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 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.
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PMID:Nonlanguage disorders of speech reflect complex neurologic apparatus. 16 83

A 66-year-old man (case 1) and a 71-year-old woman (case 2) showed systemic degeneration of the globus pallidus, substancia nigra, subthalamic nucleus, centrum medianum thalami and at times, superior colliculus in the midbrain. In the pallido-nigral system, neuronal loss was severe in both cases and an increase of pigment and granular spheroids was marked in case 2, less in case 1. Electron-microscopically, the spheroids consisted of aggregates of highly dense material, often membrane-bound, and varying amounts of groups of loosely packed filaments. Clinical symptoms were stereotyped and unique, showing severe akinesia, no rigidity in the limbs, no tremor but retropulsions, upward gaze palsy, dysarthria, dysphagia and later, nuchal stiffness. Nosological identification is discussed.
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PMID:Pallido-nigro-luysial atrophy associated with degeneration of the centrum medianum. A clinicopathologic and electron microscopic study. 84 97

The neurologic states and activities of daily life of patients with Parkinson's disease were evaluated using a rating scale with subitems, and subsequently the neurologic disturbance scores and the daily activity impairment scores were obtained. Subjects consisted of 19 normal controls, and 55 ambulatory patients without marked dyskinesia who were on various anti-parkinsonian drugs. Blink reflex was elicited by paired electrical stimulation over the supraorbital nerve. The interval time between the conditioning stimulation and the test stimulation was set at 200 ms, and 5 serial ipsilateral maximal R2 amplitudes on the stimulated side were measured. The mean of the paired maximal R2 amplitude ratio (test/conditioning), expressed as a percentage, was defined as the habituation index. The habituation indices in normal controls and those with Parkinson's disease were 17.1 +/- 7.6 and 51.9 +/- 29.3, respectively (P less than 0.01). The degree of akinesia, rigidity, balance/gait and dysarthria was positively correlated with the habituation index (P less than 0.01), while tremor was not. On the whole the habituation index was found to have a significant correlation not only with the neurologic disturbance score but also with the daily activity impairment score (P less than 0.01).
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PMID:A correlation study between blink reflex habituation and clinical state in patients with Parkinson's disease. 156 13

For the stereotactic treatment of Parkinson's disease, the target is usually located in the thalamus; this point is related to nearby structures (third ventricle). Then the position is controlled by electrophysiological recordings. The lesion of the target results in permanent suppression of the contralateral tremor and/or rigidity but it changes neither the course of the disease nor the akinesia. Owing to the risk of dysarthria with bilateral procedures, the main indication for surgery is parkinsonism with unilateral tremor or rigidity. Particularly interesting for the future are the possibilities of stimulation through implanted chronic electrodes.
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PMID:[Stereotaxic treatment in Parkinson's disease]. 265 87

This open trial is a study of the effect of adding bromocriptine (BC) to the treatment of patients who had taken a dopa-containing preparation (LD) for many years. Sixty-five patients entered the trial at an average age of 66.6 years. The mean duration of Parkinson's disease was 12.74 years and LD had been taken by one-half of them for more than 10 years and by an additional 27% for longer than 5 years. The duration of treatment with BC exceeded 2 years in 45% of cases and the average dose of BC was 19.27 mg/day. On the Hoehn and Yahr scale 70.8% of patients were classified as between stages II and IV, 24.6% were in stage I and 4.6% were in stage V. Dopa-induced involuntary movements were observed in 60% of patients at the beginning of the trial but were present in only 25% at the completion, due to the dopa-sparing effect of BC allowing a reduction of the dose of LD by an average of 34%. End-of-dose failure was reduced only slightly and on-off oscillations were not influenced by the addition of BC to LD. Tremor, rigidity, akinesia and dysarthria improved in 22% of all patients but BC offered no beneficial effect on the various gait disorders of Parkinson's disease. The conclusion of the study is that 47.7% of patients felt that the addition of BC to LD had reduced their involuntary movements and the disabilities of their disease.
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PMID:The addition of bromocriptine to long-term dopa therapy in Parkinson's disease. 270 77

In order to investigate the neuronal basis of cognitive disorders in Parkinson's disease, the neuropsychological performance of 120 patients with idiopathic Parkinson's disease was analysed in relation to motor symptoms as a function of their response to levodopa. Cognitive impairment was poorly correlated with akinesia and rigidity, symptoms which respond well to levodopa treatment, and was not correlated at all with that part of the patients' motor score that could be improved by the drug. In contrast, strong correlations were found between all neuropsychological test scores and axial symptoms such as gait disorder and dysarthria, which respond little if at all to levodopa treatment. The neuropsychological test scores were also strongly correlated with the motor score of patients estimated when clinical improvement was maximal under levodopa treatment. This score is assumed to represent residual non-dopaminergic motor dysfunctions. The correlations suggest that much of the cognitive impairment in Parkinson's disease results from the dysfunction of non-dopaminergic neuronal systems.
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PMID:Does cognitive impairment in Parkinson's disease result from non-dopaminergic lesions? 270 38

Experience with liver transplantation for patients with Wilson's disease who have major neurological impairment is limited, and this report describes the results obtained in two such patients. The first was a 30-year-old man with a 14-month history of hepatic and neurological impairment. In spite of treatment with d-penicillamine, he developed increasing dysarthria, dysphagia, akinesia and rigidity of all four limbs, and required continuous nursing care. Following transplantation, liver function was almost normal from four weeks onwards, but recovery of neurological function was much slower and was not seen until two to three months after surgery. By four months he was sufficiently mobile to be discharged, and when he returned for assessment at eight months, no abnormal neurological signs were detectable. The second patient was a 27-year-old woman with worsening liver dysfunction for eight years; one year previously she had developed dysarthria, akinesia, a fine tremor and moderate rigidity of all limbs as well as marked psychological impairment. There was no improvement on treatment with d-penicillamine or trientine, but as liver function returned to normal two months after liver grafting, her neurological and psychological function began to improve so that by three months she could be discharged.
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PMID:Reversal of severe neurological manifestations of Wilson's disease following orthotopic liver transplantation. 332 13

The motor score with and without levodopa was estimated in 193 parkinsonian patients with variable length of evolution. The effect of levodopa on akinesia, rigidity, and tremor remained quite stable during the course of the disease. In contrast, the aggravation of gait disorder, postural instability, and dysarthria was more severe, with decreased percentage of improvement on levodopa in patients with longer evolution. It is suggested that aggravation of Parkinson's disease mainly results from increasing severity of cerebral nondopaminergic lesions.
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PMID:Does long-term aggravation of Parkinson's disease result from nondopaminergic lesions? 362 54

An unusual case of Whipple's disease is reported. The diagnosis was difficult as the characteristic digestive sign and symptoms (malabsorption, diarrhea, mucosal infiltration by PAS-positive macrophages) were absent. After a ten-year history of seronegative arthritis, myocardiopathy, with aortic insufficiency, basilar pulmonary infiltrates, enlarged lymph nodes, the patient, a 56 years old man, was referred to us for a severe vegetative and neurological dysfunction: stupor, dysarthria, akinesia, hypertonia, hypothermia and abnormal thirst. A CT-scan showed a low-density area of the right hypothalamus, and PAS-positive macrophages were found in a lymph node, in the CSF and in a cerebral biopsy. The patient then received a classical antibiotic treatment, yet the neurologic dysfunction remained severe. Finally, a trial with rifampicin brought a striking improvement of the patient's condition, which has now lasted for three years.
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PMID:[Hypothalamic form of Whipple's disease. Favorable effect of rifampicin]. 619 50

A female patient, who died at the age of 61 and had suffered from several manic-depressive psychoses for more than 30 years, developed three phases of intoxication under lithium therapy. There was a 15-year history of electro- and Pentetrazol-induced convulsive therapy prior to lithium medication; neuroleptics were still administered during lithium therapy. The last lithium intoxication, 3 years prior to death was during a low-dosage therapy with normal lithium levels followed by severe lasting impairment: akinesia, rigidity, dysarthria, ataxia, and an organic alteration in character. For the first time, neuropathological findings could be established in such a case: extensive damage to granule and Purkinje cells in the cerebellum; gliosis in the dentate nucleus, the inferior olives, and the nucleus ruber; cytoplasmic inclusions in various nerve cells of the cranial nerve nuclei; cytoplasmic vacuoles, especially in the cells of the supra-optic nucleus. Surprisingly little damage could be found in the substantia nigra and in the neostriatum. The clinical course as well as the pattern and intensity of the brain damage oppose an interpretation as a consequence of preceding convulsive shock therapy.
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PMID:Clinical and neuropathological aspects of long-term damage to the central nervous system after lithium medication. 679 83


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