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

Clinical neurological examination, computed tomography (CT) scan, cerebral angiography, and cerebral blood flow-single photon emission computerized tomography (CBF-SPECT) study have been performed in 39 patients with acute ischemic stroke within 6 h from the onset of symptoms. Seven of these patients were submitted to a second CBF study after an intravenous infusion of nimodipine. A greater CBF impairment was observed in patients with severe neurological deficit at entry, poor outcome, cerebral arterial occlusion, and large hypodensity on the CT scan performed 1 week after admission. In patients treated with nimodipine, a significant increase of CBF was detected at the periphery of the ischemic zone, indicating a potential action of this Ca antagonist on the "ischemic penumbra."
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PMID:Calcium antagonists in ischemic stroke. 246 16

Fourteen patients were studied by positron emission tomography (PET) within 48 h of onset of a hemispheric ischemic stroke and again 7 days later. After the first set of PET scans, the patients were randomized to receive either nimodipine (n = 7) or a carrier solution (n = 7) by intravenous infusion. The infusions were maintained until the end of the second PET studies. CBF, cerebral blood volume (CBV), oxygen extraction ratio (OER), CMRO2, and CMRglc were measured each time. These metabolic and perfusion measurements were performed by standard methods. A surface map of each metabolic and perfusion measurement in the cortical mantle was generated by interpolating between the available slices. The various surface maps representing the physiological characteristics determined in the same or subsequent studies were aligned so that all data sets could be analyzed identically using an array of square regions of interest (ROIs). The functional status of each ROI was recorded at the two intervals following the cerebrovascular accident to characterize the evolution of the infarct, penumbra, and normal brain regions. We presumed the ischemic penumbra to be cortical regions in the proximity of the infarct and perfused at CBF values between 12 and 18 ml/100 g/min on the first PET scan, while densely ischemic regions had CBF of less than 12 nl/100 g/min and normally perfused brain greater than 18 ml/100 g/min. In the densely ischemic zone, CBF increased more in the nimodipine-treated group than in the carrier group. As well, in this region nimodipine reversed the decline in CMRO2 noted in the carrier group, the difference in the changes being significant. In the penumbra zone, comparable trends were noted in OER and CMRO2 but the difference in the changes between the two groups did not reach statistical significance. Changes in CMRglc and CBV were comparable between the two groups in both cortical regions.
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PMID:The effect of nimodipine on the evolution of human cerebral infarction studied by PET. 266 84

To study the effects of focal infarction on the capacity for functional activation of an ipsilateral somatosensory system remote from the lesion, we produced a small thrombotic infarct in the left frontal pole of male Wistar rats by a photochemical method. Five days later, the awake, restrained rats received tactile stimulation of the large whiskers (vibrissae) of the right side of the face, while a double-label 14C-autoradiographic study of local CMRglc (lCMRglc) and local CBF (lCBF) was performed. Unlesioned and unstimulated animals served as controls. In rats without frontal infarct, vibrissae stimulation led to activation of lCMRglc in the three synaptic relay stations of the barrel-field pathway (ipsilateral trigeminal medullary nucleus, contralateral ventrobasal thalamus, and contralateral barrel-field cortex). The mean increment in lCMRglc was 42% in lamina IV of barrel-field cortex and 49% in ventrobasal thalamus. Normalized lCBF tended to increase in superficial cortical laminae. In unstimulated animals with frontal infarct, lCMRglc was reduced by 20-30% throughout the ipsilateral barrel-field cortex as well as other ipsilateral cortical regions, but not in ventrobasal thalamus or other subcortical areas. In animals with frontal infarct subjected to contralateral vibrissae stimulation, a remarkable suppression of activation was observed throughout the barrel-field cortex so that left-less-than-right hemispheral lCMRglc asymmetry persisted despite stimulation. The ventrobasal thalamus, similarly, failed to increment its lCMRglc with vibrissae stimulation, whereas activation of the trigeminal nucleus was not suppressed. Similar trends were observed in the normalized lCBF data. These observations, which establish that a small frontal infarct is capable of suppressing normal physiological activation in remote ipsilateral brain structures, may have important implications with respect to suppression and recovery of function in human ischemic stroke.
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PMID:Acute thrombotic infarction suppresses metabolic activation of ipsilateral somatosensory cortex: evidence for functional diaschisis. 271 5

In a series of patients with unilateral supratentorial ischemia, clinical scores and parameters derived from computer analysis of the EEG and from measurement of the CBF were determined in the first several weeks after the stroke. Seventeen of these patients underwent a carotid-endarterectomy and 15 a STA-MCA bypass operation. Matched control patients were selected from the remaining cases. All patients, including the controls, were eligible for vascular surgery. The measurements were repeated respectively 3 months and 3 years after the first examination. Clinical improvement occurred in all groups. The degree of these clinical changes was similar for operated and non operated cases. EEG changes indicated more improvement in the cases without surgery. Finally, the CBF was remarkably stable in all patients. The overall effects of reconstructive vascular surgery on the recovery after cerebral ischemia appeared to be negligible.
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PMID:Long-term clinical and neurophysiological effects of reconstructive vascular surgery for cerebral ischemia. 272 55

CBF and somatosensory evoked potentials (SEPs) were measured in a model of moderate cerebral ischemia in anesthetized spontaneously hypertensive rats. The rats were bled to reduce SEP amplitudes to about 50% of prebleeding control. The consequent blood pressure fall reduced CBF to 77% of control as measured by the laser-Doppler technique. Naloxone (5 mg kg-1 i.v. plus 25 mg kg-1 h-1 i.v. for 30 min) caused a significant increase in SEP amplitudes, while CBF did not change significantly. In addition, the latency of the first SEP component decreased toward prebleeding values. Heart rate (HR) decreased, but MABP was held constant by a pressure-regulating reservoir. In unbled rats, naloxone (5 mg kg-1 i.v.) caused a transient small increase in MABP and SEP amplitudes and decrease in HR. These results indicate that sensory input is regulated by opioid systems. Increased opioid activity may inhibit ascending sensory pathways during relative cerebral ischemia and thereby depress SEP responses. Thus, naloxone can release this inhibition and enhances SEP independently of CBF during relative cerebral ischemia. Similar mechanisms might explain the apparently beneficial effects of naloxone in some stroke models.
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PMID:The effects of naloxone on cerebral blood flow and cerebral function during relative cerebral ischemia. 273 17

Although decreased CBF has now been reported during the prodrome of migraine, the cause of the decreased flow is still unknown. It is particularly unclear whether these phenomena are related to vasospasm and "steal" between the extracranial and intracranial circulation or to the spreading depression of Leao and the accompanying metabolic depression. In the present paper, metabolic changes in the brain during ischemia and reperfusion are reviewed and compared with CNS biochemical changes during migraine attack. In addition, the technique of Topical Magnetic Resonance (TMR) as applied to the in vivo study of energy phosphate metabolism in extracranial tissues and brain is described and the potential of this technique to evaluate shifts in energy metabolism and pH in stroke and migraine is discussed.
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PMID:Biochemical effects of cerebral ischemia: relevance to migraine. 286 8

TCD recording of flow velocities in intracranial vessels was first described by Aaslid in 1982. The utility of this instrument becomes more apparent as it is used in different clinical settings and compared with angiographic findings (Figures 1 and 2). Its importance in early detection of vasospasm in subarachnoid hemorrhage is now clearly known; increased flow velocity can be documented prior to neurologic deterioration and thus allow early institution of therapy. In patients with stroke or transient ischemic attack of unclear etiology, especially in blacks, Orientals, or females, who have a higher incidence of intracranial arterial disease, TCD can be a very important noninvasive means for detecting stenosis of intracranial vessels. Its value for assessing collateral circulation, intraoperative monitoring, and measuring CBF is quite promising. Hopefully, through further work with TCD, we will be able to clarify the spectrum of its usages as well as its limitations, though the preliminary data indicate that it should be an important addition to present noninvasive evaluations.
Stroke 1988 Jul
PMID:Transcranial Doppler. 296 90

There is still considerable controversy regarding the influence of blood viscosity upon CBF. We have measured CBF with microspheres in 23 cats. Autoregulation was disturbed in the left caudate nucleus by microsurgical occlusion of the left middle cerebral artery. Induced hypertension or hypotension was used and i.v. mannitol (1 g/kg) administered. In all cats blood viscosity decreased an average of 16% at 15 minutes and, in 16 cats, increased 10% at 75 minutes post-mannitol. CBF in the right caudate was 79 +/- 6 ml/100g/min, in the left 38 +/- 6 (p less than 0.001). Only minor changes of CBF occurred in areas with presumed normal autoregulation, including the right caudate, in conjunction with pressure or viscosity changes. In the left caudate CBF decreased 21% with hypotension and 18% with higher viscosity, more than on the right (p less than 0.01 and p less than 0.2, respectively). CBF increased in the left caudate 56% with hypertension and 47% with lower viscosity, again much more than on the right (p less than 0.001 and p less than 0.01, respectively). In the other area which is (nearly) exclusively supplied by the middle cerebral artery of the cat, i.e., the ectosylvian cortex, results were similar to those in the caudate nucleus. These results show that viscosity changes must result in compensatory readjustments of vessel diameter, but that these adjustments do not occur where autoregulation to pressure changes is known to be defective. The adjustments to viscosity changes might be called blood viscosity autoregulation of CBF. We hypothesize that pressure autoregulation and blood viscosity autoregulation share the same mechanism.
Stroke
PMID:Cerebral blood flow is regulated by changes in blood pressure and in blood viscosity alike. 308 Aug 24

The remote effects of small unilateral cerebrovascular lesions confined to subcortical structures were evaluated by single photon emission computerized tomography (SPECT) and a CBF tracer, I-123 HIPDM. A CBF study was performed in 34 patients presenting with subcortical stroke either in the acute or in the chronic stages. Twenty-one of the 34 patients showed areas of cortical hypoperfusion ipsilateral to the subcortical lesion. In 14 patients, asymmetry of perfusion was also observed at the cerebellar level, perfusion being significantly reduced in the cerebellar hemisphere contralateral to the lesion. There was no correlation between the degree and extension of these remote effects and the type of stroke (ischemic or hemorrhagic), the patency of cerebral arteries, or the size and site of the lesion by transmissive computerized tomography (TCT). Subcortical hematomas showed a correlation between occurrence of remote effects and time interval from the onset of stroke, occurring more frequently in the acute phase. A correlation was observed between cortical and cerebellar remote effects and the severity of clinical presentation. The causes of remote effects are still unclear and have been extensively debated. Our data indicate that there is a relationship of remote effect to the neurological status. It is possible to show, by noninvasive, low-cost methods, remote CBF effects after stroke that may contribute to the assessment of brain functional impairment.
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PMID:Remote effects of subcortical cerebrovascular lesions: a SPECT cerebral perfusion study. 326 May 96

Regional (r) CBF, rOEF, rCMRO2, rCBV in five cases of "moyamoya" disease in children were studied with PET scan, using 15O steady-state methods. All cases showed ischemic symptoms such as TIA, RIND and minor stroke. Intervals from the latest ictus to PET ranged from 3 days to 3 years 6 months. Control data were obtained through PET studies in 8 normal volunteers. Physiological parameters described above, in cerebral gray matter, white matter and basal ganglia were calculated and were carefully compared with normal control. Apparently low density area in X-ray CT were excluded from this analysis. Although rCBF showed a little bit higher value in all gray, white and basal ganglia, it was not statistically significant. rCBV of "moyamoya" disease significantly increased in gray, white and basal ganglia. The calculated value of CBF/CBV is considered to be an index of perfusion pressure and is the reversed value of transit time. This value was significantly decreased in "moyamoya" disease in every three region. Under the normal autoregulation, further decrease of perfusion pressure initiate increase of rOER and also decrease of rCBF. In spite of reduction of CBF/CBV, rOER was not significantly increased in every three region. Hence the cerebral circulation in children's "moyamoya" disease of ischemic type appears to be characterized by the mild decrease of perfusion pressure, dilated resistant vessels and prolonged circulation time.
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PMID:[Cerebral circulation and oxygen metabolism in children's "moyamoya" diseases]. 326 Sep 96


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