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 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 multiple sclerosis (MS) in a 39 year old Japanese female with high antibody titer to human T-lymphotropic virus type I (HTLV-I) in serum and cerebrospinal fluid (CSF) was reported. At the age of 15, gait and urinary disturbances accompanied by sensory impairment in the lower abdomen and lower extremities developed suddenly. The motor disturbance slowly progressed to tetraparesis over a period of 15 years with several remissions. At the age of 28 the patient suffered from an acute loss of visual acuity, unilateral initially, and became blind by the age of 34. On admission to our department in September, 1987, the patient was alert and had spastic paraparesis, the impairment of all sensory modalities below the level of Th 10 and urinary disturbance. Weakness of facial muscles, nystagmus, deviation of the tongue and dysarthria were also noted. By the PA method, the antibody titer to HTLV-I was measured x512 in the serum and x64 in the CSF. Western blotting analysis of the CSF disclosed the bands to p19, p24 and p28 of HTLV-I gag proteins. The CSF contained a few ATL-like atypical cells and showed mild lymphocytosis, but the total protein was not increased. The computed tomography revealed diffuse low density areas in the cerebral white matter. The magnetic resonance imaging disclosed high intensity signal areas in the cerebral white matter and in the dorsolateral portion of the medulla oblongata on the T2 weighted image. The link of HTLV-I infection to the pathogenesis of human demyelinating diseases was discussed.
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PMID:[A case of multiple sclerosis with high CSF antibody titer to HTLV-I]. 275 51

Hemifacial spasm is usually an isolated symptom resulting from facial nerve root compression. Three patients had, in addition, tinnitus, hearing loss, facial sensory loss, diminished gag reflex, dysphagia, and dysarthria. Acoustic reflexes were abnormal, and facial nerve conduction studies showed evidence of ephaptic transmission and ectopic excitation. Brain CT and metrizamide cisternography were normal. Surgical exploration showed compression of cranial nerve roots by posterior inferior cerebellar artery branches. After decompression, symptoms abated, and electrical signs of hemifacial spasm disappeared. Vascular compression of nerve roots in the cerebellopontine recess may cause multiple cranial neuropathy.
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PMID:Vascular compression, hemifacial spasm, and multiple cranial neuropathy. 399 Sep 69

A 59-year-old female was admitted with complaints of vertigo, dysarthria and dysphagia. On neurological examination, right-sided cranial nerve signs included ptosis, Bruns's nystagmus, decreased corneal sensation, diminished facial pain and temperature sensation, decreased palatal excursion and loss of gag reflex. There was no evident motor weakness, but deep tendon reflexes were slightly exaggerated on the left extremities. Coordination testing showed right cerebellar signs. Sensory examination of the remaining parts of the body was quite normal. X-ray CT scan showed multiple high density areas in the right medulla, right pons, right temporal and frontal lobes. T2 weighted MRI demonstrated these lesions as mixed signal intensity areas with marked low signal intensity rim. There were multiple black dots in the bilateral frontal and temporal lobes, cerebellar hemispheres on T2-weighted images. Carotid and vertebral angiograms showed no abnormality. This is the first report of the cavernous malformation presenting as lateral medullary syndrome.
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PMID:[Lateral medullary syndrome due to cavernous malformation in the brain stem]. 840 82

Here we report a 47-year-old man with dissecting aneurysm of the basilar artery who developed Foville's syndrome due to upper pons involvement. At first he had an abrupt onset of dysarthria and weakness in his left upper and lower extremities during his work. Neurological examination on admission revealed mild disturbance of consciousness, absent light reaction on the left side, hypesthesia of the left face, absent gag reflex, dysarthria, and left hemiparesis with ataxia. On the second hospital day he developed paralysis of conjugate eye movement to the right, left central facial palsy, and left hemiplegia, and hyperhidrosis of the left side of the body. He was diagnosed to have superior pons type of Foville's syndrome. Computed tomography showed low density area in the right upper pons, and the basilar artery had marked lateral shift, dilatation, and calcification. Vertebral angiography demonstrated dissecting aneurysm of the basilar artery. Although it is very rare that dissecting aneurysm of the basilar artery causes the brain stem symptoms, its possibility should be considered when computed tomography shows marked lateral shift, dilatation, and/or calcification of the basilar artery.
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PMID:[A case of dissecting aneurysm of the basilar artery presented as superior pons type of Foville's syndrome]. 856 44

Eight elderly men whose primary symptoms of myasthenia gravis were decreased speech and swallowing ability were seen for speech pathology evaluations and videofluoroscopic swallow studies. All patients had fatigable flaccid dysarthria and greater than expected pharyngeal phase dysphagia on videofluoroscopy; eight had decreased pharyngeal motility as demonstrated by residual material in the valleculae and pyriform sinuses bilaterally; seven had episodes of laryngeal penetration secondary to overflow of residual material; and five experienced silent aspiration despite gag reflexes and the ability to cough to command. Five patients required feeding tubes because their dysphagia responded poorly to treatment. Videofluoroscopic swallow studies revealed a common swallowing profile with pharyngeal phase dysphagia greater than expected from patient symptoms. Dysphagia did not improve at the same rate as other manifestations of myasthenia gravis.
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PMID:Dysphagia in elderly men with myasthenia gravis. 879 Dec 38

We reported a 72-year-old man with left supranuclear hypoglossal nerve palsy and right Avellis' syndrome due to a medullary small infarction. On admission, he showed slight disturbance of consciousness, ocular lateropulsion to the right side, rotatory nystagmus, dysarthria, absent right gag reflex, curtain sign, absent right palatal reflex, deviation of the uvula toward the left side, raise of only the left palate when the patient attempted to utter, paralysis of the right vocal cord and deviation of the tongue toward the left side. Neither atrophy nor fasciculation was observed on the tongue. 124 days after the onset, he had only the left supranuclear hypoglossal nerve palsy and right Avellis' syndrome. MRI showed a small lesion in the medulla, so lateral area of the medulla and a part of the reticular formation medial to the nucleus ambiguous presumed to be involved. These findings suggest that supranuclear pathway to the hypoglossal nucleus of the opposite side exists in the reticular formation near nucleus ambiguous.
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PMID:[A case of supranuclear hypoglossal nerve palsy with Avellis' syndrome due to a medullary infarction]. 890 92

We describe a case of unilateral IX, X and XI cranial and upper cervical nerve palsies involving zoster sine herpete (ZSH). A 63-year-old man experienced nausea, loss of appetite and general fatigue. On 4 days of illness, dysphagia, dysarthria and difficulty in elevation of his right arm appeared. Neurological examination showed the right curtain sign, a nasal voice and a decreased right gag reflex. He could hardly elevate his right arm laterally. Needle electromyography revealed positive sharp waves in his right trapezius muscle. Although no skin lesion was detected, anti-varicella-zoster virus antibodies were positive in both serum and cerebrospinal fluid. Acyclovir and a steroid were ineffective for these symptoms. Although case reports of unilateral IX, X and XI cranial nerve palsies with ZSH is very rare, ZSH should be kept in mind in the differential diagnosis of multiple cranial nerve palsies.
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PMID:[A case of zoster sine herpete with involvement of the unilateral IX, X and XI cranial and upper cervical nerves]. 1061 62

We present a case of bilateral medial medullary infarction demonstrated by magnetic resonance imaging (MRI) and review 12 previously reported cases. We classify these 13 cases (including the present case) into two groups according to the extent of the ischemic region: type 1, the ischemic lesion developed from the medullary pyramid to the medial longitudinal fasciculus; type 2, the lesion was confined to the medullary pyramid.A 71 year old man presented with slight disturbance of consciousness, dysarthria, disturbance of leftward gaze, no gag reflex and tetraparesis. He developed nearly complete horizontal ophthalmoplegia. MRI revealed upper medial medullary infarction bilaterally that extended to the pontomedullary junction. We propose that the prognosis of type 2 bilateral medial medullary infarction is better than that of type 1. Furthermore, the prognosis of bilateral medial medullary infarction itself may be better than previously indicated.
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PMID:Bilateral medial medullary infarction. 1102 38


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