Consequently, transient epileptic amnesia may be readily misdiagnosed as a nonepileptic memory dysfunction in older individuals. These findings support the theory of a Todd phenomenon as the underlying pathophysiological mechanism in transient epileptic amnesia.ĪB - Transient epileptic amnesia is a rare but probably underrecognized form of temporal lobe epilepsy, which typically manifests as episodic isolated memory loss. hours after the occurrence of a brief focal seizure. Prolonged postictal slowing in the mesial temporal structures was evident on invasive electroencephalography 5. We describe a patient with drug-resistant transient epileptic amnesia treated with unilateral temporal lobectomy. When appropriately recognized, it has been described as a treatment-responsive syndrome amenable to antiepileptic drugs. Conclusion: As approximately every tenth patient with suspected TGA either had an alternative diagnosis or a severe comorbidity, which had not been obvious at the time of admission, we consider in-patient treatment of all suspected TGA cases as appropriate, preferably in the setting of a stroke unit, as ischemic stroke was the by far most important diagnosis mimicking TGA.N2 - Transient epileptic amnesia is a rare but probably underrecognized form of temporal lobe epilepsy, which typically manifests as episodic isolated memory loss. Important comorbidities that had not been obvious at the time of presentation were severe sleep apnea (2 patients), triptan overuse (1 patient), and an involuntary amlodipine intoxication during TGA. Other mimics were transient epileptic amnesia (2 patients) and steroid-induced delirium (1 patient). The most important differential diagnosis was stroke (11 patients, 6.6% of all TGA suspects and 61.1% of the complicated TGA/mimic group). Eighteen patients (10.8%) either had an alternative diagnosis or a severe comorbidity that was assumed to have had an impact on the occurrence of the amnestic episode (“complicated TGA/mimic”). After the workup, the diagnosis of TGA was confirmed in 148/166 (89.2%) episodes (“simple TGA”). Results: 163 patients with 166 episodes of suspected TGA were hospitalized (3 patients twice). All patients were hospitalized and received a neurological workup including brain imaging, color-coded duplex sonography of the brain supplying arteries, electroencephalography, and laboratory studies of blood and (in selected cases) cerebrospinal fluid. Methods: We evaluated the medical records and the imaging data of an unselected consecutive cohort of patients with suspected TGA over a 7-year period. The aim of our study was to assess the frequency of a severe underlying disease or alternative diagnoses (mimics) in patients fulfilling the clinical criteria. Most neurological guidelines allow the diagnosis on the basis of clinical criteria only a more extensive evaluation is recommended only for patients with “red flags” like severe headache, nausea or vomiting, or metabolic abnormalities. Its etiology is still a matter of debate. Background: Transient global amnesia (TGA) is a syndrome featuring acute anterograde amnesia as the most striking clinical symptom.
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