Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1762617 (weakness)
 37,932 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Transient postictal hemiparesis or monoparesis is not uncommon after partial (focal) seizures. We report 2 patients who complained of severe bilateral limb weakness after generalized tonic-clonic seizures (GTCS) beginning focally. Bilateral Todd's paralysis was verified and documented in both patients. EEG and clinical evidence indicate the supplementary motor cortex as the most likely source of the seizures in both cases.
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PMID:Bilateral Todd's paralysis after focal seizures. 146 71

Although primary aldosteronism (PA) has been reported as a relatively benign form of hypertension and is associated with low incidence of vascular complications, recent reports indicate that PA complicated by cerebral vascular accidents is not rare. The authors reported here that a 57-year-old man was diagnosed as a case of PA 4 years after initial treatment of intracerebral hemorrhage (ICH) and hypertension. The patient was transferred to our department for further management of his left hemiplegia and hypertension after surgical treatment for a putaminal ICH at the age of 53. During the first 2 years of follow-up, he did well except for an episode of transient motor weakness. Diastolic hypertension was moderately good, controlled by calcium antagonists and ACE inhibitors. Laboratory data was normal, and the serum potassium levels were in the lower limits of normal. In the last 2 years, episodes of motor weakness have increased. He was admitted to our hospital, under the suspicion of recurrent Todd's paralysis. The serum potassium level ranged from 1.9 to 2.1 despite administration of potassium agents. Abdominal CT scans and 131 I-scintigraphy disclosed a left adrenal tumor. Elevation of plasma aldosterone and suppression of plasma renin were observed. The diagnosis of PA due to hypersecretion of aldosterone from an adrenal tumor was thus confirmed. We performed a total left adrenectomy 4 weeks after his admission. Histological examination showed a clear-cell type of benign adrenal adenoma. After the operation, laboratory data were normal and ACE inhibitors were able to normalize his diastolic hypertension. According to the literature, PA complicated by ICH is associated with a high rate of recurrence of cerebral vascular accidents if treatment of PA is not performed. Although diagnosis of PA in the early stage is difficult, as it was in our presented case, high suspicion of PA is essential for patients with diastolic hypertension and persistent hypopotassiumemia, particularly in young adults and middle-aged patients.
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PMID:[Primary aldosteronism presented with intracranial hemorrhage]. 1168 Oct 14

Development of dural arteriovenous fistula (dAVF) after cerebral venous sinus thrombosis (CVST) was very uncommon and for all these reported cases, the dAVF was a chronic complication. We present a case of acute development of dAVF after CVST. A 40-year-old female was admitted into our department with 2day's headache and vomiting for 9h. Head computed tomography (CT) scan showed only scattered minor hematomas over the right frontal lobe. Blood test indicated an elevated D-dimer. The patient experienced transient paralysis (Todd's paralysis) after intermittent focal epilepsy from day 3, which progressed into sustained epilepsy on day 6. Magnetic resonance imaging (MRI) on day 7 confirmed the thrombosis of the superior sagittal sinus and a large area of infarction and edema in the left frontal and parietal lobe. She was then treated with heparin and warfarin. Cerebral angiography on day 9 demonstrated a dAVF which was classified as Borden Type II and fed by the left occipital artery. Subsequently, endovascular occlusion of the fistula was conducted and the patient recovered well with only slight right limbs weakness at 1year follow up.
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PMID:Cerebral venous sinus thrombosis complicated with acute development of dural arteriovenous fistula: A case report. 2867 69

Todd's paralysis, a neurological abnormality characterized by temporary limb weakness or hemiplegia, typically occurs following a seizure, without enduring consequences. Since limb weakness or hemiplegia can also be a common symptom of an acute ischemic stroke, it is often difficult to diagnose Todd's paralysis in individuals experiencing an acute ischemic stroke if they do not have a pre-existing history of epilepsy. Given that there is a limited understanding of Todd's paralysis, this review discusses the history, prevalence, clinical manifestations, duration, etiology, and diagnosis of Todd's paralysis. A few factors that may help clinicians distinguish Todd's paralysis from other clinical indications are as follows: (1) Todd's paralysis is commonly observed after partial seizures or generalized tonic-clonic seizures. (2) The incidence of Todd's paralysis is greater if the epilepsy is associated with old age or stroke history. (3) The duration of Todd's paralysis can range from minutes to days, depending on the type of seizure or whether the patient has experienced cortical structural damage. (4) The etiology of Todd's paralysis is associated with cerebral perfusion abnormality after seizures. Further research is needed to explore factors that distinguish Todd's paralysis from other indications that may lead to limb weakness in order to improve the diagnosis of Todd's paralysis.
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PMID:Frequency and Pathophysiology of Post-Seizure Todd's Paralysis. 3213 3