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 48-year-old man, who took by mistake a sip of ointment containing dichloroethane, survived, and showed a course of two phases of toxic symptoms. After an initial narcosis and an interval with few pathological symptoms seizures, myoclonia and somnolence occurred. Irreversible final disturbances were lasting mental defects, cerebellar dysarthria, ataxia, and hydrocephalus. Concomitant diseases were acute liver dystrophy, nephropathy, and anemia. The clinical picture of dichoroethane posoning is outlines, the pathogenesis of this particular cerebral lesion described, and the therapy discussed.
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PMID:[Dichloroethane poisoning with myoclonic syndrome, seizures and irreversible cerebral defects (author's transl)]. 122 Jun 46

A 55-year-old female with progressed dementia, cerebellar ataxia was reported. There was no family history of the same symptoms although her brothers, sisters and a son showed hypoceruloplasminemia and decrease of the serum copper content. On physical examination, anemia, dementia, dysarthria, torticollis, choreic involuntary movement of respiratory muscles, hyperreflexia in extremities and cerebellar ataxia were noted. Blood analysis revealed microcytic hypochromic anemia, diabetes mellitus, decrease of copper content of the serum and urine. Serum ferritin concentration was increased. Serum ceruloplasmin could not be detected. Biopsy of the liver showed that copper content in the liver was slightly increased and iron content was remarkably increased. On MRI study, dentate nucleus of the cerebellum, the thalamus, the putamen and the caudate nucleus and the liver showed low intensity in both T1 and T2 weighted images. Based on increased iron content in the liver, the radiological findings of the brain suggested deposition of iron in the brain. This deposition was considered as caused by deficiency of function of ceruloplasmin as ferroxidase. This disorder is suggested as a new disease due to ceruloplasmin deficiency different from Wilson's disease.
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PMID:[A case of ceruloplasmin deficiency which showed dementia, ataxia and iron deposition in the brain]. 145 25

A 50-year-old man complained of lumbar pains, lack of energy, dysarthria and ataxic gait. Investigation revealed progressive anaemia (haemoglobin initially 10.5 g/dl, later 6.8 g/dl) and thrombocytopenia (initially 67,000/microliters, later 25,000/microliters). In addition he had unexplained pyrexia of up to 39.8 degrees C. Lactate dehydrogenase was 780 U/l and fragmented red cells were noted in the blood film. Because of suspicion of thrombotic thrombocytopenic purpura, treatment with fresh plasma by infusion was immediately initiated. On the third day of treatment he developed left ventricular failure; auscultation revealed a blowing early diastolic murmur over Erb's point together with a spindle-shaped early diastolic murmur over the right second intercostal space. Computed tomography of the skull showed recent haemorrhage into the left half of the cerebellum and an older right posterior infarct. The abdominal ultrasound scan suggested a haemorrhagic spleen infarct. In view of these findings the diagnosis was revised to embolizing aortic endocarditis with aortic reflux (confirmed by colour Doppler echo-cardiography). Aortic valve replacement was performed immediately, and the patient was treated with gentamycin 80 mg/d and teicoplanin 400 mg/d for four weeks. Postoperatively he was given 12 units of platelet concentrate and the platelet count remained stable thereafter (greater than 100,000/microliters). Splenectomy became necessary because the splenic haematoma increased in size during oral anticoagulant therapy. After a 6 week hospital stay the patient was discharged in good condition.
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PMID:[Embolizing aortic valve endocarditis in the differential diagnosis of thrombotic thrombocytopenic purpura]. 153 83

A patient with hepatitis B virus-associated cirrhosis manifested various symptoms such as anemia, renal damage and neurological signs including cerebellar ataxia due to long-term administration of germanium-containing food. The patient was a 40-year-old male who had taken germanium containing mineral cheese for 26 months after he was diagnosed as having cirrhosis. Twenty four months after beginning to take the mineral cheese, he began manifesting paresthesia of the extremities, dysarthria and gait ataxia. Laboratory findings revealed anemia and renal damage. Biopsy of the peripheral nerve revealed loss of the large sheathed nerve, a characteristic feature of germanium intoxication. A high concentration of germanium (GeO2) was detected in patient's hair and urine. Cerebellar ataxia was characteristic in this patient, which was not reported in the previous papers.
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PMID:[A patient with liver cirrhosis manifesting various symptoms including cerebellar ataxia due to germanium intoxication]. 155 52

Central nervous system is rarely involved in progressive systemic sclerosis (PSS) unless there are concomitant abnormalities in renal or lung function or hypertension. A 72-year-old woman with typical PSS developed cerebellar bleeding. Medical history records revealed, she had noted the onset of Raynaud's sign on her upper extremities at the age of 37. This was followed by necrosis and repeated infection, and as a result, shortening of her fingers in her 40's. The disease progressed and involved lower extremities, and then face and body in her 50's. Aortic valve stenosis was diagnosed at 69 year old, cardiac myopathy at 70 and at the age of 71 infectious dermatitis in both inguinal regions. Mild anemia, hypoalbuminemia and the decrease of serum Fe were discovered in June 1988. At the same time, prolonged ESR, positive C-reactive protein, RA, and anti-nuclear-antibody were also noticed. A chest roentgenogram revealed pulmonary fibrosis. Systemic hypertension was not noticed on the clinical course. She developed an onset of vertigo and vomiting in the morning of August 8, 1988. Consequently, she was brought to our hospital. She was alert but a physical examination showed a swallowing disturbance, dysarthria, right cerebellar ataxia, nystagmus and hypertension (192/100 mmHg). A CT examination on admission revealed a slightly low density area in right cerebellar hemisphere without mass effect. She was treated with dextran and mannitol and her condition improved on the 6th day of her admission. She was alert and blood pressure calm down to 120/70 mmHg without the use of anti-hypertension drugs on August 21.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of progressive systemic sclerosis associated with a hemorrhagic infarction of the cerebellum]. 235 21

Lead, cadmium, mercury and arsenic are widely dispersed in the environment. Adults are primarily exposed to these contaminants in the workplace. Children may be exposed to toxic metals from numerous sources, including contaminated air, water, soil and food. The chronic toxic effects of lead include anemia, neuropathy, chronic renal disease and reproductive impairment. Lead is a carcinogen in three animal species. Cadmium causes emphysema, chronic renal disease, cancer of the prostate and possibly of the lung. Inorganic mercury causes gingivitis, stomatitis, neurologic impairment and nephrosis, while organic mercurials cause sensory neuropathy, ataxia, dysarthria and blindness. Arsenic causes dermatitis, skin cancer, sensory neuropathy, cirrhosis, angiosarcoma of the liver, lung cancer and possibly lymphatic cancer.
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PMID:Occupational and community exposures to toxic metals: lead, cadmium, mercury and arsenic. 716 33

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

We report an autopsy case of multiple system atrophy (MSA) presenting with rapid progression of autonomic disturbance. He was admitted to our hospital because of gait disturbance and dysarthria. The patient was a Japanese man, who first noticed gait disturbance and dysarthria at age 58, followed by syncope 3 months later. He developed urinary incontinence and frequency of urination 8 months after the disease onset. His gait disturbance, dysarthria, syncope, and urinary symptoms progressed, and he was admitted to the department of neurology 1 year after the onset of the disease. He was clinically diagnosed as having MSA and was followed in the outpatient office. He deteriorated rapidly and was readmitted to the department of neurology 19 months after the onset of the disease. Physical examination showed orthostatic hypotension. Neurological examination revealed nystagmus, dysarthria of cerebellar type, increased deep tendon reflexes, bilateral positive Babinski signs, ataxic and spastic gait, mild right hypesthesia and hypalgesia, impotence, constipation, and urinary incontinence. Routine blood examination showed slight anemia, elevated BUN, GOT, and blood sugar. Electrocardiography revealed sinus tachycardia and chest rentogenogram showed cardiac enlargement. Brain MRI showed atrophy of cerebellum and pons, and lacunae in basal ganglia. Autonomic function tests revealed abnormal in head-up tilt test, and CVR-R in May and November 1995. However 123I-MIBG myocardial scintigraphy showed normal uptake of MIBG in May 1995 and decreased uptake in November 1995. He deteriorated rapidly and died in May 1996. Autopsy findings revealed not only prominent olivopontocerebellar and slight striatonigral lesions, but also autonomic lesions with massive appearance of glial cytoplasmic inclusions. He was pathologically verified as having MSA. In the present patient, autonomic nervous system, especially cardiac sympathetic nerve, deteriorated rapidly, which might result in short duration of the illness.
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PMID:[An autopsy case of multiple system atrophy presenting with rapid progression of autonomic disturbance]. 1022 92

The development of central pontine myelinolysis (CPM) has rarely been reported in association with hemophagocytic syndromes (HPS). Here we report a unique case of Epstein-Barr Virus (EBV)-related HPS which was accompanied with CPM. A 72-year-old man who had no significant medical history was admitted to our hospital due to high fever and progressing dysphasia and dysarthria. Physical examination revealed anisocoria of the right pupil, fixed reaction to light, and paralysis of the left vagus nerves. Magnetic resonance imaging revealed low signal intensity on T1-weighted images and high signal intensity T2-weighted images in the patient's central midpontine lesion. Initial work-up showed anemia and thrombocytopenia with elevated levels of serum ferritin, lactate dehydrogenase, and soluble IL-2 receptor. Bone marrow aspiration revealed hemophagocytosis. The EBV genome was detected in the peripheral blood using the polymerase chain reaction method. He was diagnosed as having EBV-related HPS and CPM. Despite intensive treatment with methylpredonisolone, immunoglobulin, and etoposide, he died due to progressive disease and fungal septicemia. The etiology and relation between CPM and HPS are discussed.
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PMID:EBV associated hemophagocytic syndrome accompanied by central pontine myelinolysis. 1248 7

Thrombotic thrombocytopenic purpura (TTP) is an autoimmune disorder characterised by thrombocytopenia, haemolytic anemia, fluctuating neurological deficits, fever, and renal impairment. This case report is about a young man who presented with acute onset right sided paralysis, dysarthria, and central facial paralysis, suggestive of cerebrovascular accident, but eventually diagnosed as TTP. In addition, the clinical presentation of TTP is discussed and some teaching points for the emergency physicians are emphasised.
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PMID:Thrombotic thrombocytopenic purpura mimicking acute ischemic stroke. 1692 Oct 72


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