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)

Bromisoval has been used as a hypnotic for the past several decades, and its abuse was known to cause various neurological as well as psychiatric symptoms. Three patients showed a variety of symptoms which could not be explained neuroanatomically: nystagmus, gait disturbance and hyperreflexia of the limbs in all the cases, dysarthria, double vision, hypotonia, ataxic gait and disturbance of consciousness occasionally and auditory agnosia in one case. For the purpose of determining the diagnosis, an energy dispersive X-ray microanalysis (EDX) was used to detect bromine. Five microliters of specimens were placed on the carbon-coated mesh, and using a TN-2000 analyzer, characteristic X-ray peaks of bromine were detected in the serum, urine and cerebrospinal fluid. The sensitivity to detect bromine in the serum was 30 micrograms/ml.
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PMID:Three cases of chronic bromisoval intoxication: clinical symptoms and application of energy dispersive X-ray analysis (EDX) to detect bromine in serum, urine and cerebrospinal fluid. 362 93

This work is to study the ultrastructure of the neuronal lipofuscin that occurred in the brain and the spinal cord of an autopsy case of familial Alzheimer's disease and to compare with those in several other diseases. The patient was a 46-year-old male, whose father and elder brother were diagnosed as Alzheimer's disease and died at the age of 42, respectively. He became afflicted with forgetfulness and disorientation at the age of 36. He developed a grand mal seizure at the age of 39 and thereafter, his clinical course was characterized by pyramidal signs, dysarthria and the symptoms of Gerstmann's syndrome, visuo-spatial agnosia, apraxia for dressing and constructive apraxia. He became bedridden at 45 years old and died of general prostration. The brain weighed 1,250 g, and the cerebral cortex showed mild atrophy. The neuronal loss, senile plaques and Alzheimer's neurofibrillary tangles were found throughout the cerebral cortex. The senile plaques were also found in the basal ganglia, the cerebellar medulla and cortex. There was severe amyloid angiopathy in the occipital and cerebellar cortices. The specimens for electron microscopy were taken from the cerebral cortex, the basal ganglia, the thalamus, the midbrain, the medulla oblongata, the cerebellum and the spinal cord. The ultrastructural study revealed three different types of the neuronal lipofuscin, though different stainability between these lipofuscin granules could not be manifested by several histochemical methods. Their morphological differences seemed to be based on the sites of the central nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ultrastructural study of the neuronal lipofuscin--an autopsy case of familial Alzheimer's disease]. 648 35

We presented a rare care who had right frontal lobe infarction, with left side pseudoataxia, and the mechanism, causing pseudoataxia, was considered. The patient, a 51 year-old, righ-handed male, was admitted on August 9, 1980, complaining of left-side pseudoataxia. About p.m. 7:00, July 29, 1980, he suddenly noticed numbness of the left foot, and he found himself difficulty in standing in the next morning. He had a mild paresis and tactile-tactile of the left side including the face, which was rapidly improved. However, there was pseudoataxia of the left extremities, which had not been improved. On physical examination, dysarthria, aphasia, finger agnosia, difficulty in right left orientation or muscle weakness was not recognized, and there was no sensory disturbance except for slight impairment of stereognosis, two point discrimination and vibratory sense. Demonstrable impairment of tactiletactile from was observed in the left hand. Notable dysmetria, terminal tremor and dysdiadochokinesia were seen in the left limbs, which were remarkably worsened with eyes closed. However, tapping and line-drawing tests were normal. Babinski-Weil's test disclosed typical compass gait. There was marked swaying in Romberg position. Tandem gait was impossible with a tendency to decline the left. Deep reflexies were normal except for mildly hyperactive radial reflex in the left. Carotid and vertebral angiographies revealed neither evidence of vascular occlusion nor displacement of vessels CT scan demonstrated a low density area, which included the right inferior and middle frontal gyri, the head of the right caudate nucleus and a part of anterior crus of right internal capsule. There was enlargement of anterior horn of the right lateral ventricle. Caloric test, electronystagmography, eye tracking test or optokinetic nystagmus test disclosed no abnormalities. Vibration induced falling, which is the postural reaction to muscle vibration during standing (Ekuland, G., 1972), was not recognized when the left Achiles' tendon was stimulated. Pseudoataxia of this patient differed from the typical cerebellar or vestibular ataxia. From a review of the literatures concerning frontal pseudoataxia, almost all cases had no distinct cerebellar signs, and showed positive Romberg's sign. The impairment of tactile-tactile form and postural reaction to vibratory stimulation to the left leg, appeared in this case, could be hardly explained by the lesion of parietal lobe or deconnection syndrome. Sensory perception of parietal lobe and pyramidal motor system were thought to be almost normal in this case. Therefore, these findings should be due to impairment of integration center between sensory and motor systems. The pseudoataxia in frontal lesion seems to occur as the results of involvement of this center, in which caudate nucleus maybe has important role, but not as the results of disturbances in the front-ponto-cerebellar or front vestibular pathway.
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PMID:[Frontal pseudoataxia, discussion on its mechanism (author's transl)]. 732 87

We report a 74-year-old man with a lung cancer, who developed right leg weakness, neurogenic bladder, and multiple cranial nerve palsies. The patient was well until December of 1992, when he was 74-year-old, when he noted transient double vision; in February of 1993, he noted numb sensation and weakness in his right leg. Later in the same month, he developed overflow incontinence of urine and weakness in his right face. He also noted deafness in his left ear (he had a marked loss of hearing in his right ear since childhood because of otitis media). His weakness in his right leg had progressed, and he was admitted to our service on March 19, 1993. On admission, he was afebrile and BP was 130/50 mmHg. General physical examination was unremarkable. On neurologic examination, he was alert and oriented to all spheres; no dementia was noted nor were detected aphasia, apraxia, and agnosia. His optic fundi were unremarkable; ocular movement appeared normal, however, he complained of diplopia in far vision. Sensation of the face was intact. He had right facial palsy of peripheral type; he was unable to close his right eye, and Bell's phenomenon was observed on attempted eye closure. On the left side, he had facial spasm. He had marked bilateral deafness. He had no dysarthria or dysphagia. The remaining of the cranial nerves were intact. Motor wise, he was unable to stand or walk alone; weakness did not appear to account for his difficulty in gait; manual muscle testing revealed 4/5 weakness in his tibialis anterior muscle, 1/5 in the peroneus longus, 0/5 in his extensor hallucis longus and extensor digitorum longus, all on the right side. Brachioradial and quadriceps femoris reflexes were increased to 3/4; plantar response was equivocal on the right side, and flexor on the left. Sensory examination revealed loss of touch and pain sensation in the L5 and S1 distributions in his right leg: vibration and position sensations were also diminished in his right foot. He had overflow urinary incontinence with loss of bladder sensation. Marked nuchal stiffness was noted, however, no Kernig's sign or eye ball tenderness was present. Pertinent laboratory findings were as allows; WBC 8,100/microliters, Ht 42.5%, platelet 326,000/microliters, TP 6.8 g/dl, BUN 16 mg/dl, creatinine 0.54 mg/dl, glucose 95 mg/dl, Na 136 mEq/l, K 4.4 mEq/l, Cl 100 mEq/l; liver profile was normal; CEA 436.6 ng/ml, CA19-93 U/ml; urinalysis was normal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 74-year-old man with urinary incontinence, right leg weakness and multiple cranial nerve palsies]. 766 22

Dysarthria occurs in approximately 40% of all patients with MS. When speech and voice disturbances do occur, they usually present as a spastic-ataxic dysarthria with disorders of voice intensity, voice quality, articulation, and intonation. While language disturbances such as aphasia, auditory agnosia, anomia, dysgraphia, and dyslexia are very rare in MS, cognitive deficits and swallowing disorders are common. Treating dysarthria, dysphagia, and cognitive deficits in MS patients is effective for reestablishing functional daily activities. The types, severity, and rates of deterioration in MS are highly variable; complete restoration to normal functioning is therefore not always expected. For these reasons, careful documentation of clinical-treatment outcomes and the factors influencing these outcomes should be regularly collected and reported.
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PMID:Speech-language pathology and dysphagia in multiple sclerosis. 989 14

We report a 55-year-old right-handed Japanese man with motor neuron disease and dysgraphia of kana letters. He was admitted to our hospital because of dysarthria and dysphasia. On admission, the results of general physical examination were within normal limits. Neurological examination revealed severe dysarthria, dysphasia, impaired movement of the tongue without fasciculation and slight distal muscle weakness in the bilateral upper limbs. There were no fasciculation of the muscle. Deep tendon reflexes were hyperactive without Babinski's signs. Sensation, coordination, and gait were normal. Neurophysiological studies demonstrated normal motor nerve conduction velocities and sensory action potential. The results of needle electromyography of the upper limbs were compatible with motor neuron disease (MND). Magnetic resonance imaging (MRI) showed atrophy of the bilateral temporal region of the brain. 99mTc-HMPAO SPECT (Single Photon Emission Computed Tomography) showed reduced uptake of tracer in the bilateral temporal region. On neuropsychological examination, his behavior was normal, and orientation and intelligence were also preserved, but his speech was severely impaired. Reading comprehension was slightly impaired. In regard to writing comprehension, he had no difficulty in copying of words though dictation was found to be impaired. He omitted one kana letter in a word. Agraphia is accompanied by various factors such as aphasia, dementia, agnosia, alexia. But in this case at least for early stage, agraphia existed without other higher cortical dysfunction. He did not show severe dementia in his early stage of his disease, but developed it later in the disease's progression. In this case, agraphia might be due to the atrophic changes in the temporal lobe.
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PMID:[A case of dementia with motor neuron disease associated with agraphia--the omission of kana letters]. 1556 82

Japanese encephalitis, the commonest Arbovirus encephalitis, has been endemic in many parts of Asia, the Pacific Islands, and India; also, there have been many epidemics. Most of the post JE cases have been associated with neurological and neuropsychiatric deficits but have not been properly classified and followed. Practically all the previous studies were in children or young adults. The aim of this study, involving only adult cases, the largest ever being reported, has been to follow the 688/1,199 survivors of JE patients out of 1,282 of acute cases admitted during four epidemics for a period of 14 years after properly classifying the sequelae. This prospective study was conducted in B.R.D. Medical College Gorakhpur (India), involving 665/688 post JE cases with neuropsychiatric deficits from four epidemics of 1978, 1980, 1988 and 1989 which were properly classified in nine groups. While the first epidemic of 1978 was being studied, more disastrous episodes flared up and the patients were subsequently added. Hence, the total duration of this prospective study was from November 1978 to December 2003. There were 14 defaulted initially from 688 followed (23/688 without sequelae and 665/688 with neuropsychiatric deficits), and later 130 were lost from time to time at various stages of follow up. Four out of 23/688 discharged without any deficit had to be readmitted for bizarre movements, assaultative behaviour and euphoria without fever and altered sensorium. All of them improved by symptomatic treatment. Progressive improvement occurred in all the parameters consisting of psychological disturbances, higher cerebral dysfunction, speech disorders (dysphonia, dysarthria, dysphasias, apraxia and agnosia), extra pyramidal, pyramidal features, and hypothalamic disturbances, cranial nerves including pupils and fundi and seizures. Maximum cases improved between 6 months (55%) to 1 year (78%). Only some features improved between 5 to 14 years. Four patients of hemiplegia remained bed ridden. Some non disabling features like dysarthria and corticospinal features without paralysis persisted in 5% (95% improved) and 74% (26% improved) respectively. One patient with bizarre movement and nine with marked tremors could not regain normalcy. A large number of patients of JE are left with several minor or gross residual neuropsychiatric and neurological features after the acute phase. In this series also the discharged patients with neurological deficits who were quite disabled initially and needed constant care by family members and also those who required some help intermittently improved with passage of time and eventually returned to normal life. Some of them were left with non-disabling residual neurological signs even after 14 years. Fourteen of 544 (3%) could not return to their livelihood.
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PMID:Japanese encephalitis (JE) part II: 14 years' follow-up of survivors. 2168 33