Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0494475 (tonic-clonic seizure)
1,319 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A novel antiepileptic drug, levetiracetam, has been reported to cause several psychiatric adverse effects in spite of its effectiveness on epilepsy. However, a possible relationship between levetiracetam and obsessive-compulsive behavior has only been reported in a few studies with adult epilepsy patients. We treated a pediatric patient with epilepsy without past or family history of psychiatric disorder. Levetiracetam was started to control generalized tonic-clonic seizure. Two months after initiation of levetiracetam with favorable seizure control, she started to show an obsessive-compulsive behavior such as repetitive checking of her back, pants, and chair. Based on the course of its appearance, levetiracetam administration was identified as a possible cause. After termination of levetiracetam, her obsessive-compulsive behavior completely disappeared with reappearance of seizures. This case provides clear evidence that levetiracetam may cause obsessive-compulsive behavior even in a pediatric epilepsy patient without psychiatric background, possibly mediated by modulation of the glutamate system by levetiracetam.
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PMID:Obsessive-compulsive behavior induced by levetiracetam. 2500 11

This case discusses the course of a woman with a history of epilepsy, alcohol use disorder, herpes simplex virus (HSV) encephalitis, and Wernicke encephalopathy (WE) who presented with altered mental status following approximately 48 hours of vomiting. After experiencing a tonic-clonic seizure in the emergency department, she developed a fluent aphasia. Aphasias are ordinarily attributed to structural changes in the brain parenchyma, often from stroke, neoplasm, or infection. When the magnetic resonance imaging of brain failed to show changes that could explain her fluent aphasia, the neurology team consulted psychiatry to workup psychogenic aphasia. During an admission 9 months earlier, she had been diagnosed with HSV encephalitis and possible WE. There was a high degree of suspicion for recurrent HSV infection, intermittent focal seizure activity, postictal psychosis, pseudobulbar affect, or a vascular cause of her fluent aphasia. After 3 days of treatment with levetiracetam, high-dose intravenous thiamine, and aripiprazole, the patient's fluent aphasia reversed. The authors conclude that the patient's reversible fluent aphasia was not psychiatric in etiology but likely caused by her seizures, the result of subtherapeutic phenytoin levels; her electroencephalogram showed focal seizure activity in the temporal lobes, possibly affecting her language centers. Language-related neurological conditions, or aphasias, can mimic psychiatric conditions such as conversion disorder or psychosis. In patients with substance use disorders, the line between psychiatric and neurological conditions becomes even more difficult to distinguish. The paper also discusses how unique aspects of her medications - levetiracetam conferring neuron membrane fluidity; aripiprazole, a drug shown to halt brain atrophy in mouse models; and parenteral thiamine to address her deficiency and WE - have aided in the reversal of the fluent aphasia. Levetiracetam should be considered in WE and the rare occurrence of aphasia after seizures.
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PMID:Postseizure aphasia in Wernicke's encephalopathy: a case report and review of literature. 3034 57

CSNK2B, which encodes the beta subunit of casein kinase II (CK2), plays an important role in neuron morphology and synaptic transmission. Variants in CSNK2B associated with epilepsy and/or intellectual disability (ID)/developmental delay (DD) have been reported in five cases only. Among the 816 probands suspected hereditary epilepsy whose initial report of trio-based whole exome sequencing (WES) were negative, 10 de novo pathogenic or likely pathogenic variants of CSNK2B in nine probands were identified after reanalysis of their raw Trio-WES data. Six of the nine epileptic patients had ID/DD. The age of seizure onset of these nine patients with CSNK2B variants ranged from 2-12 months. Eight patients had age of seizure onset of less than 6 months. The epilepsy of most probands (8/9) was generalized tonic-clonic seizure and clustered (6/9). Most patients had normal electroencephalogram (5/9) and brain magnetic resonance image (7/9) results. Most patients (7/9) had easy-to-control seizures. Levetiracetam was the most commonly used drug in seizure-free patients (5/7). The variants detected in five patients (5/9, 55.6%) were located in the zinc-binding domain. In summary, our research provided evidence that variants in CSNK2B are associated with epilepsy with or without ID/DD. CSNK2B-related epilepsy is relatively easy to be controlled. The zinc-binding domain appears to be the hotspot region for mutation.
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PMID:Germline de novo variants in CSNK2B in Chinese patients with epilepsy. 3178 60