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

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

The adverse effects of cerebral angiography with metrizamide and meglumine metrizoate were compared in 20 patients for each contrast medium using a double blind technic. Deterioration of the EEG and bradycardial reactions were seen more often with meglumine metrizoate than with metrizamide and these differences were statistically significant. Metrizamide also had a shorter circulation time, less influence on the blood pressure and EMG than meglumine metrizoate, but these differences were not statistically significant. The clinical examinations showed no difference in the minor adverse effects. One patient had transient hemiparesis and dysarthria after angiography with meglumine metrizoate but no serious complications were seen in the others.
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PMID:Cerebral angiography with non-ionic (metrizamide) and ionic (meglumine metrizoate) watersoluble contrast media. A comparative study with double blind technic. 33 Nov 37

Arterial hypertension causes the formation of small lacunes, or ischemic brain infarcts, which may result in transient ischemic attacks, hemiparesis, sensory loss, ataxic hemiparesis, or dysarthria. Usually these effects are reversible with physical therapy, but multiple lesions may lead to dementia. Prevention of lacunar disease is possible with vigorous control of hypertension.
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PMID:Lacunar strokes. 39 51

A case of spontaneous pontine hematoma in young boy, with remitting and relapsing clinical course of up to 11 years, suspected of having pontine glioma or multiple sclerosis is reported. Differential diagnosis of these are mentioned with reference to our cases of pontine glioma. This patient was a man aged 16. At 5 years of age he had his first episode of double vision. 20 days after first episode, gait disturbance, left facial palsy and consciousness disturbance developed. Neurological and neuroradiological examination revealed a pontine glioma and radiotherapy was administered. All signs and symptoms resolved except for bilateral abducens palsy. Four months later, he again complained of gait disturbance and facial palsy. Examination revealed bilateral conjugate ocular palsy, left facial palsy and cerebellar ataxia. These symptoms again resolved spontaneously, except for bilateral abducens palsy. At age 16 years, having been asymptomatic for 10 years, he suddenly noticed loss of taste. At that time sensory disturbance of the left side of himself, right hearing disturbance, dysarthria and retardation urinae. Neurological examination revealed bilateral optic atropy, bilateral abducens palsy, left facial palsy, right hyperacuisis, dysarthria, left hemiparesis, hypesthesia of the left side of the body and left cerebellar ataxia. The vertebral angiography was no evidences of mass lesion and vascular anomalies. The computed tomography demonstrated a pontine hematoma. Conservative therapy was performed and these symptoms cleared off except for bilateral abducens palsy.
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PMID:[A case of spontaneous pontine hematoma in patient suspected of pontine glioma and multiple sclerosis (author's transl)]. 72 72

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

A case of left atrial myxoma with repeated multiple cerebral emboli is reported. A-44-year-old man first developed a sudden right hemiparesis in October 1969. After intensive physical theraphy, strength improved and he was able to return to his work. In March 1970, he suddenly lost consciousness and remained comatose for a day. Upon waking, he had a profound right hemiparesis, motor aphasia and Gerstmann's syndrome. He was admitted to Hiroshima City Hospital on August 1, 1970. The cardiac examination, including an electrocardiogram, was entirely normal. Laboratory studies revealed a normal blood count and urinalysis; erythrocyte sedimentation rate was elevated (32mm/hour). On a left cerebral angiographic study, performed on September 6, 1971, multiple aneurysmal dilatations of the branches of the left middle cerebral artery were demonstrated. No specific diagnosis was made. In January 1973, he developed dysarthria, dysphagia and quadriplegia because of the recurrent cerebral attacks. He had a high temperature continuously for three days and died on May 30, 1974. At autopsy a myxoma with the peduncle was attached to the septal wall of left atrium, and there were old infarcts in the brain, the myocardium and the kidneys.
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PMID:[Left atrial myxoma with repeated multiple cerebral emboli]. 103 60

A case of hemihyperhidrosis and non-paralytic pontine exotropia due to brainstem infarction is reported. A 55-year-old hypertensive man developed right hemiparesis with slight dysarthria and nausea upon awaking. The right side of his face and right upper limb and trunk to the level of the Th8-9 territory showed hyperhidrosis, which disappeared in a week. Ocular motor examination revealed that during forward gaze with the left eye fixing, the right eye deviated outward. The patient was able to adduct the right eye to midposition with the right eye fixing. Rightward gaze elicited full abduction and right-beating nystagmus of the right eye, but the left eye did not adduct. When he attempted to gaze leftward, both eyes made the full excursion, but saccades were slow in that direction. Convergence was intact. Vertical gaze was full, and he did not show Horner's sign. This ocular sign, non-paralytic pontine exotropia, disappeared three days later. T2-weighted spin echo magnetic resonance imaging disclosed a small lesion with high intensity in the inner side of the left middle pons. This hyperhidrosis was thought to be caused by destruction of inhibitory fibers thermoregulating sweating. These findings suggest that at the level of the middle pons inhibitory fibers descend along the inner side of facilitatory fibers thermoregulating sweating, which are speculated to descend the dorso-lateral part of the pontine tegmentum. These findings also suggest that lesions of non-paralytic pontine exotropia may be located in the paramedian pontine reticular formation rostral to the abducens nucleus with ipsilateral medial longitudinal fasciculus lesion, but further investigation is necessary.
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PMID:[A case of hemi-hyperhidrosis and non-paralytic pontine exotropia due to brainstem infarction]. 129 Nov 62

Epithelial cysts in the posterior fossa are very rare, and only 22 cases have been reported in literatures. We report a case of epithelial cyst occurring on the anterior surface of the brain stem. A 31-year-old man was admitted to our hospital complaining of right hemiparesis and dysarthria. Plain CT showed a heterogeneous (isodense-hyperdense) mass in front of the pons, and was not enhanced after injection of contrast medium. As for findings of MRI, the tumor revealed as heterogeneous (isointense-hyperintense) mass on T1-weighted image and also heterogeneous (hypointense-hyperintense) mass on T2-weighted image. We removed partially the tumor which content was like yogurt. The histological findings of the cyst wall revealed a pseudostratified columnar ciliated epithelium.
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PMID:[Epithelial cyst occurring on the anterior surface of the brain stem--case report and review of the literatures]. 129 17

We examined six patients with an abrupt change in behavior after infarction involving the inferior genu of the internal capsule. The acute syndrome featured fluctuating alertness, inattention, memory loss, apathy, abulia, and psychomotor retardation, suggesting frontal lobe dysfunction. Contralateral hemiparesis and dysarthria were generally mild, except when the infarct extended into the posterior limb. Neuropsychological testing in five patients with left-sided infarcts revealed severe verbal memory loss. Additional cognitive deficits consistent with dementia occurred in four patients. A right-sided infarct caused transient impairment in visuospatial memory. Functional brain imaging in three patients showed a focal reduction in hemispheric perfusion most prominent in the ipsilateral inferior and medial frontal cortex. We infer that the capsular genu infarct interrupted the inferior and anterior thalamic peduncles, resulting in functional deactivation of the ipsilateral frontal cortex. These observations suggest that one mechanism for cognitive deterioration from a lacunar infarct is thalamocortical disconnection of white-matter tracts, in some instances leading to "strategic-infarct dementia."
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PMID:Confusion and memory loss from capsular genu infarction: a thalamocortical disconnection syndrome? 841 58


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