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a University of Cambridge Neurology Unit, b Department of Clinical
Neurophysiology, Addenbrooke's Hospital, Hills Road, Cambridge, UK, c MRC Applied Psychology Unit, 15 Chaucer
Rd, Cambridge, UK
Correspondence to: Professor J R Hodges, MRC Applied Psychology Unit, 15 Chaucer Rd,Cambridge CB2 2QQ, UK. Telephone 0044 1223 245151; fax: 0044 1223 336941.
Received 30 April 1997 and in revised form 21 July 1997;
Accepted 29 July 1997
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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