Objective. We aimed to study the ictal EEG patterns in patients with non‐convulsive seizures (NCS) and their relationship with underlying etiology and patient outcome.
Methods. We conducted a retrospective review of EEG studies from patients undergoing continuous EEG (cEEG) monitoring for indication of altered mental status with a suspicion of NCS. Ictal EEG findings of NCS were categorized as three patterns: focal or generalized epileptiform discharges (EDs) at frequencies >2.5 Hz (Pattern 1); EDs at frequencies of ≤2.5 Hz or rhythmic activity >0.5 Hz with spatiotemporal evolution (Pattern 2); and EDs with ≤2.5 Hz with subtle clinical correlate during the ictal EEG or clinical and EEG improvement after a trial of IV anti‐seizure drugs (Pattern 3). Patients with anoxic brain injury were excluded from the study. Associations between ictal EEG patterns and underlying etiology and their impact on in‐hospital mortality was measured.
Results. Of 487 patients included in the study, NCS was recorded on cEEG monitoring in 57 (12%). The ictal EEG Pattern 2 was the most commonly seen ictal EEG finding in our cohort of patients with NCS (70%, n=40/57), followed by Pattern 3 (15%, n=9/57) and Pattern 1(14%, n=8/57). In patients with acute brain injury, Pattern 2 (67%, n=27/40) was a commonly seen ictal EEG finding, whereas Pattern 1 (62% n=5/8) was seen in patients with underlying acute medical illness. No statistically significant difference was found between ictal EEG patterns and underlying neurological versus medical etiologies (p=0.27) or in‐hospital mortality (p=0.5).
Significance. Spatiotemporal evolution of epileptiform discharges at a lower frequency was the most commonly recorded ictal EEG pattern in our cohort. Further prospective studies with a larger sample size of patients with NCS may provide valuable clinical data that could be used to evaluate the etiologic correlate of the various ictal EEG patterns and their effect on outcome.
Central pontine myelinolysis (CPM) is an acute demyelinating neurological disorder affecting primarily the central pons and is frequently associated with rapid correction of hyponatremia. Common clinical manifestations of CPM include spastic quadriparesis, dysarthria, pseudobulbar palsy, and encephalopathy of various degrees; however, coma, “locked-in” syndrome, or death can occur in most severe cases. Rarely, CPM presents with neuropsychiatric manifestations, such as personality changes, acute psychosis, paranoia, hallucinations, or catatonia, typically associated with additional injury to the brain, described as extrapontine myelinolysis (EPM). We present a patient with primarily neuropsychiatric manifestations of CPM, in the absence of focal neurologic deficits or radiographic extrapontine involvement. A 51-year-old female without significant medical history presented with dizziness, frequent falls, diarrhea, generalized weakness, and weight loss. Physical examination showed no focal neurological deficits. Laboratory data showed severe hyponatremia, which was corrected rather rapidly. Subsequently, the patient developed symptoms of an acute psychotic illness. Initial brain magnetic resonance imaging (MRI) was unremarkable, although a repeat MRI two weeks later revealed changes compatible with CPM. This case demonstrates that acute psychosis might represent the main manifestation of CPM, especially in early stages of the disease, which should be taken into consideration when assessing patients with acute abnormalities of sodium metabolism.
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