One patient had a history of seizures on two occasions in the past, possibly related to alcohol withdrawal, but no evidence of seizure at the time of assessment. Another patient had witnessed seizure activity during transport to the emergency department, but had no history of seizures. A third patient developed a seizure disorder after evaluation for the amnestic episode. No epileptiform abnormalities were noted on electroencephalography (EEG) at the time of initial evaluation in these three patients or in eight others who underwent EEG.
Six patients had history of at least one vascular disease risk, including hypertension, dyslipidemia, diabetes, and sleep apnea. Echocardiogram performed in six patients, and vessel imaging of the head and neck performed in seven patients, did not reveal a source of thromboembolism. Electrocardiogram revealed a new diagnosis of atrial fibrillation in the two oldest patients (aged 50 and 52 years). One patient aged 36 years demonstrated pulseless electrical activity and respiratory arrest (after a documented brief response to naloxone), with resolution on prehospital resuscitation. Cerebrospinal fluid findings in five patients who underwent lumbar puncture were unremarkable. Carboxyhemoglobin and methemoglobin levels were measured in two patients and were unremarkable. Initial aspartate and alanine aminotransferase were elevated in all 13 patients tested, with both levels in one patient exceeding 500 units/liter (approximately 10 times the upper limit of normal). Otherwise, extensive work-up was unremarkable. Investigation of the 14 cases is ongoing.
Discussion
The combination of clinical findings described in this report has previously been reported rarely and in isolation, associated with isolated cocaine use, influenza, and carbon monoxide poisoning.2–6 This cluster of amnestic syndrome associated with bilateral complete hippocampal ischemia is unusual given the absence of a readily identifiable etiology, the temporospatial clustering, relatively young patient age, and extensive substance use among affected persons.
Cardiopulmonary, cerebrovascular, or other mechanisms might serve as plausible explanations underlying certain findings. Hypoxemic injury to the relatively vulnerable hippocampal regions, for example, has been raised as one possibility.10 However, further case identification and reporting are needed to determine whether these combined observations represent an emerging syndrome related to substance use or other causes (e.g., a toxic exposure).
The findings in this report are subject to at least three limitations. First, information was obtained from medical records from several different facilities, and differences in documentation and medical assessment across patients limited the consistent characterization of variables. Second, this investigation was intended to establish the existence of the case cluster and generate hypotheses about possible associated exposures. A case-control study could more rigorously test potential associations. Finally, the identification of cases required that MRI of the head had been performed during patient work-up, which might not be consistently performed by medical providers for various reasons.
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