Epilepsy and Behavior Case Reports最新文献

Focal neuroinflammation is considered one of the hypotheses for the cause of temporal lobe epilepsy (TLE) with amygdala enlargement (AE). Here, we report a case involving an adult female patient with TLE-AE characterized by late-onset seizures and cognitive impairment. Anti-N-methyl-d-aspartate receptor (NMDAR) antibodies were detected in her cerebrospinal fluid. However, administration of appropriate anti-seizure drugs (ASD), without immunotherapy, improved TLE-AE associated with NMDAR antibodies. In the present case, two clinically significant observations were made: 1) anti-NMDAR antibody-mediated autoimmune processes may be associated with TLE-AE, and 2) appropriate administration of ASD alone can improve clinical symptoms in mild cases of autoimmune epilepsy.

A 27-year-old man with a diagnosis of new onset refractory status epilepticus (NORSE) was treated with five anti-seizure drugs (ASDs) including clobazam, levetiracetam and topiramate. He received plasma exchange (PE) for presumed autoimmune etiology. Serum ASD levels were serially monitored in two sessions. Levels of clobazam, levetiracetam and topiramate were significant reduced by PE. Serum clobazam level dropped down to at least 85% and 75% of the baseline during and after the procedure respectively; levetiracetam dropped down to 83% and 83%; and topiramate dropped to 86% and 79%. The results may imply a theoretical risk of breakthrough seizure during PE due to low ASD levels.

Brain tumor-related epilepsy is a common complication of primary and metastatic brain tumors with seizures often representing the first manifestation of the tumor. The size and location of the tumor can make detection of epileptiform discharges on scalp electroencephalogram and safe surgical resection challenging. We describe a case of a patient with glioblastoma multiforme presenting as dominant temporal lobe epilepsy. Seizures were manifest as episodes of speech arrest on a background of long-standing history of episodic speech difficulty and headache. In this case, recognizing a change in semiology allowed diagnosis of a high-grade glioma. Use of electrocorticography during surgical excision of the tumor guided safe maximal excision without damage to eloquent cortex and helped confirm the diagnosis of brain tumor-related epilepsy.

Extreme delta brush (EDB) is an EEG pattern unique to anti-NMDA encephalitis. It is correlated with seizures and status epilepticus in patients who have a prolonged course of illness. The etiology of the underlying association between EDB and seizures is not understood. We present a patient with anti-NMDA encephalitis who developed status epilepticus evolving from the high frequency activity of the extreme delta brush. This case demonstrates that EDB is not only a marker for a greater propensity for seizures but also directly implicated in seizure generation.

Sodium valproate is a commonly used antiseizure drug with broad indications for different seizuretypes and epilepsy syndromes. Well-recognised side effects include weight gain, tremor, dizziness, and unsteadiness. Non-hyperammonaemic parkinsonism, with or without cognitive impairment, is a rare adverse effect of sodium valproate. We present the case of a sixty year-old lady with a generalized seizure disorder, treated with phenytoin, valproate, lamotrigine and clonazepam. Following withdrawal of phenytoin she developed an akinetic-rigid syndrome, with ataxia and marked cognitive impairment. Extensive investigation failed to identify a cause. Serum ammonia and valproate levels were normal. Hypothesizing this might be valproate encephalopathy, valproate was rapidly substituted with levetiracetam. Her severe motor symptoms resolved within two weeks and cognitive impairment markedly improved. Valproate-induced encephalopathy, with or without hyperammonaemia and liver toxicity are typically recognizable for their temporal relation between the start of therapy with valproate and emergence of the clinical syndrome. Reversible disorders of motor function and cognition attributable to valproate are well described, but few cases have been reported presenting years after starting treatment. Given the insidious progression, delayed onset, lack of association with drug levels or presence of hyperammonaemia, a high index of suspicion is needed to make the diagnosis.

We report a case with therapeutic hypothermia after cardiac arrest where meaningful recovery far exceeded anticipated negative endpoints following cardiac arrest with loss of brainstem reflexes and subsequent status epilepticus. This man survived and recovered after an out-of-hospital cardiac arrest followed by a 6-week coma with absent motor responses and 5 weeks of burst suppression. Standard criteria suggested no chance of recovery. His recovery may relate to the effect of burst-suppression on EEG to rescue neurons near neuronal cell death. Further research to understand the mechanisms of therapeutic hypothermia and late restoration of neuronal functional capacity may improve prediction and aid end-of-life decisions after cardiac arrest.

The focal and network concepts of epilepsy present different aspects of electroclinical phenomenon of seizures. Here, we present a 23-year-old man undergoing surgical evaluation with left fronto-temporal electrocorticography (ECoG) and microelectrode-array (MEA) in the middle temporal gyrus (MTG). We compare action-potential (AP) and local field potentials (LFP) recorded from MEA with ECoG. Seizure onset in the mesial-temporal lobe was characterized by changes in the pattern of AP-firing without clear changes in LFP or ECoG in MTG. This suggests simultaneous analysis of neuronal activity in differing spatial scales and frequency ranges provide complementary insights into how focal and network neurophysiological activity contribute to ictal activity.

We present a teenage boy with recent onset of seizures, who was erroneously treated with a large dose of an antiseizure medication as a result of drug mix-up. The ensuing drug toxicity caused vertical gaze palsy, an unusual manifestation related to overdose of the agent. Timely recognition of the error and discontinuation of the drug resulted in complete recovery to baseline.

This prospective uncontrolled study evaluated the effect of low-dose adjunctive perampanel therapy (4 mg/day for 3 months) on the sleep-wake cycle and daytime somnolence in adult patients (n = 10) with focal seizures. A > 50% reduction in the number of seizures was reported in 80% of the study patients; treatment had no significant effect on any sleep parameters as evident by the Maintenance of Wakefulness Test, Pittsburgh Sleep Quality Index and Epworth Sleepiness Scale scores. Two patients reported dizziness with treatment. In conclusion, low-dose perampanel may improve seizure control without affecting the sleep characteristics or daytime somnolence in patients with epilepsy.