Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Tetrabenazine (TBZ) is widely used to treat hyperkinetic movement disorders in adults; however, published experience with the drug in children is limited. Common side effects of TBZ include drowsiness, sedation, weakness, Parkinsonism, depression, and acute akathisia, all of which are reversible with decreased doses. We report here a 7-year-old girl with rheumatic chorea who developed acute akinesia of all four limbs and dysarthria due to TBZ therapy. Withdrawal of the drug led to rapid improvement within 18 hours.
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PMID:Quadriparesis and dysarthria due to tetrabenazine therapy in a child with rheumatic chorea. 2202 10

A 55-year-old woman with a 3-year and 4-month history of liver metastasis from breast cancer underwent chemotherapy with capecitabine and cyclophosphamide for following 10-months. She did not have hypertension and was not pregnant. She showed dysarthria and mild somnolence, and her conscious level developed to semicoma after 6 days. She had pyrexia. Cerebrospinal fluid (CSF) demonstrated increased cell-count and elevated protein but no evidence of positive cytological finding and cultivation of bacteria was found in the CSF. Brain magnetic resonance imaging (MRI) revealed multiple lesions with hyperintensity in the brain stem, bilateral middle cerebellar peduncles, left splenium of corpus callosum, bilateral basal ganglia, bilateral thalami, bilateral corona radiata, and bilateral subcortical white matters of parietal lobes on the T(2) weighted and fluid attenuated inversion recovery (FLAIR) images. These lesions demonstrated mild hyperintensity on the diffusion weighted images but did not demonstrate hypointensity on the T(1) weighted images. Capecitabine and cyclophosphamide were discontinued at 4th day after onset of symptoms, and her conscious disturbance showed improvement slowly since day 12 after cessation of these drugs and hyperintensity areas detected on FLAIR image of MRI showed decreasing intensity after three weeks of onset. Capecitabine is an oral prodrug converted to 5-fluorouracil (5-FU). 5-FU and cyclophosphamide are known to induce leukoencephalopathy. Reversible multiple lesions with leukoencephalopathy on brain MRI which is called as a posterior reversible encephalopathy syndrome (PRES). Capecitabine is also reported to induce PRES in rare cases. Combination of these drugs was considered for the possible cause to induce leukoencephalopathy like PRES. Usually leukoencephalopathy occurs in relatively early time after start of chemotherapy with capecitabine or cyclophosphamide, but we consider that late-onset leukoencephalopathy can be induced by long-term chemotherapy with these drugs. It is necessary to observe leukoencephalopathy by brain MRI regularly when these drugs are used.
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PMID:[Late-onset leukoencephalopathy induced by long-term chemotherapy with capecitabine and cyclophosphamide for liver metastasis from breast cancer]. 2253 58

A 56-year-old woman with a history of alcohol abuse was found at home amidst empty wine bottles with somnolence and severe dysarthria. MRI of the brain revealed selective demyelination of the corpus callosum, consistent with Marchiafava-Bignami disease.
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PMID:[A woman without speech]. 2255 54

Soporific acute hyperammonemic hepatic encephalopathy (aHE) can induce considerable changes in cerebral white and gray matter. This report describes a patient in the subacute phase of aHE grade I without disturbed consciousness and with reversible fine laminar cortical involvement on magnetic resonance imaging (MRI). The 59-year-old patient had esophageal varices bleeding due to primary biliary cirrhosis (ammonium blood level: 140 mmoL/L) and presented with sensory Jacksonian seizures, dysarthria, and increased drowsiness and fatigue. MRI revealed patchy hyperintense (T2-weighted, T2w) white-matter lesions and bilateral signal intensities in the striatum (T1w). During a rise of ammonium blood level to 220 mmoL/L, the patient had increased drowsiness, persistent dysarthria and mild temporary hemiparesis without loss of consciousness. Two weeks later, the patient was asymptomatic and blood ammonium level had reverted to normal value. MRI at that time revealed bihemispheric fine laminar subcortical hyperintensities on T2w and fluid-attenuated inversion recovery (FLAIR) imaging, and partially on T1w sequences, with no swelling or restricted diffusion; the hyperintensities were fully reversible a month later. Such a distinct cortical signal increase not only on T2w images, but also on T1w, in a patient after a mild form of aHE is a new MR finding.
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PMID:Reversible laminar signal intensity in deep cortical gray matter in T1-weighted images and FLAIR after mild acute hyperammonemic hepatic encephalopathy. 2265 36

Burkitt lymphoma is a type of B-cell lymphoma that occurs mostly in children, and rarely in adults. The sporadic type is known to occur mostly at the ileum and cecum. Cytarabine, which is used for central nervous system prophylaxis during chemotherapy for Burkitt lymphoma, has known neurotoxicity, and its side effects include motor ataxia due to cerebellar injury, ataxic dysarthria, dysfunction of ocular movement, confusion, somnolence and lethargy. This case report is about a patient diagnosed with Burkitt lymphoma who manifested motor ataxia after chemotherapy that included cytarabine.
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PMID:Rehabilitation for ataxia following chemotherapy for burkitt lymphoma involving the rectum. 2297 88

A 66-year-old man with hypertension presented with complaints of excessive daytime sleepiness (Epworth Sleepiness Score 14/24), dyspnea upon exertion, and episodes of noninjurious dream-enacting behavior. He reported tongue biting when sleeping in the right lateral decubitus position. Medications included atenolol 12.5 mg, lovastatin 20 mg, doxazosin 2 mg, amlodipine 5 mg, isosorbide mononitrate 60 mg, and aspirin 81 mg. He denied headaches, visual changes, dysarthria, dysphagia, or localized weakness. He denied use of alcohol, tobacco, or drugs.
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PMID:Positional central apnea and vascular medullary compression. 2313 63

A 50-year-old woman presented with drowsiness, severe dysarthria, left facial palsy, and left hemiparesis. Diffusion-weighted MRI showed cerebral infarction in the left pontine tegmentum and right cerebellum and angiography revealed basilar artery occlusion. Altered consciousness and hemiparesis fully resolved following successful recananlisation of the basilar artery by emergent intra-arterial thrombolysis. However, about 8 months later, obvious wasting of the left temporal and buccal area without sensory signs was detected. Electrophysiological evaluation revealed a chronic denervation process in the left masseter and temporalis muscles. We suggest that a small infarction in the trigeminal nucleus of the pontine tegmentum can cause an isolated trigeminal motor neuropathy with masticatory muscle atrophy.
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PMID:Pure motor trigeminal neuropathy in a woman with tegmental pontine infarction. 2383 66

A 69-year-old woman was admitted due to gradual progression of daytime sleepiness and forgetfulness over a period of approximately 1 month. Bradycardia and hypothermia were observed on admission, and neurological examination revealed memory disturbance, mild dysarthria, and bradykinesia. Fluid-attenuated inversion recovery (FLAIR) images of the brain magnetic resonance imaging (MRI) indicated signal hyperintensity in the region bordering the lateral and third ventricles. Serum anti-aquaporin 4 (AQP4) antibody was detected. The patient had no history or findings of optic neuritis or myelitis, and she was diagnosed as anti-AQP4 antibody-associated disorder. Diencephalon lesion and/or symptoms are rarely observed at the onset of neuromyelitis optica. Differential diagnosis of this disorder is necessary in cases manifesting diencephalon symptoms or involving lesions bordering the third ventricle without evidence of previous optic neuritis or myelitis.
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PMID:[Hypothermia and memory disturbance as initial manifestations associated with lesions of the diencephalon in a patient with anti-aquaporin 4 antibody-associated disorder: a case report]. 2514 37

Tumefactive multiple sclerosis (MS) is an aggressive form of MS that can be difficult to treat with standard therapies. In severe MS relapses, plasma exchange (PLEX) has shown some benefit, but reports of its use in patients with tumefactive MS are limited. This article describes the successful use of PLEX in a patient with tumefactive MS. A 46-year-old right-handed woman with a recent diagnosis of MS presented with drowsiness, dysarthria, horizontal nystagmus, and quadriparesis. Her brain magnetic resonance images demonstrated multiple tumefactive demyelinating lesions in the medulla, bilateral periventricular white matter, and corona radiata white matter. She was initially treated with a 10-day course of intravenous methylprednisolone without benefit; therefore, PLEX was initiated. After the second exchange, the patient started to improve and was discharged initially to rehabilitation and then home. She was started on disease-modifying therapy with natalizumab and did not experience further relapses but had slow clinical decline during the next year, which led to discontinuation of natalizumab treatment. PLEX may be used as second-line treatment in corticosteroid-resistant MS relapses, but there are limited reports of its use in patients with tumefactive MS. This patient presented with aggressive disease with multiple tumefactive lesions and did not respond to standard treatment with corticosteroids. PLEX was successful in improving her symptoms, allowing her to return home, although the disease progressed during the next year.
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PMID:Plasma Exchange in a Patient with Tumefactive, Corticosteroid-Resistant Multiple Sclerosis. 2647 44

Acute onset of encephalopathy is often due to infections or intoxications, but a high index of suspicion should exist for metabolic or autoimmune causes particularly in recurrent cases. A 6-year-old previously healthy Caucasian male presented with confusion and somnolence. He had several days of fever, myalgia, headaches, and rhinorrhea and was influenza-A positive. He was noted to have new urinary incontinence, inability to follow commands, and was responsive only to noxious stimuli. His neurological examination revealed bilateral ankle clonus. Laboratory results were significant for hypoglycemia and high anion gap metabolic acidosis. Cerebrospinal fluid was unremarkable and cultures remained negative. A magnetic resonance imaging (MRI) of the brain showed diffuse gray matter restricted diffusion. His presentation was attributed to acute influenza-A encephalitis. Four months later, he presented with emesis, abdominal pain, dehydration, and hypoglycemia. He subsequently developed dysarthria and confusion. A brain MRI was similar to his previous presentation. A repeat lumbar puncture was normal. A urine organic acid profile showed elevations of ketones and branched chain ketoacids, with mild elevations of N-acetylleucine and N-acetyl isoleucine. This pattern is consistent with maple syrup urine disease (MSUD). Genetic testing revealed that he is a heterozygote for 2 pathogenic variants in the BCKDHB gene (P200X and G278S), confirming MSUD. This case highlights the importance of broadening workup to include inborn errors of metabolism in cases of unexplained encephalopathy. Providers should be aware that diseases such as MSUD can occur in intermittent forms that may not be detected until early childhood.
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PMID:Recurrent Encephalopathy During Febrile Illnesses in a 6-Year-Old Boy. 3001 8


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