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

A 61-year-old hypertensive diabetic man awoke with a numb, heavy right arm and leg; symptoms progressed within 30 hours to a dense right hemisensory syndrome involving head, face, trunk, arm, and leg, accompanied by a right hemiparesis, involving tongue, face, arm, and leg with extensor plantar response, leaving him barely able to move the arm and leg against gravity. No impairment in alertness, memory, language, praxic, or visual functions was evident at any time. Improvement in motor function began in 24 hours and progressed to walking status by discharge on day 23. Eight days passed before the sensory deficit showed improvement, and it was still prominent at discharge. Autopsy three months later showed a 4 X 2 X 4-mm lacune in the ventral posterior nucleus of the left thalamus, with a zone of pallor on stained microscopic sections extending into the immediately adjacent posterior limb of the internal capsule. This case appears to be unique in that a sensorimotor stroke has been produced by a confirmed thalamocapsular infarct.
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PMID:Sensorimotor stroke due to thalamocapsular ischemia. 58 93

Younger gerbils have been found to be more resistant than adults to cerebral infarction after carotid ligation. In this study, the perfused cerebral area after bilateral common carotid occlusion was evaluated in infant, young, and adult Mongolian gerbils by the carbon black perfusion method to assess the existence and significance of collateral blood vessels between the vertebrobasilar and carotid circulations. Nineteen gerbils were divided into three groups (i.e., infant, young and adult gerbils aged 3-4, 5-7, and 10-17 weeks, respectively). After bilateral common carotid artery occlusion, carbon black was injected directly into the left ventricle by cardiac puncture through the closed thorax. In five of eight infant gerbils, the whole brain was perfused by carbon black, while in the remaining three, only the cerebellum and brainstem were stained well, and marked bilateral cerebral pallor was observed. On the other hand, carbon black did not perfuse the brain region supplied by the carotid arteries, both in young and adult gerbils (11 animals in total). These results suggest that infant gerbils might have a more highly developed network of collateral blood vessels between the vertebrobasilar and carotid circulations, and the existence of such a significant network might be the basis for the fact that infant gerbils are resistant to cerebral infarction following carotid ligation. We propose that gerbils should be used as a stroke model only when they are 5 weeks old or older.
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PMID:Why are infant gerbils more resistant than adults to cerebral infarction after carotid ligation? 619 32

We report a 91-year-old man who had a stroke and died of renal failure. He had been treated for hypertension since 20 years before the onset of the present illness. In addition, he was operated on a gastric cancer 17 years previously. Otherwise he was doing well until May 29, 1991 (when he was 87-year-old) when he had sudden onset of dysarthria and right facial weakness. He was admitted to our hospital. On admission, general physical examination was unremarkable, and neurologic examination revealed a mentally sound man with slight dysarthria, right facial weakness, orolingual dyskinesia, and dysequilibrium in which he showed difficulty in tandem gait; however, no cerebellar ataxia was noted. A cranial CT scan revealed leukoaraiosis with multiple low density areas in the cerebral white matter. His BUN was 37 mg/dl and Cr 2.2 mg/dl. His neurologic symptoms cleared within the next few weeks and he was discharged with ticlopidine 100 mg q.d.. He had been doing well after the discharge except for gradual worsening of his renal function; his BUN was 65 mg/dl and Cr 3.27 mg/dl in April of 1994. On March 10, 1995, he fell down and hit his back; he became unable to walk because of pain, and he was admitted again on March 16, 1995. On admission, his blood pressure was 170/80 mmHg. There was an 1 + pitting pretibial edema; otherwise general physical examination was unremarkable. Neurologic examination revealed an alert and oriented man, however, Hasegawa's dementia scale was 23/30. Higher cerebral functions as well as cranial nerves were intact. He showed some unsteadiness of gait, however, no motor weakness or ataxia was noted. Deep tendon reflexes were diminished, but Chaddock sign was positive bilaterally. Vibration was diminished in the feet, however, pain and touch sensations were intact. Laboratory examination revealed a compression fracture of the twelfth thoracic vertebra. Blood count and chemistries were as follows; Hb 7.6 g/dl, Hct 23.3%, TP 6.0 g/dl, Alb 3.6 g/dl, BUN 87 mg/dl, Cr 4.53 mg/dl, T-Chol 174 mg/dl, HDL-Chol 49 mg/dl, Glu 156 mg/dl, Na 142 mEq/L, K 5.4 mEq/L, Cl 115 mEq/L. A urine specimen contained 1 + protein and 1 + glucose, and the sediments contained hyaline casts. A cranial CT scan was essentially same as that taken four years ago. His hospital course was complicated with pneumonia, congestive heart failure, and progressive renal failure. He was treated with intravenous fluid, chemotherapy, and other supportive measures, however, he expired from respiratory failure on April 30, 1995. He was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had Binswanger's disease in the brain, benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were divided regarding the question as to whether or not this patient had Binswanger's disease. Although his cranial CT scan revealed leukoaraiosis, his dementia and gait disturbance was only mild until his fall on March, 1995. Clinical features did not conform to those of Binswanger's disease. Postmortem examination of the right hemisphere revealed wide spread atherosclerosis and arteriolosclerosis. The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries and the left middle cerebral artery with 70% stenosis. Myelin stain showed diffuse myelin pallor of the cerebral white matters with scattered small infarcts. Arterioles in the white matter showed arteriolosclerosis. Small infarcts were also seen in the putamen and in the thalamus. This patient appeared to have had circulatory disturbance of the white matter which is the basic abnormality causing Binswanger's disease. However, white matter changes in this patient were not quite severe enough to make a pathologic diagnosis of Binswanger's disease.
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PMID:[A 91-year-old man with a stroke, hypertension, and renal failure]. 899 Apr 84

A 67-year-old man was referred to us for tonic-clonic convulsions. A review of his history revealed that he had been hospitalized for loss of consciousness, hypotension, and suspected apoplexy at age 67. He had experienced prior tonic-clonic convulsions at age 72 and age 74. He had malaria and tuberculosis in his history but had been otherwise generally well. Physical examination was normal, and his blood pressure was 100/80 mmHg. Laboratory findings were normal except alcalinephosphatase (292 U/l) and gamma-glutamyl transpeptidase(60 U/l). Neurological examination showed alert consciousness, mild upper gaze palsy, slight right-side hemiparesis and left Babinski signs was present. Cranial magnetic resonance imaging showed no abnormality, but cerebral angiography revealed bilateral carotid artery occlusion. There were abundant leptomeningeal anastomoses, and the posterior communicating artery was supplied by the left vertebral artery. Electroencephalography showed a spike wave in the temporal lobe and rebuild-up phenomenon in the right hemisphere. Brain atrophy in the anterior and temporal lobes progressed, and the patient experienced gradual disorientation, delirium and hypobulia. He was eventually bedridden. He also demonstrated repetitive tonic-clonic convulsions. After one convulsion, he remained unconscious and died of pneumonia. Autopsy revealed thickening of the intima and internal elastic lamina in the occluded internal carotid artery. The anterior and middle cerebral arteries showed the same pathological changes. Multiple small infarctions restricted to grey matter were present in the cerebral cortex and may have caused the progressive brain atrophy. There was no myelin pallor in the white matter of the cerebrum. Atherosclerotic changes, senile plaque, and neurofibrillary tangles were seen but were within normal limits. These pathological findings were strongly suggestive of moyamoya disease.
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PMID:[An autopsy case of bilateral carotid artery occlusion with repetitive epilepsy and brain atrophy in a senile patient]. 1068 97

The pattern of acute illness was determined in 102 adolescents and adults with sickle cell anaemia who presented to the emergency unit of a Lagos hospital. The patients had a mean age of 20.5 years (SD 13.1) and a male-female ratio of 1.5. The symptoms included fever (72%), fatigue and weakness (59%), anorexia (59%) and pain (57.5%) while major clinical signs were pallor (100%), jaundice (71%) and hepatomegaly (68%). Sixty-eight per cent of patients had sickle cell crises, including one with hemiplegic stroke, 10% with combined anaemia and pain crises, 33% with anaemia crises only and 23.5% with pain crises only. Sixty-three per cent had infection which was malaria in 24.5%, bacterial in 17% and viral in 6%. Of 16 patients with pyrexia of unknown origin, seven responded to treatment with chloroquine and eight to antibiotics. Infection was detected in 50% of the patients with sickle cell crises. The association between anaemia crises and malaria was significant (P < 0.05). Of the eight deaths, seven (88%) had anaemia crises. In contrast to studies conducted two decades ago in the same hospital, the prevalence of anaemia crises now exceeds that of pain crises and malaria now exceeds that of bacterial infection. Severe symptomatic anaemia (anaemia crisis) was more frequently associated with infection (mostly malaria) than was bone pain crisis. The Girdle pain crisis more frequently resulted in a fatal outcome than the uncomplicated bone pain crisis.
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PMID:Acute sickle cell syndromes in Nigerian adults. 1093 Nov 63

A clinicopathological study of 41 cases of pituitary apoplexy in a series of 324 surgically treated pituitary adenomas is presented. In 23 patients, the predominant operative finding was hemorrhage with or without necrosis. However, there were 15 (37.7%) cases where pale, necrotic tissue with no evidence of hemorrhage was found at surgery. Pale, necrotic material was particularly found when there was a long interval between the acute clinical event and surgery. It is concluded that the pale, necrotic debris represents one stage in the resorption process of blood after hemorrhagic necrosis of pituitary adenomas. This entity needs to be kept in mind especially since the material closely resemble the pultaceous material seen in craniopharyngiomas and epidermoid cysts.
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PMID:Hemorrhagic necrosis of pituitary adenomas. 1257 4

Cerebellar syndromes and radiologic cerebellar atrophy after hyperpyrexia have occasionally been reported, mostly in neuroleptic malignant syndromes, but neuropathologic studies are extremely rare. We studied 3 patients (a 74-year-old woman, a 63-year-old man, and an 80-year-old man) who had heat stroke during heat waves in France. One patient had generalized seizures and died 28 hours after admission. The other patients survived one month and 2 months after admission; both had palatal myoclonus, and in one case, magnetic resonance imaging showed high signal intensity in the cerebral peduncles. The main neuropathology in the 3 cases was severe diffuse loss of Purkinje cells associated with heat shock protein 70 expression by Bergmann glia. In situ end labeling was negative in surviving Purkinje cells, suggesting that the mechanism of neuronal death was not apoptosis. Degeneration of Purkinje cells axons resulted in myelin pallor of the white matter of the folia and of the hilum of the dentate nuclei. DNA internucleosomal breakages were identified by in situ end labeling in the dentate nuclei and centromedian nuclei of the thalamus and were associated with degeneration of the cerebellar efferent pathways: superior cerebellar peduncles, decussation of the superior cerebellar peduncles (Wernekinck commissure), and dentatothalamic tract. These findings suggest that the mechanisms of neuronal death in the dentate nuclei and centromedian nuclei of the thalamus was different from that in Purkinje cells and more likely resulted from deafferentation. Ammon's horn and other areas susceptible to hypoxia were spared. These observations confirm the selective vulnerability of Purkinje cells to heat-induced injury and involvement of the cerebellar efferent pathways in palatal myoclonus.
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PMID:Brain damage after heat stroke. 1625 91

Acute vascular- and neuroprotective effects of simvastatin were evaluated in a rat model of transient, focal cerebral ischemia. Male, Wistar rats (n=12) underwent transient middle cerebral artery (MCA) occlusion for 3 hours followed by 3 hours of reperfusion. After 30 minutes of MCA occlusion, four rats each were subcutaneously injected with either 20 or 40 mg/kg of simvastatin. At the end of 3 hours of reperfusion, tissue injury and blood-brain barrier (BBB) opening were quantified by histology and [(14)C]-alpha-aminoisobutyric acid (AIB)-based quantitative autoradiography (QAR), respectively. Compared with untreated rats, those treated with simvastatin (20 mg/kg) had reduced volumes of AIB leakage, tissue pallor and distribution space for AIB (p<0.05). No additional effects were seen with the higher drug dose (40 mg/kg). These data suggest that the acute neuroprotective effects of statins are in part owing to attenuation of stroke-induced changes in BBB permeability.
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PMID:Acute neurovascular unit protection by simvastatin in transient cerebral ischemia. 1728 39

Oxcarbazepine is a commonly used antiepileptic and mood stabilizer medication with a considerably good safety profile. Medication-induced side effects are a common cause of morbidity in the geriatric population. We describe a patient presenting with hemolytic anemia attributed to oxcarbazepine that resolved after discontinuation of the drug. A 75-year-old male was brought into the hospital because of lethargy for the previous few days. His medical history included diet-controlled diabetes mellitus, mild essential hypertension, ischemic stroke with no residual deficit, seizure disorder, and dementia. He was taking only trileptal for the previous 3 months. His other history was insignificant. Physical examination was remarkable for generalized pallor and impaired memory. Laboratory results showed hemoglobin of 4.6 g/dL. Serum lactate dehydrogenase was 1314 u/L, and total bilirubin was 3.4 mg/dL, with indirect bilirubin of 2.9 mg/dL. Peripheral blood smear revealed microspherocytes, polychromasia, and a few nucleated red blood cells. Urinalysis showed 12RBCs/high power field (HPF), hemosiderinuria, and moderate bilirubin. Coombs test, cold agglutinins, antinuclear antibodies, and cultures were negative. Computerized tomographic scan of the chest, abdomen, and pelvis was also normal. After exclusion of other causes of hemolysis, drug-induced hemolytic anemia was suspected, and oxcarbazepine was discontinued. The patient's symptoms and laboratory parameters improved. He was in a usual state of health at 7 months follow-up. To our knowledge, this is the first reported case of oxcarbazepine-induced hemolytic anemia in the medical literature, and it was reported to the manufacturing pharmaceutical company.
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PMID:Oxcarbazepine-induced hemolytic anemia in a geriatric patient. 1835 42

The phenomenon of erythrocyte sickling observed in sickle cell anaemia is responsible for ischaemia and tissue infarction compromising several organs and systems including the mouth and face. This brief paper reports the case of a 17- year-old female with a complicated sickle cell anaemia, hypertension and paraplegia (after an ischaemic stroke at the age of six years). Oral examination revealed the absence of tooth 12, fractures of teeth 11, 21 and 22 (from trauma), active caries lesions in the enamel of teeth 36, 37 and 46, mucosal pallor, and a smooth tongue. Oral radiographs revealed bone rarefaction and trabecular bone coarsening. Dental surgeons and physicians should be aware of the general and oral abnormalities that can be present in individuals with sickle cell anaemia to allow for preventive measures and implementation of effective treatment options.
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PMID:Oral considerations in the management of sickle cell disease: a case report. 2297 72


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