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)

A 62-year-old man developed recurrent TIAs presenting as mild unconsciousness, dysarthria and weakness of the right upper extremity lasting for 15 to 20 minutes. He was found to have severe iron deficiency anemia (hemoglobin: 5.5-5.9g/dl; hematocrit: 18.4-19.5%) which insidiously developed through the chronic bleeding from the gastric ulcer. He had slight hypertension (184/86mmHg), but no orthostatic hypotension. DSA and MR angiography showed severe stenosis at the origin of the bilateral internal carotid arteries and of the left vertebral artery. There was also hypoplasia of the right vertebral artery. Blood circulation detected by 123I-IMP-SPECT was markedly decreased in the whole brain and in the right hemisphere of the cerebellum. TIA was, however, completely disappeared following to the recovery of anemia. The present case suggested that the presence of severe anemia accelerated the occurrence of hemodynamic TIA (regional cerebral anemic hypoxia), which is probably the consequence of the reduced oxygen-transporting capacity of the blood.
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PMID:[Hemodynamic TIA associated with severe anemia--a case report]. 799 47

Here, we present the first instance of Guillain-Barre syndrome variant in a patient with beta thalassemia and iron overload who had a history of transfusion before the onset of symptoms. Our patient was a 50- year-old Persian woman with history of intermediate thalassemia who had been treated with pack cells because of low hemoglobin level. Ten days after transfusion, she developed numbness of arms, left sided ptosis, and afterwards dysarthria, dysphagia, and bilateral ptosis. Electrodiagnosis on day 12 revealed reduced repetition of f-waves in the upper limbs and reduced recruitment with 1+ fibrillation in facial muscles. Electromyography and nerve conduction velocities in the limbs were normal. After excluding other causes and according to electrodiagnosis, the pharyngeal-cervical-brachial variant of Guillain- Barre syndrome was considered and plasma exchange began. Following exchanges, significant clinical improvement was attained. Iron overload and possible transmission of infections from blood products might have contributed in the development of syndrome.
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PMID:Pharyngeal-cervical-brachial variant of Guillain-Barre syndrome in a patient with thalassemia intermedia. 2104 78

We report a 37-year-old woman with no history of alcohol consumption or malnutrition who had Marchiafava-Bignami disease (MBD) as a complication of diabetes mellitus. The patient suddenly developed dizziness and could not speak words fluently. Neurological examination revealed acalculia, agraphia, left blepharoptosis, and mild left facial palsy. Her blood glucose was 391 mg/dL, and her glycated hemoglobin (HbA1c) was 16.0%. Her brain MRI revealed hyperintense changes in the corpus callosum on T2-weighted, fluid-attenuated inversion recovery and diffusion-weighted images. In addition to therapy for diabetes mellitus, prednisolone was commenced. All of the symptoms gradually improved, and after three months, only slight dysarthria, acalculia, and agraphia were observed. Brain MRI also revealed a reduction in lesion size. In conclusion, MBD may occur even with metabolic disorders. It is important to diagnose MBD in the early stages with MRI and to treat the symptoms with cortico steroids.
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PMID:A patient with Marchiafava-Bignami disease as a complication of diabetes mellitus treated effectively with corticosteroid. 2232 74

A 74-year-old man noted dysarthria and right hemiparesis. His history included a gastric ulcer 2 years previously, and he had gradually lost 10 kg over a 2-year period due to appetite loss. He daily consumed 120 mg of alcohol. Upon arrival, he had clear consciousness and stable vital signs. He was malnourished. Neurologic findings included a positive finding of Barre sign in the right hand and dysarthria. A venous blood gas analysis demonstrated the following: pH 7.059; PCO2, 21.5 mm Hg; PO2, 59.1 mm Hg; HCO(3-), 5.8 mmol/L; base excess, -22.7 mmol/L; lactate,17 mmol/L; and glucose, 4 mg/dL. After the administration of an infusion of thiamine and glucose, his abnormal neurologic findings subsided completely. Head magnetic resonance image (MRI; diffusion weighted image) disclosed 3 spotty, high-intensity signals in the brain. The main results of biochemical analyses of the blood collected on arrival were as follows: hemoglobin, 5.5 g/dL; glucose, 5 mg/dL; aspartate aminotransferase, 89 IU/L. He was admitted for further examination and was diagnosed as having alcoholic ketoacidosis with hypoglycemic encephalopathy and anemia due to colon cancer.
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PMID:A patient with clear consciousness even with a glucose level of 5 mg/dL (0.2 mmol/L). 2652 Nov 93

A 70-year-old woman noticed difficulty in speech and weakness of the left upper and lower limb upon awakening. Neurological examination showed dysarthria and left hemiparesis. No sensory disturbance was observed. Brain MRI revealed acute infarction in the right posterior limb of the internal capsule. On the hospital day 1, she developed the abnormal sensations restricted to the bilateral shoulders, resulting in difficulty initiating sleep. On laboratory data, renal function and serum hemoglobin and ferritin levels were normal. When four essential features of restless legs syndrome (RLS) were applied to her shoulders, the patient met RLS criteria. Following low dose pramipexole treatment, the abnormal sensation of the shoulders and insomnia significantly improved. We should be aware of the possibility of RLS or its variant, including "restless shoulder" of our patient, for the cause of insomnia following acute ischemic infarction.
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PMID:[A 70-year-old woman presenting with restless shoulder following posterior internal capsule infarction]. 2907 Jul 54

BACKGROUND Autoimmune cerebellar ataxia can be paraneoplastic in nature or can occasionally present without evidence of an ongoing malignancy. The detection of specific autoantibodies has been statistically linked to different etiologies. CASE REPORT A 55-year-old African-American woman with hypertension and a past history of morbid obesity and uncontrolled diabetes status post gastric bypass four years prior to the visit (with significantly improved body mass index and hemoglobin A1c controlled at the time of the clinical encounter) presented to the office complaining of gradual onset of unsteadiness and recurrent falls for the past three years, as well as difficulties coordinating routine daily activities. The neurologic exam showed moderate dysarthria and ataxic gait with bilateral dysmetria and positive Romberg test. Routine laboratory test results were only remarkable for a mild elevation of erythrocyte sedimentation rate, and most laboratory and imaging tests for common causes of ataxia failed to demonstrate an etiology. Upon further workup, evidence of anti-voltage-gated calcium channel and anti-glutamic acid decarboxylase antibody was demonstrated. She was then treated with intravenous immunoglobulins with remarkable clinical improvement. CONCLUSIONS We present a case of antibody-mediated ataxia not associated with malignancy. While ataxia is rarely related to autoantibodies, in such cases it is critical to understand the etiology of this disabling condition in order to treat it correctly. Clinicians should be aware of the possible association with specific autoantibodies and the necessity to rule out an occult malignancy in such cases.
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PMID:A Rare Case of Cerebellar Ataxia Due to Voltage-Gated Calcium Channel and Glutamic Acid Decarboxylase Autoantibodies. 2917 43

A 79-year-old woman came to us because of sudden onset of dysarthria. She had taken apixaban due to her non-valvular atrial fibrillation. A neurological examination revealed mild facial palsy of her right side, and magnetic resonance imaging showed acute brain infarction at the left frontal lobe. There were no stenotic lesions on intracranial or extracranial magnetic resonance angiography, and she was diagnosed with cardioembolic stroke. Intravenous infusion of heparin and edaravone was initiated, and her neurological symptoms improved. However, she gradually developed jaundice and anemia. Gastro-intestinal bleeding was not observed, and her blood test met the diagnostic criteria for hemolytic anemia. Because both the direct Coombs test and cold agglutinin were positive, she was diagnosed with mixed-type autoimmune hemolytic anemia. Although her serum hemoglobin level decreased to 7.0 g/dl on the 12th hospital day, her anemia gradually improved after steroidal therapy with transfusion. It was revealed that she had shown mild anemia (hemoglobin: 9.2-10.9 g/dl) and hyperbilirubinemia (total bilirubin: 1.8-2.6 mg/dl) for 6 months. Therefore, her latent autoimmune hemolytic anemia became activated with the occurrence of cardioembolic stroke. Autoimmune hemolytic anemia might have promoted cardiac thrombus formation despite the administration of an anticoagulant in this case. It should be noted that autoimmune hemolytic anemia can develop as thrombotic disease. In the present case, autoimmune hemolytic anemia was diagnosed based on the development of cardioembolic stroke.
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PMID:[A case of autoimmune hemolytic anemia diagnosed by occurrence of cardioembolic stroke]. 3136 54