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)

The speech of three groups of Parkinson patients--nonsurgical, postunilateral and postbilateral thalamotomy--was evaluated. Dysarthria, bulbar motility and pyramidal tract indexes were determined for each patient. There was a statistically significant greater impairment in dysarthria and pyramidal tract indexes of patients with thalamotomy. L-Dopa and carbidopa therapy failed to significantly improve speech in any group.
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PMID:Effect of thalamotomy and levodopa therapy on the speech of Parkinson patients. 85 63

A three-year-old boy developed gait instability, nausea, vomiting, cranial nerve disturbances, hypotonus and dysarthria. Angiography of the four main cranial arteries showed complete obstruction of both vertebral arteries at the level of C1 to C2. Abundant collateral circulation was observed, which by-passed the obstruction to the vertebral arteries before their enterance into the posterior cranial fossa. The left vertebral artery was hypoplastic and both internal carotid arteries showed coiling in their extracranial portions. A high erythrocyte sedimentation rate at the beginning of the disease suggests an inflammatory alteration of both dysplastic vertebral arteries. The child recovered completely one month after the onset of symptoms. All other reported cases of childhood vertebro-basilar obstruction are reviewed and it is emphasized that the site of arterial obstruction has an important bearing on the clinical outcome.
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PMID:Bilateral obstruction of the vertebral arteries in a three-year-old child. 87 Mar 61

Dysarthria and aphasia represent primary symptoms of cerebral nerve dysfunction, and may particularly involve the facial and the hypoglossal nerves. In order for management to be effective, careful examination of the muscular functions of the oral cavity is required, with particular emphasis placed on the movements of the tongue and velum. Such evaluation, which utilizes both neuropsychologic and linguistic determinations, permit an accurate differentiation of the possible causes of aphasia to be made. During the evaluation, both verbal and non-verbal responses by the patient are included for proper diagnosis and therapy. Of great value in obtaining an accurate differential diagnosis is the exclusion of disturbances of hearing or buccofacial apraxia.
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PMID:[Applied phoniatry. VI. The dysarthria and aphasia syndromes as a result of cranial nerve palsies (author's transl)]. 89 62

A systematic search for cases of adult-onset hereditary ataxia was conducted on location in Scotland. The investigation resulted in the discovery of eight pedigrees with 42 patients of whom 16 were alive in 1975. Nine patients were examined by the authors and recent hospital records were available on the remaining seven. The clinical features were quite variable. In declining order of frequency, findings were gait and limb ataxia, dysarthria, hyperreflexia, extrapyramidal motor disturbances, impaired vibratory sense, spasticity, defects of extraocular movements and nystagmus, reflex depression, Babinski signs, impaired joint position sense, muscle weakness, optic atrophy, and mental abnormalities. Foot deformity occurred only once. Inheritance was compatible with autosomal dominant transmission, but complicated by consanguinity in two families. The minimum prevalence was calculated as 0.31/100,000. Autopsy in two members in one family revealed olivopontocerebellar degeneration.
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PMID:Adult-onset hereditary ataxia in Scotland. 90 33

Most ophthalmologists are aware of the cranial nerve dysfunctions that have been associated with the facial diplegias of Mobius syndrome. However, many are not aware of the combined limb deficiencies and cranial nerve dysfunctions. Limb malformations have been associated with a spectrum of oral facial anomalies consisting of micrognathia, hypoglossia, microstomia, hypodontia, oral bands, and dysarthria. It has been suggested that the differences which exists between these entities may in fact represent a common etiology. The variability may be related to an intrauterine insult at slightly different times. The oral-facial anomalies associated with absence of limbs or of limb anomalies suggests a correlation between the limbs and the first visceral arch possibly within the second month of gestation.
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PMID:Mobius syndrome and limb abnormalities. 91 40

A case of hypertensive intracerebellar hematoma surgically treated and cured was reported. The 41-year-old male had two cerebrovascular attacks with headache and vomiting followed by left hemiparesis. Drowsiness and dysarthria appeared the next day. The patient was admitted to a hospital, where right facial palsy, loss of right gag reflex and paralytic hemiplegia on the left side were noted. On the 7th day, the patient's consciousness became clear byt the other neurological evidences did not change. On the 14th day, bradycardia and central hyperventilation appeared and he became drowsy again. The patient was transferred to the authors' clinic. When the patient was admitted, he showed typical cerebellar signs such as nystagmus, ataxia, and slurring speech with pyramidal sign on left side and cranial nerves paralysis on right side, and also showed the changes of vital signs as a medullary syndrome in the late stage of the course. The vertebral angiogram revealed a space taking process in the right cerebellar hemisphere. The old blood (30g) was removed by suboccipital craniectomy. The hematoma cavity had a communication with the IVth ventricle through a small perforation in the medial wall of the hematoma. Spontaneour intracerebellar hematoma including of hypertensive origin is not rare in the reports of autopsy but surgically treated case has only rarely been reported. The main reason of few survivals should be in its fulminate course.
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PMID:[A cured case of hypertensive intracerebellar hematoma (author's transl)]. 94 80

An autosomal dominant striatonigral degeneration is present in a family of Portuguese ancestry numbering in excess of 329 persons in eight generations. The illness begins in the second, third, or fourth decade, and progresses for about 15 years with parkinsonian rigidity, spasticity, spastic dysarthria, and abnormalities of eye movement. Neuropathologic findings are severe neuronal loss and astrocytic gliosis in the corpus striatum and substantia nigra, with a moderate neuronal loss in the dentate nucleus of the cerebellum and nucleus ruber of the midbrain. This is a new genetic entity, distinct from other autosomal dominant neurologic disorders such as nigrospinodentatal degeneration, olivopontocerebellar degeneration, dystonia musculorum deformans, Machado's disease, and Huntington's disease.
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PMID:Autosomal dominant striatonigral degeneration. A clinical, pathologic, and biochemical study of a new genetic disorder. 94 67

Autosomal dominant olivopontocerebellar degeneration was diagnosed in a family of Scottish ancestry by clinical examination and autopsy. In addition to having progressive cerebellar ataxia, head titubation, and severe dysarthria, the patients are unable to initiate saccadic eye movements. Slow pursuit movements are normal. Reflex movements of the eyes caused by passive rotation or caloric labyrinthine stimulation are not impaired but are not associated with nystagmus. The phenomenon can be classified as supranuclear pseudo-ophthalmoplegia. It differs from congenital ocular motor apraxia in age at onset and the absence of random eye movements. The anatomic lesion responsible for the defect of saccadic eye movements remains to be established.
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PMID:Supranuclear ophthalmoplegia in olivopontocerebellar degeneration. 94 71

Side effects of orally administered bismuthic salts have been known for many years. Many systems are involved, including the digestive and urinary. The authors discuss a recently discovered effect on the central nervous system, termed "bismuth encephalopathy". In the light of the medical literature reviewed, two original aspects are stressed: the clinical symptoms are stereotyped and completely reversible, and the distribution of the disease is almost epidemic, being limited in time and space. The prodromes include confusion, asthenia, slowing of mental functions and disturbance of gait. The clinical picture is dominated by four major symptoms: confusion (again), ataxia, dysarthria and, above all, myoclonic jerks. In conclusion, various pathogenetic hypotheses are considered. The purpose of this study is to enable the general practitioner to detect the development of this condition early in treatment with oral bismuthic salts. Withdrawal of the medication always results in normalization of the patient's condition.
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PMID:[Encephalopathy during oral treatment with bismuth salts]. 98 34

Twelve members of a family with hereditary cerebellar ataxia of late onset were examined and, in 5, quantitative recording of eye movements were obtained. The initial and most severe symptom in all patients was ataxia of gait, followed by dysarthria and later by dysmetria of the limbs. Clinical examination did not reveal involvement of structures other than the cerebellum. Ocular motor examination showed: (1) inability to hold eccentric gaze resulting in gaze-paretic nystagmus; (2) downward beating nystagmus, accentuated on lateral gaze; (3) defective smooth pursuit, with relative preservation of optokinetic nystagmus induced by full-field stimulation; (4) rebound nystagmus; (5) enhanced gain (eye velocity/head velocity) of the vestibulo-ocular reflex during rotation in darkness; (6) decreased ability to suppress the vestibulo-ocular reflex during fixation of an object rotating with the patient; (7) saccadic dysmetria, especially downward overshoot; and (8) square wave-jerks. Although each of these signs can probably occur with lesions elsewhere in the brain, in combination they are highly suggestive of cerebellar involvement. With the reservation that we do not yet have pathological confirmation of the location of our patients' lesions, our results support the suggestion that the cerebellum specifically: (1) helps maintain eccentric gaze; (2) produces smooth pursuit eye movements; and (3) modulates the amplitude of saccadic eye movements. Many of the characteristics of the altered vestibulo-ocular responses and rebound nystagmus could be explained by the underlying anomaly in the smooth pursuit system.
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PMID:Ocular motor abnormalities in hereditary cerebellar ataxia. 99 Aug 97


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