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)

Nine cases of multiple sclerosis with paroxysmal disorders were treated with acetazolamide. In most cases a brain-stem origin of the seizures was suggested by their particular pattern: crossed syndromes (facial spasm associated with contralateral weakness of the arm and leg, paroxysmal paraesthesiae in one side of the face and weakness of the contralateral leg), paroxysmal dysarthria, and ataxia. One patient with a Brown-Sequard syndrome complained of paroxysmal paraesthesiae in the lower limbs, for which a spinal origin was admitted. In all patients the paroxysmal disorders were promptly suppressed or markedly reduced by acetazolamide.
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PMID:Treatment with acetazolamide of brain-stem and spinal paroxysmal disturbances in multiple sclerosis. 115

The authors report a case of glioblastoma in which MR images with Gd-DTPA enhancement changed rapidly during the early stage. A 61 year-old male presented with sudden right facial spasm and dysarthria. However, both a plain and an enhanced CT failed to demonstrate any abnormal lesions. On the other hand, T2 weighted MR image revealed a well circumscribed high intensity lesion in the left frontal lobe without mass effect. This lesion could not be differentiated from cerebral infarction, since no contrast enhanced lesion was able to be observed in T1 weighted MR image with Gd-DTPA. His symptoms gradually became aggravated and at 3 months from the onset, MR image with Gd-DTPA disclosed a small enhanced lesion in the left frontal lobe near the cortical surface. After 6 months from the onset, he suffered from right hemiparesis and motor aphasia. The MR image with Gd-DTPA at this time showed a large enhanced lesion in the left frontal lobe with mass effect. He was admitted to our hospital, and subtotal removal of the tumor and intraoperative radiation was carried out. The patient did well postoperatively without additional neurological deficit, and then he received additional radiation therapy. It should be noted that Gd-DTPA enhanced MR image might fail to reveal the lesion of glioblastoma in its early stage, while T1 weighted image discloses only the gyral swelling.
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PMID:[A case of glioblastoma in which early diagnosis was difficult by MRI]. 194 85

Various types of associated movements of eyeballs with other cranial muscles have been described in the literature. Only a few observations, however, have been reported on the relation of ocular movements and facial muscles innervated by the facial nerve, especially the orbicularis oculi muscles. We report two cases presenting gaze-evoked involuntary contraction of the orbicularis oculi muscle and unilateral eyelid closure. Case 1 was a 38-year-old housewife who was admitted to our hospital because of gait disturbance and sensory deficits below the neck. She had a 5-year history of left facial palsy, disturbed horizontal eye movements, retrobulbar optic neuritis, spastic paraparesis and bladder and rectal disturbances, some of which had relapsed a few times. Neurological abnormalities were summarized as follows: bilateral pale discs, right Horner's sign, horizontal nystagmus, left facial nerve palsy of peripheral type, spastic paraparesis with left-sided predominance, sensory disturbances below the third cervical segment, truncal and limb ataxia, and bladder and rectal disturbances. Gaze-linked synchronized contraction of the left facial muscles was observed and on the left lateral gaze marked spasm of the left orbicularis oculi muscle with occasional lid closure was evoked. Case 2 was a 72-year-old female with cerebellar hemorrhage. Neurological abnormal findings included mild disorientation, meningeal irritation signs, horizontal nystagmus on lateral gaze, reduced response of reflex eye movement to the left, minimal weakness of the left facial muscles, ataxic dysarthria, mild left hemiparesis and hemisensory deficits with face, truncal and limb ataxia. She could move eyeballs to any direction but with effort to the left.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Gaze-evoked eyelid closure. Report of two cases]. 261 99

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 17 year old high school boy experienced fever and diarrhea, which subsided within 4 days by appropriate medications. Six days later, however, he developed unsteadiness and limb spasm. On the morning of admission, he was found to have drowsiness, dysarthria, gait disturbance and involuntary jerks. When he was brought to the hospital, he was lethargic but could follow simple verbal commands. Frequent involuntary movements manifested by facial grimacings, limb spasms and twitchings with dystonic features were seen. Decorticate posturing was readily elicited by painful stimuli. There was no meningeal irritation sign or gross sensory impairment. The deep tendon reflexes were symmetrically exaggerated with bilateral Babinski signs. Bilateral lateral rectus muscle weakness was found together with mild ptosis and upward gaze limitation. Nystagmus was not present and the funduscopic examination was normal. Immediately he was placed on anticonvulsants, steroid hormone, gamma-globulin and antibiotics as well. A brain CT scan and a CSF examination revealed no abnormality. Meanwhile he continued to show a progressive deterioration associated with fever and status epilepticus, and within 24 hours he lapsed into coma in decorticate posture. An EEG obtained at the 3rd hospital day was compatible with spindle coma. In spite of aggressive treatment he remained febrile and comatous. Therefore, vidarabine (adenine arabinoside) was initiated from the 3rd hospital day for 5 days. Then he began to groan and show frequent choreic movements. For the subsequent 2 weeks he made a slow recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of brain stem encephalitis with complete recovery (Bickerstaff's encephalitis)]. 620 73

Thirty-four patients were submitted to the conventional cervical myelography by administration of metrizamide (Amipaque) through three routes (lumbar 23, suboccipital 6, C1-C2 lateral 5). After the injection of metrizamide (4-11 ml, 170-250 mgI/ml), all procedures of the cervical myelography were done as soon as possible within 9 minutes. The adverse reactions of Amipaque were observed in 29 cases (85%) out of 34 cases initially 1 hour after cervical myelography and disappeared completely in an average of 16 hours. The total number of the side effects was 140 incidences such as meningeal irritation (headache 18, nausea 17, vomiting 17), cerebellar signs (dizziness 11, dysarthria 8, tremor 5, bradylalia 2, dysmetria 2, tipsy feeling 2, dysdiadochokinesis 1), autonomic signs (flushing 7, pale face 4, fever 4, sweating 2, hiccup 2, fatigability 2, micturition disturbance 1), sensory signs (exacerbation of numbness 6, perioral numbness 3, back pain 1, chest pain 1), motor signs (focal muscle spasm 5, exacerbation of paresis 4, areflexia 1), psychiatric signs (dysphasia 3, disturbance of consciousness 2, euphoria 1, persecutory delusion 1) and muddiness 7. We observed that waxing and waning of side effects correlated tightly with transient cortical penetration of dye in CT and cortical dysfunction mainly slowing of the background activity and slow wave burst in EEG. According to high frequency of side effects in our study, we suggest that a greater incidence of side effects may result when high concentration of Amipaque comes in contact with the cerebral cortex by using an inadequate fluoroscopic table which has only fixed one plane image and rough positioning control. Slow absorption into blood stream may affect appearance and maintenance of side effects. In order to decrease side effects after Amipaque cervical myelography, we propose that we should introduce a mobile rotating chair coupled with high power image and chose C1-C2 lateral route using 1500-1700mgI of Amipaque.
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PMID:[Side effects of metrizamide (Amipaque) cervical myelography (author's transl)]. 711 May 15

We administered local botulinum toxin injections on the leg adductors of 12 patients with spastic paraparesis (9 patients with HAM, 2 patients with spinal spastic paraparesis, 1 patient with an identified degenerative disease). Two of them were wheelchair-bound and the other patients could walk with or without help. The patients were assessed by the time to walk 10 m and the spasticity score which was derived from the degree of muscle tone and spasm frequency of leg adductors. After the initial injection, 7 of the 12 patients improved spasticity scores and 8 of the 10 patients could walk 10 m within a shorter time. The time to walk 10 m was markedly shortened in moderate cases. However, one patient complained of leg weakness and the time to walk 10 m was prolonged. Five of the 12 patients received injections 3 to 7 times, and were followed up for a mean of 16.2 months. In 4 of the 5 patients, repeated injections could maintain the improvement of spasticity score and time to walk 10 m. However, injection was discontinued in one patient because of leg weakness. The other side effects were pain and swelling at the injected site and dysarthria. However, these side effects were slight and transient and did not require treatment. No other systemic side effects were observed. In conclusion, the beneficial effects of botulinum injections to spastic paraparesis were (1) improvement of objective symptoms in mild cases, (2) improvement of ADL in moderate cases, and (3) improvement of objective symptoms and ease of nursing care in severe cases. Furthermore, we confirmed the long-term efficacy and safety of botulinum toxin.
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PMID:[Treatment of spastic paraparesis with botulinum toxin with reference to beneficial effects, disease severity and long-term treatment]. 761 46

We report a 74-year-old man with a lung cancer, who developed right leg weakness, neurogenic bladder, and multiple cranial nerve palsies. The patient was well until December of 1992, when he was 74-year-old, when he noted transient double vision; in February of 1993, he noted numb sensation and weakness in his right leg. Later in the same month, he developed overflow incontinence of urine and weakness in his right face. He also noted deafness in his left ear (he had a marked loss of hearing in his right ear since childhood because of otitis media). His weakness in his right leg had progressed, and he was admitted to our service on March 19, 1993. On admission, he was afebrile and BP was 130/50 mmHg. General physical examination was unremarkable. On neurologic examination, he was alert and oriented to all spheres; no dementia was noted nor were detected aphasia, apraxia, and agnosia. His optic fundi were unremarkable; ocular movement appeared normal, however, he complained of diplopia in far vision. Sensation of the face was intact. He had right facial palsy of peripheral type; he was unable to close his right eye, and Bell's phenomenon was observed on attempted eye closure. On the left side, he had facial spasm. He had marked bilateral deafness. He had no dysarthria or dysphagia. The remaining of the cranial nerves were intact. Motor wise, he was unable to stand or walk alone; weakness did not appear to account for his difficulty in gait; manual muscle testing revealed 4/5 weakness in his tibialis anterior muscle, 1/5 in the peroneus longus, 0/5 in his extensor hallucis longus and extensor digitorum longus, all on the right side. Brachioradial and quadriceps femoris reflexes were increased to 3/4; plantar response was equivocal on the right side, and flexor on the left. Sensory examination revealed loss of touch and pain sensation in the L5 and S1 distributions in his right leg: vibration and position sensations were also diminished in his right foot. He had overflow urinary incontinence with loss of bladder sensation. Marked nuchal stiffness was noted, however, no Kernig's sign or eye ball tenderness was present. Pertinent laboratory findings were as allows; WBC 8,100/microliters, Ht 42.5%, platelet 326,000/microliters, TP 6.8 g/dl, BUN 16 mg/dl, creatinine 0.54 mg/dl, glucose 95 mg/dl, Na 136 mEq/l, K 4.4 mEq/l, Cl 100 mEq/l; liver profile was normal; CEA 436.6 ng/ml, CA19-93 U/ml; urinalysis was normal.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 74-year-old man with urinary incontinence, right leg weakness and multiple cranial nerve palsies]. 766 22

Superficial hemosiderosis (SH) of the CNS is a rare disease caused by repeated subarachnoid hemorrhage, with progressive superficial siderosis of the CNS. We report a patient with SH whose clinical picture was marked by progressive gait ataxia, hearing loss, dysarthria, and recurrent episodes of hemifacial spasm. Iron and ferritin levels in the CSF were significantly higher than in a control group of patients. Six month's treatment with the iron-chelating agent trientine dihydrochloride led to clinical improvement, with a concomitant reduction of CSF iron level. We suggest that, in addition to magnetic resonance imaging findings, CSF levels of iron and ferritin should be used as diagnostic criteria for SH, as well as to estimate the efficacy of iron chelation treatment.
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PMID:Superficial hemosiderosis of the central nervous system. 855 30

When a child does not speak, this may be because there is no wish to do so (elective or selective mutism), or the result of lesions in the brain, particularly in the posterior fossa. The characteristics of the former children are described, especially their shyness; and it is emphasized that mild forms are quite common and a definitive diagnosis should only be made if the condition is significantly affecting the child and family. In the case of mutism due to organic causes, the commonest of these is trauma to the cerebellum. Operations on the cerebellum to remove tumours can be followed by mutism, often after an interval of a few days, and it may last for several months or longer, to be followed by dysarthria. Other rarer causes are discussed, and also the differential diagnosis. The so-called posterior fossa syndrome consists of mutism combined with ataxia, cranial nerve palsies, bulbar palsies, hemiparesis, cognitive impairment and emotional lability, but the post-operative symptoms are often dominated by the lack of speech. The most accepted cause for the condition is vascular spasm with involvement of the dentate nucleus and the dentatorubrothalamic tracts to the brain-stem, and subsequently to the cortex. Diaschisis may be involved in causing the loss of higher cerebral functions, and possibly, complicating hydrocephalus. The treatment of elective mutism is reviewed, either using a psychotherapeutic approach or a variety of drugs, or both. These may well be ineffective, and it must be remembered that the condition often resolves on its own. The former treatment must concentrate on the training of social skills and activities of daily life and must be targeted to both the child, the family, and the school. Also, all kinds of punishment and insistence on speech must be discouraged. The drug, which seems to be most effective, is fluoxetine. Discovering more about the causes of mutism due to organic causes may well depend on studies using such techniques as magnetic resonance imaging and single photon emission tomography.
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PMID:Mutism: elective or selective, and acquired. 1124 56


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