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Query: UMLS:C0013362 (dysarthria)
 3,768 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mute or nearly mute patient who is alert and has good understanding of speech and a right hemiparesis could have Broca's aphasia, akinesia of speech (transcortical motor aphasia), or aphemia. The patient who has Broca's aphasia does not write well, and his speech does not improve greatly with repetition. The speech of a patient with akinesia of speech improves with repetition. The aphemic patient writes normally, but his speech does not improve with repetition. The mute patient whose eyes are open but who is poorly responsive and moves little or not at all could be an akinetic mute (with either a cingulate or a thalamomesencephalic lesion) or have a locked-in syndrome. The latter is diagnosed by asking the patient to look up and down or to open and close his eyes. If he obeys these commands, the physician questions him using a code of eye movement responses. If the patient fails to respond at all, he is an akinetic mute; intense stimulation may result in speech or movement. If the patient is drowsy and has third nerve involvement, the lesion is in the thalamomesencephalic reticular formation. If the patient appears alert and has episodes of agitation, he probably has bilateral lesions in the gyri cinguli. Patients with weakness of the bulbar musculature (facial, palatal, and tongue weakness and dysphonia) may have either upper motor neuron or lower motor neuron lesions. Only bilateral upper motor neuron lesions produce permanent dysarthria. As a typical example, a patient has a transient left hemiparesis with dysarthria and almost completely recovers. Later, however, a right hemiparesis develops and the patient experiences severe bilateral facial weakness, drooling, dysphagia, and severe dysarthria. The absence of atrophy of the bulbar musculature, a hyperactive jaw jerk and gag reflex and, sometimes, inappropriate laughing or crying episodes indicate that the lesion is located above the medulla in the corticobulbar tracts. Flaccid paralysis, absence of the jaw jerk or gag reflex, and absence of other upper motor neuron signs, such as upgoing toes, indicate a lower motor neuron or neuromuscular junction problem. Appropriate tests to rule out myasthenia gravis should be done. The other conditions discussed here are often obvious from their clinical presentation. Although the specific disorder of speech sometimes is helpful in localizing the cause, in most patients, the associated deficits on neurologic examination are of greatest value.
Geriatrics 1975 Sep
PMID:Nonlanguage disorders of speech reflect complex neurologic apparatus. 16 83

The cases presented with psychic troubles and repeated somnolence episodes accompanied by dysarthria in 5 cases, myoclonic jerks in 4 cases and epileptic seizures in 1 case. In all cases the EEG was disturbed. It showed symetrical, paroxystic, bilateral, monomorph slow activity with more or less frequent paroxysms. The average serum aluminium level was at 407 microgram/l in the acute phase, at 161 microgram/l in the remission phase and at 123 microgram/l three months later. After interruption of oral and dialytic aluminium intake the remission is maintained. However in 2 cases the transitory readministration of aluminium gel was followed by reversible recurrency. The role of both aluminium gel and dialysate aluminium as the origin of encephalopathy is discussed.
Nouv Presse Med 1979 Sep 10
PMID:[Reversible dialytic encephalopathy after interruption of aluminium intake. 6 cases (author's transl)]. 49 78

Amyotrophic lateral sclerosis (ALS) is a degenerative neurologic disease having both upper and lower motor neuron signs and symptoms. When the speech musculature is involved, a mixed dysarthria and dysphagia usually result. In a 49-year-old man with ALS, dysarthria and dysphagia progressed from mild to severe forms over 17 months. Eleven months after the patient first experienced symptoms, neurologic examination showed fasciculations of the extremities and tongue, limb weakness, and hyperreflexia of the limbs and velopharyngeal mechanism. Tongue strength was one-fourth that of normal. Lingual alternate motions rates for consonant-vowel syllables were also reduced. To enhance lingual strength and swallowing, a tongue-strengthening program was developed for use with articulation training; to augment velopharyngeal function, a palatal lift was fitted; and to increase extremity strength, physical therapy was initiated. Six months after the initial neurologic examination, medical and speech reevaluation showed progressive weakness of the body parts affected initially; continued decline in tongue strength and lingual alternate motion rate; hypoactive reflex activity, indicative of progressive involvement of the lower motor neuron system; and continued deterioration of articulation and phonation owing to the progressive nature of the disease.
Arch Phys Med Rehabil 1979 Sep
PMID:Progressive speech deterioration and dysphagia in amyotrophic lateral sclerosis: case report. 49 10

The speech of five individuals with cerebellar disease and ataxic dysarthria was studied with acoustic analyses of CVC words, words of varying syllabic structure (stem, stem plus suffix, stem plus two suffixes), simple sentences, the Rainbow Passage, and conversation. The most consistent and marked abnormalities observed in spectrograms were alterations of the normal timing pattern, with prolongation of a variety of segments and a tendency toward equalized syllable durations. Vowel formant structure in the CVC words was judged to be essentially normal except for transitional segments. The greater the severity of the dysarthria, the greater the number of segments lengthened and the degree of lengthening of individual segments. The ataxic subjects were inconsistent in durational adjustments of the stem syllable as the number of syllables in a word was varied and generally made smaller reductions than normal subjects as suffixes were added. Disturbances of syllable timing frequently were accompanied by abnormal contours of fundamental frequency, particularly monotone and syllable-falling patterns. These dysprosodic aspects of ataxic dysarthria are discussed in relation to cerebellar function in motor control.
J Speech Hear Res 1979 Sep
PMID:Acoustic characteristics of dysarthria associated with cerebellar disease. 50 19

A 64-year-old hypertensive man presented with the dysarthria--clumsy hand syndrome, manifested by dysarthria, dysphagia, central facial weakness, deviation of the tongue on protrusion, incoordination of the affected hand, and mild imbalance on walking. A computed tomograpphic scan demonstrated a resolving acute infarction in the vicinity of the genu of the internal capsule.
Ann Neurol 1979 Sep
PMID:Dysarthria--clumsy hand syndrome produced by capsular infarct. 53 26

The author presents a case report of a manic-depressive patient who developed dysarthria and ataxia while on lithium maintenance. These symptoms were erroneously attributed to lithium toxicity occurring at therapeutic serum levels. However, the symptoms persisted despite diminution in lithium dosage and a neurological consultation revealed the diagnosis of multiple sclerosis. The author concludes that lithium therapy is effective with manic-depressive patients, that adverse side effects are infrequent and can occur at toxic or therapeutic serum lithium levels, and that the exceptional patient may have a second illness incorrectly attributed to lithium toxicity.
J Nerv Ment Dis 1978 Sep
PMID:Multiple sclerosis masquerading as lithium toxicity. 69 Jun 25

A study of chronic proximal spinal muscular atrophy was undertaken with the main aim of obtaining empirical recurrence risks for genetic counselling. Thirty-eight patients and their families were studied. Of these, 33 had similar clinical features and onset of disease in infancy or childhood. A division of these 33 patients by onset before or after 2 years (which was equivalent to whether or not they ever walked normally) gave recurrence risks for sibs which were higher with early onset. Among the sibs of patients with onset before 2 years, the incidence of disease was 1 in 5, due to most patients having an autosomal recessive disorder. A few patients, however, were thought to represent new dominant mutations. Among the families of index patients with onset after 2 years, the incidence of disease in sibs was only 1 in 15, but among their children it as 1 in 8. Both autosomal recessive and autosomal dominant forms therefore occurred in this age group, but it was concluded that nearly half the patients with onset after 2 had non-genetic motor neuron disease. The autosomal recessive form of chronic spinal muscular atrophy generally had onset before 2 years, but occasionally after 2. About a third of the patients never walked, and about half were in wheelchairs by age 10. No genetic heterogeneity within this form was demonstrated. Three remaining patients had distinctive clinical features associated with their proximal weakness, external ophthalmoplegia in one, dysarthria in another, and joint contractures in a third. Only 2 patients had onset in adult life, one of a probable recessive disorder and the other a probable dominant disorder.
Brain 1975 Sep
PMID:A clinical and genetic study of chronic proximal spinal muscular atrophy. 118 87

Neuropathological study of the visual pathway from the retina to the occipital cortex in Creutzfeldt-Jakob disease (CJD) has been scarcely performed. In the present study, pathological involvement of the visual pathway was observed in a 54-year-old man with CJD. The patient had the onset of visual disturbances in December 1985. He subsequently developed progressive dementia, right hemiparesis, ataxia and dysarthria, and rapidly fell into decerebrate posture in February 1986. In March 1986, myoclonus appeared on the whole body and EEG revealed periodic synchronous discharges, while brain CT and CSF findings showed no abnormalities. Myoclonus was observed most frequently from May to October 1986, and then reduced gradually. Brain atrophy on CT started from April 1986, and was progressive till the end stage of the disease. He died in January 1988, and the total clinical course was about 24 months. Neuropathological examination revealed severe degeneration of the cerebral cortex and the white matter. In the cerebral cortex, marked loss of neurons, astrogliosis, and spongiform changes were observed. In the cerebral white matter, the destruction of myelin sheaths and axons were evident. The cerebellum showed prominent loss of granule cells. These findings are consistent with those of the panencephalopathic type of CJD. In the visual pathway, loss of ganglion cells and bipolar cells in the retina, mild demyelination of the optic nerve, neuronal loss in the lateral geniculate body, and severe degeneration in the visual cortex were observed. The present case suggests that the neuropathological investigation in the visual pathway from the retina to the occipital cortex is important for clarifying the pathological processes in the visual system in CJD.
Hokkaido Igaku Zasshi 1992 Sep
PMID:[A case of the panencephalopathic type of Creutzfeldt-Jakob disease with retinal involvement]. 142 8

A 70-year-old man was admitted to our hospital because of fever and progressive dyspnea in December 1989. He was already diagnosed as having erythrocytosis secondary to pulmonary fibrosis 4 years previously and the values of his hematocrit (Ht) were maintained between 44.5 and 62.9% by repeated phlebotomy. Immediately after admission, severe diarrhea developed and the Ht value was 61.5%. Around 1:30 a.m. of the 3rd hospital day, he developed disturbance of consciousness. In addition, the serum levels of LDH, CPK, aldolase, and myoglobin of muscle origin increased markedly and the Ht value showed 78.5%. While the level of consciousness was gradually restored by 600 ml phlebotomy and 1,500 ml saline infusion, dysarthria and hemiplegia became evident. The Ht value early in the morning of the 3rd hospital day was reduced to 59.4%. Although cranial CT and MRI performed 74 days and 15 months, respectively, after the onset of the symptoms failed to reveal any abnormal shadow, he was clinically suspected to have cerebral infarction. These findings emphasize that abrupt increase in Ht or blood viscosity is a possible factor triggering cerebral infarction, and adequate control of Ht value is recommended for the prevention of such a condition in the aged.
Nihon Ronen Igakkai Zasshi 1991 Sep
PMID:[Cerebral infarction and high serum levels of muscle-derived enzymes associated with abrupt increase in hematocrit in a patient with secondary erythrocytosis]. 175 34

An 85-year-old housewife was admitted owing to the sudden onset of amnestic syndrome on June 27, 1986. There was no history of abulia or somnolence. Though she showed severe amnesia, her understanding was not impaired. There was no aphasia, no dysarthria or other focal sings. The CT showed a low density area in the genu of the left internal capsule. The patient's amnestic syndrome did not improve during the following four years and thus she was readmitted for further examination in July, 1990. Although her WAIS scores were fairly good and intelligence was considered normal, she showed very poor performance on the Wechsler memory scale-R and Benton visual retention test. MRI of the brain showed infarction which extended from the genu to the anterior limb of the left internal capsule. The longstanding amnesia in the present case was induced probably by the infarction of the genu of the left internal capsule, where some fibers of memory pathways, such as the anterior thalamic peduncle, ansa peduncularis, and stria terminalis, may pass.
Rinsho Shinkeigaku 1991 Sep
PMID:[Persistent amnestic syndrome due to infarction of the genu of the left internal capsule]. 176 47


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