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 surgically treated case of ventrally exophytic pontine glioma is reported. A 49-year-old woman, complaining of dysarthria, dysphagia and gait disturbance, was admitted to our department. Her past history included bronchial asthma. Plain skull x-p and tomography revealed destruction of the dorsum sellae and upper clivus. CT demonstrated an enhanced oval mass at the ventral side of the upper brainstem. The mass was severely compressing the brainstem dorsally. MRI revealed a low-intensity band between the tumor and the brainstem. Dynamic MRI demonstrated a pattern of rapid increasing and slow reduction. Cerebral angiogram demonstrated a paradoxical sign that pontine branches were located anterior to the basilar artery. The finding demonstrated that the tumor was an intraaxial mass. The first operation was performed by the orbitofrontomalar approach. On the trans-sylvian route, the tumor was removed partially with CUSA and neuronavigation system. Its histology was astrocytoma grade III. Radiation therapy was added. The patient's symptoms aggravated again. On the second operation, the transtemporal route with tentorial resection was chosen. Under a wide visual field, intracapsular subtotal resection of the tumor was performed. Interferon therapy was added. She was discharged to her home with no neurological deficits. Ventrally exophytic pontine glioma is very rare. Low-intensity band of MRI, a sign of extraaxial mass, was visualised in our case. On the other hand, cerebral angiogram demonstrated a paradoxical sign. This sign suggested that the tumor originated from the brainstem. With update skull base surgery and neuronavigation system, surgical therapy of ventrally exophytic pontine glioma is safe and effective.
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PMID:[A surgically treated case of ventrally exophytic pontine glioma]. 747 14

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

Varicella-zoster virus can cause neurological disease in primary and reactivated latent forms, with a wide spectrum of disorders throughout a person's lifetime. 35-year-old male with AIDS; histoplasmosis; mild, intermittent asthma; and hypertension presented to hospital with left-sided weakness and slurred speech. Exam showed left hemiparesis with left upper motor neurons facial palsy and dysarthria. Acute right basal ganglia infarct was detected in head CT without contrast. A subsequent MRI showed acute non-hemorrhagic infarct, right basal ganglia; fusiform dilatation, and proximal right middle cerebral artery. A CT angiogram of the bilateral carotid arteries revealed occlusion of the right anterior cerebral artery with conical dilatation at the origin; significant stenosis, and dilatation of the right middle cerebral artery. These findings were consistent with vasculitis. Patient was successfully treated with IV acyclovir. Rapid diagnosis of VZV vasculopathy is important because it is a treatable cause of stroke. Mortality rate is 25% without treatment.
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PMID:Varicella zoster vasculopathy. 2143 Feb 39