cohort of 65 patients is described and combined with the original 50 patients in order to clarify and more fully describe the demographic, clinical and neuropsychological features of this condition. Through this largest ever cohort of TEA patients it is shown that the mean age of onset of TEA is 61.7 years, and that men are more commonly diagnosed than women. Seizures in TEA typically last from 15 to 30 minutes and frequently occur on a monthly basis. 93% of patients in this study reported cessation of seizures following the initiation of medication. Despite this, interictal memory concerns are common: including autobiographical amnesia, accelerated long-term forgetting and topographical amnesia.
In comparing these two groups it is shown that patients who experience TEA are younger than those who experience epileptic seizures as a feature of MCI or dementia. They perform better on cognitive testing and neuroradiological investigations are more likely to be normal. In TEA, ictal amnesia is more likely to be the sole feature of a seizure, and olfactory hallucinations are more common. Patients with dementia are more likely to experience periods of unresponsiveness. Patients who develop epileptic seizures as a feature of MCI or dementia demonstrate significant cognitive decline over time, whereas cognitive performance is typically stable in patients with TEA.
Abstract.
Zeman A (2020). Aphantasia. Adam Zeman. Chapter in the Cambridge Handbook of the Imagination, ed Anna Abraham, Cambridge University Press, 2020. In Abraham A (Ed) The Cambridge Handbook of the Imagination, ed Anna Abraham, Cambridge University Press, 2020, Cambridge University Press, 692-710.
Baker J, Savage S, Zeman A (2020). DIFFERENTIATING TRANSIENT EPILEPTIC AMNESIA FROM EPILEPSY IN DEMENTIA AND MILD COGNITIVE IMPAIRMENT.
Author URL.
Romiszewski S, May FEK, Homan EJ, Norris B, Miller MA, Zeman A (2020). Medical student education in sleep and its disorders is still meagre 20 years on: a cross-sectional survey of UK undergraduate medical education.
J Sleep Res,
29(6).
Abstract:
Medical student education in sleep and its disorders is still meagre 20 years on: a cross-sectional survey of UK undergraduate medical education.
Sleep is a pillar of health, alongside adequate nutrition and exercise. Problems with sleep are common and often treatable. Twenty years ago, UK medical school education on sleep disorders had a median teaching time of 15 min; we investigate whether education on sleep disorders has improved. This is a cross-sectional survey, including time spent on teaching sleep medicine, subtopics covered and forms of assessment. Thirty-four medical degree courses in the UK were investigated via a questionnaire. We excluded responses not concerned with general undergraduate education (i.e. optional modules). Twenty-five (74%) medical schools responded. Time spent teaching undergraduates sleep medicine was: median, 1.5 hr; mode,
Abstract.
Author URL.
Argyropoulos GPD, Moore L, Loane C, Roca-Fernandez A, Lage-Martinez C, Gurau O, Irani SR, Zeman A, Butler CR (2020). Pathologic tearfulness after limbic encephalitis. Neurology, 10.1212/WNL.0000000000008-10.1212/WNL.0000000000008.
Zeman AZJ, Milton F, Della Sala S, Dewar M, Frayling T, Gaddum J, Hattersley A, Heuerman-Williamson B, Jones K, Mackisack M, et al (2020). Phantasia - the psychological significance of lifelong visual imagery vividness extremes. Cortex, 130, 426-440.
Zeman A (2020). THE EYE'S MIND: PERSPECTIVES ON VISUAL IMAGERY.
Author URL.
2019
Baker J, Libretto T, Henley W, Zeman A (2019). A Longitudinal Study of Epileptic Seizures in Alzheimer's Disease.
Front Neurol,
10Abstract:
A Longitudinal Study of Epileptic Seizures in Alzheimer's Disease.
The prevalence of epileptic seizures is increased in patients in the clinical stages of Alzheimer's disease (AD) when compared to age-matched cognitively normal populations. In previously reported work from the Presentation of Epileptic Seizures in Dementia (PrESIDe) study, we identified a clinical suspicion of epilepsy in between 12.75 and 28.43% of patients with AD recruited from a memory clinic. EEGs were not performed in this study. Patients with epilepsy performed similarly to patients without epilepsy on cognitive testing at the time of recruitment but were more impaired on two measures of everyday functioning [Cambridge Behavioral Inventory-Revised and Clinical Dementia Rating (CBI-R and CDR)]. On repeated testing in this 12-month follow-up study, patients in whom a suspicion of epilepsy was identified performed significantly worse on cognitive function testing (p = 0.028) in addition to maintaining a difference on the informant questionnaires (CBI-R p < 0.001, CDR p = 0.020). These findings suggest that seizures in this population could be a marker of a more rapid decline and worse prognosis.
Abstract.
Author URL.
Hoefeijzers S, Zeman A, Della Sala S, Dewar M (2019). Capturing real-life forgetting in transient epileptic amnesia via an incidental memory test.
Cortex,
110, 47-57.
Abstract:
Capturing real-life forgetting in transient epileptic amnesia via an incidental memory test
Transient epileptic amnesia (TEA) is an epileptic syndrome characterized by recurrent, brief episodes of amnesia. Patients with TEA often complain of interictal (between attacks) retention deficits, characterised by an ‘evaporation’ of memories for recent events over days to weeks. Clinical tests of anterograde memory often fail to corroborate these complaints as TEA patients commonly perform within the normal range after the standard 10–30-min delay period. Modified laboratory tests that include a 1–3 week delay period frequently reveal clear evidence of ‘accelerated long-term forgetting’ (ALF). However, they are not used routinely and lack ecological validity. In the present study we examined whether ‘real-life’ ALF can be captured via a controlled incidental memory test in TEA patients. To this end, the experimenter told 27 TEA patients and 32 controls a well-rehearsed amusing story, apparently as a way of making light conversation before starting a set of research experiments. Without prior warning, the experimenter subsequently probed the participants' memory of this story via tests of free recall and forced choice recognition after 30 min or 1 week. After 30 min retention was comparable in TEA patients and controls. After 1 week TEA patients retained significantly less story material than controls, and significant ALF was revealed in the TEA patients in the recognition test. Our data show that ALF in a ‘real-life’ situation can occur even when standard memory tests indicate normal memory function. Moreover, our data suggest that incidental memory tests can capture real-life ALF, and that forced-choice recognition tests might be more sensitive than free recall tests for the detection of real-life ALF.
Abstract.
Zeman A, Baker J, Savage S (2019). Cognitive Assessment. https://doi.org/10.1017/9781108593946.003. In Butler R, Katona C (Eds.) Seminars in Old Age Psychiatry, ed. Rob Butler and Cornelius Katona, Cambridge University Press, December 20, 2019, 27-40.
Bowman P, Day J, Torrens L, Shepherd MH, Knight BA, Ford TJ, Flanagan SE, Chakera A, Hattersley AT, Zeman A, et al (2019). Cognitive, Neurological, and Behavioral Features in Adults with KCNJ11 Neonatal Diabetes.
Diabetes Care,
42(2), 215-224.
Abstract:
Cognitive, Neurological, and Behavioral Features in Adults with KCNJ11 Neonatal Diabetes.
OBJECTIVE: Central nervous system (CNS) features in children with permanent neonatal diabetes (PNDM) due to KCNJ11 mutations have a major impact on affected families. Sulfonylurea therapy achieves outstanding metabolic control but only partial improvement in CNS features. The effects of KCNJ11 mutations on the adult brain and their functional impact are not well understood. We aimed to characterize the CNS features in adults with KCNJ11 PNDM compared with adults with INS PNDM. RESEARCH DESIGN AND METHODS: Adults with PNDM due to KCNJ11 mutations (n = 8) or INS mutations (n = 4) underwent a neurological examination and completed standardized neuropsychological tests/questionnaires about development/behavior. Four individuals in each group underwent a brain MRI scan. Test scores were converted to Z scores using normative data, and outcomes were compared between groups. RESULTS: in individuals with KCNJ11 mutations, neurological examination was abnormal in seven of eight; predominant features were subtle deficits in coordination/motor sequencing. All had delayed developmental milestones and/or required learning support/special schooling. Half had features and/or a clinical diagnosis of autism spectrum disorder. KCNJ11 mutations were also associated with impaired attention, working memory, and perceptual reasoning and reduced intelligence quotient (IQ) (median IQ KCNJ11 vs. INS mutations 76 vs. 111, respectively; P = 0.02). However, no structural brain abnormalities were noted on MRI. The severity of these features was related to the specific mutation, and they were absent in individuals with INS mutations. CONCLUSIONS: KCNJ11 PNDM is associated with specific CNS features that are not due to long-standing diabetes, persist into adulthood despite sulfonylurea therapy, and represent the major burden from KCNJ11 mutations.
Abstract.
Author URL.
Helbig KL, Lauerer RJ, Bahr JC, Souza IA, Myers CT, Uysal B, Schwarz N, Gandini MA, Huang S, Keren B, et al (2019). De Novo Pathogenic Variants in CACNA1E Cause Developmental and Epileptic Encephalopathy with Contractures, Macrocephaly, and Dyskinesias.
Am J Hum Genet,
104(3).
Author URL.
Atherton KE, Filippini N, Zeman AZJ, Nobre AC, Butler CR (2019). Encoding-related brain activity and accelerated forgetting in transient epileptic amnesia.
Cortex,
110, 127-140.
Abstract:
Encoding-related brain activity and accelerated forgetting in transient epileptic amnesia.
The accelerated forgetting of newly learned information is common amongst patients with epilepsy and, in particular, in the syndrome of transient epileptic amnesia (TEA). However, the neural mechanisms underlying accelerated forgetting are poorly understood. It has been hypothesised that interictal epileptiform activity during longer retention intervals disrupts normally established memory traces. Here, we tested a distinct hypothesis-that accelerated forgetting relates to the abnormal encoding of memories. We studied a group of 15 patients with TEA together with matched, healthy control subjects. Despite normal performance on standard anterograde memory tasks, patients showed accelerated forgetting of a word list over one week. We used a subsequent memory paradigm to compare encoding-related brain activity in patients and controls. Participants studied a series of visually presented scenes whilst undergoing functional MRI scanning. Recognition memory for these scenes was then probed outside the scanner after delays of 45 min and of 4 days. Patients showed poorer memory for the scenes compared with controls. In the patients but not the controls, subsequently forgotten stimuli were associated with reduced hippocampal activation at encoding. Furthermore, patients demonstrated reduced deactivation of posteromedial cortex regions upon viewing subsequently remembered stimuli as compared to subsequently forgotten ones. These data suggest that abnormal encoding-related activity in key memory areas of the brain contributes to accelerated forgetting in TEA. We propose that abnormally encoded memory traces may be particularly vulnerable to interference from subsequently encountered material and hence be forgotten more rapidly. Our results shed light on the mechanisms underlying memory impairment in epilepsy, and offer support to the proposal that accelerated forgetting may be a useful marker of subtle dysfunction in memory-related brain systems.
Abstract.
Author URL.
Berkovic SF, Oliver KL, Canafoglia L, Krieger P, Damiano JA, Hildebrand MS, Morbin M, Vears DF, Sofia V, Giuliano L, et al (2019). Kufs disease due to mutation of CLN6: clinical, pathological and molecular genetic features.
Brain,
142(1), 59-69.
Abstract:
Kufs disease due to mutation of CLN6: clinical, pathological and molecular genetic features.
Kufs disease is the major adult form of neuronal ceroid lipofuscinosis, but is rare and difficult to diagnose. Diagnosis was traditionally dependent on the demonstration of characteristic storage material, but distinction from normal age-related accumulation of lipofuscin can be challenging. Mutation of CLN6 has emerged as the most important cause of recessive Kufs disease but, remarkably, is also responsible for variant late infantile ceroid lipofuscinosis. Here we provide a detailed description of Kufs disease due to CLN6 pathogenic variants. We studied 20 cases of Kufs disease with CLN6 pathogenic variants from 13 unrelated families. Mean age of onset was 28 years (range 12-51) with bimodal peaks in teenage and early adult life. The typical presentation was of progressive myoclonus epilepsy with debilitating myoclonic seizures and relatively infrequent tonic-clonic seizures. Patients became wheelchair-bound with a mean 12 years post-onset. Ataxia was the most prominent motor feature. Dementia appeared to be an invariable accompaniment, although it could take a number of years to manifest and occasionally cognitive impairment preceded myoclonic seizures. Patients were usually highly photosensitive on EEG. MRI showed progressive cerebral and cerebellar atrophy. The median survival time was 26 years from disease onset. Ultrastructural examination of the pathology revealed fingerprint profiles as the characteristic inclusions, but they were not reliably seen in tissues other than brain. Curvilinear profiles, which are seen in the late infantile form, were not a feature. of the 13 unrelated families we observed homozygous CLN6 pathogenic variants in four and compound heterozygous variants in nine. Compared to the variant late infantile form, there was a lower proportion of variants that predicted protein truncation. Certain heterozygous missense variants in the same amino acid position were found in both variant late infantile and Kufs disease. There was a predominance of cases from Italy and surrounding regions; this was partially explained by the discovery of three founder pathogenic variants. Clinical distinction of type a (progressive myoclonus epilepsy) and type B (dementia with motor disturbance) Kufs disease was supported by molecular diagnoses. Type a is usually caused by recessive pathogenic variants in CLN6 or dominant variants in DNAJC5. Type B Kufs is usually associated with recessive CTSF pathogenic variants. The diagnosis of Kufs remains challenging but, with the availability of genetic diagnosis, this will largely supersede the use of diagnostic biopsies, particularly as biopsies of peripheral tissues has unsatisfactory sensitivity and specificity.
Abstract.
Author URL.
May F, Romiszewski S, Norris B, Miller M, Zeman A (2019). MEDICAL STUDENT EDUCATION IN SLEEP AND ITS DISORDERS: HAS IT IMPROVED OVER 20 YEARS?.
Author URL.
Savage SA, Irani S, Leite MI, Zeman A (2019). NMDA receptor antibody encephalitis presenting as Transient Epileptic Amnesia. Journal of Neuroimmunology
Davis P, Corcoran R, Rylance R, Zeman A, Kidd D, de Bezenac C (2019). Reading: Brain, mind and body. In (Ed) Reading and Mental Health, 293-320.
Savage S, Hoefeijzers S, Milton FN, Streatfield C, Dewar M, Zeman A (2019). The evolution of accelerated long-term forgetting: Evidence from the TIME study. Cortex, 110, 16-36.
Baker J, Libretto T, Henley W, Zeman A (2019). The prevalence and clinical features of epileptic seizures in a memory clinic population. Seizure, 71, 83-92.
2018
Weston PSJ, Nicholas JM, Henley SMD, Liang Y, Macpherson K, Donnachie E, Schott JM, Rossor MN, Crutch SJ, Butler CR, et al (2018). Accelerated long-term forgetting in presymptomatic autosomal dominant Alzheimer's disease: a cross-sectional study.
LANCET NEUROLOGY,
17(2), 123-132.
Author URL.
Helbig KL, Lauerer RJ, Bahr JC, Souza IA, Myers CT, Uysal B, Schwarz N, Gandini MA, Huang S, Keren B, et al (2018). De Novo Pathogenic Variants in CACNA1E Cause Developmental and Epileptic Encephalopathy with Contractures, Macrocephaly, and Dyskinesias.
Am J Hum Genet,
103(5), 666-678.
Abstract:
De Novo Pathogenic Variants in CACNA1E Cause Developmental and Epileptic Encephalopathy with Contractures, Macrocephaly, and Dyskinesias.
Developmental and epileptic encephalopathies (DEEs) are severe neurodevelopmental disorders often beginning in infancy or early childhood that are characterized by intractable seizures, abundant epileptiform activity on EEG, and developmental impairment or regression. CACNA1E is highly expressed in the central nervous system and encodes the α1-subunit of the voltage-gated CaV2.3 channel, which conducts high voltage-activated R-type calcium currents that initiate synaptic transmission. Using next-generation sequencing techniques, we identified de novo CACNA1E variants in 30 individuals with DEE, characterized by refractory infantile-onset seizures, severe hypotonia, and profound developmental impairment, often with congenital contractures, macrocephaly, hyperkinetic movement disorders, and early death. Most of the 14, partially recurring, variants cluster within the cytoplasmic ends of all four S6 segments, which form the presumed CaV2.3 channel activation gate. Functional analysis of several S6 variants revealed consistent gain-of-function effects comprising facilitated voltage-dependent activation and slowed inactivation. Another variant located in the domain II S4-S5 linker results in facilitated activation and increased current density. Five participants achieved seizure freedom on the anti-epileptic drug topiramate, which blocks R-type calcium channels. We establish pathogenic variants in CACNA1E as a cause of DEEs and suggest facilitated R-type calcium currents as a disease mechanism for human epilepsy and developmental disorders.
Abstract.
Author URL.
Romiszewski S, Croft D, Veale J, Matthews L, Ryland H, May F, Zeman A (2018). Neurological sleep medicine: a case note audit from a specialist clinic.
Progress in Neurology and Psychiatry,
22(2), 9-17.
Abstract:
Neurological sleep medicine: a case note audit from a specialist clinic
On average, humans sleep for a third of their lives, and sleep disorders are common and treatable. However, services for most sleep disorders are highly variable across the UK, and sleep medicine is neglected in the medical curriculum. We report the findings of an audit of patients with neurological sleep disorders seen in a combined cognitive neurology and sleep disorder clinics over a seven‐year period, 75 with hypersomnias, 67 with parasomnias and 39 with insomnia. Also, the results of a pilot of a cognitive behavioural therapy service for insomnia undertaken in the same population are analysed.
Abstract.
Zeman A, MacKisack M, Onians J (2018). The Eye's mind – Visual imagination, neuroscience and the humanities. Cortex, 105, 1-3.
Fulford J, Milton F, Salas D, Smith A, Simler A, Winlove C, Zeman A (2018). The neural correlates of visual imagery vividness – an fMRI study and literature review.
Cortex,
105, 26-40.
Abstract:
The neural correlates of visual imagery vividness – an fMRI study and literature review
Using the Vividness of Visual Imagery Questionnaire we selected 14 high-scoring and 15 low-scoring healthy participants from an initial sample of 111 undergraduates. The two groups were matched on measures of age, IQ, memory and mood but differed significantly in imagery vividness. We used fMRI to examine brain activation while participants looked at, or later imagined, famous faces and famous buildings. Group comparison revealed that the low-vividness group activated a more widespread set of brain regions while visualising than the high-vividness group. Parametric analysis of brain activation in relation to imagery vividness across the entire group of participants revealed distinct patterns of positive and negative correlation. In particular, several posterior cortical regions show a positive correlation with imagery vividness: regions of the fusiform gyrus, posterior cingulate and parahippocampal gyri (BAs 19, 29, 31 and 36) displayed exclusively positive correlations. By contrast several frontal regions including parts of anterior cingulate cortex (BA 24) and inferior frontal gyrus (BAs 44 and 47), as well as the insula (BA 13), auditory cortex (BA 41) and early visual cortices (BAs 17 and 18) displayed exclusively negative correlations. We discuss these results in relation to a previous, functional imaging study of a clinical case of ‘blind imagination’ and to the existing literature on the functional imaging correlates of imagery vividness and related phenomena in visual and other domains.
Abstract.
Winlove CIP, Milton F, Ranson J, Fulford J, MacKisack M, Macpherson F, Zeman A (2018). The neural correlates of visual imagery: a co-ordinate-based meta-analysis.
Cortex,
105, 4-25.
Abstract:
The neural correlates of visual imagery: a co-ordinate-based meta-analysis
Visual imagery is a form of sensory imagination, involving subjective experiences typically described as similar to perception, but which occur in the absence of corresponding external stimuli. We used the Activation Likelihood Estimation algorithm (ALE) to identify regions consistently activated by visual imagery across 40 neuroimaging studies, the first such meta-analysis. We also employed a recently developed multi-modal parcellation of the human brain to attribute stereotactic co-ordinates to one of 180 anatomical regions, the first time this approach has been combined with the ALE algorithm. We identified a total 634 foci, based on measurements from 464 participants. Our overall comparison identified activation in the superior parietal lobule, particularly in the left hemisphere, consistent with the proposed ‘top-down’ role for this brain region in imagery. Inferior premotor areas and the inferior frontal sulcus were reliably activated, a finding consistent with the prominent semantic demands made by many visual imagery tasks. We observed bilateral activation in several areas associated with the integration of eye movements and visual information, including the supplementary and cingulate eye fields (SCEFs) and the frontal eye fields (FEFs), suggesting that enactive processes are important in visual imagery. V1 was typically activated during visual imagery, even when participants have their eyes closed, consistent with influential depictive theories of visual imagery. Temporal lobe activation was restricted to area PH and regions of the fusiform gyrus, adjacent to the fusiform face complex (FFC). These results provide a secure foundation for future work to characterise in greater detail the functional contributions of specific areas to visual imagery.
Abstract.
2017
Zeman AZJ, Baker J (2017). Accelerated Long-Term Forgetting in Epilepsy - and Beyond. Cognitive Neuroscience of Memory Consolidation, Studies in Neuroscience, Psychology and Behavioural Economics, 401-417.
Vossel KA, Tartaglia MC, Nygaard HB, Zeman AZ, Miller BL (2017). Epileptic activity in Alzheimer's disease: causes and clinical relevance.
The Lancet Neurology,
16(4), 311-322.
Abstract:
Epileptic activity in Alzheimer's disease: causes and clinical relevance
Epileptic activity is frequently associated with Alzheimer's disease; this association has therapeutic implications, because epileptic activity can occur at early disease stages and might contribute to pathogenesis. In clinical practice, seizures in patients with Alzheimer's disease can easily go unrecognised because they usually present as non-motor seizures, and can overlap with other symptoms of the disease. In patients with Alzheimer's disease, seizures can hasten cognitive decline, highlighting the clinical relevance of early recognition and treatment. Some evidence indicates that subclinical epileptiform activity in patients with Alzheimer's disease, detected by extended neurophysiological monitoring, can also lead to accelerated cognitive decline. Treatment of clinical seizures in patients with Alzheimer's disease with select antiepileptic drugs (AEDs), in low doses, is usually well tolerated and efficacious. Moreover, studies in mouse models of Alzheimer's disease suggest that certain classes of AEDs that reduce network hyperexcitability have disease-modifying properties. These AEDs target mechanisms of epileptogenesis involving amyloid β and tau. Clinical trials targeting network hyperexcitability in patients with Alzheimer's disease will identify whether AEDs or related strategies could improve their cognitive symptoms or slow decline.
Abstract.
Zeman AZJ (2017). Foreword to Aphantasia – experiences, perceptions and insights. Alan Kendle, Dark River, Bennion Kearny 2017. In (Ed) Aphantasia – experiences, perceptions and insights. Alan Kendle, Dark River, Bennion Kearny 2017.
Day JO, Flanagan SE, Shepherd MH, Patrick AW, Abid N, Torrens L, Zeman AJ, Patel KA, Hattersley AT (2017). Hyperglycaemia-related complications at the time of diagnosis can cause permanent neurological disability in children with neonatal diabetes. Diabetic Medicine, 34(7), 1000-1004.
Cuttle G, Burn W, Zeman A (2017). INTEGRATING NEUROSCIENCE INTO PSYCHIATRIC TRAINING - AND VICE VERSA.
Author URL.
Savage SA, Butler CR, Baker J, Hodges JR, Zeman AZ (2017). LONG-TERM FOLLOW-UP IN TRANSIENT EPILEPTIC AMNESIA: PROGNOSIS OVER 10-20 YEARS.
Author URL.
Savage S, Baker J, Butler C, Hodges J, Zeman A (2017). Long-term prognosis of transient epileptic amnesia: Evidence from the time project.
Author URL.
Zeman A (2017). Michael R. Trimble, the Intentional Brain (Baltimore, MD: John Hopkins University Press, 2016), pp. x, 308, $29.95, hardback, ISBN: 978-1-4214-1949-7.
Med Hist,
61(2), 329-330.
Author URL.
Zeman AZJ, Byruck M, Tallis P, Vossel K, Tranel D (2017). NSY-D-17-00057R1 Touching the Void. Neuropsychologia
Savage SA, Butler CR, Milton F, Han Y, Zeman AZ (2017). On the nose: olfactory disturbances in transient epileptic amnesia. Epilepsy and Behavior, 66, 113-113.
Baker J, Savage S, Zeman A (2017). TIME 2: a REPLICATION STUDY OF TRANSIENT EPILEPTIC AMNESIA.
Author URL.
Zeman A (2017). The syndrome of transient epileptic amnesia: Diagnose "psychogenic" causation carefully: Remember that "standard tests" can sometimes miss the point, and discuss difficult cases with colleagues when in doubt. In (Ed) Neuropsychiatry Case Studies, 121-125.
2016
Day J, Torrens L, Bowman P, Shepherd M, Chakera A, Hattersley A, Zeman A (2016). KCNJ11 MUTATIONS CAUSE SEVERE NEUROPSYCHOLOGICAL DEFICITS.
Author URL.
Day JO, Torrens L, Bowman P, Shepherd M, Chakera A, Hattersley AT, Zeman AJ (2016). KCNJ11 mutations can result in severe cognitive and behavioural problems as well as neonatal diabetes: evaluation of seven adult patients.
Author URL.
Weston P, Liang Y, Henley S, Nicholas J, Ryan N, Schott J, Rossor M, Butler C, Zeman A, Fox N, et al (2016). LONG-TERM FORGETTING IN PRECLINICAL FAMILIAL ALZHEIMER'S DISEASE.
Author URL.
Day JO, Zeman AJ (2016). Limbic encephalitis driven by a pleural mesothelioma: a paraneoplastic complication.
Middle East Journal of Cancer,
7(4), 221-223.
Abstract:
Limbic encephalitis driven by a pleural mesothelioma: a paraneoplastic complication
Paraneoplastic neurological syndromes have only been described with pleural mesothelioma in five cases. We have described a 72-year-old man who developed anterograde amnesia 27 months after diagnosis of epithelioid pleural mesothelioma. Investigations revealed a limbic encephalitis with no alternative causes identified. Limbic encephalitis is a classical paraneoplastic syndrome and presentation within five years of a cancer with no other causes identified is sufficient to diagnose a paraneoplastic etiology. This is the first case of isolated paraneoplastic limbic encephalitis driven by a pleural mesothelioma.
Abstract.
MacKisack M, Aldworth S, Macpherson F, Onians J, Winlove C, Zeman A (2016). On picturing a candle: the prehistory of imagery science.
Frontiers in Psychology,
7(APR), 515:1-16.
Abstract:
On picturing a candle: the prehistory of imagery science
© 2016 MacKisack, Aldworth, Macpherson, Onians, Winlove and Zeman.The past 25 years have seen a rapid growth of knowledge about brain mechanisms involved in visual mental imagery. These advances have largely been made independently of the long history of philosophical - and even psychological - reckoning with imagery and its parent concept 'imagination'. We suggest that the view from these empirical findings can be widened by an appreciation of imagination's intellectual history, and we seek to show how that history both created the conditions for - and presents challenges to - the scientific endeavor. We focus on the neuroscientific literature's most commonly used task - imagining a concrete object - and, after sketching what is known of the neurobiological mechanisms involved, we examine the same basic act of imagining from the perspective of several key positions in the history of philosophy and psychology. We present positions that, firstly, contextualize and inform the neuroscientific account, and secondly, pose conceptual and methodological challenges to the scientific analysis of imagery. We conclude by reflecting on the intellectual history of visualization in the light of contemporary science, and the extent to which such science may resolve long-standing theoretical debates.
Abstract.
Zeman A, Zaiwalla Z (2016). Prescribing sodium oxybate for narcolepsy.
BMJ,
353 Author URL.
Zeman A, Dewar M, Della Sala S (2016). Reflections on aphantasia.
Cortex,
74, 336-337.
Author URL.
Atherton KE, Nobre AC, Lazar AS, Wulff K, Whittaker RG, Dhawan V, Lazar ZI, Zeman AZ, Butler CR (2016). Slow wave sleep and accelerated forgetting.
Cortex,
84, 80-89.
Abstract:
Slow wave sleep and accelerated forgetting
We investigated whether the benefit of slow wave sleep (SWS) for memory consolidation typically observed in healthy individuals is disrupted in people with accelerated long-term forgetting (ALF) due to epilepsy. SWS is thought to play an active role in declarative memory in healthy individuals and, furthermore, electrographic epileptiform activity is often more prevalent during SWS than during wakefulness or other sleep stages. We studied the relationship between SWS and the benefit of sleep for memory retention using a word-pair associates task. In both the ALF and the healthy control groups, sleep conferred a memory benefit. However, the relationship between the amount of SWS and sleep-related memory benefits differed significantly between the groups. In healthy participants, the amount of SWS correlated positively with sleep-related memory benefits. In stark contrast, the more SWS, the smaller the sleep-related memory benefit in the ALF group. Therefore, contrary to its role in healthy people, SWS-associated brain activity appears to be deleterious for memory in patients with ALF.
Abstract.
Zeman A, Hoefeijzers S, Milton F, Dewar M, Carr M, Streatfield C (2016). The GABAB receptor agonist, baclofen, contributes to three distinct varieties of amnesia in the human brain - a detailed case report.
Cortex,
74, 9-19.
Abstract:
The GABAB receptor agonist, baclofen, contributes to three distinct varieties of amnesia in the human brain - a detailed case report.
We describe a patient in whom long-term, therapeutic infusion of the selective gamma-amino-butyric acid type B (GABAB) receptor agonist, baclofen, into the cerebrospinal fluid (CSF) gave rise to three distinct varieties of memory impairment: i) repeated, short periods of severe global amnesia, ii) accelerated long-term forgetting (ALF), evident over intervals of days and iii) a loss of established autobiographical memories. This pattern of impairment has been reported in patients with temporal lobe epilepsy (TLE), in particular the subtype of Transient Epileptic Amnesia (TEA). The amnesic episodes and accelerated forgetting remitted on withdrawal of baclofen, while the autobiographical amnesia (AbA) persisted. This exceptional case highlights the occurrence of 'non-standard' forms of human amnesia, reflecting the biological complexity of memory processes. It suggests a role for GABAB signalling in the modulation of human memory over multiple time-scales and hints at its involvement in 'epileptic amnesia'.
Abstract.
Author URL.
Dewer B, Rogers P, Ricketts J, Mukonoweshuro W, Zeman A (2016). The radiological diagnosis of frontotemporal dementia in everyday practice: an audit of reports, review of diagnostic criteria, and proposal for service improvement.
Clin Radiol,
71(1), 40-47.
Abstract:
The radiological diagnosis of frontotemporal dementia in everyday practice: an audit of reports, review of diagnostic criteria, and proposal for service improvement.
AIM: to investigate how commonly valuable diagnostic information regarding the frontotemporal dementias (FTDs) may be missed on routine radiological reporting. MATERIALS AND METHODS: the magnetic resonance imaging (MRI) examination results of a series of 39 consecutive patients in whom the diagnosis was initially thought to be a form of FTD were audited. Twenty-two patients satisfied formal diagnostic criteria for subtypes of FTD. The initial non-specialist radiological reports of the MRI examinations were compared with those of a radiologist who specifically examined the images for the possibility of atypical dementia. RESULTS: Six of the 22 original reports provided a full and accurate description of the radiological findings, while two provided a fully accurate interpretation. CONCLUSION: Valuable diagnostic information may be missed unless clinicians and radiologists jointly review and discuss brain imaging in cases of dementia. The use of standardised scales may enhance the reporting of MRI examinations for dementia.
Abstract.
Author URL.
Savage SA, Butler CR, Hodges JR, Zeman AZ (2016). Transient Epileptic Amnesia over twenty years: Long-term follow-up of a case series with three detailed reports. Seizure, 43, 48-55.
2015
Hoefeijzers S, Dewar M, Della Sala S, Butler C, Zeman A (2015). Accelerated long-term forgetting can become apparent within 3-8 hours of wakefulness in patients with transient epileptic amnesia.
Neuropsychology,
29(1), 117-125.
Abstract:
Accelerated long-term forgetting can become apparent within 3-8 hours of wakefulness in patients with transient epileptic amnesia.
OBJECTIVE: Accelerated long-term forgetting (ALF) is typically defined as a memory disorder in which information that is learned and retained normally over standard intervals (∼30 min) is forgotten at an abnormally rapid rate thereafter. ALF has been reported, in particular, among patients with transient epileptic amnesia (TEA). Previous work in TEA has revealed ALF 24 hr - 1 week after initial memory acquisition. It is unclear, however, if ALF observed 24 hr after acquisition reflects (a) an impairment of sleep consolidation processes taking place during the first night's sleep, or (b) an impairment of daytime consolidation processes taking place during the day of acquisition. Here we focus on the daytime-forgetting hypothesis of ALF in TEA by tracking in detail the time course of ALF over the day of acquisition, as well as over 24 hr and 1 week. METHOD: Eleven TEA patients who showed ALF at 1 week and 16 matched controls learned 4 categorical word lists on the morning of the day of acquisition. We subsequently probed word-list retention 30 min, 3 hr, and 8 hr postacquisition (i.e. over the day of acquisition), as well as 24-hr and 1-week post acquisition. RESULTS: ALF became apparent in the TEA group over the course of the day of acquisition 3-8 hr after learning. No further forgetting was observed over the first night in either group. CONCLUSIONS: the results of this study show that ALF in TEA can result from a deficit in memory consolidation occurring within hours of learning without a requirement for intervening sleep.
Abstract.
Author URL.
Dewer B, Rogers P, Ricketts J, Mukonoweshuro W, Zeman A (2015). DIAGNOSING FRONTOTEMPORAL DEMENTIA IN OUTPATIENTS: AN AUDIT OF RADIOLOGICAL REPORTS AND REVIEW OF DIAGNOSTIC CRITERIA.
Author URL.
Dewar M, Hoefeijzers S, Zeman A, Butler C, Della Sala S (2015). Impaired picture recognition in transient epileptic amnesia.
Epilepsy Behav,
42, 107-116.
Abstract:
Impaired picture recognition in transient epileptic amnesia.
Transient epileptic amnesia (TEA) is an epileptic syndrome characterized by recurrent, brief episodes of amnesia. Transient epileptic amnesia is often associated with the rapid decline in recall of new information over hours to days (accelerated long-term forgetting - 'ALF'). It remains unknown how recognition memory is affected in TEA over time. Here, we report a systematic study of picture recognition in patients with TEA over the course of one week. Sixteen patients with TEA and 16 matched controls were presented with 300 photos of everyday life scenes. Yes/no picture recognition was tested 5min, 2.5h, 7.5h, 24h, and 1week after picture presentation using a subset of target pictures as well as similar and different foils. Picture recognition was impaired in the patient group at all test times, including the 5-minute test, but it declined normally over the course of 1week. This impairment was associated predominantly with an increased false alarm rate, especially for similar foils. High performance on a control test indicates that this impairment was not associated with perceptual or discrimination deficits. Our findings suggest that, at least in some TEA patients with ALF in verbal recall, picture recognition does not decline more rapidly than in controls over 1week. However, our findings of an early picture recognition deficit suggest that new visual memories are impoverished after minutes in TEA. This could be the result of deficient encoding or impaired early consolidation. The early picture recognition deficit observed could reflect either the early stages of the process that leads to ALF or a separable deficit of anterograde memory in TEA. Lastly, our study suggests that at least some patients with TEA are prone to falsely recognizing new everyday visual information that they have not in fact seen previously. This deficit, alongside their ALF in free recall, likely affects everyday memory performance.
Abstract.
Author URL.
Zeman A, Dewar M, Della Sala S (2015). Lives without imagery - Congenital aphantasia.
Cortex,
73, 378-380.
Author URL.
Zeman A (2015). NEW THEORIES OF MEMORY SYSTEMS AND NETWORKS.
Author URL.
Dharia S, Zeman A, Devon R (2015). SLEEP-DEPRIVATION AMNESIA.
Author URL.
Atherton K, Lazar A, Wulff K, Nobre K, Zeman A, Butler C (2015). Slow wave sleep is detrimental for memory consolidation in transient epileptic amnesia.
Author URL.
Butler C, Zeman A (2015). Syndromes of Transient Amnesia. In Laureys S, Tononi G (Eds.) The Neurology of Consciousness.
Zeman A (2015). The origins of subjectivity. In Jeeves M (Ed) In the Emergence of Personhood. Eerdmans.
Hoefeijzers S, Zeman A (2015). Transient Epileptic Amnesia. In (Ed)
International Encyclopedia of the Social & Behavioral Sciences: Second Edition, 554-561.
Abstract:
Transient Epileptic Amnesia
Abstract.
Hoefeijzers S, Zeman A (2015). Transient Epileptic Amnesia. In: James D Wright (editor-in-chief), International Encyclopedia of the Social & Behavioral Sciences. In (Ed) , 554-561.
2014
Zeman A (2014). Brain imaging - what it can (and cannot) tell us about consciousness.
Neuropsychol Rehabil,
24(1), 144-146.
Author URL.
Bäumer D, East SZ, Tseu B, Zeman A, Hilton D, Talbot K, Ansorge O (2014). FTLD-ALS of TDP-43 type and SCA2 in a family with a full ataxin-2 polyglutamine expansion.
Acta Neuropathol,
128(4), 597-604.
Abstract:
FTLD-ALS of TDP-43 type and SCA2 in a family with a full ataxin-2 polyglutamine expansion.
Polyglutamine expansions in the ataxin-2 gene (ATXN2) cause autosomal dominant spinocerebellar ataxia type 2 (SCA2), but have recently also been associated with amyotrophic lateral sclerosis (ALS). We present clinical and pathological features of a family in which a pathological ATXN2 expansion led to frontotemporal lobar degeneration with ALS (FTLD-ALS) in the index case, but typical SCA2 in a son, and compare the neuropathology with a case of typical SCA2. The index case shares the molecular signature of SCA2 with prominent polyglutamine and p62-positive intranuclear neuronal inclusions mainly in the pontine nuclei, while harbouring more pronounced neocortical and spinal TDP-43 pathology. We conclude that ATXN2 mutations can cause not only ALS, but also a neuropathological overlap syndrome of SCA2 and FTLD presenting clinically as pure FTLD-ALS without ataxia. The cause of the phenotypic heterogeneity remains unexplained, but the presence of a CAA-interrupted CAG repeat in the FTLD case in this family suggests that one potential mechanism may be variation in repeat tract composition between members of the same family.
Abstract.
Author URL.
Fred A, De Marsico M, Tabbone A (2014). Foreword.
Zeman A, Rickards H, White P (2014). Integrating alienists.
LANCET PSYCHIATRY,
1(5), 333-333.
Author URL.
Warren-Gash C, Zeman A (2014). Is there anything distinctive about epileptic déjà vu?.
Journal of Neurology, Neurosurgery and Psychiatry,
85(2), 143-147.
Abstract:
Is there anything distinctive about epileptic déjà vu?
Background Déjà vu can occur as an aura of temporal lobe epilepsy and in some psychiatric conditions but is also common in the general population. It is unclear whether any clinical features distinguish pathological and physiological forms of déjà vu. Methods 50 epileptic patients with ictal déjà vu, 50 non-epileptic patients attending general neurology clinics and 50 medical students at Edinburgh University were recruited. Data were collected on demographic factors, the experience of déjà vu using a questionnaire based on Sno's Inventory for Déjà Vu Experiences Assessment, symptoms of anxiety and depression using the Hospital Anxiety and Depression Scale as well as seizure characteristics, anti-epileptic medications, handedness, EEG and neuroimaging findings for epileptic patients. Results 73.5% of neurology patients, 88% of students and (by definition) all epilepsy patients had experienced déjà vu. The experience of déjà vu itself was similar in the three groups. Epileptic déjà vu occurred more frequently and lasted somewhat longer than physiological déjà vu. Epilepsy patients were more likely to report prior fatigue and concentrated activity, associated derealisation, olfactory and gustatory hallucinations, physical symptoms such as headaches, abdominal sensations and fear. After controlling for study group, anxiety and depression scores were not associated with déjà vu frequency. Conclusions Déjà vu is common and qualitatively similar whether it occurs as an epileptic aura or normal phenomenon. However ictal déjà vu occurs more frequently and is accompanied by several distinctive features. It is distinguished primarily by 'the company it keeps'.
Abstract.
Zeman A (2014). Mirrors in the Brain.
AMERICAN JOURNAL OF PSYCHOLOGY,
127(2), 264-268.
Author URL.
Zeman A (2014). Neurology is psychiatry--and vice versa.
Pract Neurol,
14(3), 136-144.
Abstract:
Neurology is psychiatry--and vice versa.
This paper explores the relationship between neurology and psychiatry. It marshals evidence that disorders of the brain typically have neurological and psychological-cognitive, affective, behavioural-manifestations, while disorders of the psyche are based in the brain. Given the inseparability of neurological and psychiatric disorders, their disease classifications should eventually fuse, and joint initiatives in training, service and research should be strongly encouraged.
Abstract.
Author URL.
Wells CE, Moulin CJA, Ethridge P, Illman NA, Davies E, Zeman A (2014). Persistent psychogenic déjà vu: a case report.
J Med Case Rep,
8Abstract:
Persistent psychogenic déjà vu: a case report.
INTRODUCTION: Déjà vu is typically a transient mental state in which a novel experience feels highly familiar. Although extensively studied in relation to temporal lobe epilepsy as part of simple partial seizures, déjà vu has been less studied in other clinical populations. A recent review of temporal lobe epilepsy suggested a possible link between clinical levels of anxiety and debilitating déjà vu, indicating further research is required. Here, for the first time in the literature, we present a case study of a young man with anxiety and depersonalisation who reported experiencing persistent and debilitating déjà vu. This report therefore adds to the limited literature on the relationship between anxiety and déjà vu. CASE PRESENTATION: a 23-year-old White British man presented with a form of persistent déjà vu in 2010, approximately 3 years since symptom onset. He reported a history of anxiety and experiencing feelings of depersonalisation. Neurological assessment (electroencephalogram and magnetic resonance imaging) did not indicate any abnormalities. We assessed his recognition memory with a task used in patients with dementia who report similar experiences but lack awareness of their falseness. CONCLUSIONS: Our case's memory performance was more conservative than controls but did not indicate a memory deficit. Unlike other patients with chronic déjà vu (for example, in dementia), he is fully aware of the false nature of his déjà vu and this presumably leads to his intact recognition memory performance. We suggest that his persistent déjà vu is psychogenic and conclude that déjà vu should be further studied in psychiatric disorders.
Abstract.
Author URL.
Atherton KE, Nobre AC, Zeman AZ, Butler CR (2014). Sleep-dependent memory consolidation and accelerated forgetting.
Cortex,
54(1), 92-105.
Abstract:
Sleep-dependent memory consolidation and accelerated forgetting
Accelerated long-term forgetting (ALF) is a form of memory impairment in which learning and initial retention of information appear normal but subsequent forgetting is excessively rapid. ALF is most commonly associated with epilepsy and, in particular, a form of late-onset epilepsy called transient epileptic amnesia (TEA). ALF provides a novel opportunity to investigate post-encoding memory processes, such as consolidation. Sleep is implicated in the consolidation of memory in healthy people and a deficit in sleep-dependent memory consolidation has been proposed as an explanation for ALF. If this proposal were correct, then sleep would not benefit memory retention in people with ALF as much as in healthy people, and ALF might only be apparent when the retention interval contains sleep. To test this theory, we compared performance on a sleep-sensitive memory task over a night of sleep and a day of wakefulness. We found, contrary to the hypothesis, that sleep benefits memory retention in TEA patients with ALF and that this benefit is no smaller in magnitude than that seen in healthy controls. Indeed, the patients performed significantly more poorly than the controls only in the wake condition and not the sleep condition. Patients were matched to controls on learning rate, initial retention, and the effect of time of day on cognitive performance. These results indicate that ALF is not caused by a disruption of sleep-dependent memory consolidation. Instead, ALF may be due to an encoding abnormality that goes undetected on behavioural assessments of learning, or by a deficit in memory consolidation processes that are not sleep-dependent. © 2014 the Authors.
Abstract.
Baker S, Williams H, Sharp D, Gardner A, Harris A, Zeman A, Fulford J (2014). Sports-related concussion and diffusion tensor imaging findings in rugby players.
BRAIN INJURY,
28(5-6), 686-686.
Author URL.
Butler C, Zeman A (2014). Transient Epileptic Amnesia. In Aminoff MJ, Daroff RB (Eds.) Encyclopedia of the Neurological Sciences, Oxford: Academic Press, 485-488.
2013
Hoefeijzers S, Dewar M, Della Sala S, Zeman A, Butler C (2013). Accelerated long-term forgetting in transient epileptic amnesia: an acquisition or consolidation deficit?.
Neuropsychologia,
51(8), 1549-1555.
Abstract:
Accelerated long-term forgetting in transient epileptic amnesia: an acquisition or consolidation deficit?
Accelerated Long-term Forgetting (ALF) is the rapid loss of newly acquired memories over days to weeks despite normal retention at standard (~30 min) intervals. It has recently been described in association with epilepsy, particularly the syndrome of Transient Epileptic Amnesia (TEA). The cognitive mechanisms underlying ALF remain uncertain, but disruption either of memory acquisition or consolidation processes has been postulated. To arbitrate between these accounts, we reanalysed data from an existing word-list recall data set to investigate whether ALF can be observed for words learned under precisely matched conditions in TEA patients and controls. We reanalysed the data of 24 patients with TEA and 24 matched healthy controls who learnt a 15-item word list to a learning criterion of 90% with a minimum of five learning trials. Free recall of the words was probed at delays of 30 min and 1 week and 3 weeks after learning. In addition, a 'yes-no' recognition test was conducted after the 3-week free recall. Forgetting rates across the first 30 min delay and the subsequent 1 week and 3 week delay were compared between patients and controls. To ensure that learning conditions were closely matched between patients and control participants, we excluded exceptionally fast (N(TEA)=1, N(controls)=4) and slow (N(TEA)=6, N(controls)=2) learners. Furthermore, we analysed only words that were presented five or six times during learning and retrieved successfully on four or five occasions during learning. Recall performance on the last learning trial and 30 min after acquisition were indistinguishable between TEA patients and controls. Over the delay interval of 30 min to 1 week, however, accelerated forgetting of this newly learned verbal material was observed in TEA patients. This severe forgetting is also reflected in the three-week recognition test, where TEA patients performed significantly worse than controls. Moreover, whereas recall on the last learning trial correlated significantly with the 30 min delayed recall in both groups, recall on the last learning trial correlated significantly with 1 week and 3 week delayed recall only in the controls. In both groups, the three-week free recall performance correlated with the three-week recognition test. Patients with TEA demonstrate ALF even for verbal material that is learned under precisely matched conditions. These results are consistent with the hypothesis that ALF represents a disruption of memory consolidation rather than an acquisition deficit.
Abstract.
Author URL.
Charland-Verville V, Bruno MA, Bahri MA, Demertzi A, Desseilles M, Chatelle C, Vanhaudenhuyse A, Hustinx R, Bernard C, Tshibanda L, et al (2013). Brain dead yet mind alive: a positron emission tomography case study of brain metabolism in cotard's syndrome. Cortex, 49(7), 1997-1999.
Zeman AZJ, Milton FN, Smith A, Rylance R (2013). By heart. An fMRI study of brain activation by poetry and prose. Journal of Consciousness Studies, 20(9-10), 132-158.
Zeman AZJ, Beschin N, Dewar M, Della Sala S (2013). Imagining the present: Amnesia may impair descriptions of the present as well as of the future and the past.
Cortex,
49(3), 637-645.
Abstract:
Imagining the present: Amnesia may impair descriptions of the present as well as of the future and the past
Recent evidence suggests that in some patients with amnesia the capacity to imagine the future is impaired in parallel with the capacity to remember the past. This paper asks whether descriptions of the present may be similarly affected. We recruited 7 patients with amnesic syndromes of varying aetiologies who were matched for age, sex and education with 7 control participants. Patients showed no deficits on subjective measures of visual imagery. They were impaired by comparison with controls on measures of imagination and future thinking. However there was an even more marked impairment on tasks requiring them to give descriptions of their current experience. Potential explanations include effects of amnesia on narrative construction or on the texture of experience itself, and the confounding influence of cognitive impairments outside the memory domain. We conclude that tasks requiring descriptions of current experience provide a valuable control condition in studies examining the relationship between memory and imagination. © 2012 Elsevier Ltd.
Abstract.
Butler C, van Erp W, Bhaduri A, Hammers A, Heckemann R, Zeman A (2013). Magnetic resonance volumetry reveals focal brain atrophy in transient epileptic amnesia.
Epilepsy Behav,
28(3), 363-369.
Abstract:
Magnetic resonance volumetry reveals focal brain atrophy in transient epileptic amnesia.
Transient epileptic amnesia (TEA) is a recently described epilepsy syndrome characterized by recurrent episodes of isolated memory loss. It is associated with two unusual forms of interictal memory impairment: accelerated long-term forgetting (ALF) and autobiographical amnesia. We investigated the neural basis of TEA using manual volumetry and automated multi-atlas-based segmentation of whole-brain magnetic resonance imaging data from 40 patients with TEA and 20 healthy controls. Both methods confirmed the presence of subtle, bilateral hippocampal atrophy. Additional atrophy was revealed in perirhinal and orbitofrontal cortices. The volumes of these regions correlated with anterograde memory performance. No structural correlates were found for ALF or autobiographical amnesia. The results support the hypothesis that TEA is a focal medial temporal lobe epilepsy syndrome but reveal additional pathology in connected brain regions. The unusual interictal memory deficits of TEA remain unexplained by structural pathology and may reflect physiological disruption of memory networks by subclinical epileptiform activity.
Abstract.
Author URL.
Zeman A, Butler C, Muhlert N, Milton F (2013). Novel forms of forgetting in temporal lobe epilepsy.
Epilepsy and Behavior,
26(3), 335-342.
Abstract:
Novel forms of forgetting in temporal lobe epilepsy
Transient Epileptic Amnesia (TEA) is a recently defined subtype of temporal lobe epilepsy, principally affecting people in middle age with a male predominance. Its key manifestation is the occurrence of recurring episodes of transient amnesia, usually lasting less than an hour and often occurring on waking. One-third of patients have exclusively amnestic attacks, while in two-thirds, at least some attacks are accompanied by other manifestations of epilepsy, especially olfactory hallucinations. Several lines of evidence point to a seizure focus in the medial temporal lobes. Transient Epileptic Amnesia is accompanied by a striking loss of autobiographical memories in two-thirds of sufferers, accelerated loss of memories which had been acquired successfully in around one half, and topographical amnesia in around one-third. This paper reviews the findings of the TIME project (The Impairment of Memory in Epilepsy - http://sites.pcmd.ac.uk/time/tea.php) in relation to TEA, accelerated long-term forgetting, and remote memory impairment.This article is part of a Special Issue entitled "The Future of Translational Epilepsy Research". © 2012.
Abstract.
Sabah M, Zeman A (2013). Oculo-Dento-Digital Dysplasia (ODDD). Advances in Clinical Neuroscience and Rehabilitation, 13, 16-17.
Brázdil M, Zeman A (2013). The boundaries of epilepsy: Where is the limit? a reply to Labate and Gambardella. Cortex, 49(4), 1163-1164.
Zeman A, Coebergh JA (2013). The nature of consciousness.
Handb Clin Neurol,
118, 373-407.
Author URL.
Zeman A, Dewar B, Butler C (2013). Transient epileptic amnesia: the contribution of the british neurological surveillance unit.
J Neurol Neurosurg Psychiatry,
84(11).
Abstract:
Transient epileptic amnesia: the contribution of the british neurological surveillance unit.
Transient Epileptic Amnesia (TEA) is a subtype of temporal lobe epilepsy characterised by recurrent episodes of transient amnesia, usually in middle aged people, often occurring on waking, which prove to be due to epilepsy. Attacks are sometimes accompanied by other more familiar manifestations of epilepsy, especially olfactory hallucinations. The epilepsy typically responds very well to anticonvulsant treatment but interictal memory disturbance often persists despite abolition of the seizures, in particular an extensive autobiographical amnesia (AA), and a tendency for memories to fade more rapidly than usual over days to weeks (accelerated long-term forgetting, ALF). The TIME project (The Impairment of Memory in Epilepsy: see http://www.exeter.ac.uk/time/) was established in 2003 to study TEA and its associated interictal memory disturbance. It has since generated around 20 publications describing the clinical, neuropsychological and radiological features of TEA, AA and ALF.(1-4) the British Neurological Surveillance Unit (BNSU) contributed to patient recruitment in 2003-2005 and again recently (2011-present). In 2003-5, 32 patients were referred via the BNSU. 16 were included in the patient cohort described in our 2007 report,(1) nine were excluded as they did not satisfy our diagnostic criteria, seven were potentially suitable but study resources did not allow us to assess them fully. 22 cases have been referred recently. Details are awaited for 13, one refused consent, four have been assessed, three await assessment, one was excluded after assessment. The BNSU has made a major contribution to the success of the TIME project. The recruitment process would work more smoothly if participating neurologists i) asked patients for consent to pass on demographical and clinical details at the time of the clinic visit on which they are identified, ii) communicated these immediately to the researcher or iii) kept a note of patient details if i) and ii) are not feasible. The current system works well, and helps greatly in the recruitment of series of cases of moderately rare disorders, but its efficiency could be improved.
Abstract.
Author URL.
Butler C, Zeman A (2013). Transient global amnesia. In Reuber M, Schacter S (Eds.) In the Borderlands of Epilepsy, Oxford University Press.
2012
Milton F, Butler CR, Benattayallah A, Zeman A (2012). An fMRI study of autobiographical memory deficits in transient epileptic amnesia.
Journal of Neurology, Neurosurgery and Psychiatry,
83(10).
Abstract:
An fMRI study of autobiographical memory deficits in transient epileptic amnesia
Objective:
to identify the neural basis of autobiographical memory deficits in transient epileptic amnesia (TEA).
Method:
11 people (mean age: 65.91; SD=7.63) diagnosed with transient epileptic amnesia, all of whom complained of extensive autobiographical memory loss, and 17 age and IQ matched controls were recruited. Participants were matched on standard measures of anterograde memory. Participants recalled 32 previously identified autobiographical memories, specific in time and place, from four different time periods (childhood, young adult, middle aged and recent), during fMRI scanning. Activations were analysed using SPM8 software, effective connectivity using dynamic causal modelling (DCM). Post-scan ratings of the subjective vividness, level of detail, pleasantness, personal significance and frequency of retrieval of the memories were recorded.
Results:
Both patients and controls activated core regions of the autobiographical memory network. However, patients had reduced activation in the right posterior parahippocampal gyrus (pPHG), particularly for more recent memories, together with decreased engagement of the right temporoparietal junction and the right cerebellum. In addition, we found reduced effective connectivity in patients between the right pPHG and the right middle temporal gyrus. There were no differences in the subjective ratings of memories between patients and control participants.
Conclusion:
the reduction of activity in the right pPHG is consistent with other evidence that TEA is a disorder of the medial temporal lobes (MTL) and further implicates the pPHG as a key region for contextual information. These MTL differences were most marked for recent and mid-life periods suggesting that, at least at the neural level, remote memories are more robust than recent memories. We also found reduced effective connectivity in patients between the right pPHG and the right middle temporal gyrus. This may reflect persisting effects of the seizures, the continued presence of sub-clinical epileptiform activity or the sequelae of subtle structural changes in the MTL in our patient group.
Abstract.
White PD, Rickards H, Zeman AZJ (2012). Classifying mental and neurological conditions together: Authors' reply to letters. BMJ (Online), 345(7867).
Zeman A, Kapur N, Jones-Gotman M (2012).
Epilepsy and Memory - a comprehensive multi-author review of the interactions between epilepsy and memory. , Oxford University Press.
Abstract:
Epilepsy and Memory - a comprehensive multi-author review of the interactions between epilepsy and memory.
Abstract.
Butler C, Kapur N, Zeman A, Weller R, Connelly A (2012). Epilepsy-related long-term amnesia: Anatomical perspectives.
Neuropsychologia,
50(13), 2973-2980.
Abstract:
Epilepsy-related long-term amnesia: Anatomical perspectives
There are few clues as to the neural basis of selective long-term amnesia. We report group and single-case data to shed light on this issue. In a group study of patients with transient epileptic amnesia, there were no significant correlations between volumetric measures of the hippocampus and indices of accelerated long-term forgetting or longer-term autobiographical memory loss. Post-mortem investigations in a patient with temporal lobe epilepsy who showed accelerated long-term forgetting, together with a degree of autobiographical memory loss, yielded evidence of neuronal loss and gliosis in regions of both the right and the left hippocampus. Neuronal loss and gliosis were more evident in anterior than posterior hippocampus. These results indicate that the unusual forms of long-term forgetting seen in some patients with temporal lobe epilepsy have no gross anatomical correlate. The findings leave open the possiblities that subtle structural damage or subtle functional disturbance, perhaps in the form of subclinical epileptiform activity, underly epilepsy-related long-term amnesia. © 2012 Elsevier Ltd.
Abstract.
Sabah M, Mulcahy J, Zeman A (2012). Herpes simplex encephalitis. Praxis, 101(22), 1437-1440.
Sabah M, Mulcahy J, Zeman A (2012). Herpes simplex encephalitis. BMJ, 344:e3166, 47-49.
Butler CR, van Erp W, Bhaduri A, Hammers A, Heckemann R, Zeman AZ (2012). Magnetic Resonance Volumetry Reveals Focal Brain Atrophy in Transient Epileptic Amnesia.
Author URL.
White PD, Rickards H, Zeman AZ (2012). Mental and neurological illnesses should be classified together as conditions of the nervous system. British Medical Journal, 344:e3454, 26-28.
Jung HH, Geser F, Haybaeck J, Bader B, Danek A, Fuhr P, Neumann M, Reichard R, Udd B, Zeman A, et al (2012). Neuropathology of McLeod neuroacanthocytosis syndrome.
Author URL.
Carson A, Stone J, Zeman A (2012). Neuropsychiatry for liaison psychiatrists. In Guthrie E, Rao S, Temple M (Eds.) Seminars in Liaison Psychiatry, RCPsych publications.
Zeman A, Butler CR (2012). The Syndrome of Transient Epileptic Amnesia (TEA).
Author URL.
Muhlert N, Zeman A (2012). The enigma of long-term forgetting.
Seizure,
21(2), 77-78.
Author URL.
Ryland H, Williams WH, Zeman A, Murray J, Turner M (2012). The impact of neurological indicators of severity of concussion on neurocognitive performance in a sports population.
BRAIN INJURY,
26(4-5), 627-628.
Author URL.
Milton FN, Butler CR, Benattayallah A, Zeman, A.Z.J. (2012). The neural basis of autobiographical memory deficits in transient epileptic amnesia. Neuropsychologia, 50(14), 3528-3541.
Brazdil M, Marecek R, Urbanek T, Kasparek T, Mikl M, Rektor I, Zeman A (2012). UNVEILING THE MYSTERY OF DEJA VU.
Author URL.
Brázdil M, Mareček R, Urbánek T, Kašpárek T, Mikl M, Rektor I, Zeman A (2012). Unveiling the mystery of déjà vu: the structural anatomy of déjà vu.
Cortex,
48(9), 1240-1243.
Abstract:
Unveiling the mystery of déjà vu: the structural anatomy of déjà vu
Déjà vu (DV) is a widespread, fascinating and mysterious human experience. It occurs both in health and in disease, notably as an aura of temporal lobe epilepsy. This feeling of inappropriate familiarity has attracted interest from psychologists and neuroscientists for over a century, but still there is no widely agreed explanation for the phenomenon of non-pathological DV. Here we investigated differences in brain morphology between healthy subjects with and without DV using a novel multivariate neuroimaging technique, Source-Based Morphometry. The analysis revealed a set of cortical (predominantly mesiotemporal) and subcortical regions in which there was significantly less gray matter in subjects reporting DV. In these regions gray matter volume was inversely correlated with the frequency of DV. Our results demonstrate a structural correlate of DV in healthy individuals for the first time and support a neurological explanation for the phenomenon. We hypothesis that the observed local gray matter decrease in subjects experiencing DV reflects an alteration of hippocampal function and postnatal neurogenesis with resulting changes of volume in remote brain regions. © 2012 Elsevier Srl.
Abstract.
2011
Pal S, Zeidler M, Ironside JW, Zeman A (2011). 31st Advanced Clinical Neurology Course, Edinburgh 2009: progressive cognitive impairment, behavioural change and upper motor neuron signs in a 57-year-old woman.
Pract Neurol,
11(2), 71-80.
Author URL.
Butler CR, Zeman A (2011). The causes and consequences of transient epileptic amnesia.
Behav Neurol,
24(4), 299-305.
Abstract:
The causes and consequences of transient epileptic amnesia.
Transient epileptic amnesia (TEA) is a recently recognised syndrome of epilepsy in which the principle manifestation of seizures is recurrent episodes of isolated memory loss. In this article, we describe the clinical and cognitive profile of this emerging syndrome, and present new data that provide at most weak support for its proposed relationship to cerebrovascular disease. TEA is often associated with two unusual forms of interictal memory impairment: accelerated long-term forgetting and remote memory impairment. We discuss the clinical and theoretical implications of these relatively novel cognitive deficits.
Abstract.
Author URL.
Milton F, Muhlert N, Butler C, Zeman A (2011). The neural correlates of everyday recognition memory at a six month delay. Memory, 19, 733-744.
Milton F, Muhlert N, Butler CR, Benattayallah A, Zeman AZJ (2011). The neural correlates of everyday recognition memory.
Brain and Cognition,
76(3), 369-381.
Abstract:
The neural correlates of everyday recognition memory.
We used a novel automatic camera, SenseCam, to create a recognition memory test for real-life events.
Adapting a ‘Remember/Know’ paradigm, we asked healthy undergraduates, who wore SenseCam for 2
days, in their everyday environments, to classify images as strongly or weakly remembered, strongly
or weakly familiar or novel, while brain activation was recorded with functional MRI. Overlapping, widely
distributed sets of brain regions were activated by recollected and familiar stimuli. Within the medial
temporal lobes, ‘Remember’ responses specifically elicited greater activity in the right anterior and posterior
parahippocampal gyrus than ‘Know’ responses. ‘New’ responses activated anterior parahippocampal
regions. A parametric analysis, across correctly recognised items, revealed increasing activation in the
right hippocampus and posterior parahippocampal gyrus (pPHG). This may reflect modulation of these
regions by the degree of recollection or, alternatively, by increasing memory strength. Strong recollection
elicited greater activity in the left posterior hippocampus/pPHG than weak recollection indicating that
this region is specifically modulated by the degree of recollection.
Abstract.
Milton F, Butler CR, Zeman AZJ (2011). Transient epileptic amnesia: déjà vu heralding recovery of lost memories. Journal of Neurology, Neurosurgery, & Psychiatry, 82, 1178-1179.
2010
Muhlert N, Milton F, Butler CR, Kapur N, Zeman AZJ (2010). Accelerated forgetting of real life events in Transient Epileptic Amnesia. Neuropsychologia, 48, 3235-3244.
Butler C, Muhlert N, Zeman A (2010). Accelerated long-term forgetting. In (Ed) Forgetting, 211-234.
Zeman A, Torrens L (2010). Cognitive Assessment. In Puri B, Treasaden I (Eds.) Psychiatry: an Evidence-based Text, Hodder Arnold.
Zeman AZJ, Della Sala S, Torrens LA, Gountouna VE, McGonigle DJ, Logie RH (2010). Loss of imagery phenomenology with intact visuo-spatial task performance: a case of 'blind imagination'.
NEUROPSYCHOLOGIA,
48(1), 145-155.
Abstract:
Loss of imagery phenomenology with intact visuo-spatial task performance: a case of 'blind imagination'
The capacity for imagery, enabling us to visualise absent items and events, is a ubiquitous feature of our experience. This paper describes the case of a patient, MX, who abruptly lost the ability to generate visual images. He rated himself as experiencing almost no imagery on standard questionnaires, yet performed normally on standard tests of perception, visual imagery and visual memory. These unexpected findings were explored using functional MRI scanning (fMRI). Activation patterns while viewing famous faces were not significantly different between MX and controls, including expected activity in the fusiform gyrus. However, during attempted imagery, activation in MX's brain was significantly reduced in a network of posterior regions while activity in frontal regions was increased compared to controls. These findings are interpreted as suggesting that MX adopted a different cognitive strategy from controls when performing the imagery task. Evidence from experimental tasks thought to rely on mental imagery, such as the Brooks' matrices and mental rotation, support this interpretation. Taken together, these results indicate that successful performance in visual imagery and visual memory tasks can be dissociated from the phenomenal experience of visual imagery. (C) 2009 Elsevier Ltd. All rights reserved.
Abstract.
Zeman AZJ (2010). Mind and Brain: building bridges between neurology, psychiatry and psychology. In (Ed) Oxford Textbook of Medicine, Oxford University Press.
Shankar R, Jalihal V, Walker M, Zeman A (2010). Pseudocataplexy and transient functional paralysis: a spectrum of psychogenic motor disorder.
J Neuropsychiatry Clin Neurosci,
22(4), 445-450.
Abstract:
Pseudocataplexy and transient functional paralysis: a spectrum of psychogenic motor disorder.
The authors describe and discuss a syndrome of transient psychogenic weakness usually mistaken for cataplexy but which has a close association with a depressive mental state. Four patients were referred to the authors with suspected neurological causes of transient weakness, including cataplexy in three cases, for whom the eventual diagnosis was of a functional or psychogenic motor disorder, related in most cases to depression. This variety of transient functional weakness is related to conditions such as nonepileptic attack disorder, persistent functional weakness, catatonia, and depressive motor retardation. These cases point to the existence of a syndrome of transient motor weakness which resembles cataplexy and has features in common with other forms of mood induced psychogenic weakness such as psychomotor retardation and catatonia. Psychogenic "pseudocataplexy" is a diagnostic consideration in patients with atypical cataplexy, especially in the context of mood disturbance. Despite its close resemblance to cataplexy, pseudocataplexy has a different pathogenesis and requires a different approach to management.
Abstract.
Author URL.
Milton F, Muhlert N, Pindus D, Butler CR, Kapur N, Graham KS, Zeman AZJ (2010). Remote memory deficits in transient epileptic amnesia. Brain, 133, 1368-1379.
Smith A, Milton F, Rylance R, Zeman AZJ (2010). Rhyme and reason: the neural correlates of reading poetry and prose. Journal of Neurology, Neurosurgery, & Psychiatry, 81, e9-e9.
Benattayallah A, Milton F, Muhlert N, Butler CR, Zeman AZJ (2010). The neural correlates of everyday recognition memory. 18th Proceedings of the International Society for Magnetic Resonance in Medicine. 1st May 2020 - 7th May 2010.
Zeman A, Butler C (2010). Transient epileptic amnesia.
Curr Opin Neurol,
23(6), 610-616.
Abstract:
Transient epileptic amnesia.
PURPOSE OF REVIEW: Case reports over the past 100 years have raised the possibility that epilepsy can manifest itself in episodes of amnesia. Recent research has established that this is indeed the case, and indicates that characteristic varieties of interictal memory disturbance co-occur with this form of epilepsy. RECENT FINDINGS: Transient epileptic amnesia is a distinctive syndrome of temporal lobe epilepsy principally affecting middle-aged people, giving rise to recurrent, brief attacks of amnesia, often occurring on waking. It is associated with novel forms of interictal memory disturbance: accelerated long-term forgetting, remote memory impairment, especially affecting autobiographical memory, and topographical memory impairment. The seizure focus lies in the medial temporal lobes. The seizures respond promptly to treatment, whereas the interictal impairments generally persist. Further work is required to establish whether the interictal memory impairment is due to physiological or structural disturbance. SUMMARY: Transient epileptic amnesia is an under-recognized but treatable cause of transient memory impairment. Accelerated long-term forgetting and autobiographical amnesia, which are invisible to standard memory tests, help to explain the discrepancy between normal test performance and prominent memory complaints among patients with epilepsy. Further investigation of these forms of memory impairment promises to shed light on processes of human memory.
Abstract.
Author URL.
Laureys S, Celesia GG, Cohadon F, Lavrijsen J, León-Carrión J, Sannita WG, Sazbon L, Schmutzhard E, von Wild KR, Zeman A, et al (2010). Unresponsive wakefulness syndrome: a new name for the vegetative state or apallic syndrome.
BMC Med,
8Abstract:
Unresponsive wakefulness syndrome: a new name for the vegetative state or apallic syndrome.
BACKGROUND: Some patients awaken from coma (that is, open the eyes) but remain unresponsive (that is, only showing reflex movements without response to command). This syndrome has been coined vegetative state. We here present a new name for this challenging neurological condition: unresponsive wakefulness syndrome (abbreviated UWS). DISCUSSION: Many clinicians feel uncomfortable when referring to patients as vegetative. Indeed, to most of the lay public and media vegetative state has a pejorative connotation and seems inappropriately to refer to these patients as being vegetable-like. Some political and religious groups have hence felt the need to emphasize these vulnerable patients' rights as human beings. Moreover, since its first description over 35 years ago, an increasing number of functional neuroimaging and cognitive evoked potential studies have shown that physicians should be cautious to make strong claims about awareness in some patients without behavioral responses to command. Given these concerns regarding the negative associations intrinsic to the term vegetative state as well as the diagnostic errors and their potential effect on the treatment and care for these patients (who sometimes never recover behavioral signs of consciousness but often recover to what was recently coined a minimally conscious state) we here propose to replace the name. CONCLUSION: Since after 35 years the medical community has been unsuccessful in changing the pejorative image associated with the words vegetative state, we think it would be better to change the term itself. We here offer physicians the possibility to refer to this condition as unresponsive wakefulness syndrome or UWS. As this neutral descriptive term indicates, it refers to patients showing a number of clinical signs (hence syndrome) of unresponsiveness (that is, without response to commands) in the presence of wakefulness (that is, eye opening).
Abstract.
Author URL.
2009
Muhlert N, Milton FN, Butler CR, Zeman A (2009). ACCELERATED LONG TERM FORGETTING OF REAL LIFE EVENTS IN PATIENTS WITH TRANSIENT EPILEPTIC AMNESIA.
Author URL.
Zeman AZJ (2009). Do you remember the TIME?. Transient Epileptic Amnesia: the TIME Project. Epilepsy Professional, 13, 10-14.
Demertzi A, Liew C, Ledoux D, Bruno M-A, Sharpe M, Laureys S, Zeman A (2009). Dualism persists in the science of mind.
Ann N Y Acad Sci,
1157, 1-9.
Abstract:
Dualism persists in the science of mind.
The relationship between mind and brain has philosophical, scientific, and practical implications. Two separate but related surveys from the University of Edinburgh (University students, n= 250) and the University of Liège (health-care workers, lay public, n= 1858) were performed to probe attitudes toward the mind-brain relationship and the variables that account for differences in views. Four statements were included, each relating to an aspect of the mind-brain relationship. The Edinburgh survey revealed a predominance of dualistic attitudes emphasizing the separateness of mind and brain. In the Liège survey, younger participants, women, and those with religious beliefs were more likely to agree that the mind and brain are separate, that some spiritual part of us survives death, that each of us has a soul that is separate from the body, and to deny the physicality of mind. Religious belief was found to be the best predictor for dualistic attitudes. Although the majority of health-care workers denied the distinction between consciousness and the soma, more than one-third of medical and paramedical professionals regarded mind and brain as separate entities. The findings of the study are in line with previous studies in developmental psychology and with surveys of scientists' attitudes toward the relationship between mind and brain. We suggest that the results are relevant to clinical practice, to the formulation of scientific questions about the nature of consciousness, and to the reception of scientific theories of consciousness by the general public.
Abstract.
Author URL.
Zeman AZJ (2009). Epilepsy, Deja vu, Automatisms. In Wilken P, Bayne T, Cleeremans A (Eds.) The Oxford Companion to Consciousness, Oxford University Press.
Butler C, Zeman A (2009). Syndromes of transient amnesia. In (Ed) The Neurology of Consciousness, 339-351.
Butler CR, Zeman AZJ (2009). TRANSIENT EPILEPTIC AMNESIA: a CASE REPORT WITH RADIOLOGICAL LOCALISATION.
Author URL.
Butler CR, Bhaduri A, Acosta-Cabronero J, Nestor PJ, Zeman A (2009). TRANSIENT EPILEPTIC AMNESIA: REGIONAL BRAIN ATROPHY AND ITS RELATION TO MEMORY DEFICITS.
Author URL.
Zeman A (2009). The problem of unreportable awareness.
Prog Brain Res,
177, 1-9.
Abstract:
The problem of unreportable awareness.
We tend to regard consciousness as a fundamentally subjective phenomenon, yet we can only study it scientifically if it has objective, publicly visible, manifestations. This creates a central, recurring, tension in consciousness science which remains unresolved. On one 'objectivist' view, consciousness is not merely revealed but endowed by the process of reporting which makes it publicly accessible. On a contrasting 'subjectivist' view, consciousness, per se, is independent of the possibility of report, and indeed will always remain beyond the reach of direct observation. I shall explore this tension with examples drawn from clinical neurology, cognitive neuroscience and philosophy. The underlying aim of the paper is to open up the simple but profoundly difficult question that lurks in the background of consciousness science: what is it that are studying?
Abstract.
Author URL.
Butler CR, Bhaduri A, Acosta-Cabronero J, Nestor PJ, Kapur N, Graham KS, Hodges JR, Zeman AZ (2009). Transient epileptic amnesia: regional brain atrophy and its relationship to memory deficits.
Brain,
132(Pt 2), 357-368.
Abstract:
Transient epileptic amnesia: regional brain atrophy and its relationship to memory deficits.
Transient epileptic amnesia (TEA) is a recently recognised form of epilepsy of which the principle manifestation is recurrent, transient episodes of isolated memory loss. In addition to the amnesic episodes, many patients describe significant interictal memory difficulties. Performance on standard neuropsychological tests is often normal. However, two unusual forms of memory deficit have recently been demonstrated in TEA: (i) accelerated long-term forgetting (ALF): the excessively rapid loss of newly acquired memories over a period of days or weeks and (ii) remote autobiographical memory loss: a loss of memories for salient, personally experienced events of the past few decades. The neuroanatomical bases of TEA and its associated memory deficits are unknown. In this study, we first assessed the relationship between subjective and objective memory performance in 41 patients with TEA. We then analysed MRI data from these patients and 20 matched healthy controls, using manual volumetry and voxel-based morphometry (VBM) to correlate regional brain volumes with clinical and neuropsychological data. Subjective memory estimates were unrelated to performance on standard neuropsychological tests but were partially predicted by mood, ALF and remote autobiographical memory. Manual volumetry identified subtle hippocampal volume loss in the patient group. Both manual volumetry and VBM revealed correlations between medial temporal lobe atrophy and standard anterograde memory scores, but no relation between atrophy and ALF or remote autobiographical memory. These results add weight to the hypothesis that TEA is a syndrome of mesial temporal lobe epilepsy. Furthermore, they suggest that although standard anterograde memory test performance is related to the degree of mesial temporal lobe damage, this is not true for ALF and autobiographical amnesia. It is possible that these unusual memory deficits have a more diffuse physiological basis rather than being a consequence of discrete structural damage.
Abstract.
Author URL.
Zeman A (2009). When a patient with epilepsy complains about poor memory.
Pract Neurol,
9(2), 85-89.
Abstract:
When a patient with epilepsy complains about poor memory.
Patients with epilepsy often complain of "poor memory". The first step in managing this complaint is a clinical evaluation to define and, if possible, quantify the problem. The memory difficulty may be entirely unconnected to the epilepsy. But if the two appear to be linked, establish whether the memory problem is due to the seizures themselves, the pathology that underlies the seizures, their treatment, or their psychological sequelae such as anxiety or depression. Further management depends on the cause, while practical advice on the amelioration of poor memory can be useful.
Abstract.
Author URL.
2008
Zeman A (2008). A Portrait of the Brain. London, Yale University Press.
Butler CR, Zeman A (2008). A case of transient epileptic amnesia with radiological localization.
Nat Clin Pract Neurol,
4(9), 516-521.
Abstract:
A case of transient epileptic amnesia with radiological localization.
BACKGROUND: a 54-year-old man presented to a cognitive disorders clinic having experienced recurrent episodes of transient amnesia over a number of years. The attacks often occurred on waking, did not affect other cognitive abilities such as perception, language or judgment, and typically lasted about half an hour. The attacks were sometimes associated with olfactory hallucinations. Between amnestic episodes, the patient noticed a gradual deterioration in his recall of remote events, despite normal performance on standard memory tests. INVESTIGATIONS: Physical examination, laboratory tests, EEG, MRI brain scan, PET imaging, and neuropsychological assessment. DIAGNOSIS: Transient epileptic amnesia. MANAGEMENT: Anticonvulsant medication.
Abstract.
Author URL.
Zeman A (2008). Consciousness: concepts, neurobiology, terminology of impairments, theoretical models and philosophical background. Handb Clin Neurol, 90, 3-31.
Zeman AZJ (2008). Does consciousness spring from the brain?. Dilemmas of awareness in practice and in theory. In Davies M, Weiskrantz L (Eds.) The Frontiers of Consciousness. Chichele Lectures, Oxford University Press.
Zeman AZJ (2008). Foreword. In Olins Alpert B (Ed) The Creative Ice Age Brain: cave art in the light of neuroscience, M.A.T. Foundation.
Ambrose T, Butler C, Myles L, Zeman A (2008). Pitfalls in the diagnosis of hydrocephalus.
Br J Hosp Med (Lond),
69(4), 192-195.
Abstract:
Pitfalls in the diagnosis of hydrocephalus.
Hydrocephalus is a life-threatening condition presenting with a wide range of symptoms to a variety of specialties. Resulting delays in diagnosis can be hazardous. Doctors in all specialties should be familiar with the protean presentations of hydrocephalus.
Abstract.
Author URL.
Shankar R, Jalihal V, Zeman A (2008). Pseudo-cataplexy.
Author URL.
Butler CR, Zeman AZ (2008). Recent insights into the impairment of memory in epilepsy: transient epileptic amnesia, accelerated long-term forgetting and remote memory impairment.
BRAIN,
131, 2243-2263.
Abstract:
Recent insights into the impairment of memory in epilepsy: transient epileptic amnesia, accelerated long-term forgetting and remote memory impairment
Complaints of memory difficulties are common among patients with epilepsy, particularly with temporal lobe epilepsy where memory-related brain structures are directly involved by seizure activity. However, the reason for these complaints is often unclear and patients frequently perform normally on standard neuropsychological tests of memory. In this article, we review the literature on three recently described and interrelated forms of memory impairment associated with epilepsy: (i) transient epileptic amnesia, in which the sole or main manifestation of seizures is recurrent episodes of amnesia; (ii) accelerated long-term forgetting, in which newly acquired memories fade over days to weeks and (iii) remote memory impairment, in which there is loss of memories for personal or public facts or events from the distant past. Accelerated long-term forgetting and remote memory impairment are common amongst patients with transient epileptic amnesia, but have been reported in other forms of epilepsy. Their presence goes undetected by standard memory tests and yet they can have a profound impact on patients lives. They pose challenges to current theoretical models of memory. We discuss the evidence for each of these phenomena, as well as their possible pathophysiological bases, methodological difficulties in their investigation and their theoretical implications.
Abstract.
Torrens L, Burns E, Stone J, Graham C, Wright H, Summers D, Sellar R, Porteous M, Warner J, Zeman A, et al (2008). Spinocerebellar ataxia type 8 in Scotland: frequency, neurological, neuropsychological and neuropsychiatric findings.
Acta Neurol Scand,
117(1), 41-48.
Abstract:
Spinocerebellar ataxia type 8 in Scotland: frequency, neurological, neuropsychological and neuropsychiatric findings.
OBJECTIVES: the objectives of this study were to: (i) establish whether the spinocerebellar ataxia type 8 (SCA 8) expansion is associated with ataxia in Scotland; (ii) test the hypothesis that SCA 8 is associated with neuropsychological impairment; and (iii) review neuroradiological findings in SCA 8. METHODS: the methods included: (i) measurement of SCA 8 expansion frequencies in ataxic patients and healthy controls; (ii) comprehensive neuropsychological assessment of patients with SCA 8 and matched controls, neuropsychiatric interview; and (iii) comparison of patient and matched control magnetic resonance imaging (MRI) scans. RESULTS: (i) 10/694 (1.4%) unrelated individuals with ataxia had combined CTA/CTG repeat expansions >100 compared to 1/1190 (0.08%) healthy controls (P < 0.0005); (ii) neuropsychological assessment revealed a dysexecutive syndrome among SCA 8 patients, not readily explained by motor or mood disturbance; neuropsychiatric symptoms occurred commonly; (iii) cerebellar atrophy was the only salient MRI abnormality in the patient group. CONCLUSIONS: the SCA 8 expansion is associated with ataxia in Scotland. The disorder is associated with a dysexecutive syndrome.
Abstract.
Author URL.
Butler C, Zeman A (2008). Transient epileptic amnesia: Old syndrome or new? Reply.
ANNALS OF NEUROLOGY,
63(3), 409-409.
Author URL.
2007
Zeman A, McGonigle D, Gountouna E, Torrens L, Della Sala S, Logie R (2007). "Blind imagination'': Brain activation after loss of the mind's eye.
Author URL.
Zeman AZJ (2007). Conscience and Consciousness. In Walker G (Ed) The Science of Morality, Royal College of Physicians.
Zeman AZJ (2007). Diagnosis of brain death and persistent vegetative state. In (Ed) Reviews in Neurology, Continuing Medical Education Program of the Indian Academy of Neurology.
Stone J, Zeman A, Simonotto E, Meyer M, Azuma R, Flett S, Sharpe M (2007). FMRI in patients with motor conversion symptoms and controls with simulated weakness.
Abstract:
FMRI in patients with motor conversion symptoms and controls with simulated weakness.
Abstract.
Author URL.
Carson A, Zeman A, Myles L, Sharpe M (2007). Neurological Disorders. In Guthrie E, Lloyd G (Eds.) The Handbook of Liaison Psychiatry, University Press, Cambridge.
Carson AJ, Zeman A, Myles L, Sharpe M (2007). Neurology and Neurosurgery. In Levenson J (Ed) Essentials of Psychosomatic Medicine, American Psychiatric Publishing Incorporated, Washington DC.
Kalra S, Chancellor A, Zeman A (2007). Recurring déjà vu associated with 5-hydroxytryptophan.
Acta Neuropsychiatrica,
19(5), 311-313.
Abstract:
Recurring déjà vu associated with 5-hydroxytryptophan
Background: Déjà vu occurs both in normal experience and as a neuropsychiatric symptom. Its pathogenesis is partially understood. We describe an iatrogenic case with implications for the neuropharmacological basis of déjà vu. Case presentation: a 42-year-old woman received 5-hydroxytryptophan, in combination with carbidopa, as treatment for palatal tremor, on two occasions, separated by 1 week. On each occasion, she experienced intense, protracted déjà vu, lasting for several hours. We discuss her case in relation to the neuroanatomical and neuropharmacological basis of déjà vu. Conclusion: the serotonergic system is involved in the genesis of déjà vu. © 2007 Blackwell Munksgaard.
Abstract.
Zeman A (2007). Sherrington's philosophical writings--a 'zest for life'.
Brain,
130(Pt 8), 1984-1987.
Abstract:
Sherrington's philosophical writings--a 'zest for life'.
Sherrington's late writings are often described as dualistic, yet Sherrington was deeply uneasy with theories that radically separate mind and brain. His questioning, open-minded and historically-informed approach to their relationship eschews dogmatic solutions.
Abstract.
Author URL.
Butler CR, Graham KS, Hodges JR, Kapur N, Wardlaw JM, Zeman AZJ (2007). The syndrome of transient epileptic amnesia.
ANNALS OF NEUROLOGY,
61(6), 587-598.
Author URL.
2006
Zeman A, Carson A, Rivers C, Nath U (2006). A case of evolving post-ictal language disturbance secondary to a left temporal arteriovenous malformation: jargon aphasia or formal thought disorder?.
Cogn Neuropsychiatry,
11(5), 465-479.
Abstract:
A case of evolving post-ictal language disturbance secondary to a left temporal arteriovenous malformation: jargon aphasia or formal thought disorder?
INTRODUCTION: Wernicke's dysphasia and formal thought disorder are regarded as distinct diagnostic entities although both are linked to pathology in the left superior temporal gyrus (STG). We describe a patient with focal pathology in the left STG, giving rise acutely to a fluent dysphasia, which gradually evolved into formal thought disorder. METHOD: Clinical, neuropsychological, neuropsychiatric, and neuroradiological assessment. RESULTS: a right-handed patient, AJ, presented acutely with a fluent dysphasia. His speech output gradually evolved from undifferentiated jargon, through neologistic jargon, to an intelligible but bizarre form of discourse. Comprehension was relatively well preserved. Radiology revealed an arteriovenous malformation in the left middle, and inferior temporal gyri, with reduced perfusion of the left STG. Six months later his overt dysphasia had recovered, but his speech retained some of its previous characteristics, in particular a tendency to a loose association of ideas which now suggested a disorder of thought. CONCLUSIONS: AJ's case illustrates that comprehension may be unexpectedly preserved in jargon aphasia, and that an overtly linguistic impairment can gradually evolve to an apparent disorder of thought. Indistinguishable formal thought disorders can result from "structural" and "functional" pathology in the dominant temporal lobe.
Abstract.
Author URL.
Zeman AZJ (2006). Consciousness. In Hallett M (Ed) Psychogenic Movement Disorders, Lipincott, Williams and Wilkins, Philadelphia.
Wright H, Wardlaw J, Young AW, Zeman A (2006). Prosopagnosia following nonconvulsive status epilepticus associated with a left fusiform gyrus malformation.
Epilepsy Behav,
9(1), 197-203.
Abstract:
Prosopagnosia following nonconvulsive status epilepticus associated with a left fusiform gyrus malformation.
A 67-year-old, right-handed woman became unable to recognize familiar faces following a period of nonconvulsive status epilepticus. Neuropsychological assessment revealed a relatively selective impairment of familiar face recognition in the absence of low-level visual deficits or widespread cognitive impairment. MRI scanning demonstrated an isolated lesion, probably a venous angioma, involving the left fusiform gyrus, mirror-symmetrical to the site typically linked to prosopagnosia. Potential explanations for the patient's prosopagnosia include seizure-related damage to a left fusiform region required for fully competent face recognition and damage to the contralateral fusiform gyrus via interhemispheric connections. Focal neuropsychological deficits in patients with refractory partial epilepsy who develop nonconvulsive status epilepticus may be underdiagnosed.
Abstract.
Author URL.
Butler C, Zeman A (2006). Syndromes of transient amnesia. Advances in Clinical Neuroscience and Rehabilitation, 6, 13-14.
Zeman A (2006). What do we mean by "conscious" and "aware"?.
Neuropsychol Rehabil,
16(4), 356-376.
Abstract:
What do we mean by "conscious" and "aware"?
The concepts of consciousness and awareness are multifaceted, and steeped in cultural and intellectual history. This paper explores their complexities by way of a series of contrasts: (1) states of consciousness, such as wakefulness and sleep are contrasted with awareness, a term that picks out the contents of consciousness: these range across all our psychological capacities; the scientific background of the two concepts is briefly outlined; (2) consciousness is contrasted to self-consciousness, itself a complex term embracing self-detection, self-monitoring, self-recognition, theory of mind and self-knowledge; (3) "narrow" and "broad" senses of consciousness are contrasted, the former requiring mature human awareness capable of guiding action and self-report, the latter involving the much broader capacity to acquire and exploit knowledge; (4) an "inner" conception of consciousness, by which awareness is essentially private and beyond the reach of scientific scrutiny, is contrasted with an "outer" conception which allows that consciousness is intrinsically linked with capacities for intelligent behaviour; (5) finally "easy" and "hard" questions of consciousness are distinguished, the former involving the underlying neurobiology of wakefulness and awareness, the latter the allegedly more mysterious process by which biological processes generate experience: Whether this final distinction is valid is a focus of current debate. Varied interests converge on the study of consciousness from the sciences and the humanities, creating scope for interdisciplinary misunderstandings, but also for a fruitful dialogue. Health professionals treating disorders of consciousness should be aware both of its scientific complexities and of its broad cultural background, which influences the public understanding of these conditions.
Abstract.
Author URL.
2005
Zeman A, Torrens L, Sala SD, Logie R (2005). A case of blind imagination?.
Author URL.
Manes F, Graham KS, Zeman A, de Luján Calcagno M, Hodges JR (2005). Autobiographical amnesia and accelerated forgetting in transient epileptic amnesia.
J Neurol Neurosurg Psychiatry,
76(10), 1387-1391.
Abstract:
Autobiographical amnesia and accelerated forgetting in transient epileptic amnesia.
BACKGROUND: Recurrent brief isolated episodes of amnesia associated with epileptiform discharges on EEG recordings have been interpreted as a distinct entity termed transient epileptic amnesia (TEA). Patients with TEA often complain of autobiographical amnesia for recent and remote events, but show normal anterograde memory. OBJECTIVE: to investigate (a) accelerated long term forgetting and (b) autobiographical memory in a group of patients with TEA. METHODS: Seven patients with TEA and seven age matched controls were evaluated on a range of anterograde memory tasks in two sessions separated by 6 weeks and by the Galton-Crovitz test of cued autobiographical memory. RESULTS: Patients with TEA showed abnormal long term forgetting of verbal material, with virtually no recall after 6 weeks. In addition, there was impaired recall of autobiographical memories from the time periods 1985-89 and 1990-94 but not from 1995-1999. CONCLUSIONS: TEA is associated with accelerated loss of new information and impaired remote autobiographical memory. There are a number of possible explanations including ongoing subclinical ictal activity, medial temporal lobe damage as a result of seizure, or subtle ischaemic pathology. Future analyses should seek to clarify the relationship between aetiology, seizure frequency, and degree of memory impairment.
Abstract.
Author URL.
Zeidler M, Zeman A (2005). Can brain biopsy aid the diagnosis of dementia?.
NATURE CLINICAL PRACTICE NEUROLOGY,
1(2), 82-83.
Author URL.
Zeman A, Daniels G, Tilley L, Dunn M, Toplis L, Bullock T, Poole J, Blackwood D (2005). McLeod syndrome: life-long neuropsychiatric disorder due to a novel mutation of the XK gene.
Psychiatr Genet,
15(4), 291-293.
Abstract:
McLeod syndrome: life-long neuropsychiatric disorder due to a novel mutation of the XK gene.
A 50-year-old man presented with worsening, virtually lifelong, chorea and progressive behavioural disturbance, involving disinhibition and hoarding, over 10 years. Clinical assessment revealed chorea, dysarthria, areflexia, an inappropriately jovial, impulsive manner and neuropsychological evidence of frontosubcortical dysfunction. Investigation results included an elevated creatine kinase, caudate atrophy and hypoperfusion, acanthocytes in the peripheral blood and the McLeod phenotype. DNA studies demonstrated a single-base deletion at position 172 in exon 1 of the XK gene, giving rise to a premature stop codon at position 129 in exon 2.
Abstract.
Author URL.
Zeman A, Butler C (2005). Neurological syndromes which can be mistaken for psychiatric conditions. Journal of Neurology Neurosurgery & Psychiatry, 76(suppl_1), 31-38.
Carson A, Zeman A, Myles L, Sharpe M (2005). Neurology and Nuerosurgery. In Levenson J (Ed) The American Psychiatric Textbook of Psychosomatic Medicine, Washington: American Psychiatric Press Incorporated.
Zeman A (2005). Tales from the temporal lobes.
N Engl J Med,
352(2), 119-121.
Author URL.
Zeman A, Reading P (2005). The science of sleep.
Clin Med (Lond),
5(2), 97-101.
Author URL.
Butler CR, Zeman AZJ (2005). Time - a study of epileptic amnesia.
Author URL.
Zeman A (2005). What in the world is consciousness?. In Laureys S (Ed) The Boundaries of Consciousness, Amsterdam: Elsevier.
2004
Zeman A (2004). Conference report - ASSC 8. Journal of Consciousness Studies, 11(9), 70-75.
Zeman A, Britton T, Douglas N, Hansen A, Hicks J, Howard R, Meredith A, Smith I, Stores G, Wilson S, et al (2004). Narcolepsy and excessive daytime sleepiness.
BMJ,
329(7468), 724-728.
Author URL.
Zeman A, Shenton G (2004). Neuroacanthocytosis. Practical Neurology, 4, 298-301.
Carson A, Zeman A, Brown TM, Sharpe M (2004). Organic Psychiatry. In Jonstone EC (Ed) Companion to Psychiatric Studies, Edinburgh: Churchill Livingstone.
Zeman A (2004). Soul made flesh - the discovery of the brain - and how it changed the world.
NEW YORK TIMES BOOK REVIEW, 16-16.
Author URL.
Zeman A, Burns E, Porteus M, Stone J (2004). Spinocerebellar ataxia type 8 in Scotland: genetic and clinical features in 7 unrelated cases and a review of the literature. Journal of Neurology Neurosurgery & Psychiatry, 75(3), 459-465.
Zeman A (2004). The concept of consciousness.
Author URL.
Zeman A (2004). Theories of visual awareness. In (Ed) Progress in Brain Research, Elsevier, 321-329.
Zeman A (2004). Theories of visual awareness. In (Ed)
, 321-329.
Abstract:
Theories of visual awareness.
Abstract.
Author URL.
2003
Warren-Gash C, Zeman A (2003). A study of deja vu in patients with temporal lobe epilepsy, students, and neurology outpatients.
Author URL.
Louis-Auguste J, Zeman A (2003). A study of impaired awareness due to stroke.
Author URL.
Warren-Gash C, Zeman A (2003). Déjà vu. Practical Neurology, 3(2), 106-109.
. (2003). The Vegetative State. Guidance on diagnosis and management. Report of a working party of the Royal College of Physicians, RCP.
Zeman A (2003). What is consciousness and what does it mean for the persistent vegetative state?. Advances in Clinical Neuroscience and Rehabilitation, 3, 12-14.
2002
Al-Shahi R, Scolding NJ, Bell JE, Zeman AZ, Warlow CP (2002). A young man with a fatal encephalopathy. Practical Neurology, 2(1), 26-35.
Zeman AZJ (2002). Consciousness. In Nadel L (Ed) Macmillan Encyclopaedia of Cognitive Science, Nature Publishing.
Zeman A (2002). Consciousness: a User's Guide. Yale, Yale University Press.
Stone J, Zeman A, Sharpe M (2002). Functional weakness and sensory disturbance.
J Neurol Neurosurg Psychiatry,
73(3), 241-245.
Abstract:
Functional weakness and sensory disturbance.
In the diagnosis of functional weakness and sensory disturbance, positive physical signs are as important as absence of signs of disease. Motor signs, particularly Hoover's sign, are more reliable than sensory signs, but none should be used in isolation and must be interpreted in the overall context of the presentation. It should be borne in mind that a patient may have both a functional and an organic disorder.
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Zeman AZJ (2002). Guidelines for the Management of Narcolepsy in Children and Adults. Report of an interdisciplinary working party. Taylor Patten Communications.
Zeman A (2002). The persistent vegetative state: conscious of nothing?. Practical Neurology, 2, 214-217.
2001
Zeman A (2001). Consciousness.
BRAIN,
124, 1263-1289.
Author URL.
Stone J, Zeman A (2001). Conversion hysteria: the view from neurology. In Halligan P, Bass C, Marshall J (Eds.) Conversion Hysteria, Oxford: Oxford University Press.
Zeman A, Narcolepsy MGW (2001). Evidence based guidelines for the management of narcolepsy.
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY,
71(3), 424-424.
Author URL.
Manes, F. Hodges, J.R. Graham, K.S. (2001). Focal autobiographical amnesia in association with transient amnesia. Brain, 124(3), 499-509.
Stone J, Smith L, Watt K, Barron L, Zeman A (2001). Incoordinated thought and emotion in spinocerebellar ataxia type 8.
J Neurol,
248(3), 229-232.
Author URL.
Zeman A, Douglas N, Aylward R (2001). Narcolepsy mistaken for epilepsy. British Medical Journal, 322(7280), 216-217.
Zeman A, Stone J, Porteous M, Barron L, Warner J (2001). Study of the neurological, cognitive, and behavioural features of spinocerebellar ataxia type 8.
JOURNAL OF NEUROLOGY NEUROSURGERY AND PSYCHIATRY,
71(3), 420-420.
Author URL.
2000
Zeidler M, Hughes T, Zeman A (2000). Confused by arteritis.
Lancet,
355(9201).
Author URL.
Zeman AZJ, Emanuel L (2000). Ethical Dilemmas in Neurology. In (Ed) Major Problems in Neurology, W B Saunders, London.
Zeman A, Hodges J (2000). Transient global amnesia and transient eplieptic amnesia. In Berrios G, Hodges J (Eds.) Memory Disorders in Psychiatric Practice, Cambridge: Cambridge University Press.
1999
Graham NL, Zeman A, Young AW, Patterson K, Hodges JR (1999). Dyspraxia in a patient with corticobasal degeneration: the role of visual and tactile inputs to action.
J Neurol Neurosurg Psychiatry,
67(3), 334-344.
Abstract:
Dyspraxia in a patient with corticobasal degeneration: the role of visual and tactile inputs to action.
OBJECTIVES: to investigate the roles of visual and tactile information in a dyspraxic patient with corticobasal degeneration (CBD) who showed dramatic facilitation in miming the use of a tool or object when he was given a tool to manipulate; and to study the nature of the praxic and neuropsychological deficits in CBD. METHODS: the subject had clinically diagnosed CBD, and exhibited alien limb behaviour and striking ideomotor dyspraxia. General neuropsychological evaluation focused on constructional and visuospatial abilities, calculation, verbal fluency, episodic and semantic memory, plus spelling and writing because impairments in this domain were presenting complaints. Four experiments assessed the roles of visual and tactile information in the facilitation of motor performance by tools. Experiment 1 evaluated the patient's performance of six limb transitive actions under six conditions: (1) after he described the relevant tool from memory, (2) after he was shown a line drawing of the tool, (3) after he was shown a real exemplar of the tool, (4) after he watched the experimenter perform the action, (5) while he was holding the tool, and (6) immediately after he had performed the action with the tool but with the tool removed from his grasp. Experiment 2 evaluated the use of the same six tools when the patient had tactile but no visual information (while he was blindfolded). Experiments 3 and 4 assessed performance of actions appropriate to the same six tools when the patient had either neutral or inappropriate tactile feedback-that is, while he was holding a non-tool object or a different tool. RESULTS: Miming of tool use was not facilitated by visual input; moreover, lack of visual information in the blindfolded condition did not reduce performance. The principal positive finding was a dramatic facilitation of the patient's ability to demonstrate object use when he was holding either the appropriate tool or a neutral object. Tools inappropriate to the requested action produced involuntary performance of the stimulus relevant action. CONCLUSIONS: Tactile stimulation was paramount in the facilitation of motor performance in tool use by this patient with CBD. This outcome suggests that tactile information should be included in models which hypothesise modality specific inputs to the action production system. Significant impairments in spelling and letter production that have not previously been reported in CBD have also been documented.
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Zeman AZ (1999). Episodic memory in transient global amnesia.
J Neurol Neurosurg Psychiatry,
66(2).
Author URL.
Halligan PW, Zeman A, Berger A (1999). Phantoms in the brain. British Medical Journal, 319(7210), 587-588.
1998
Zeman A (1998). The consciousness of sight.
BMJ,
317(7174), 1696-1697.
Author URL.
Zeman AZ, Boniface SJ, Hodges JR (1998). Transient epileptic amnesia: a description of the clinical and neuropsychological features in 10 cases and a review of the literature.
J Neurol Neurosurg Psychiatry,
64(4), 435-443.
Abstract:
Transient epileptic amnesia: a description of the clinical and neuropsychological features in 10 cases and a review of the literature.
OBJECTIVES: to clarify the clinical and neuropsychological aspects of transient epileptic amnesia (TEA) based on 10 personally studied cases as well as review of 21 previously published cases; and to propose tentative diagnostic criteria for the diagnosis of TEA. METHODS: all 10 patients and informants underwent a standardised clinical interview. The radiological and neurophysiological (EEG) data were also reviewed in all cases. The diagnosis of transient epileptic amnesia was made on the basis of the following criteria: (1) there was a history of recurrent witnessed episodes of transient amnesia; (2) cognitive functions other than memory were judged to be intact during typical episodes by a reliable witness; (3) there was evidence for a diagnosis of epilepsy. This evidence was provided by either (a) wake or sleep EEG, or (b) the co-occurrence of other seizure types (if their roughly concurrent onset or close association with episodes of transient amnesia suggested a connection), or (c) a clear cut response to anticonvulsant therapy, or by a combination of these three factors. In addition all patients were administered a comprehensive neuropsychological test battery designed to assess verbal and non-verbal anterograde memory and retrograde memory for famous personalities and personal events. Their results were compared with those of 25 age and IQ matched normal controls. RESULTS: TEA usually begins in later life, with a mean age of 65 years in this series. Episodes are typically brief, lasting less than one hour, and recurrent, with a mean frequency of three a year. Attacks on waking are characteristic. Repetitive questioning occurs commonly during attacks. The anterograde amnesia during episodes is, however, often incomplete so that patients may later be able to "remember not being able to remember". The extent of the retrograde amnesia during attacks varies from days to years. Most patients experience other seizure types compatible with an origin in the temporal lobes, but transient amnesia is the only manifestation of epilepsy in about one third of patients. Epileptiform abnormalities arising from the temporal lobes are most often detected on interictal sleep EEG. Despite normal performance on tests of anterograde memory, many patients complain of persistent interictal disturbance of autobiographical memory, involving a significant but variable loss of recall for salient personal episodes. The epochs affected may predate the onset of epilepsy by many years. CONCLUSIONS: TEA is an identifiable syndrome and comprises episodic transient amnesia with an epileptic basis, without impairment of other aspects of cognitive function. Future studies should consider the question of whether TEA reflects ictal activity or a postictal state, and the mechanism of the persistent autobiographical amnesia. It is hypothesised that the latter may result in part from impairment of very long term memory consolidation as a result of epileptic activity in mesial temporal structures.
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1997
Zeman AZ, Grayling AC, Cowey A (1997). Contemporary theories of consciousness.
J Neurol Neurosurg Psychiatry,
62(6), 549-552.
Author URL.
Zeman A (1997). Persistent vegetative state.
Lancet,
350(9080), 795-799.
Author URL.
Zeman AZ, Hodges JR (1997). Transient global amnesia.
Br J Hosp Med,
58(6), 257-260.
Abstract:
Transient global amnesia.
Transient global amnesia is an alarming but benign disorder of middle age, which prevents both the formation of new memories, and the retrieval of recently formed ones, for some hours. Research over the last 10 years has shed light on the epidemiology, neuropsychology, functional anatomy and differential diagnosis of this distinctive condition, and clarified its management.
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1994
ZEMAN AZJ, KEIR G, LUXTON R, THOMPSON EJ, MILLER D, MCDONALD WI (1994). OLIGOCLONAL BANDS IN MULTIPLE-SCLEROSIS - RECENT FINDINGS, FUTURE USES.
ANNALS OF NEUROLOGY,
36(2), 325-325.
Author URL.
1993
Zeman A, McLean B, Keir G, Luxton R, Sharief M, Thompson E (1993). The significance of serum oligoclonal bands in neurological diseases.
J Neurol Neurosurg Psychiatry,
56(1), 32-35.
Abstract:
The significance of serum oligoclonal bands in neurological diseases.
The presence of oligoclonal bands (OCBs) of immunoglobulin G (IgG) in CSF provides evidence for the occurrence of a humoral immune response, but it is not always appreciated that the oligoclonal IgG may have originated in the serum. To determine the diagnostic significance of serum OCBs 146 patients with serum OCBs were identified among 1874 patients with suspected neurological disorders (7.6%). Clear diagnoses had been made in 112 of these patients: in 56 identical CSF and serum bands were present, revealing a systemic immune response, while in 46 additional unique CSF bands indicated that intrathecal IgG synthesis was also occurring. In the first group neoplasia and peripheral neuropathies accounted for over 50% of the diagnoses, infections and systemic inflammatory disorders for 32%, and multiple sclerosis was diagnosed in only one case. These figures contrast considerably with those reported for patients with CSF OCBs alone. Diagnoses in the second group of patients, with unique CSF OCBs in addition to serum OCBs, resembled those among patients with CSF OCBs alone. Examining CSF and serum in parallel for OCBs of IgG provides more diagnostic information than examining CSF alone, and the latter is potentially misleading.
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