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 78-year-old Caucasian man was admitted in the Department of Neurology for visual disturbances, started two days before. The next day the patient experienced headache, fever and gait disturbances. He had hypertension, diabetes mellitus, an ischemic stroke 13 years ago, longstanding seronegative rheumatoid arthritis (17 years), polynodular goiter, right ischio-pubian fracture and right femoral vein thrombosis a year ago due to a car accident, since he is treated with oral anticoagulants associated to antiaggregant, hypotensors, statin and oral antidiabetics. The neurologic examination had evidenced nuchal rigidity, left homonymous hemianopsia, left central facial palsy, ataxia of the inferior limbs with wide-based gait, achilean reflexes abolished bilaterally, bilaterally abolished plantar reflexes, ideomotor apraxia, dysarthria, hypoprosexia, and preserved consciousness patient. A non-contrast cerebral CT scan had shown right temporal and parieto-occipital intraparenchymatous hemorrhages, a right frontal sequelar lesion, multiple old lacunar infarets, cortical atrophy. Laboratory findings included an inflammatory syndrome, absence of rheumatoid arthritis positive serology, normal coagulogram, an elevated proteinuria. The cerebral IRM performed on the seventh day of hospitalisation was suggestive for subacute right parietal hemorrhage, old cerebral infarction in the right anterior cerebral artery area, old lacunar infarcts and cerebral atrophy. The anticoagulant and antiaggregant treatment was stopped after a generalized tonic-clonic seizure occurred. Antiedematous, hypotensor, anticonvulsivant, beta-blocker, and symptomatic treatment was started, while the antidiabetic treatment was continued. All symptoms remitted. Arguments for amyloid angiopathy in our patient are previous non-cardioembolic ischemic stroke and a chronic inflammatory disease- rheumatoid arthritis in his personal medical history.
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PMID:Multiple Intracerebral Hemorrhages in an Old Patient with Rheumatoid Arthritis. 2693 15

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

Cortical atrophy has been identified using magnetic resonance imaging (MRI) in humans and dogs with Lafora disease (LD). In humans, proton magnetic resonance spectroscopy (1HMRS) of the brain indicates decreased N-acetyl-aspartate (NAA) relative to other brain metabolites. Brain 1HMRS findings in dogs with LD are lacking. A 6-year-old female Beagle was presented with a history of a single generalized tonic-clonic seizure and episodic reflex myoclonus. Clinical, hematological, and neurological examination findings and 3-Tesla MRI of the brain were unremarkable. Brain 1HMRS with voxel positioning in the thalamus was performed in the affected Beagle. It identified decreased amounts of NAA, glutamate-glutamine complex, and increased total choline and phosphoethanolamine relative to water and total creatine compared with the reference range in healthy control Beagles. A subsequent genetic test confirmed LD. Abnormalities in 1HMRS despite lack of changes with conventional MRI were identified in a dog with LD.
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PMID:Brain proton magnetic resonance spectroscopy findings in a Beagle dog with genetically confirmed Lafora disease. 3241 79