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

In a retrospective study, pathological tissue enhancement was found in nearly two fifths of patients with acute SAH on contrast-enhanced cranial computed tomography. By means of absorption measurements with the region of interest technique over the basal ganglia, it was proved indirectly that pathological tissue enhancement should be brought about not only by hyperaemia, i.e., a blood volume increase, but also by extravasation of the contrast material, i.e., blood-brain barrier (BBB) disruption. A similar conclusion was drawn from the retrospective isotope brain scintigraphy study. It was further established that, although the pathological contrast enhancement was most obvious in the cortex, and particularly in the neighbourhood of the subarachnoid spaces, the phenomenon is probably widespread throughout the brain. Patients with abnormal enhancement are likely to be in less favourable clinical grades, have a high incidence of marked or diffuse spasm, have a poorer outcome independent of surgical or conservative treatment, and develop cerebral infarction more frequently. Systemic arterial hypertension was associated with an increased incidence of abnormal enhancement. Pathological tissue contrast enhancement or isotope accumulation in the first few days of SAH may serve as prognostic signs indicative of the late development of vasospasm and ischaemia. As ischaemic disruption of the capillary system is not prominent in the initial days following any stroke, vasoactive substances arising from the breakdown of the blood clot should play important part in the BBB damage in the acute stage of SAH. The "cortical SAH" model developed in the animal experiments ensured a constant subarachnoid blood volume with minimal local brain damage. The intracranial pressure and mean arterial blood pressure did not change significantly, and perfusion defects did not arise. Thus, this model proved suitable for studying the influence on the BBB of vasoactive blood breakdown products (responsible for arterial spasm) without the accompanying effects of pathological conditions such as raised intracranial pressure, systemic hypertension, non-reflow phenomena, which also disrupt the BBB. Measurements on the water, electrolyte, albumin contents of brain tissue, as well as the immunohistochemical localization of albumin, clearly indicated that the brain oedema developing at the acute stage of experimental SAH could be classified as having a primary vasogenic component in addition to the cytotoxic component. This increased capillary permeability was found to be brought about by opening of tight junctions and pinocytosis in the endothelial cells. The pathological capillary permeabilit
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PMID:The pathogenetic and prognostic significance of blood-brain barrier damage at the acute stage of aneurysmal subarachnoid haemorrhage. Clinical and experimental studies. 407 81

We tested the hypothesis that cerebral arteriospasm developing after rupture of a subarachnoid aneurysm may be due to the vasoconstrictor effect of locally generated angiotensin II. Ten dogs had subarachnoid hemorrhage simulated by intracisternal introduction of 2 ml autologous blood, and were followed by cineangiography. Thirty minutes later, when acute arteriospasm was established, seven dogs received injection of the angiotensin converting enzyme inhibitor teprotide and 3 control dogs received normal saline. Repeat angiography at 30 and 90 minutes after injection, showed total or partial release of spasm in the experimental dogs and no change or further intensification of spasm in the control animals. We concluded that angiotensin converting enzyme inhibition may be a potentially useful approach for the reversal or prevention of cerebral arteriospasm after subarachnoid hemorrhage.
Stroke
PMID:Reversal of experimental acute cerebral vasospasm by angiotensin converting enzyme inhibition. 617 64

A 12 year old boy who was a habitual glue sniffer developed a dense hemiparesis in association with an episode of glue sniffing. Occlusion of the right middle cerebral artery was found. It is postulated that the stroke was precipitated by an episode of vascular spasm.
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PMID:Glue sniffing and cerebral infarction. 646 42

We have studied the effects of the calcium antagonist verapamil on the epicerebral arteriovenous transit time and regional epicerebral circulation of dogs by direct measurement of arterial diameters, fluorescein angiography, and krypton-85 regional epicerebral blood flow analysis. A large craniectomy was performed and vasoconstriction was induced by the subarachnoid injection of human platelet-rich plasma (PRP) pretreated with 25 mu M of ADP to cause maximum aggregation. Once vasoconstriction was established, verapamil (0.1 mg/kg) was topically applied to the perforated arachnoid. The PRP-ADP produced a mean decrease in the arterial diameters of 38.2 +/- 1.6% (p less than 0.01) at 10 minutes after its injection and verapamil produced a mean dilatation of 19.5 +/- 2.5% (p less than 0.01), compared to control values. Regional epicerebral blood flow was 54.9 +/- 3.4 ml/100 g/min in the control state, 34.8 +/- 3.2 ml/100 g/min (p less than 0.01) during vasospasm, and 78.2 +/- 4.5 ml/100 g/min (p less than 0.01) after verapamil. Fluorescein angiography, after verapamil, demonstrated a mean acceleration of the arteriovenous circulation time of 4.5 +/- 0.8 seconds (p less than 0.01) compared to the spasm value. We concluded that the topical application of verapamil can dilate previously constricted cortical arteries and that this dilatation is associated with acceleration of the epicerebral transit time and increased cerebral blood flow.
Stroke
PMID:The effects of calcium antagonism on the epicerebral circulation in early vasospasm. 650 12

The authors describe case histories of patients with brain involvement--extensive brain strokes with blood breakthrough to the ventricles. The development of myocardial lesions (from extensive hemorrhages to the heart muscle till the development of large myocardial infarction) attests to the possibility of centrally caused disorders of coronary circulation. It is necessary to note that the development of myocardial lesion is masked, as a rule, by the clinical picture of a grave brain stroke and is not adequately detectable at ECG studies. It is believed that the development of hemorrhages in the myocardium is consequent on the reperfusion syndrome, whereas formation of myocardial infarction is the result of the spasm of the coronary arteries.
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PMID:[The cerebrocardiac syndrome]. 652 63

Three partially paralyzed patients were unable to walk even after maximal rehabilitation attempts at a major rehabilitation center. One 36-year-old man had transverse myelitis, a 57-year-old man had had a stroke, and the third patient, a 35-year-old man, had incurred a traumatic brain injury. The three patients were unable to flex the hips, had adductor spasm and weak hip and knee extension, and lacked ankle dorsiflexion. Intramuscular stainless steel wire electrodes activated by timers were placed in the quadriceps, hip flexors, extensors, and abductors, as needed. Muscle force and foot contact evaluations were done using the Cybex and the Cleveland Veterans Administration Gait Laboratory. After implantation of intramuscular electrodes, all three patients had improved function but still desired some supervision in walking. A ten-fold increase in knee torque was noted in one patient, thereby providing him with nearly normal strength. No implant complications were noted. The study demonstrated the feasibility of functional neuromuscular stimulation (FNS) gait augmentation in a previously nonwalking patient outside the laboratory. Further improvements will require the development of an implantable, multichannel, programmable microprocessor-controlled stimulator.
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PMID:Functional walking in paralyzed patients by means of electrical stimulation. 660 57

Occlusion of the anterior cerebral artery is a rare condition. A review of CT scans from 413 patients with ischemic infarction confirmed this low relative incidence: only 3% of CT scans evidencing infarction involved the territory of the anterior cerebral artery. Four major mechanisms of anterior cerebral artery occlusion have been identified in this series: Emboli in unusual hemodynamic circumstances such as patients presumed to have increased flow through the anterior communicating artery because of unilateral internal carotid artery occlusion. Propagation of thrombotic material from an occluded internal artery into the intracranial branches. Spasm, emboli or propagating thrombosis associated with anterior communicating aneurysm.
Stroke
PMID:Occurrence and mechanisms of occlusion of the anterior cerebral artery. 665

Two patients developed paraplegia associated with the use of the intraaortic balloon pump. In one patient, transient spinal ischemic episodes ceased after removal of the intraaortic balloon and the second patient apparently sustained spinal cord infarction. Possible etiologic mechanisms include vascular occlusion due to balloon position, arterial spasm, thromboembolic phenomena, hypotension, hypoxia and arterial dissection.
Stroke
PMID:Paraplegia associated with intraaortic balloon pump counterpulsation. 665 4

Eleven freshly removed brains and 20 lenticulostriate arteries (collected at emergency surgery for intracerebral hemorrhage) were examined by electron microscopy in a search for the mechanism of arterial rupture in hypertensive intracerebral hemorrhage. Forty-six of 48 ruptured arteries examined showed severe arteriosclerosis including degenerative changes of the media at or near bifurcations. Atrophy and fragmentation of smooth muscle cells gave them a moth-eaten appearance. Material resembling basement membrane and cell debris was also present in the arterial walls. The above findings were restricted to the middle and distal portions of the perforating arteries. Rupture from a miliary aneurysm was observed in only 2 of the 48 specimens examined. These resembled saccular aneurysms, ultrastructurally. They seemingly formed at a cavity which we strongly felt may have been formed by complete or incomplete subclinical hemorrhages; reabsorption of the hemorrhage from the dissection resulted in the aneurysms seen. Degeneration of smooth muscle cells may be the result of prolonged tension or spasm of the arterial wall as a result of longstanding hypertension.
Stroke
PMID:Electron microscopic studies of ruptured arteries in hypertensive intracerebral hemorrhage. 682 83

All contributory factors to the unusual occurrence of stroke in young people were evaluated in patients under age 40 admitted to the Stroke Unit of the Austin Hospital in Melbourne, Australia. Over the August 1977 to December 1980 period there were 700 admissions. Of these 14 patients were under the age of 40. There were 7 males and 7 females whose ages ranged from 17-38 years. Each patient was screened for factors which might contribute to premature vascular disease including hypertension, diabetes, smoking, obesity, and hyperlipidemia. In addition, the following tests were performed to exclude an arteritic process: full blood examination; ESR; protein electrophoresis; syphilis serology; and the presence of antinuclear factor. Each of the 14 patients suffered cerebral infarction. A summary of each case is presented in a table. In 9 patients, infarction occurred in the carotid territory of supply. Large cortical infarcts with or without subcortical involvement occurred in cases 1-8, of whom 5 had major vessel occlusion demonstrated angiographically and another had stenosing and ulcerative atheromatous disease at the extracranial carotid bifurcation. In a further 4 patients, infarction occurred within the vertebrobasilar territory and was either confined to the brain stem, the occiptal cortex, or involved both. Angiograms were performed in 2 of these patients and showed irregular narrowing of the vertebral artery which was interpreted as spasm and segmentally narrowing of the basilar artery. The final patient had several ischemic events which included right sided amaurosis fugax, and left frontal, right parieto-occipital and left occipital infarctions. Angiography was normal. All patients survived the stroke and were able to go home. There may be an interrelationship between the pathological findings of Irey et al. (1978) and the effect oral contraceptives (OCs) has on migraine. This is relevant to Case 13. Sustained exposure to OCs may produce the pathological changes described (visible as segmental narrowing angiographically). In 2 patients cerebral infarction was caused by atheromatous or hypertensive occlusive vascular disease. In Case 3 an embolus occluded the middle cerebral artery. Infarction complicating migraine was diagnosed confidently in 4 patients on the basis of typical migrainous symptomatology in the past and accompanying the stroke. Of the 12 patients fully evaluated, there were no cases of polycythemia or thrombocytosis. There were no abnormalities of the clotting factors. Almost every patient had some form of emotional upset, and there were 7 who had significant psychiatric illness and emotional problems of extreme magnitide.
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PMID:Stroke syndromes in young people. 692 82


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