Tatum, W. O. IV DO; Ross, J. MD; Cole, A. J. MD
Dementia is a frequent cause of memory loss with aging. The incidence of complex partial seizures sharply rises after age 60. Complex partial seizures that occur with subtle clinical signs or loss of awareness, or occur during sleep may defy identification. We report five elderly patients fearing dementia in whom memory dysfunction was due to unrecognized complex partial seizures.
Dementia is a common neuropsychiatric condition occurring in 5 to 11% of the population by age 65 and up to 50% beyond age 85.1 Alzheimer's disease (AD) is the fourth leading cause of death, a major cause of morbidity, and a significant concern for the aged population. Multiple medical conditions are known to result in dementia. Evaluation to exclude treatable causes of cognitive dysfunction is essential for proper diagnosis and treatment.
The prevalence of seizures is highest early in life and peaks again after age 60.2 Complex partial seizures represent more than 50% of new seizure cases in the elderly. Complex partial seizures manifest some combination of altered awareness and amnesia during an attack. Recurrent partial seizures causing transient amnesia have previously been recognized.3,4
We report five elderly patients who presented with memory impairment masquerading as dementia caused by serial complex partial seizures. Ictal recordings confirmed the diagnosis after initial EEGs were nondiagnostic. Multiple complex partial seizures were recorded in three patients. Four patients improved with antiepileptic drugs (AEDs).
|Table Summary of clinical data on patients with epileptic pseudodementia|
|Figure. Representative EEG taken from Patient 2.|
Representative case report. A 70-year-old man presented to a memory disorders clinic with memory loss and confusion. He had no significant past medical history and was taking no medication. He complained of increasing emotional lability with periods when he would feel "spacey" and mumble, with facial flushing. Impaired consciousness was absent. This occurred one to two times per month initially and then became continuous at the time of presentation. Neurologic examination was normal except for mild declarative memory deficits on mental status testing. Brain MRI revealed mild white matter changes and two lacunar infarcts. EEG demonstrated intermittent left temporal slowing. Repeat EEG captured an electrographic partial seizure emanating from the left temporal region appearing clinically as prominent amnesia. Treatment with carbamazepine resulted in resolution of memory loss and confusion.
Discussion. Amnesia for the ictus is a feature of complex partial seizures with variable periods of anterograde amnesia postictally. Blum et al.,5 during presurgical evaluation of intractable epilepsy with inpatient video EEG, found that 30% of patients were unaware of their seizures. Gallassi et al.3 reported 13 patients with brief "epileptic amnesic attacks" that appeared to be a distinct form of temporal lobe epilepsy. Halgren et al.6 reproduced disruption of memory formation and retrieval with bitemporal electrical stimulation. Bridgman et al.7 using intracranial electrodes found that recurrent focal hippocampal subclinical seizures were capable of limiting memory recall.
Amnesia as an isolated manifestation of seizures is rare. Palmini et al.4 postulated that "pure amnestic seizures" resulted from selective ictal inactivation of the mesial temporal structures without cortical involvement. Epileptic amnesia has been viewed as a Todd's paralysis of the limbic system with neocortical recovery. Clinical assessment during long-term monitoring demonstrated persistent subjective memory complaints in our patients despite return of baseline EEG between electrographic seizures. Our findings agree with Tassinari et al.,8 who previously described "epileptic transient global amnesia" as a postictal phenomenon in a patient using video EEG monitoring. Various degrees of peri-ictal anterograde an retrograde memory disturbance may occur.
All our patients initially complained of memory difficulties fearing AD. Memory loss with a waxing and waning course was described by all. Patients 3 and 5 had more discrete episodes of memory impairment lasting from 30 to 45 minutes to several days. These identifiable episodes are similar to"epileptic amnestic attacks." However, the duration of memory deficit in our patients was more prolonged and less discrete. Patients 2 and 4 had nocturnal seizures recognized only by the daytime sequelae. The heterogeneity of presentation supports the concept of an epileptic amnestic syndrome defined by Gallassi et al.3 Three of our patients had resolution of memory deficits with AED treatment. One patient improved with treatment, and one required an assisted care living facility because of memory impairment after declining AED treatment.
Formal neuropsychological testing in Patients 1 and 3 and the Mini-Mental State Examination in Patients 2, 4, and 5 demonstrated immediate memory deficits without global cognitive dysfunction. No progression of memory dysfunction was noted on follow-up testing in Patients 2 and 3, and no patient had objective evidence for dementia despite memory impairment.
Declarative memory likely involves hippocampal-entorhinal cortical connections for maintaining information; however, integration, indexing, processing, and storage depend on additional cortical projections. Hippocampal neuropathology coexisting with diffuse neocortical atrophy may be the neuroanatomic substrate for compromised retrieval and deficient storage mechanisms. Recurrent Complex partial seizures may therefore lead to prolonged episodes of postictal memory dysfunction in elderly patients. Our first patient had right hippocampal atrophy on MRI with complex partial seizures originating from the left temporal lobe. Although atrophy may occur with aging, the possibility of bilateral hippocampal dysfunction created by both a structural and epileptogenic mechanism together may exist. Two of our patients demonstrated atrophy on brain MRI, and two patients had white matter ischemic changes. Such findings are frequent in elderly populations where unrecognized anatomic abnormalities may become clinically evident when complex partial seizures occur.
Seizures are usually diagnosed based on historical information supported with EEG. Approximately half of epilepsy patients have interictal epileptiform discharges (IEDs) on initial EEG. Still, some may not reveal IEDs despite repeated recording.9 All our patients had initial nondiagnostic EEGs. Electrographic partial seizures suggesting left temporal origin were captured in four patients. Seizure awareness has been noted to be lowest for left temporal seizures in one series.5 In one patient (Patient 3), ictal recording was obscured by artifact during an event designated as "memory lapse" on event diary. Subsequently, 24-hour inpatient video EEG captured no episodes.
We conclude that memory dysfunction may be caused by complex partial seizures and may present in two ways: discrete episodes of amnesia may occur or, alternatively, an insidious fluctuating course of memory dysfunction may simulate dementia. Prolonged EEG may help define an epileptogenic basis in patients with atypical or fluctuating dementia even when a routine EEG is normal. Subclinical, clinically subtle, or purely nocturnal partial seizures with amnesia may be detected by EEG. Frequent electrographic seizures may exist without apparent clinical signs. We recommend that a heightened level of suspicion for complex partial seizures in the elderly should be maintained. Epileptic pseudodementia represents a potentially reversible cause of memory dysfunction.
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