Aphasic status epilepticus in a tertiary referral center in Turkey: Clinical features, etiology, and outcome

De novo aphasic status epilepticus: Finally making the diagnosis by long-term EEG

“…In a small group of patients ( N = 5) with normal EEG and brain MRI, in which aphasic SE was suspected, fluorodeoxyglucose positron emission tomography (FDG–PET) confirmed the diagnosis by revealing hypermetabolism in language areas [9] . Two groups [9] , [10] suggested, in the case of clinical suspicion of aphasic SE in which EEG failed to show clear ictal activity and conventional MRI was normal, other methods, such as FDG–PET or, in acute situations, CT-perfusion (CTP). The findings of hypermetabolism in the epileptogenic zone on FDG–PET or hyperperfusion on CTP in the dominant hemisphere can lead to the diagnosis.…”

Verbal and memory deficits caused by aphasic status epilepticus after resection of a left temporal lobe glioma

“…[ 2 , 4 , 12 ] However, in a recent study, approximately 30% of patients with ASE developed mild-to-moderate aphasia, which is consistent with our case. [ 1 ] Given that the etiology of ASE includes malignant brain tumors, stroke, and encephalitis, it is usually difficult to determine whether verbal disturbance is solely due to epileptic activities. However, our case demonstrated that ASE can induce verbal deficits, as there were no obvious exacerbations other than the epileptic events.…”

“…In support of this result, a previous study indicated that ASE lasting for 8 h can induce neurological deficits. [ 1 ] Therefore, the critical period before stopping ASE, which may be shorter than that previously assumed, should be identified. Other key determinants for ASE treatment include its etiology, the efficacy of nonaggressive treatment, and mortality due to aggressive treatment.…”

“…[ 15 ] In addition, regional hyperperfusion in computed tomography perfusion imaging and hypermetabolism in 18 F-fluorodeoxyglucose positron emission tomography are helpful in distinguishing the postictal state from the ictal state. [ 1 , 3 , 7 , 8 ] These modalities allow differentiation of NCSE from Todd paresis, which can last up to 36 h as a postictal symptom. [ 13 ] Furthermore, the etiology can contribute to the prediction of NCSE, because gliomas, metastatic brain tumors, and stroke each tend to induce ASE in neurosurgical diseases.…”

“…[ 13 ] Furthermore, the etiology can contribute to the prediction of NCSE, because gliomas, metastatic brain tumors, and stroke each tend to induce ASE in neurosurgical diseases. [ 1 ] In practice, it may be difficult to perform all these tests promptly. Therefore, if ASE is suspected, early aggressive intervention should be considered without waiting for all the test results.…”