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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A diagnosis based on the presumed mechanism of stroke onset is useful for management strategies in acute ischemic stroke. Ninety-two patients with embolic (cardiac or artery-to-artery) and 107 with non-embolic (thrombotic or hemodynamic) stroke were diagnosed on strict cerebral angiographic criteria alone. To clearly discriminate between these two groups, the neurological and computed tomographic (CT) findings were then compared. Rapidity of onset, vomiting, urinary incontinence, level of consciousness, cervical bruit, anisocoria, tongue deviation, sensory disturbance, and CT findings (location of hypodense area, findings of brain edema and hemorrhagic transformation) were discriminatory factors between the two groups (p<0.01). According to these 11 items, we prepared a numerical table for quantitative differential diagnosis. A diagnostic accuracy of 98.9% for embolic and 87.9% for non-embolic stroke in internal verification, and 90.0% and 82.9%, respectively, in external verification was observed. The differences in clinical features and CT findings between embolic and non-embolic stroke may reflect the pathophysiological mechanisms of the occlusive process of cerebral artery as well as the extent and severity of ischemia.
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PMID:Differences in clinical features and computed tomographic findings between embolic and non-embolic acute ischemic stroke: a quantitative differential diagnosis. 955 May 93

Acute infarction confined to the territory of the white matter medullary arteries is a poorly characterised acute stroke subtype. 22 patients with infarction confined to this vascular territory on CT and/or MRI were identified from a series of 1,800 consecutive admissions to our stroke unit (1.2%) between August 1993 and March 1997. 19 patients had small infarcts (< 1.5 cm maximum diameter) and 3 large infarcts (> 1.5 cm). Small infarcts were associated with a history of smoking (69%), hypertension (58%), and hyperlipidaemia (37%), and less frequently with atrial fibrillation (21%). Significant (>50%) ipsilateral carotid stenosis (16%) was a less frequent finding in this group. Patients most commonly presented with weakness and/or sensory disturbance affecting mainly the upper limbs, but dysarthria, dysphasia, and ataxia were also seen. Large infarcts were infrequent in our series, but did not differ significantly from small infarcts with respect to clinical presentation or risk factor profiles (p > 0.05 for all comparisons). The majority of symptomatic patients with white matter medullary infarcts are associated with small (< 1.5 cm diameter) lesions and a risk factor profile consistent with small vessel disease. More data are required to elucidate the mechanism of larger (> 1.5 cm) infarcts. Because of the potential overlap between white matter medullary infarcts and internal watershed infarcts, suggested criteria for each are presented.
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PMID:White matter medullary infarcts: acute subcortical infarction in the centrum ovale. 971 27

A 52-year-old man with diabetes mellitus, hyperlipidemia and smoking habit, experienced transient ischemic attacks (TIAs) with symptoms of left orbital pain, left blepharoptosis and hoarseness lasting for five minutes on March 10, 1997. Subsequently, the same symptoms repeated once or twice daily. On March 28, he had dysphagia, numbness and disturbance of pain and temperature sensation (segmental dissociated sensory disturbance) on the right side of the body above the level of the Th10, the right upper limb and face. The deficits persisted for more than 24 hours. Angiographic studies revealed an occlusion of the left vertebral artery immediately after branching of the posterior inferior cerebellar artery. MRI demonstrated a hyperintense lesion on MRI T2 weighted image in the left lateral medulla. About three months after the completed stroke, he had six episodes of TIAs of left Horner's sign and hoarseness. To our knowledge, this is the rare case that had frequent TIAs presenting the Wallenberg syndrome before and after the onset of lateral medullary infarction. We speculate that the TIAs resulted from microembolism from the proximal end of occluted left vertebral artery and failure of the microcirculation in and around the lateral portion of the medulla oblongata.
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PMID:[A case with frequent episodes of transient ischemic attack presenting the Wallenberg syndrome before and after the onset of brain infarction]. 1042 53

A 60-year-old hypertensive woman had a pontine hemorrhage that caused slight right hemiplegia, deep sensory disturbance on her right side and dysarthria. Three months after the stroke, she was transferred to our hospital for rehabilitation. Approximately 6 months later, she gradually began to complain of the visual oscillation. Continual, unceasing conjugate vertical/rotatory eye movements were observed. Fixation was momentary at best because of an inability to dampen the spontaneous eye movements. Electrooculography (EOG) showed bilateral vertical/rotatory sinusoidal eye movements of 2.5 Hz frequency and 10- to 35-degree amplitude. Both vertical and horizontal optokinetic nystagmus were absent. Caloric stimulation did not evoke any responses bilaterally. There were no rhythmical movements at similar frequencies in other parts of the body such as palatal myoclonus. MRI revealed not only hematoma mainly at the dorsal pontine tegmentum but also hypertrophy of the inferior olive nucleus, suggesting disruption of the central tegmental tract. Lesions of this tract may be one cause of pendular nystagmus. Several drug therapies were investigated for the nystagmus. There was no response to baclofen 15 mg. Trihexyphenidyl 4 mg was discontinued because of drug-induced hallucinations. Tiapride 600 mg and phenobarbital 90 mg were each slightly effective in reducing both frequency and amplitude of nystagmus. Treatment with clonazepam 1 mg resulted in the striking disappearance of nystagmus. She was aware of this and no longer experienced oscillopsia. Despite the visual benefit, however, the patient did not wish to continue this drug because of drowsiness and muscle relaxation. The potential long-term therapeutic application of clonazepam should be further investigated. To our knowledge, there have been no reports of successful treatment in acquired pendular nystagmus with clonazepam. Therefore, based on this favorable experience, it is suggested that clonazepam should be added to the list of potential therapies for pendular nystagmus.
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PMID:[Acquired pendular nystagmus after pontine hemorrhage]. 1065 2

A 15-year-old woman with a history of transient dysarthria two years before, suddenly developed weakness of right upper extremity, right facial palsy, and dysarthria. She was admitted to our hospital on the third day. She had no hypertension, heart murmur and oedema. On neurological examination, she had mild right hemiparesis including face muscles and mild dysarthria. The right knee jerk was brisk with no Babinski's sign. Ataxia and sensory disturbance were not present. T2-weighted MRI showed a hyperintensity at the posterior limb of the left internal capsule. Cerebral angiography was unremarkable. Ultracardiography and 24-hour electrocardiography were normal. Laboratory data revealed no inflammatory findings, liver dysfunction, hyperglycemia and hyperlipidemia. Antinuclear and anticardiolipin antibodies were negative. Prothrombin time was normal, but activated partial thromboplastin time was slightly prolonged (35.4 sec, normal 25.2-34.4). Protein C, protein S and antithrombin III were normal. Heparin cofactor II (HC II) activity was decreased (44%) with normal HC II antigen (79%) and so she was diagnosed as heparin cofactor II deficiency type II (heparin cofactor II abnormality). Her father manifesting thromboangitis obliterans also had low HC II activity with normal HC II antigen. However, on her genetic analysis, we didn't detect any mutations in the coding region of HC II gene. Until now she has no recurrence of cerebrovascular attacks. On the basis of these results, we suspect that HC II deficiency was a possible risk factor of cerebral infarction in this case because she was so young and had no general risk factors except for HC II. No stroke associated with HC II deficiency type II has been reported up to date. This case is worth considering etiologies of juvenile cerebral infarction.
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PMID:[Juvenile cerebral infarction associated with heparin cofactor II abnormality. A case report]. 1096 62

We studied clinical symptomatology and somatosensory evoked potentials(SEP) of 7 pure sensory stroke patients due to pontine lesions. Clinical symptoms were examined by modality(pinprick, touch, vibration and joint position sense), intensity and distribution of the sensory disturbance. SEP were recorded by the median nerve stimulation in the upper extremities, and the posterior tibial nerve stimulation in the lower extremities. Patients 1-4 were characterized by decreased contra-lesional fingers or fingers, toes joint position sense, normal pinprick and vibration sense. We think that these patients' lesions were localized in the lemniscus medialis. Patients 5-7 were characterized by decreased contra-lesional upper extremity or upper and lower extremity vibration sense, decreased pinprick sense and normal joint position sense. We think that these patients' lesions involved spinothalamic tract. There was no abnormal finding of SEP with upper extremity stimulation, but disappearance or very low amplitude of P38 with lower extremity stimulation in 4 of the 7 patients. We conclude that 1) the vibration sense may be conducted also through the spinothalamic tract, 2) SEP findings are abnormal only with lower extremity stimulation in pontine pure sensory infarction.
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PMID:[Pure sensory stroke due to a pontine lesion: a study of clinical symptomatology and somatosensory evoked potential findings]. 1107 Sep 23

We evaluated consecutive stroke patients with an acute, unilateral lesion, in order to elucidate the anatomical correlates and the clinical course of sensory extinction phenomenon as well as its relation with unilateral spatial neglect (USN) and anosognosia for hemiplegia (AHP). Subjects consisted of 76 patients with right cerebral hemispheric lesions (RHL) and 43 with left cerebral hemispheric lesions (LHL). Twelve of 76 patients with RHL and 18 of 43 patients with LHL were excluded from this study, because of consciousness disturbance, aphasia, severe sensory disturbance, hemianopia, or severe dementia. All of the patients included in this study had an ischemic or hemorrhagic stroke, who admitted to our hospital within 24 hours after the onset of stroke. We repeatedly examined the patients to detect the presence of sensory extinction phenomenon, USN, and AHP from their acute to chronic stage. The incidence of extinction phenomenon in RHL was 33% (11/19 with cortical lesions and 10/45 with deep-seated lesions). When we excluded the patients with a lacunar stroke or TIA, 10 of 13 patients with subcortical lesions had sensory extinction phenomenon. Nineteen of 21 patients with RHL who showed sensory extinction phenomenon also accompanied USN, and twelve had associated AHP. The sensory extinction phenomenon disappeared within 20 days in 6 of 10 patients with subcortical lesions and 3 of 11 with cortical lesions. In contrast, three of 25 (12%) patients with LHL showed extinction phenomenon, the incidence being much rarer than the lesion in the right. Of these, two had USN and one had AHP together. All the deficits disappeared within 20 days after the onset of stroke in patients with LHL. Our studies may show that subcortical lesions present with extinction phenomenon more frequently than cortical lesions, although the phenomenon caused by the subcortical lesions of often disappear in a few weeks.
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PMID:[Sensory extinction phenomenon of double simultaneous stimulation: the analysis of consecutive stroke series with acute and unilateral lesions]. 1196 39

We analyzed clinical characteristics of central post-stroke pain (CPSP), constant and burning pain, in 32 patients with Wallenberg syndrome due to infarction. CPSP developed in 44% (14/32) of the patients; 8 in acute stage (within 4 days after the stroke) and 8 in chronic stage(10-120 days after the stroke). Apart from one exceptional case, CPSP was present in the hypalgesic side of face and extremities. In 9 cases of typical type (Currier's distribution of sensory disturbance), CPSP occurred in the ipsilateral face to the lesion during acute stage. Among them, 2 cases developed severe lancinating pain in chronic stage. In 5 cases of ventral type, it occurred in the contralateral extremities during chronic stage. Spino- and trigemino-thalamic tract are injured but medullary reticular formation is intact in Wallenberg syndrome. It is, therefore, considered that CPSP in Wallenberg syndrome is caused by denervation sensitivity of "paleo-reticulothalamic" tract within the reticular formation.
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PMID:[Central post-stroke pain in Wallenberg syndrome]. 1527 95

Lesions affecting localized regions of the cerebral cortex may result in pseudoperipheral neurologic deficits. Such deficits have not been reported in association with subcortical lesions. A 60-year-old man with a history of hypertension presented with an acute sacral pseudoradiculopathy corresponding to an S1-S2 dermatomal distribution. The presence of hyperreflexia in the affected limb suggested an intracranial lesion. A brain magnetic resonance imaging scan revealed an isolated, small area of infarction localized to the centrum semiovale deep to the primary motor and sensory cortices. This case serves to illustrate that stroke can mimic a sacral radiculopathy. The distribution of the present patient's sensory disturbance suggests that thalamocortical projections maintain a dermatomal organization as they pass through the centrum semiovale.
J Stroke Cerebrovasc Dis
PMID:Sacral pseudoradiculopathy due to centrum semiovale stroke. 1789 64

In paramedian caudal pontine infarctions, the medial lemniscus is often affected. This typically leads to dissociated sensory symptoms. We present a case in which a patient suffering from a bilateral caudal pontine infarction experienced a marked bilateral sensory disorder of the hands and distal arms.
J Stroke Cerebrovasc Dis
PMID:Bilateral paramedian pontine base infarction. 1790 45


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