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)

A 44-year-old man presented with symptoms of periodic ataxia, dysarthria, nausea and excessive sweating during the last twenty years. These symptoms could be provoked by physical or emotional stress and disappeared after bedrest for several hours. No other members of his family were known to have such complaints. Acetazolamide (Diamox) proved effective in preventing these symptoms. A disturbance of tryptophan metabolism is suggested as a cause of this disorder.
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PMID:Non-familial periodic ataxia responding to acetazolamide. 398 40

It has been recognized that small intracerebral hemorrhage not uncommonly produced lacunar syndromes. In this study, we examined cases of intracerebral hemorrhage presenting as lacunar syndromes. Of 174 cases with recent intracerebral hemorrhage, 19 presented with a lacunar syndrome: 4 presented with pure motor hemiparesis, 5, ataxic hemiparesis, 3, dysarthria-clumsy hand syndrome, 7, sensorimotor stroke, and, none, pure sensory stroke. The sites of hemorrhage were capsular in 11, putamenal in 6, and pontine in 2. In these 19 patients, 17 were hypertensive, and the signs characteristic of parenchymal hemorrhage, e.g., gradual onset, headache, nausea, vomiting and stiff neck, were absent or very rare. Computed tomography revealed that one third of the patients had one or more non-symptomatic lacunae in the basal ganglia, the corona radiata or the anterior limb of the internal capsule. These observations suggests that hypertensive intracerebral hemorrhage causes lacunar syndrome more often than previously considered and is apt to manifest ataxic hemiparesis and sensorimotor stroke. Computed tomography is the only way of differentiating hemorrhagic "lacunar" syndrome from lacunar infarct.
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PMID:Lacunar syndrome due to intracerebral hemorrhage. 400 60

A 46-year-old man developed sudden dysarthria and atactic gait and was noted to be unable to get up even on the bed about one year prior to his death. By following several days, he started to have scanning speech, nausea, trancal ataxia and dysmetria in succession. The cerebro-spinal fluid yielded moderate pleocytosis. There were no sensory disturbance, pathological reflexes and Romberg's sign. Half a year later, submandibular tumor was noted. The biopsy showed metastatic small cell undifferentiated carcinoma, presumably of pulmonary origin, and paraneoplastic cerebellar degeneration was suspected. He died of bronchopneumonia, superimposed on lung cancer on February 25 in 1979. The necropsy showed a large tumor in the right lung which was histologically verified small cell undifferentiated carcinoma (so-called oat-cell carcinoma). The cerebellum disclosed diffuse cortical atrophy, chiefly of Purkinje cell type. Moderate demyelination with reparative gliosis and foamy macrophages was seen in the white matter, which was considered secondary to cortical devastation. The morphometric study on Purkinje cell loss showed interesting distribution of the lesions. The severely affected portions were the central lobe and culmen in the vermis, and the ala lobuli centralis and quadrangular lobe in the hemisphere, respectively. The lingula was strikingly spared. The finding was compared with that of other cerebellar disease in reviewing the literature.
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PMID:[An autopsy case of carcinomatous subacute cerebellar degeneration--on distribution of cerebellar cortical lesions]. 609 6

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

Clinical features of cerebellar infarction in the territory of the superior cerebellar artery (SCA) were investigated in six male patients, ranging in age from 50 to 69 years. In all patients, there were MR images of infarction located in the area supplied by the SCA. The lesion was on the left-side in 2, right-side in 3 and bilateral (recurrent) in 1 patient. The onset of disease occurred with nausea, vomiting and floating sensation, with no overt brain stem signs other than symptoms of unilateral cerebellar ataxia and dysarthria. Five of the 6 patients had heart disease and cerebral angiography without definite evidence of SCA occlusion, strongly suggesting occlusion of the artery at its periphery due to cardiogenic embolism. A comparison of these 6 patients with those reported previously in Japan suggests that patients with SCA occlusion may be divided into two distinct subgroups: one manifesting diffuse brain stem signs in addition to cerebellar signs, and the other showing cerebellar signs as the only neurologic manifestation. In the former group, comprising the vast majority of patients, SCA occlusion occurred at the origin of the vessel due to a thrombus under a state of hypertension, diabetes mellitus or malignancy, producing signs of brain stem involvement, such as dissociating sensory disturbance and Horner's sign. While in the latter group, which included these 6 patients, paucity of brain stem signs, absence of definite cerebral angiographic evidence of SCA occlusion, and the presence of heart disease were distinguishing clinical features. Cardiogenic cerebral embolism was probably the underlying pathology in many of the cases and the functional prognosis was favorable.
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PMID:[Cerebellar infarction in the territory of the superior cerebellar artery, presenting a predominant cerebellar symptom--with special reference to its pathophysiology]. 761 47

We report a 78-year old woman with 30 years history of rheumatoid arthritis and nephrotic syndrome, who developed right hemiparesis and renal failure recently. The patient was diagnosed as having rheumatoid arthritis in 1965, and had been treated with gold -sol, steroid hormone, and non-steroidal anti-inflammatory drugs intermittently. Later on her clinical course was complicated by nephrotic syndrome, however, her renal function was well compensated. Otherwise, she was apparently doing well until October of 1988 when she had an onset of anomic aphasia; she was 73-year-old at that time. She was admitted to our hospital; a cranial CT scan at that time revealed a low density area in the left temporal region, and she was diagnosed as suffered from an atherothrombotic infarction involving the left middle cerebral artery territory. She recovered soon and was discharged for out patient follow up with ticlopidine 100 mg/day. She was doing well until December 15, 1990, when she had an acute onset of nausea, vomiting, and speech disturbance; she was admitted to our hospital for the second time. On admission, she was alert, but she had motor aphasia, right hemiparesis, and dysarthria. A cranial CT scan revealed a low density area in the left temporal region extending into adjacent frontal and parietal areas including the angular gyrus; in addition, leukoaraiosis, cortical atrophy, and ventricular dilatation were noted (Fig. 1A, B). She was treated supportively, and she showed improvement in her aphasia, however, moderate weakness remained in her right upper and lower extremities. She was discharged for out patient follow up. She was doing well until May 21, 1993, when she developed difficulty in swallowing and speech. She became unable to take foods orally and she was admitted again on May 31. On admission, she was afebrile and BP was 120/80 mmHg. General physical examination was unremarkable except for pitting edema and multiple contracture of her joints. On neurologic examination, she was alert but appeared to have aphasia and dementia; she could utter only a few simple words, and was able to understand only simple questions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[A 78-year-old woman with rheumatoid arthritis, right hemiparesis, and renal failure]. 789 38

The frequency of cerebellar infarctions over two and a half years was 2.7% of the 1300 hospitalized patients over that period. Sixteen patients with cerebellar infarctions were studied by using clinical manifestations and magnetic resonance imaging (MRI). Ages ranged from 41-87 (mean 63.5) years; 13 were men and 3, women. Risk factors included: hypertension (50%), diabetes (44%), prior stroke (44%), cardiac disease (38%), and hyperlipidemia (19%). Common symptoms and signs were dizziness/vertigo (75%), unsteadiness (69%), dysarthria (69%), and nausea/vomiting (50%). Infarcts mainly involved the posterior inferior cerebellar artery (PICA) territory and tended to be associated with brainstem infarcts in 14 of the 16 patients. Most cerebellar infarctions had a benign course, especially the small ones. No mortality was noted in this series. The short-term outcome of the cerebellar infarctions seemed to depend on the size of the infarcts and the sites of the artery occlusion. It was concluded that diagnosis of cerebellar infarctions requires a high index of clinical suspicion, especially when patients present with a sudden onset of ataxia, dizziness/vertigo, nausea/vomiting and dysarthria; and that MRI is a useful tool for the detailed study of cerebellar infarctions and can elucidate associated brainstem infarcts.
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PMID:A clinical and MRI study of cerebellar infarctions. 829 26

Listeria monocytogenes rhombencephalitis has never been studied in a significant group of patients. We describe 14 adult cases who were seen over a 10-year period. A biphasic illness was characteristic: (1) prodromes (5-15 days) with malaise, fatigue, headache, nausea or vomiting, and fever; (2) cranial nerve palsy with facial palsy, diplopia, dysphagia, dysarthria, usually multiple. Meningism and hemi- or tetraparesis were present in 11 patients and cerebellar dysfunction in 9 patients. In 4 cases, CT showed widening of the brain stem with disappearance of the surrounding cisterns. The cerebrospinal fluid was abnormal in all patients in whom this investigation was done (pleocytosis, elevation in protein content). The patients received antibiotic therapy for 2-6 weeks. In the 9 patients who recovered, the neurological dysfunction improved within 2 days to 1 week of the initiation of therapy. There were 5 deaths. At autopsy in 2 cases, there was severe purulent meningitis and rhombencephalitis with predominantly polymorphonuclear cellular infiltration in 1 case, while numerous microabscesses in the midbrain, pons and medulla were observed in the other. We conclude that L. monocytogenes infection should be considered in patients who develop fever and focal neurological signs particularly localized to the brain stem.
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PMID:Early symptoms and outcome of Listeria monocytogenes rhombencephalitis: 14 adult cases. 849 12

Fabry's disease (FD) is a rare, sex-linked disorder resulting from alpha-galactosidase deficiency. Cerebrovascular complications have been reported in the literature but have not been systematically analyzed. We report 2 patients and review 51 previously reported cases (descriptive meta-analysis) to clarify the clinical, radiologic, and pathologic features. The average age at onset of cerebrovascular symptoms was 33.8 years for hemizygous individuals (n = 43) and 40.3 years of heterozygotes (n = 10). The most frequent symptoms and signs were as follows (in descending order of frequency): hemiparesis, vertigo/dizziness, diplopia, dysarthria, nystagmus, nausea/vomiting, head pain, hemiataxia, and ataxia of gait, in the hemizygote group; and memory loss, dizziness, ataxia, hemiparesis, loss of consciousness and hemisensory symptoms, in the heterozygote group. The vertebrobasilar circulation was symptomatic in 67% of the hemizygotes and 60% of the heterozygotes. Intracerebral hemorrhage was found in 4 patients (3 hemizygotes and 1 heterozygote). Elongated, ectatic, tortuous vertebral and basilar arteries were the most common angiographic and pathologic features. For the hemizygotes, the recurrence rate for cerebrovascular disease was 76% and the death rate was 55%; 86% of the heterozygotes had recurrent cerebrovascular event(s) and 40% died. The cerebrovascular manifestations of FD, in both hemizygotes and heterozygotes, are predominantly due to dilative arteriopathy of the vertebrobasilar circulation, frequently recur, and portend a poor prognosis.
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PMID:Cerebrovascular complications of Fabry's disease. 868 96

Medial medullary infarctions (MMI) were reported in less than 40 patients with satisfactory clinicotopographic documentation. We studied seven patients with MRI-proven acute MMI seen in two neurologic departments over a 5-year period (1990-1994). MMI represented less than 1% of ischemic strokes in the posterior circulation. Five patients had an infarction above the pyramidal decussation. All patients had contralateral hemiparesis and lemniscal sensory loss, accompanied by ipsilateral lingual palsy (Dejerine's syndrome) in three. Two patients had infarction below the pyramidal decussation, with ipsilateral hemiparesis and lemniscal sensory loss. Accompanying symptoms and signs of MMI were vertigo and nausea (n = 5), mild ipsi- or contralateral decrease in pain sensation (n = 6), headache (n = 4), ipsilateral limb ataxia (n = 6), contralateral truncal lateropulsion (n = 5), mild ipsilateral ptosis (n = 4), nystagmus (n = 4), dysarthria (n = 3), and somnolence (n = 2). Presumed causes of MMI were stenosis, occlusion or dissection of the ipsilateral vertebral artery (n = 5), and cardioembolism (n = 1). Outcome at 3 months was favorable in five patients. In conclusion, the clinical features of MMI are more heterogeneous than commonly thought, whereas its etiology seems fairly constant (vertebral artery disease).
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PMID:Medial medullary stroke: report of seven patients and review of the literature. 971 65


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