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

Six patients with bilateral paramedian thalamic infarction were seen in a general hospital over a 4 year period. This distinct stroke syndrome was recognized by the features of disturbed vigilance, often episodic, with vertical gaze disorder. Other signs included an amnesic syndrome, convergence difficulty, third nerve palsies, eyelid retraction, dysarthria, ataxia and involuntary limb movements. Diagnosis was confirmed by CT brain scan or magnetic resonance imaging. A variety of risk factors for stroke were present. All patients improved but two had significant residual disabilities.
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PMID:Bilateral paramedian thalamic infarction: a distinct but poorly recognized stroke syndrome. 143 69

Spontaneous dissections of the internal carotid arteries are uncommon but are not rare. They constitute a fairly common cause of ischemic stroke in young patients (young in terms of the age at which strokes generally occur). The common presenting manifestations are (1) unilateral headaches followed after a period of delay by focal cerebral ischemic symptoms or (2) unilateral headaches and ipsilateral incomplete Horner's syndrome. These may or may not be associated with subjective or objective bruits. In rare instances, spontaneous dissections of the internal carotid arteries may present as lower cranial nerve palsies and cause dysphonia, dysarthria, dysphagia, and numbness of the throat. Affected patients may initially present to the otolaryngologist or be referred to one. This article describes eight patients with spontaneous dissections of the internal carotid arteries and lower cranial nerve palsies, and the pertinent literature is reviewed.
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PMID:Spontaneous dissection of the cervical internal carotid artery. Presentation with lower cranial nerve palsies. 155 74

We studied the correlations between the pattern of weakness, stroke type, topography, and etiology in 255 patients whose first stroke was manifested by isolated hemiparesis. They represented 14% of consecutively admitted stroke patients. The weakness distributions were as follows: face, upper limb, and lower limb (FUL) (50%); face and upper limb (FU) (29%); upper limb (U) (10%); and upper and lower limb (UL) (9%). Twenty-nine percent of the patients had dysarthria, which was of no localizing value. Less than one half of the patients had a deep infarct, and one third had a potential embolic source from the heart or large arteries. Logistic regression analysis showed that history of hypertension and type of weakness distribution were the main factors accounting for lesion localization: patients with FUL distribution and hypertension had a 90% probability of deep infarct; patients either with FUL distribution but no hypertension or with UL distribution and hypertension each had 70% probability of deep infarct. Pure motor monoparesis was almost never caused by a deep infarct. We suggest that the assumption of a lacunar etiology to a pure motor stroke should be applied only to patients with FUL involvement.
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PMID:Pure motor stroke: a reappraisal. 842

Nine cases (seven men and two women, mean age 64.5 years) of classical lacunar syndromes due to intracerebral hemorrhage are reported. Three patients presented with pure motor hemiparesis (two putaminal hematomas with proportional weakness and one cortical hemorrhage with brachio-crural hemiparesis). Four patients presented with sensorimotor stroke due to thalamo-capsular hemorrhage. The last two patients had thalamic hemorrhage causing ataxic hemiparesis or dysarthria-clumsy hand syndrome. Four subjects had arterial hypertension, one was diabetic, and two were treated with anti-vitamin K. Abrupt onset was noted in all instances. Only one patient experienced moderate inaugural headaches. Good recovery occurred in all cases. Lacunar syndromes are a very uncommon presentation of intracerebral bleeding. Hemorrhages are yet the second etiology of such syndromes. Distinguishing hemorrhage from infarction is not clinically possible and needs early unenhanced CT scan.
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PMID:[Lacunar syndromes due to intracerebral hemorrhage]. 163 70

Stroke as a presenting manifestation of sarcoidosis has rarely been reported. This contrasts with the frequent anatomopathological findings of cerebrovascular involvement in neurosarcoidosis. We present a patient who developed acutely a right brachiofacial weakness and dysarthria. Pulmonary sarcoidosis was found. A brain CT and magnetic resonance imaging (MRI) scan disclosed multiple bilateral ischemic, mainly subcortical lesions. Despite a favorable clinical evolution under adequate corticotherapy, an MRI performed 3 months later showed an increased number of the previously observed lesions. This observation suggests that in some cases the evolution of central nervous system sarcoid lesions occurs independently from corticotherapy, and that MRI, in spite of its known great sensitivity in detecting those lesions, may not play a role in the follow-up of some patients with neurosarcoidosis.
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PMID:Focal neurological deficit with sudden onset as the first manifestation of sarcoidosis: a case report with MRI follow-up. 175 60

We investigated the types of clinical syndrome, location, sizes and presumed causes of 49 patients with capsular lacunar infarction. Clinical syndromes were classified according to Fisher's criteria into pure motor hemiparesis (PM), sensorimotor stroke (SM) and ataxic hemiparesis (AH) including dysarthria clumsy hand syndrome. Cases who had higher brain dysfunctions or brainstem syndromes were excluded. The size of infarcts was expressed as the volume on brain CT. All patients underwent 12-lead ECG and 2-dimension echocardiography. Twenty three patients (47%) underwent angiography or carotid ultrasonography. Lesion sites on CT were divided into three groups, i.e., perforating branch of ACA (PACA), perforating branch of MCA (PMCA) and anterior choroidal artery (AC). Lesion sizes of AH were significantly smaller than those of SM and tended to be smaller than those of PM. In AH patients, no cardioembolic sources nor large arterial lesions could be detected, whereas 40% in SM patients and 30% in PM patients had cardioembolic sources and 33% in SM patients and 75% of PM patients had large arterial lesions. The lesion volume was classified into two groups, larger and smaller than 1 ml. The larger volume group had more frequent cardioembolic sources than the small volume group (42% and 17% respectively, p less than 0.05), but no significant difference in frequency of large artery lesions was found among the two groups. Patients with "large striatocapsular infarct" had frequent cardiac and arterial lesions (60% and 40% respectively). Patients with AC territory infarction had more infrequent but not significant cardiac and arterial lesions than patients with PMCA territory infarction. All patients with PACA territory infarction presented PM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Type of syndrome, location, size and etiology of capsular lacunar infarction]. 180 63

Three cases of anterior choroidal artery territorial infarction, diagnosed by computerized tomography, with the triad of hemiplegia, hemianaesthesia and hemianopia, pure motor stroke and ataxic hemiparesis are described. Major and minor (lacular) infarctions in the territory of the anterior choroidal artery involve almost exclusively the basal segment of the posterior limb of the internal capsule and manifest themselves by symptoms of long pathway lesion. Based on the published case reports and the authors' own observations, the complete capsular syndrome characterized by the triad of hemiplegia, hemianaesthesia and hemianopia was differentiated from partial capsular syndromes including the following forms: pure motor stroke, pure sensory stroke, sensorimotor stroke, sensory stroke with hemiataxia, ataxic hemiparesis, dysarthria and/or clumsy hand, and homonymous hemianopia (quadrantanopia or sectoranopia). The characteristic features of the above types of capsular syndromes were analyzed. Distant symptoms of territorial infarctions involving the anterior choroidal artery are transcortical sensory or motor aphasias and construction apraxia in the dominant hemisphere, left side perception failure and visual-construction apraxia in the non-dominant hemisphere, and cerebellar hemiataxia. These distant symptoms are a manifestation of distant cortical or cerebellar metabolic depression due to the mechanism of diaschisis.
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PMID:[Anterior choroidal artery syndromes]. 180 18

Neurologic manifestations, afflicting up to 70% of SLE patients, include psychosis, seizures, chorea, neuropathies, and stroke. MRI is useful in evaluation of lupus patients and several reports have documented cerebral atrophy or focal hyperintensities. We report an unusual MRI appearance in a 56-year-old woman with SLE, diagnosed on the basis of pleuritis, lymphopenia, anti-DNA antibodies, and neurologic involvement. She reported recent onset of Raynaud's phenomenon and generalized macular rash. She presented after two months of gradual deterioration with memory loss, flattened affect, dysphagia, dysarthria, anomia, and somnolence, without focal neurologic signs. Investigations included elevated ESR, reduced complement, normal CSF without oligoclonal bands, negative viral serology, normal hormone and vitamin levels, normal renal and hepatic function. Neuropsychologic testing showed widespread impairment (WAIS-R: FSIQ-63; WMS-69; DRS-98; RCPM-14; WAB AQ-78.8). CT was normal but MRI showed strikingly symmetric, confluent hyperintensities extensively involving cerebral and cerebellar white matter on T1 and T2 weighted scans. Basal ganglia and subependymal and subcortical white matter were spared. Treated with prednisone, the patient made a gradual, but incomplete, recovery. These MRI findings may reflect widespread vasculopathy or direct immunologic brain insult with or without immunologic blood-brain barrier disruption.
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PMID:Dementia with leukoencephalopathy in systemic lupus erythematosus. 191 71

We report 9 patients with an isolated infarct of the anterior part of the rostral cerebellum, ie, the territory of the lateral branch of the superior cerebellar artery. Clinicoanatomic correlations are based on CT, MRI, or both in 8 patients and on pathologic data in the ninth. The main clinical features were ipsilateral dysmetria and axial lateropulsion, dysarthria, and unsteadiness. In 1 patient, the clinical presentation mimicked a lacunar stroke (dysarthria and clumsy hand syndrome). There were no edematous cerebellar infarcts with signs of brainstem compression, and all patients spontaneously improved without significant sequellae. Angiography in 2 patients and pathologic examination of arteries in 1 patient disclosed no occlusion in the vertebrobasilar system. Six patients had a cardiac source of emboli. In conclusion, infarcts of the anterior part of the rostral cerebellum can be regarded as a benign condition in which there is, frequently, a cardiac source of emboli.
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PMID:Infarction in the anterior rostral cerebellum (the territory of the lateral branch of the superior cerebellar artery). 199 70


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