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 59-year-old woman had chronic hyponatremia from inappropriate secretion of antidiuretic hormone (SIADH) and malnutrition after recurrent cholecystitis for 2 months. She developed dysarthria, dysphagia, bilateral ptosis, clonic convulsions and delayed onset Parkinsonian features. Magnetic resonance imaging showed increased signal density in the central pons on T2-weighted images. She was also later diagnosed as having systemic lupus erythematosus (SLE). This case is reported because central pontine myelinolysis (CPM) developed in chronic hyponatremia without correction, and manifested with atypical, delayed-onset Parkinsonian features. The patient recovered well from her neurological illness, unlike the poor outcome in previously reported cases of CPM. In addition, the coincidence of CPM and SLE has not, to knowledge, been reported before.
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PMID:Central pontine myelinolysis in chronic hyponatremic patient: a case report. 771 99

In a 21-year-old woman with a smaller and sloppy handwriting, drooling especially when stooping, sporadic choking, clumsiness, and frequent stumbling, Wilson's disease was diagnosed. The medical history disclosed a short period of haemolytic anaemia with transient hepatic failure, and irregular menstruation periods with infertility. On examination there were no signs of liver or spleen enlargement. She was slow, had an expressionless face and mild dysarthria, and slight impairment of the coordination of the limbs. Magnetic resonance imaging of the brain showed bilateral hyperintensive lesions of the basal ganglia on T2W images. Zinc therapy induced a good biochemical response and there was also some clinical improvement. Linkage analysis within the family identified one other asymptomatic homozygotically affected sister. A diagnostic delay occurs frequently due to relative unfamiliarity with this rare disease and due to its variable clinical expression.
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PMID:[Wilson's disease; diagnosis with the aid of magnetic resonance tomography]. 772 83

We reported a rare case of marked dilatation of the bilateral common carotid artery (CCA) associated with stenosis of the left middle cerebral artery (MCA). A 64-year-old female was admitted with right hemiparesis and dysarthria. She was hospitalized 2 years ago for cholecystitis. For 5 years, she has been under medical treatment for hypertension, diabetes mellitus, hyperlipidemia, cardiac failure associated with hypertrophic cardiomyopathy, and atrial fibrillation. Brain CT scan showed infarction of the left corona radiata. Angiography revealed marked dilatation of the bilateral CCA and the internal carotid artery (ICA), moderate dilatation of the innominate artery and the right subclavian artery, kinking of the right CCA, diverticular outpouching of the left ICA, and stenosis of the right external carotid artery and the left MCA. Breast CT scan revealed moderate dilatation and marked calcification of the ascending aorta and the aortic arch. Laboratory examination did not show any sign of inflammation, rheumatoid factor (RA), antistreptolysis-O (ASLO) and antinucleotic antibody. Based on the clinical course, radiological findings and laboratory data, possible diagnosis of the dilatation of the bilateral CCA was discussed with particular emphasis on arteriosclerotic aneurysm and aortitis syndrome.
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PMID:[Marked dilatation of the bilateral common carotid artery: a case report]. 773 79

We report a 65-year-old woman with progressive dysarthria, dysphagia, weakness, and gait disturbance. The patient was well until 59 years of age (January of 1986) when she noted bilateral ptosis. One year later, she noted a gradual onset of difficulty in speech (articulation). Her speech slowly deteriorated and she noted weakness in chewing power and difficulty in swallowing in addition. In October 1987, she developed emotional incontinence. In January of 1988, she started to drag her left foot. She was admitted to our hospital on June 13 of 1988. On admission, she was alert and general physical examination was unremarkable. Neurologic examination revealed no dementia; her higher cerebral functions appeared intact. Ptosis was present bilaterally more on the right. She showed difficulty in opening her eyes on command; no contraction of the frontal muscles was seen upon attempted eye opening. There was a moderate limitation in the vertical gaze. Forced laughing and crying were seen. Facial muscles were moderately weak without apparent atrophy. The movement of the soft palate was very weak, and swallowing disturbance was more prominent for liquid staff. The tongue appeared somewhat small, however, no fasciculation was noted. Her step was small and the posture was stooped. Retropulsion was present, however, Romberg's sign was absent. No muscle atrophy was apparent, however, diffuse mile to moderate muscle weakness was noted in all four limbs. Cerebellar sign was absent. Deep tendon reflexes were exaggerated bilaterally, and Babinski sign was present on the left side. Sensation was intact. Routine blood tests were unremarkable as was a cranial CT scan. Her ptosis did not improve after 10 mg of edrophonium injection. CSF was also normal. She was transferred to another hospital but her neurological disabilities further progressed. In 1989, she was totally unable to move her limbs; she could only move her eyes; still consciousness was clear without dementia. She developed respiratory difficulty and expired on July 25, 1992. She was discussed in a neurological CPC, and the opinions were divided into ALS and primary lateral sclerosis (PLS). The chief discussant arrived at the conclusion that the patient might have had the pyramidal form of ALS. Postmorten examination revealed marked myelin pallor in the anterior as well as lateral corticospinal tracts. Pyramidal tract degeneration was prominent starting at the level of the cerebral peduncle and was continued to be seen until the level of lumbar cord. The number of anterior horn cells showed only slight decrease in the cervical level, however, it was normal in the lumbar cord.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 65-year-old woman with dysarthria, dysphagia, weakness, and gait disturbance]. 777 10

We report the successful management of cerebral vasculitis in a 46-year-old woman with longstanding rheumatoid arthritis with low-dose methotrexate. She suddenly developed dysarthria and left hemiparesis. Magnetic resonance imaging disclosed ischemia of the right pons, and angiography demonstrated cerebral vasculitis of vertebro-basilar arteries. The vasculitis was refractory with high-dose steroid therapy, which had only transient clinical benefit, and evolution to the pontine infarction followed. Her clinical status showed marked improvement in association with recovery of the vascular abnormalities after the initiation of the methotrexate therapy.
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PMID:Recovery from rheumatoid cerebral vasculitis by low-dose methotrexate. 782 78

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

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 25-year-old woman suffered from hyperemesis gravidarum when she was seven weeks pregnant. Since her vomiting continued, she received intravenous dextrose and electrolytes without thiamine in a hospital. One month later, she developed gait disturbance, followed by confusion and dysarthria. On admission to our department, she was confusional and had ataxic dysarthria. Spontaneous and gaze evoked nystagmus was present. Limb coordination was bilaterally ataxic. Based on her clinical course and symptoms, she was diagnosed as having Wernicke's encephalopathy. From the admission day, intravenous infusion of vitamin B1 (600 mg/day) was started. A few days later, her consciousness and limb ataxia began to improve. However, truncal ataxia and polyneuropathy became evident. Eight weeks after onset, she developed Korsakoff's psychosis such as anterograde and retrograde amnesia, disorientation and confabulation. We administered large amounts of corticosteroid (methylprednisolone 500 mg/day) in order to reduce brain edema or stabilize the impaired blood-brain barrier. Soon after, her psychosis began to improve gradually. She recovered remarkably from the psychosis, but she was left with persistent nystagmus, mild ataxic gait and polyneuropathy. The present case suggests that corticosteroid may have the beneficial effect on Wernicke-Korsakoff syndrome.
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PMID:[Beneficial effect of steroid pulse therapy on Wernicke-Korsakoff syndrome due to hyperemesis gravidarum]. 795 22

We report a 75-year-old woman with multiple cranial nerve palsies. The patient was well until January, 1992 when she had an onset of deafness in her left ear; she developed left facial pain in September, 1992, and came to the ENT clinic of our Izunagaoka Juntendo Hospital. She had chronic sinusitis; she was referred to neurology clinic on September 25 because of decrease in the superficial sensation in the second division of the left trigeminal nerve. She developed blurring of her left vision, and was admitted to the neurology service of Juntendo Izunagaoka Hospital on December 7th, 1992. On admission, general physical examination was unremarkable. Neurologic examination revealed alert and mentally sound woman; higher cerebral functions were intact. In the cranial nerves, olfactory sensation was normal; the left vision was reduced to discriminate light and dark; the right vision was normal. Pupils were round and isocoric, but the light reflex was sluggish on the left side; the abduction of the left eye was impossible; other ocular muscles appeared intact. Sensation of the left face was almost completely lost; the corneal reflex was lost on the left side; no jaw deviation was noted. She had near complete left facial palsy of the peripheral type; the left ear was deaf. The movement of the left soft palate was slightly weak, but no deviation of the uvula was noted; she had no dysarthria or dysphagia.2/
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PMID:[A 75-year-old woman with multiple cranial nerve palsies and a paranasal mass]. 806 43

The authors present the clinico-pathological findings in a member of a family residing in Akita Prefecture located in the north-eastern region of Japan. Four members in three generations of the family developed ataxia. The autopsied patient was a 42-year-old woman, who, at the age of 25, had developed progressive cerebellar ataxia with pyramidal spasticity and increased deep tendon reflexes predominant in the lower extremities. However, she retained fine movement of the hands and fingers and showed no dysarthria until the age of 35. She could no longer walk unassisted at 38 years old. She showed cerebellar ataxia in both hands and legs, dysarthria, bulging eyes, progressive extraoculomotor palsy with nystagmus, bradykinesia, sensory disturbance, and dystonia in the face, upper extremities, and fingers. Deep tendon reflexes were decreased, especially in the lower extremities. Subacute generalized muscular atrophy developed at the age of 39. She became bedridden and died of pneumonia. The clinical diagnosis was Type-2 of the entity known in Japan as Machado-Joseph disease. At neuropathological examination, the brain weight was 1,250 g. The spinocerebellar system including Clarke's column and the spinocerebellar tracts were degenerated, but the cerebellar cortex and inferior olivary nucleus were spared. Slight-to-moderate degeneration was observed in the pontocerebellar system. In the dentate nucleus, most of the neurons showed what is known in Japan as "grumose degeneration", but there was no neuronal loss or gliosis. The hilus of the dentate nucleus and the superior cerebellar peduncle were intact.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[An autopsied case of type 2 Machado-Joseph's disease or spino-pontine degeneration]. 821 97


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