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)

We report a 78-year old woman with 30 years history of rheumatoid arthritis and nephrotic syndrome, who developed right hemiparesis and renal failure recently. The patient was diagnosed as having rheumatoid arthritis in 1965, and had been treated with gold -sol, steroid hormone, and non-steroidal anti-inflammatory drugs intermittently. Later on her clinical course was complicated by nephrotic syndrome, however, her renal function was well compensated. Otherwise, she was apparently doing well until October of 1988 when she had an onset of anomic aphasia; she was 73-year-old at that time. She was admitted to our hospital; a cranial CT scan at that time revealed a low density area in the left temporal region, and she was diagnosed as suffered from an atherothrombotic infarction involving the left middle cerebral artery territory. She recovered soon and was discharged for out patient follow up with ticlopidine 100 mg/day. She was doing well until December 15, 1990, when she had an acute onset of nausea, vomiting, and speech disturbance; she was admitted to our hospital for the second time. On admission, she was alert, but she had motor aphasia, right hemiparesis, and dysarthria. A cranial CT scan revealed a low density area in the left temporal region extending into adjacent frontal and parietal areas including the angular gyrus; in addition, leukoaraiosis, cortical atrophy, and ventricular dilatation were noted (Fig. 1A, B). She was treated supportively, and she showed improvement in her aphasia, however, moderate weakness remained in her right upper and lower extremities. She was discharged for out patient follow up. She was doing well until May 21, 1993, when she developed difficulty in swallowing and speech. She became unable to take foods orally and she was admitted again on May 31. On admission, she was afebrile and BP was 120/80 mmHg. General physical examination was unremarkable except for pitting edema and multiple contracture of her joints. On neurologic examination, she was alert but appeared to have aphasia and dementia; she could utter only a few simple words, and was able to understand only simple questions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 78-year-old woman with rheumatoid arthritis, right hemiparesis, and renal failure]. 789 38

Demyelinating disease may present with clinical and radiological features mimicking brain tumor. A 43-year-old man was admitted because of progressive right hemiparesis, facial weakness and dysarthria. Computed tomographic scans revealed two expansive lesions in the left frontal lobe and midbrain, respectively. A brain tumor or metastatic lesion was suspected. The patient underwent left frontal craniotomy and the surgical biopsy revealed a demyelinating process. The patient, however, had a poor response to steroid treatment and died two months later. The possible nature of demyelinating disease in this case is discussed.
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PMID:A case of demyelinating disease with clinical and radiological features mimicking cerebral tumor. 791 91

A 39-year-old man was admitted because of an abrupt onset of right-side weakness and dysarthria. During the 2 years before admission, he had suffered from insomnia, depressed mood and progressive memory disturbance. Neurological and psychiatric examination revealed severe intellectual impairment in addition to the neurological deficits. Neuroradiological examinations revealed multiple brain infarcts. He had no risk factor for stroke except for lupus anticoagulant. He was diagnosed as having multi-infarct dementia associated with antiphospholipid antibodies. This case suggests that it is necessary to investigate antiphospholipid antibodies in addition to neuroradiological examination when relatively young patients present with unexplained cognitive or behavioral symptoms.
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PMID:A young case with multi-infarct dementia associated with lupus anticoagulant. 791 28

A 45-year-old woman was administered oral and intravenous diphenhydramine 25 mg for the treatment of an allergic reaction. Within 2 minutes she rapidly developed trismus, dysarthria, tremors of the upper extremities, left-sided weakness, and diminished consciousness. She was treated with intravenous diazepam and benztropine with good response. After approximately 12 hours the patient's condition was completely resolved except for minor subjective weakness of her left extremities. Her hospital stay was uneventful, and she was discharged after 4 days after refusing rechallenge with the drug. Several cases of acute dystonic reactions secondary to antihistamines have been reported in the literature, four of which involved diphenhydramine. Such reactions may occur after short- or long-term therapy. Most patients experienced rapidly developing trismus, facial dystonia, dysarthria, and occasionally, decreases in consciousness, motor incoordination, and weakness. Because of the widespread availability of diphenhydramine and other antihistamines to the general public, awareness of this effect is of great importance.
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PMID:Diphenhydramine-induced acute dystonia. 793 88

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 a 54-year-old man with progressive generalized muscle atrophy and ophthalmoparesis in the terminal stage. He was well until 44 years of age (1982) when he noted weakness in his right hand and muscle atrophy; in May of 1985, he noted weakness in his left hand and in both legs. His weakness had become progressively worse, and he became unable to walk in November of 1985. He noted dysarthria one month later, and dysphagia in March of 1986. His difficulty in swallowing had also become worse; he regurgitated foods into the trachea in September of that year, and he developed a low grade fever on the same day. He was admitted to our service on September 24, 1987. On physical examination, general findings were unremarkable, except for low grade fever (37.3 degrees C). On neurologic examination, he was alert and mentally sound. He had normal vision and visual fields; ocular movements were normal. He had moderate weakness in facial muscles, dysarthria, dysphagia, and atrophy in his tongue. He had marked generalized muscle atrophy with fasciculation. He was unable to stand or walk. His muscle strength was not more than 1/6 in any part. The lower extremities were spastic. Deep reflexes were exaggerated in both lower extremities but were normal in upper extremities. Sensation was intact. Laboratory examination was unremarkable, and so was the cranial CT scan. He was treated with nasogastric feeding. He was able to communicate smoothly using his eyes, but a restriction in the vertical gaze was noted in February of 1989. The range of ocular movement was better in the oculocephalic reflex compared with his spontaneous vertical eye movements. In April of 1990, his horizontal gaze also had become slow, and he was complicated by bronchial asthma. He was treated with 20 mg/day of prednisolone; after the institution of prednisolone, his horizontal eye movement showed much improvement. In the terminal stage, he was able to move his eyes only very slowly; vertical gaze was impossible. His subsequent course was complicated by respiratory tract infection and septicemia, and he expired on July 15, 1992. The patient was discussed in a neurological CPC, and the chief discussant arrived at the conclusion that this patient had amyotrophic lateral sclerosis with oculomotor paresis. Post-mortem examination revealed spongy change involving the posterior column and the posterior spinocerebellar tract, in addition to severe degenerative change in the upper and the lower motoneurons, which were consistent with amyotrophic lateral sclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 54-year-old man with generalized muscle atrophy and oculomotor paresis]. 799 50

A 3-year-old girl with left hemiparesis suffered from bilateral paresis, motor rigidity, gait disturbance, axial hypotonia, dysarthria, apathy, and incontinence. After steroid therapy, mild improvement occurred, but muscle weakness, gait disturbance, and rigidity remained. Leigh encephalopathy was excluded on the basis of muscle biopsy and laboratory findings. Computed tomography and serial magnetic resonance imaging at an early stage revealed right-sided dominant lesions in the putamen and caudate nucleus and later bilateral striatal lesions, appearing as hyperintense signals on T2-weighted images and mixtures of hypo- and hyperintense signals on T1-weighted images. This is the first demonstration of serial magnetic resonance imaging findings in infantile bilateral striatal necrosis.
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PMID:Serial MRI in infantile bilateral striatal necrosis. 802 66

We report a patient with small cell lung cancer associated with Lambert-Eaton myasthenic syndrome (LEMS) and subacute cerebellar degeneration (SCD). The patient was a 71-year-old man suffering from weakness of the limbs and a gait disturbance who developed limb ataxia and dysarthria one month after admission. Electrophysiologic studies confirmed the diagnosis of Lambert-Eaton myasthenic syndrome. Chest X-rays 2 months after admission revealed an abnormal shadow, and small cell lung cancer was diagnosed on the basis of biopsy specimens. Anti-voltage-gated calcium channel antibody was positive. Anti-Yo and -Hu antibodies were negative. The patient was treated by plasmapheresis and chemotherapy, which resulted in a transient improvement in the LEMS symptoms but not in the SCD. Fifteen cases of LEMS associated with SCD have been reported in the Japanese literature, and all were accompanied by small cell lung cancer. We discuss the frequency of association with LEMS and SCD and the effects of plasmapheresis and chemotherapy in both diseases.
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PMID:[Report of a case of small cell lung cancer associated with Lambert-Eaton myasthenic syndrome and subacute cerebellar degeneration--with a review of the Japanese literature]. 819 44

We present a case of a 10-year-old boy who presented to the emergency department with high fever, acute choreoathetosis, weakness, and dysarthria. An EEG showed generalized slowing, and serologies defined an acute case of Mycoplasma pneumoniae encephalitis. This report describes the most common presentations, therapy, and outcomes of M pneumoniae encephalitis.
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PMID:Choreoathetotic movement disorder in a boy with Mycoplasma pneumoniae encephalitis. 819 17

A 23-year-old female was admitted to our hospital because of unilateral calf enlargement. On neurological examination, she was mentally retarded with mild dysarthria. Grip myotonia was bilaterally present. Muscle weakness including those of face, neck and extremities was noted. The right calf tight and firm on palpation, was markedly enlarged with a circumference of 35.0 cm compared with 30.0 cm on the other side. Computed tomographic scans of the skeletal muscles revealed marked hypertrophy in the right triceps surae muscle. Electromyographic studies demonstrated persistent myotonic discharge in the hypertrophied gastrocnemius muscle. A muscle biopsy specimen obtained from the right gastrocnemius showed many hypertrophied muscle fibers, with prominent internal and sarcolemmal nuclei. Histographic analysis indicated a hypertrophy factor of 2,025 for type 1 fibers and 1,102 for type 2 fibers. DNA analysis by Southern hybridization technique showed large DNA fragment, consistent with congenital myotonic dystrophy. In the present patient, unilateral calf enlargement was an unusual feature associated with myotonic dystrophy. Neuroradiological and pathological studies confirmed true muscle hypertrophy of unilateral calf muscle. A search of the literature failed to reveal any case similar to our patient.
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PMID:[True muscle hypertrophy of the unilateral calf in congenital myotonic dystrophy--a case report]. 829 16


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