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

Broca's aphasia is characterized by disorders on the phonemic, syntactic and lexical level of linguistic description. It is not only the patient's speech which is impaired; abilities to comprehend, read and write are likewise impaired. Articulatory disorders (dysarthria) which are due to an impaired innervation of the phonatory and articulatory musculature may exist. However these disorders do not account for all the linguistic deficits found in cases of Broca's aphasia. The characteristic feature enabling a differential diagnosis of Broca's aphasia is agrammatism.
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PMID:[Broca's aphasia. The clinical picture and a consideration of the neurolinguistic structure (author's transl)]. 7 59

Eight attacks of transient global amnesia were observed in a female patient who suffered from livedo reticularis and a series of other neurological symptoms, which were transient in most stances. The neurological deficits include focal epileptic attacks, unilateral loss of vision, paresis of left arm and/or leg and dysarthria. The first amnestic attack was seen at the age of 19. The episodes lasted from a few to 3 days. The intervals between the amnestic episodes varied between a few days and 11 years. The livedo reticularis became more obvious during each neurological episode and was less pronounced during the time of remission. A benign type of essential hypertension and parproteinemia (gamma-M) was found. The investigations failed to show any evidence of essential thrombocythemia, polyarteriitis nodosa, lupus erythematodes and other immune complex diseases. The underlaying disease remained unclear.
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PMID:Recurrent transient global amnesia in a case with cerebrovascular lesions and livedo reticularis (Sneddon Syndrome). 9 41

Eight macaques were trained on one of two isometric force regulation tasks. Six animals were trained to maintain a static force for a 2-sec period, and two animals were trained to make a rapid series of bites on a force transducer four times in succession. Electromyographic (EMG) electrodes were chronically implanted into temporalis and masseter muscles. Lesions were made in the cerebellum in seven monkeys and a control surgery with no neural damage was performed on one monkey. Following cerebellar lesions, the abilities of the monkeys to maintain a static isometric force for 2 sec were impaired. Animals overshot the correct force band and force tremors increased in amplitude following the lesions. Cerebellar lesions were followed also by a reduction in biting frequency from about 3 Hz to 2 Hz. Measurements of the temporalis EMG indicated that the reduced biting rate was associated primarily with a prolongation of the inter-EMG interval and secondarily with a prolongation of the EMG duration. Changes in jaw-force regulation following the lesions appear to be similar to the types of changes observed in arm control in monkeys, and in the speech of persons with ataxic dysarthria.
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PMID:Effects of cerebellar lesions on monkey jaw-force control: implications for understanding ataxic dysarthria. 10 Jun 57

The authors report the case of an 8 year-old boy who, when he was 2 1/2 years old, suffered from spasmodic mouth twitches. At the age of four, various other symptoms appeared: psychomotor backwardness, frequent fails and a photomyoclonic response on electroencephalogram. At the age of 5 1/2, noticeable difficulties appeared in walking with a broad-based gait, hypotonia, and intentional trembling associated with hypokinesia and dysarthria. When he was six, the first convulsive seizure appeared, then myoclonies which became continuous. The child gradually became bedridden. The family history tends to show these disorders can be linked with a Huntington chorea affecting six generations. This case is very similar to that previously described by the authors, in an 8 year-old girl where an anatomic examination revealed the existence of lesions characteristic of Huntington's disease associated with lesions of the cerebellum. The authors, on the basis of the data provided by the literature, discuss the myoclonic and cerebellous aspect of this infantile form. Lacking anatomic evidence, they stress the interest of the biochemical disturbances affecting the cerebral monoamines noted in this observation.
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PMID:[Myoclonic type of Huntington's chorea (author's transl)]. 14 49

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

Two adult Ashkenazi Jewish siblings have had slowly progressive deterioration of gait and posture since early childhood, distal to proximal muscle atrophy, pes cavus, foot drop, spasticity, mild ataxia of limbs and trunk, dystonic features, and dysarthria. Vision and optic fundi are normal, verbal intelligence is stable, and no seizures have occurred. The sister of the patients died at 16 years of age with the same illness. Autopsy showed diffuse neuronal storage, predominating in subcortical areas, consisting of membranocytoplasmic bodies, zebra bodies, and complex lamellar structures. GM2 ganglioside was increased in her brain. Hexosaminidase A was decreased in serum and leukocytes of the living patients, and was in the range for carriers of Tay-Sachs disease in their parents. The disease found in this family represents a new, more indolent variant of GM2 gangliosidosis.
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PMID:Adult (chronic) GM2 gangliosidosis. Atypical spinocerebellar degeneration in a Jewish sibship. 17 70

Two cases of progressive supranuclear palsy (PSP) are reported in two men (49 and 75years old) who for one and four years respectively had sudden falling while walking. Rigidity of the neck was an carly feature that prgressed to involve the upper trunk while "subcortical dementia", dysarthria and dysphagia appeared. They had a complete paralysis of vertical eye movements and slow horizontal voluntary eye movements. Oculocephalic reflexes were intact. On caloric stimulation vestibulo-ocular responses were present but only slow saccadic eye movements were observed. With surface electrodes eye movements were studied during the REM phase of sleep. Our patients had both vertical and horizontal eye movements during paradoxal sleep. This findings is in keeping with a supranuclear ophtalmoplegia, and may help in antemorten diagnosis of PSP.
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PMID:Progressive supranuclear palsy: report of two cases (author's transl). 18 May 89

Antecubital venous blood was sampled from stroke patients in the presence of disodium ethylenediamine tetraacetate. Plasma was analyzed for cyclic AMP applying a competitive protein binding method without any special pretreatment. In mild hemispheric infarction as manifested by moderate hemiparesis and/or dysarthria, plasma cyclic AMP remained in the normal range (8-18 picomoles/ml). In most of the cases with moderate infarction, the cyclic AMP level was distinctly below the normal range several days after the onset of symptoms. However, cyclic AMP remained in the normal range in severe infarction with signs of brain edema, and in two cases with moderately severe symptoms. One of the two cases suffered from later development of brain edema, and the other revealed a large lesion in brain scintigrams. The sizes of the lesion revealed in brain scintigrams were smaller in the moderate cases and larger in the severe cases, except in one of the cases mentioned above. It appeared that with plasma cyclic AMP levels we could predict the extent of the lesion, and perhaps the subsequent development of impending brain edema in a few days after the onset of cerebral infarction. In moderate cases of cerebral hemorrhage, judged from the consciousness, cyclic AMP decreased to a subnormal level 2-4 days after the onset. In severe cases it remained in the normal range. Subarachnoid hemorrhage showed significantly elevated cyclic AMP levels in the early stage.
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PMID:Venous plasma cyclic AMP in acute cerebrovascular disease. 18 49

This report presents some of the underlying neuromuscular mechanisms of dysarthric speech production as they are manifested in selected individuals with parkinsonism. Earlier explanations of parkinsonian dysarthria emphasized that the balanced hypertonus of rigidity formed the basis of reduced range of movements in speech. The present data reveal two problems in the neuromuscular control signals that can result in a reduced range of speech movements in the absence of rigidity. These neuromuscular problems are described as acceleration and weakness. The implication of these findings for the evaluation and treatment of parkinsonian dysarthria is discussed.
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PMID:Acceleration and weakness in parkinsonian dysarthria. 18 32

An unusual neurovisceral lipid storage disorder in two unrelated juvenile patients manifested itself by dystonia and involuntary movements, with facial grimacing, dysarthria, gait difficulty, and impaired manual dexterity. Supranuclear paresis of vertical gaze and splenomegaly were present. Absent were seizures, major intellectual deterioration, spasticity, or blindness. Histiocytes showed lysosomal storage of various phospholipids, cholesterol, neutral lipids, and autofluorescent material. Appendiceal neurons showed only an increse of phospholipids by histochemistry. Neuronal deposits differed ultrastructurally from these in histiocytes. Leukocyte sphingomyelinase activity was normal. The nosology of this disease and its relationship to so-called juvenile types of Niemann-Pick disease is discussed. The primary metabolic defect in these patients remains unknown.
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PMID:Juvenile dystonic lipidosis: an unusual form of neurovisceral storage disease. 18 51


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