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)

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.
Stroke 1991 Feb
PMID:Clinical-computed tomographic correlations of lacunar infarction in the Stroke Data Bank. 200 81

Nine patients with pure dysarthria underwent computed tomography or magnetic resonance imaging. Eight patients had infarcts of lacunar or larger size in the internal capsule: four in the superior portion of the anterior limb or adjacent corona radiata and four in the superior portion of the genu or the adjacent corona radiata. In one patient, there was a small infarct in the bulbar motor cortex. Dysarthria was transient and characterized by poor articulation in all cases. Five patients also had contralateral facial weakness, and three patients with lesions in the genu had minimal and transient involvement of the contralateral fingers. These three cases appeared to be variants of the dysarthria-clumsy hand syndrome. We submit that this syndrome should sometimes be regarded as a stroke syndrome rather than always as a lacunar syndrome.
Stroke 1991 Jun
PMID:Clinical anatomic study of pure dysarthria. 205 82

We report 5 patients with unilateral infarct and 1 with hemorrhage limited to the genu of the internal capsule. The most prominent finding was contralateral facial and lingual hemiparesis with dysarthria. Three patients also showed unilateral mastication-palatal-pharyngeal weakness, and 1 had unilateral vocal cord paresis. Mild limb involvement was limited to hand weakness in 4 patients. Our findings suggest that the majority of motor corticopontine and corticocobulbar fibers are located in the genu of the internal capsule. The faciolingual syndrome and its variants are highly suggestive of capsular genu stroke.
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PMID:Capsular genu syndrome. 179 70

Although spontaneous thrombosis of a giant intracranial aneurysm is relatively common, occlusion of its parent artery is rare. We describe two recent patients in whom the parent artery spontaneously occluded. One patient had severe stenosis of the left internal carotid artery, with delayed appearance of a faint shadow of vascular widening near the posterior clinoid process. One month later, complete occlusion of the left internal carotid artery was shown angiographically. The second patient had dysarthria and left hemiparesis, resulting in the diagnosis of a left internal carotid artery giant aneurysm. He had suffered an episode of visual disturbance of the right eye 5 years before. Angiography showed the right cervical internal carotid artery to be occluded. We believe the mechanism of parent artery occlusion in our two patients to be due first to stretching of the internal carotid artery by the enlarged aneurysm, followed by compression of the internal carotid artery by the aneurysm itself. Next, the anterior clinoid process and the optic nerve are involved, and, finally, thrombosis of the aneurysmal cavity extends into the internal carotid artery itself.
Stroke 1990 Oct
PMID:Two cases of spontaneous internal carotid artery occlusion due to giant intracranial carotid artery aneurysm. 221 19

Symptoms compatible with vertebrobasilar ischemia have been reported in patients with unilateral or bilateral carotid occlusive disease. Intracranial steal phenomena have been proposed to explain the symptoms. In a review of 54 patients with angiographically documented severe bilateral carotid stenosis (less than or equal to 2 mm residual lumen) or occlusion, eight had symptoms suggesting vertebrobasilar insufficiency. Five patients were identified retrospectively, and the other three were evaluated prospectively. Symptoms included various combinations of hemodynamically mediated, transient bilateral motor, sensory, or visual impairment. Dysarthria, dysphagia, and diplopia were generally absent. Each patient also described additional symptoms compatible with transient hemispheric or retinal ischemia. The anatomic regions subserving the bilateral vertebrobasilar-like symptoms could be correlated with angiographically estimated arterial border zones in both hemispheres and may thus represent bilateral hemispheric border zone ischemia rather than brain stem ischemia. An intracranial steal need not be invoked.
Stroke 1990 Dec
PMID:The syndrome of bilateral hemispheric border zone ischemia. 226 72

Two patients presented with a unilateral supranuclear facial palsy. Additional dysarthria was attributed to the pontine origin documented by magnetic resonance imaging on the contralateral side. The pontine disorder also was indicated by an isolated delay of the blink reflex R1 component or of the masseter reflex. We attribute the facial palsy to a lesion of a supranuclear fiber bundle supplying the facial nucleus. The location of the lesions favors these fibers taking a separate course from the main pyramidal tract at the mid- to upper pontine level.
Stroke 1990 Dec
PMID:Pontine supranuclear facial palsy. 226 85

We describe an analysis of 227 patients with lacunar infarcts; 177 were inpatients and the remaining 50 were outpatients. The group comprised 11% of all inpatients with cerebrovascular pathology and 16% of all consecutive inpatients with brain infarcts studied at the Department of Neurology of the Hospital de la Santa Creu i Sant Pau. The main risk factors identified in these patients were arterial hypertension in 164 (72%), diabetes mellitus in 64 (28%), and heart disease in 58 (26%). The most common clinical syndromes were pure motor hemiparesis in 125 (55%), pure hemisensory stroke in 42 (18%), the sensorimotor deficit syndrome in 34 (15%), ataxic hemiparesis in seven (3%), and the dysarthria-clumsy hand syndrome in four (2%); atypical syndromes were observed in 15 patients (7%). Lacunes were demonstrated by computed tomography in 100 patients (44%) and by magnetic resonance imaging in 35 (78%) of the 45 patients in which it was applied. Magnetic resonance imaging was significantly better (p less than 0.001) than computed tomography for imaging lacunes, especially those located in either the pons (p less than 0.005) or the internal capsule (p less than 0.001). After the acute phase, mild or no neurologic disability was detected in 178 patients (78.4%), moderate disability persisted in 48 patients (21.1%), and severe disability was recorded in one case (0.4%). Lacunar infarcts are a clearly defined entity with characteristic clinical features and an excellent short-term prognosis. Magnetic resonance imaging is the current method of choice for demonstrating these small brain lesions.
Stroke 1990 Jun
PMID:Clinical study of 227 patients with lacunar infarcts. 234 85

Acute mutism with paralysis of the bulbar and facial muscles following discrete bilateral internal capsular infarction is a rare stroke syndrome. We describe a 62 year-old male who suddenly became unable to speak or swallow. The paucity of facial expression and inability to voluntarily move the facial, lingual and pharyngeal muscles were persistent and contrasted with a relatively mild limb paresis which recovered. High resolution CT scan revealed infarcts in the posterior limbs of both internal capsules. It is important to recognise this stroke syndrome because of the permanence of dysarthria and dysphagia associated with it.
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PMID:Persistent mutism and dysphagia of acute onset due to bilateral internal capsule infarction. 239 43

We reviewed the medical records and cranial computed tomograms of 74 patients with acute capsular infarcts to investigate the correlation between infarct size and clinical symptoms. Average infarct size varied significantly by clinical syndrome; patients with sensorimotor stroke had the largest infarcts, patients with pure motor hemiparesis had middle-sized infarcts, and patients with ataxic hemiparesis or the dysarthria-clumsy hand syndrome had the smallest infarcts. Although it has been proposed that the type of lacunar syndrome is determined entirely by the infarct location, our results suggest that infarct size is another important factor influencing the clinical presentation of lacunar syndromes.
Stroke 1990 Sep
PMID:Effect of capsular infarct size on clinical presentation of stroke. 239 59

The term lacuna or lacunar cavity defines the pathological lesion while the clinical pictures due to lacuna or lacunes are referred to as 'lacunar syndromes'. The lacunar syndromes include: (1) the typical lacunar syndromes or lacunar syndromes proper--pure motor hemiplegia, pure sensory stroke, ataxic hemiparesis including dysarthria and clumsy hand, sensorimotor stroke and abnormal movement syndromes, (2) reversible ischemic attacks (TIA and/or PTIA or RIND), (3) other clinical syndromes which may be due to lacunar lesions such as suprabulbar palsy; lacunar dementia, or subacute arteriosclerotic encephalopathy (or Binswanger's disease). The different clinical pictures are reviewed, some mechanisms underlying the lacunar lesion are briefly discussed and the old label 'small vessel diseases' in cases with lacunes is reconsidered.
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PMID:The lacunar syndromes. 269 95


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