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)

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

Cerebral infarcts in children are rather rare and in most cases no precise etiology is established. The authors describe a case of cryptogenetic cerebral infarction in a 9-year-old boy. The child presented an acute onset of hemiplegia in the right arm and leg, central facial palsy, dysarthria and steppage. The infarction was proved by Computed Tomography (CT) and Magnetic Resonance Imaging (MRI). Laboratory and instrumental studies rule out all known causes of brain infarction. The only possible etiopathogenetic hypothesis was a varicella arteritis which occurred 45 days before the clinical manifestation.
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PMID:Cerebral infarction in a child. A case report. 140 87

A 70-year-old man was admitted to our hospital because of fever and progressive dyspnea in December 1989. He was already diagnosed as having erythrocytosis secondary to pulmonary fibrosis 4 years previously and the values of his hematocrit (Ht) were maintained between 44.5 and 62.9% by repeated phlebotomy. Immediately after admission, severe diarrhea developed and the Ht value was 61.5%. Around 1:30 a.m. of the 3rd hospital day, he developed disturbance of consciousness. In addition, the serum levels of LDH, CPK, aldolase, and myoglobin of muscle origin increased markedly and the Ht value showed 78.5%. While the level of consciousness was gradually restored by 600 ml phlebotomy and 1,500 ml saline infusion, dysarthria and hemiplegia became evident. The Ht value early in the morning of the 3rd hospital day was reduced to 59.4%. Although cranial CT and MRI performed 74 days and 15 months, respectively, after the onset of the symptoms failed to reveal any abnormal shadow, he was clinically suspected to have cerebral infarction. These findings emphasize that abrupt increase in Ht or blood viscosity is a possible factor triggering cerebral infarction, and adequate control of Ht value is recommended for the prevention of such a condition in the aged.
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PMID:[Cerebral infarction and high serum levels of muscle-derived enzymes associated with abrupt increase in hematocrit in a patient with secondary erythrocytosis]. 175 34

A case of persistent primitive proatlantal intersegmental artery (PPPIA) is reported. A 65-year-old male with treated hypertension was admitted to our clinic complaining of dysarthria and hemiparesis of sudden onset two days after the ictus. CT revealed spotty low-density lesions in the left corona radiata and bilateral thalami with bilateral watershed infarction. MRI findings were also compatible with cerebral infarction. Left common carotid angiography demonstrated a large anastomosis between the external carotid artery and the vertebral artery at the proatlantal region. Neither of the vertebral arteries were visualized on digital subtraction aortography. All the blood circulation of the vertebro-basilar system was through this anastomotic artery (PPPIA). A flow study revealed hypoperfusion in the territory of the left middle cerebral artery on 133Xe SPECT. Bone window CT of cervical vertebrae revealed hypoplasia of the left transverse foramen in C2, C3, C4, C5, C6 vertebrae. This case is very suggestive of an anaplasia or hypoplasia of the vertebral arteries. The etiology of his left frontal infarction seemed to be a blood-stealing phenomenon of long standing, from the anterior to the posterior circulation through the PPPIA.
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PMID:[Persistent primitive proatlantal intersegmental artery (PPPIA) presenting with cerebral infarction]. 188 24

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

Lacunar stroke was diagnosed in 337 (26%) of the 1,273 patients with cerebral infarction among the 1,805 total in the Stroke Data Bank. We analyzed the 316 patients with classic lacunar syndromes. Among these, 181 (57%) had pure motor hemiparesis, 63 (20%) sensorimotor syndrome, 33 (10%) ataxic hemiparesis, 21 (7%) pure sensory syndrome, and 18 (6%) dysarthria-clumsy hand syndrome. No striking differences were found among the risk factors for the lacunar subtypes, but differences were found between lacunar stroke as a group and other types of infarcts. Compared to 113 patients with large-vessel atherosclerotic infarction, those with lacunar stroke had fewer previous transient ischemic attacks and strokes. Compared to 246 with cardioembolic infarction, patients with lacunar stroke more frequently had hypertension and diabetes and less frequently had cardiac disease. We found a lesion in 35% of the lacunar stroke patients' computed tomograms, with most lesions located in the internal capsule and corona radiata. The mean infarct volume was greater in patients with pure motor hemiparesis or sensorimotor syndrome than in those with the other lacunar stroke subtypes. In patients with pure motor hemiparesis and infarcts in the posterior limb of the internal capsule, there was a correlation between lesion volume and hemiparesis severity except for the few whose infarct involved the lowest portion of the internal capsule; in these patients severe deficits occurred regardless of lesion volume. Taken together, the computed tomographic correlations with the syndromes of hemiparesis showed only slight support for the classical view of a homunculus in the internal capsule.
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PMID:Clinical-computed tomographic correlations of lacunar infarction in the Stroke Data Bank. 200 81

A case of rigid spine syndrome associated with rimmed vacuoles in muscle biopsy is reported. A 36-year-old man was admitted to our hospital because of gait disturbance and limited mortality of the spine. His family was free from any neuromuscular disorders. He was born in normal pregnancy and delivery. His physical development was normal. At age 7, he was unable to run fast. At age 36, he had right hemiparesis and dysarthria. He was diagnosed as cerebral infarction of the left basal ganglia by brain CT. Neurological examination revealed moderate proximal dominant muscular atrophy and weakness. His spine was straight, showing loss of physiological cervical and lumbar lordosis. The neck flexion was limited but the extension was full. And he had contracture of bilateral ankle joint. Laboratory findings were all normal. The electrocardiogram showed negative T wave in V4, V5 and QT interval elongation. The echocardiogram showed diffuse decrease of ventricular wall motion. Respiratory function test revealed decrease of vital capacity. Arterial blood gases on room air showed that the PaO2 and PaCO2 were 70 mmHg and 49 mmHg, respectively. The findings of electromyogram were compatible with myopathic change. Biopsy specimen of the biceps brachii muscle showed marked variation in fiber size, type 1 fiber predominancy and atrophy, and type 2B fiber deficiency. Numerous rimmed vaculoes were found in the same muscle. Four cases of the rigid spine syndrome with rimmed vacuoles have been described. Among them, three patients died in young ages and two suffered from constrictive respiratory failure. In rigid spine syndrome with rimmed vacuole formation, the cardiac and respiratory problems must be taken account intensively.
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PMID:[A case of rigid spine syndrome with rimmed vacuole]. 220 33

With the great progress in the imaging technique of cerebro-cerebellar perfusion and metabolism, it has been revealed that supratentorial cerebrovascular disorders often cause some reduction of contralateral cerebellar blood flow and metabolism. The phenomenon, termed crossed cerebellar diaschisis (CCD), is interpreted to be brought about by transneuronal deactivation of cerebellum via the corticopontocerebellar pathway and usually not to accompanied by limb-incoordination. We have experienced 2 cases presenting ataxia clinically and CCD in positron emission tomography (PET) which are thought to be caused by the interruption of two distinctive neural pathways, the corticopontocerebellar and cerebellorubrothalamic pathways. Case 1 was a 34-year-old housewife with cerebral infarction which magnetic resonance imaging disclosed in the left parietal cortex and subcortical white matter. She showed mild right-sided hemiataxia featured by dysarthria, hypermetria, dysrhythmia, decomposition, dysdiadochokinesis and rebound phenomenon. Cheirooral syndrome, a hand-pronation sign and defects of combined sensation were present on the right but not accompanied by any disturbances of deep sensation. PET with 15O-labeled CO2 and O2 demonstrated the left frontoparietooccipital and contralateral cerebellar hypoperfusion and hypometabolism. Case 2 was a 69-year-old female suffering from aftereffects of old thalamic hemorrhage. Neurological examination revealed moderate degree of right-sided hemiataxia suggesting a cerebellar type of dysfunction like in case 1. Muscle power and sensory system were well-preserved. Brain CT revealed a small and restricted low density area in the left posterolateral thalamus indicating destruction of the Vim nucleus. PET study confirmed reduced blood flow and oxygen metabolism in the left thalamus and contralateral cerebellar hemisphere.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical and etiological study of crossed cerebellar diaschisis. Report of two cases]. 261

Fifty-three patients with infarction of the corona radiata adjacent to the body of the lateral ventricle were clinically evaluated in order to determine the clinical characteristics of this infarction and localization of the pyramidal tract in this area, as well as its somatotopy and etiology. Clinical characteristics included the following: (1) this type of infarction was observed in 9.1% of all patients with cerebral infarction; (2) although 81.1% of the patients of this type had clear consciousness and neuropsychological symptoms in some patients; (3) motor paralysis usually occurred in the upper limbs; (4) monoplegia occurred in 13.2% of patients, with monoplegia of upper and lower limbs being associated with infarction of the anterior and posterior portion, respectively, of the corona radiata adjacent to the body of the lateral ventricle; (5) pure motor hemiplegia was observed in 45.3% of patients; (6) facial paralysis and dysarthria were observed in 54.7% and 58.5% of patients, respectively, and the incidence of these symptoms was the highest in the infarction of the anterior portion of the corona radiata; (7) sensory disturbance, which was usually recognized as a mild subjective feeling of abnormality and localized to the limbs, was reported by 47.2% of patients; (8) risk factors included hypertension, diabetes and high hematocrit and triglyceride levels; (9) arteriosclerosis was often noted in areas between the siphon of the internal carotid artery and the main stem of the anterior and middle cerebral arteries; (10) 64.2% of patients were able to conduct independent activities of daily life (ADL) 1 month after the onset of the disease and more marked paralysis remained in the infarction of the middle portion than in the anterior or posterior portion.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical characteristics of infarction of the corona radiata adjacent to the body of the lateral ventricle]. 275 54

Different dosages, varying from 250 to 500 mg/die, of ticlopidine per os have been employed in 46 patients (32 men and 14 women), average age 66, who had been admitted for acute non-embolic cerebral infarction. In the two clinical examinations, effected on average 5.4 and 18.3 days after the admission, significant alterations in 9 among the considered items have been noticed, i.e.: central deficit of the VIIth cranial nerve, motor function and gait impairment, Babinski's sign, loss of sensibility, dysarthria, visual field defect, cerebellar signs, motor and/or receptive dysphasia. A global improvement of these clinical signs has been noticed on average in 48.2% of the patients, while an exacerbation has occurred in 2.1% of the cases. None of the patients who have been considered in this study has decreased or has shown relapses of ischemic cerebral attacks during the observation. The treatment with ticlopidine has been discontinued in 3 cases (6.5%) for the occurrence of temporary adverse side-effects.
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PMID:[Use of ticlopidine in patients with acute non-embolic cerebral infarcts]. 401 94


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