European Journal of Neurology 2005, 12: 805–806
SHORT COMMUNICATION
Temporal lobe epileptic activity mimicking dementia: a case report M. Tombinia,b, G. Kocha,c, F. Placidia,c, G. Sancesarioa, M. G. Marciania,c and G. Bernardia,c a
Dipartimento di Neuroscienze, Universita` di Roma Tor Vergata, V.le Oxford 81, Rome, Italy; bDipartimento di Neurologia, Universita`
Campus Bio-Medico, Rome, Italy; and cFondazione Santa Lucia, IRCCS, Rome, Italy
Keywords:
arachnoid cysts, dementia, electroencephalogram, memory, temporal lobe epileptic activity Received 15 May 2004 Accepted 4 October 2004
Epileptic activity is an underdiagnosed cause that can determine a disruption of memory and cognitive performance, leading an incorrect diagnosis of dementia. We report a 68-year-old man, referred with a 5-year history of subtle behavioral changes and a subjective memory impairment, who was admitted to our department because of recurrent episodes of confusional state lasting from 1 week. Neuropsychological evaluation demonstrated a marked impairment of all cognitive domains examined. Electroencephalogram (EEG) recording showed frequent almost continuous sharp waves localized on the bilateral posterior temporal regions with mild right side predominance. Treatment with phenytoin reversed his cognitive dysfunction and behavioral disturbances. We presume that ictal temporal lobe epileptiform activity is the cause of his confusional episodes and cognitive dysfunction, showing an electroclinical picture of complex partial status epilepticus. However, we hypothesize that the interictal discharges and ictal and postictal effects of subclinical seizures could be involved in the behavioral changes and memory impairment complained by our patient in the last years.
Epileptic activity is an underdiagnosed cause that can determine a disruption of memory and cognitive performance, leading an incorrect diagnosis of dementia. We report a 68-year-old man admitted to our department because of recurrent episodes of confusional state lasting from 1 week. His medical history was unremarkable apart from a recent diagnosis of hypertension. Five years ago he started showing subtle behavioral changes with tendency to apathy and indifference, and a subjective memory impairment. A provisional diagnosis of mild deterioration of cognitive function was made. At the time of our observation he appeared perplexed, confused and disoriented. He did not speak fluently and he scored 15/30 on the Mini-Mental State Examination (MMSE). Remaining neurological and general examinations were normal. The day after the admission he underwent neuropsychological evaluation, which demonstrated a marked impairment of all cognitive domains examined. Blood tests exploring kidney, liver and thyroid function, B 12 and folate levels, serologic tests for syphilis and cerebrospinal fluid analysis did not reveal any significant alteration. Brain magnetic resonance imaging showed a mild ischemic periventricular leukoencephalopathy with cortical atrophy and an enlargement of overlying subCorrespondence: Mario Tombini MD, Policlinico Universitario ÔCampus Bio-MedicoÕ, Via dei Compositori, 130–132, 00128 Trigoria, Rome, Italy (tel.: +39 06 2254 1600; fax: +39 06 2254 1602; e-mail:
[email protected]).
Ó 2005 EFNS
arachnoid spaces; two bilateral arachnoid cysts localized in the left insular cistern and right anterior temporal region were also revealed. Electroencephalogram (EEG) recording showed frequent almost continuous sharp waves localized on the bilateral posterior temporal regions with mild right side predominance, with superimposed spikes of little amplitude (Fig. 1). As the patient did not show convulsive symptoms dangerous for his life, oral administration of phenytoin (200 mg/day) was started, in order to avoid possible risks of hypotension and cardiac arrhythmias associated with parenteral treatment. Since the next day he showed a progressive electroclinical improvement up to
Figure 1 EEG performed the day after the admission, showing frequent, almost continuous sharp waves localized on the bilateral posterior temporal regions with mild right side predominance, with superimposed spikes of little amplitude. Eye opening (EO) does not modify abnormal activity evident at rest with eyes closed (EC) (high frequency filter 50 Hz and time constant 0.3 s).
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a nearly complete normalization; at discharge he scored 30/30 on the MMSE. Reassessment of cognitive function after 1 month revealed normal performances in all domains examined except a mild impairment of longterm verbal memory. Disturbance of memory with temporal lobe epileptic activity is consistent with the postulated role of the medial temporal lobe structures in episodic memory function (Høgh et al., 2002). Interictal temporal lobe epileptiform activity has been also related with autobiographical memory and cognitive impairment observed in some patients (Tatum et al., 1998; Zeman et al., 1998). Both the ictal effects of the seizures themselves, postictal effects and the effects of the interictal epileptiform EEG discharges may have an impact on cognitive performance (Aldenkamp et al., 1996). In our patient treatment with phenytoin reversed his cognitive dysfunction and behavioral disturbances; only a mild long-term memory deficit persisted after therapy. We presume that ictal temporal lobe epileptiform activity is the cause of his confusional episodes and cognitive dysfunction, showing an electroclinical picture of complex partial status epilepticus. However, we hypothesize that the interictal discharges and ictal and postictal effects of subclinical seizures could be
involved in the behavioral changes and memory impairment complained by our patient in the last years, leading an incorrect diagnosis of dementia. Moreover, according to previous reports (Arroyo and Santamaria, 1997) the EEG ictal abnormalities do not seem to be closely related to the arachnoid cysts. The ischemic leukoencephalopathy could be the most probably cause of the epileptic activity.
References Aldenkamp AP, Overweg J, Gutter TH, Beun AM, Diepman L, Mulder OG (1996). The effect of epilepsy, seizures and epileptiform EEG discharges on cognitive function. Acta Neurol Scand 93:253–259. Arroyo S, Santamaria J (1997). What is the relationship between arachnoid cysts and seizure foci? Epilepsia 38:1098–1102. Høgh P, Smith SJ, Scahill RI et al. (2002). Epilepsy presenting as AD: neuroimaging, electroclinical features, and response to treatment. Neurology 58:298–301. Tatum WO, Ross J, Cole AJ (1998). Epileptic pseudodementia. Neurology 50:1472–1475. 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 64:435–443.
Ó 2005 EFNS European Journal of Neurology 12, 805–806
