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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The efficacy of the calcium channel blocker nimodipine in the prevention of chronic cerebral vasospasm (VSP) and delayed ischemia after subarachnoid hemorrhage (SAH) in monkeys was examined in a blind, randomized, placebo-controlled trial. The primate model developed in this laboratory reliably induces chronic cerebral vasospasm and can induce pathologically proven delayed ischemic neurological deficits (DINDs). With standard microsurgical procedures, an average 6.4-ml autologous hematoma was placed directly against the major anterior cerebral vessels in the right basal subarachnoid spaces of 24 monkeys. The monkeys were randomized to one of four groups and were treated orally q8h for 7 days with nimodipine (3, 6, or 12mg/kg)or placebo. An additional 2 monkeys underwent the surgical procedure without clot placement. Drug administration began between 14 and 20 hours after clot placement. Indices monitored before and after SAH included neurological status, angiographic cerebral vessel caliber, and cerebral blood flow. Significant VSP (25 to 100% reduction in vessel caliber) was present on Day 7 on the clot side in 83% of the animals (P less than or equal to 0.001). There was no significant difference (P greater than 0.05) in the incidence of VSP among the four groups. Similarly, there was no significant difference (P greater than 0.05) in the mean vessel caliber reduction after SAH among the four treatment groups. There was no VSP present on Day 7 in the sham-operated animals. One animal receiving high dose nimodipine (12 mg/kg p.o. q8h) developed a DIND on Day 5 after SAH. A second animal in the 12-mg/kg group developed a transient neurological deficit between Days 4 and 7.
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PMID:Nimodipine and chronic vasospasm in monkeys: Part 1. Clinical and radiological findings. 397 22

Periventricular arteriovenous malformations (AVMs) have often been deemed inoperable because of their location in critical structures. Furthermore, the excision of large lesions may be complicated by the potential for serious brain swelling and hemorrhage due to "autoregulation breakthrough." Nonetheless, the unfavorable natural history of the untreated disease in a symptomatic young patient has induced us to approach these lesions using staged microsurgical excision combined with elective barbiturate coma for maximal cerebral protection. Between 1979 and 1983, six patients (four female, aged 12 to 60 years, and 2 male, aged 14 and 29) who harbored large AVMs in the basal ganglia, thalamic, and hypothalamic areas presented with subarachnoid hemorrhage (2 cases), progressive neural deficits (3 cases), and intractable headache (1 case). Nineteen staged operations were performed for the complete excision of these lesions. Among the first three patients, there was one death due to "autoregulation breakthrough" hemorrhage into the lateral ventricle during the excision of a lesion approached through the sylvian fissure using standard anesthesia techniques. This led to the adoption of the transventricular surgical approach and elective barbiturate coma to facilitate exposure of the lesion and to protect the adjacent vital structures from potential ischemia. Three patients were treated in this fashion uneventfully. Of the five successfully treated patients, two have returned to their preoperative status and one has completely recovered from global hemispheric ischemia and hemiplegia. The hemiparesis in one patient worsened as a result of postoperative hypertensive intraventricular hemorrhage, and one patient developed mild dysphasia and hemiparesis. This experience suggests that this approach offers a valid therapeutic regimen for the treatment of this disease. During the same period, three patients--one man (age 23) and two women (aged 29 and 22)--harboring four intraventricular AVMs presented with intraventricular hemorrhage. After the acute effects of chemical ventriculitis and hydrocephalus were overcome with cerebrospinal fluid diversion, all four lesions were excised microsurgically using the transtemporal approach. One patient demonstrated significant and progressive improvement of her preoperative memory deficit. The remaining two patients have both returned to their preoperative employment.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Microsurgical excision of paraventricular arteriovenous malformations. 398 6

A leukotriene-like immunoreactivity was measured by radioimmunoassay in the gerbil forebrain following ischemia and reperfusion, subarachnoid hemorrhage (SAH), or nonlethal concussive brain injury. In each paradigm an increase in immunoreactivity levels was found. Peak levels were reached 15 to 30 minutes after each insult, and slowly returned to baseline over the next 24 hours. The study supports the suggestion that cerebral vessels and circulating blood are capable of producing leukotrienes, and that a major source of production is a nonvascular component within gray matter, possibly the cortical neuron. Leukotrienes may play a role in the pathophysiology of cerebral edema formation, cerebral vasospasm, seizure activity, and other central nervous system abnormalities. These studies are the first to demonstrate leukotriene production in gerbil brain following SAH or concussive brain injury.
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PMID:Leukotriene production in gerbil brain after ischemic insult, subarachnoid hemorrhage, and concussive injury. 399 37

The levels of two calcium-binding proteins, S-100 protein and calmodulin, were measured serially in the cerebrospinal fluid (CSF) of patients after subarachnoid hemorrhage (SAH) and aneurysm surgery. These two proteins have a similar molecular structure and are highly concentrated in the central nervous system (CNS). The levels of S-100 protein found in the earliest postoperative CSF samples correlated with the preoperative SAH grades. High S-100 protein levels in the CSF were found in patients with poor SAH grades. Moreover, the prognosis of the patients correlated with the S-100 protein levels in the CSF samples taken during the immediate postoperative period and with the daily changes of the S-100 protein levels. Severe diffuse cerebral vasospasm was followed by a sharp S-100 protein increase. These results suggest that S-100 protein levels in the CSF provide a useful index of organic damage in the CNS, and furthermore that S-100 protein levels and their changes may have prognostic value for patients after SAH. On the other hand, there was a lack of correlation between the calmodulin levels and the preoperative grade or outcome. It would be inappropriate, however, to speculate from the results of this study that these calcium-binding proteins in the CSF play any causative role in pathological processes such as cerebral vasospasm or brain ischemia after SAH, since changes in the levels of these proteins followed the onset of clinical signs of deterioration.
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PMID:S-100 protein and calmodulin levels in cerebrospinal fluid after subarachnoid hemorrhage. 402 Apr 69

Aneurysmal subarachnoid hemorrhage is a neurosurgical emergency. Early medical intervention is axiomatic for minimizing rebleeding and ischemia from vasospasm and achieving optimum results. The purpose of this study was to document the length and causes of the delay in referral which occur in patients following aneurysmal subarachnoid hemorrhage. The case histories of 150 consecutive patients admitted to The University of Iowa with proven ruptured aneurysms were studied. Medical records from The University of Iowa and referring hospitals were reviewed, and patients, families, and referring physicians interviewed. Overall, only 36% were referred within 48 hours of their first clear cut, recognizable sign or symptom of subarachnoid hemorrhage. Median time to referral was 3.6 days. Delay was due to physician diagnostic problems in 37%, delayed referral policy in 23%, unstable patient condition in 7%, failure of patients to recognize severity of illness in 8%, and logistical reasons in 12%. These data suggest that a large proportion of patients have a delay in achieving definitive neurosurgical care following aneurysm rupture, and that for the most part this delay is avoidable. More emphasis must be placed on public health and primary physician education regarding subarachnoid hemorrhage.
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PMID:Delay in referral of patients with ruptured aneurysms to neurosurgical attention. 402 72

110 patients with ruptured aneurysms were operated on within 4 to 96 hours after subarachnoid hemorrhage. Clinical grades (Hunt) were: 1-2-3 in 93 cases and 4-5 in 17 cases. Among the patients grades 1-2-3, 81% had a good out come without any neurological abnormality, among the patients graded 4-5, only 27% had a fair out come. Cerebral ischemia has been noted (CTS can + neurological deficits) in 7 cases only among patients graded 1-2-3 (93 cases). The results, concerning ischemia, are better than the natural course of ruptured aneurysms and better than the course in series with delayed operation. Probably vasospasm is not alone to create ischemia.
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PMID:[Early surgery of ruptured aneurysms. A factor in preventing ischemia]. 408 96

Acute subarachnoid hemorrhage (SAH) over the cerebral cortex causes single or multiple waves of cellular depolarization, which may occur in a self-propagating, reverberating fashion. This process is characterized by a massive K+ release and transient depression in electrocortical activity. The K+ levels in the extracellular space reach magnitudes known to substantially affect the membrane potentials of neurons and glia, and may cause a release of neurotransmitters from depolarized presynaptic terminals. The release of K+ may be the initial step in the development of cellular edema and, together with a multitude of other chemical and biochemical changes taking place at the cellular level, may underlie the loss of autoregulation. Cortical cells rather than blood vessels are the primary targets in the initial stages of SAH, and ischemia does not play a causal role in the pathogenesis of cellular dysfunction during this stage.
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PMID:Cortical cellular response in acute subarachnoid hemorrhage. 610 23

Sixty-five patients with ruptured aneurysms were operated upon within 48 to 72 hours after subarachnoid hemorrhage (SAH) and were treated with a regimen of intra- and postoperative nimodipine for the prevention of symptomatic vasospasm. The clinical grading (Hunt and Hess) was I to III in 49 patients and IV or V in 16. The SAH was mild in 15 patients, moderate in 27, and severe in 23; 12 patients harbored an intracerebral hematoma, and 6 had intraventricular bleeding. Acute hydrocephalus was observed on preoperative computed tomography (CT) in 19 patients. On CT 3 days postoperatively (i.e., Day 3-4 after SAH), 30 of 65 patients still had subarachnoid blood; however, severe symptomatic vasospasm as the deciding threatening event during the delayed postoperative period was not encountered in this series. Transient symptoms of ischemia were noted in 2 patients (3%) and were accompanied by angiographic spasm in 1. Irreversible neurological deficit occurred in 2 patients (3%); in 1 of these, it was a complication of postoperative control angiography. Of the patients preoperatively graded I or II, 96% had an excellent to fair outcome 6 months postoperatively, and 1 patient (4%) had died because of a surgical complication. Among patients preoperatively graded III or IV, 86% had an excellent to fair outcome, and the remaining 14% had a poor outcome. Shunt-dependent hydrocephalus developed in 7% of the patients. Acute surgical repair of ruptured cerebral aneurysms and preventive topical and intravenous administration of nimodipine reduce management complications and improve outcome; above all, ischemic lesions from symptomatic vasospasm are reduced to a minimum.
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PMID:Acute operation and preventive nimodipine improve outcome in patients with ruptured cerebral aneurysms. 647 95

The role of computed tomography (CT) in the management of vasospasm from subarachnoid hemorrhage was evaluated in 242 consecutive cases with CT performed within 7 days after hemorrhage. Only 20% of these cases did not show a detectable subarachnoid hemorrhage on CT. Subsequent angiograms showed vessel narrowing in 56% of the cases; associated clinical deterioration was noted in 34% of the cases. On later CT, clear ischemic areas were detected in 20% of the cases. A strict correlation between the amount of cisternal blood and the subsequent development of vasospasm was observed: although absent or thin cisternal depositions were rarely associated with vasospasm, consistent or thick depositions were frequently linked to vasospasm (72% of the cases) and to ischemic disturbances (51% of the cases), as well as to clear ischemic areas on later CT (30% of the cases). Regarding the morphology of the cisternal blood collection, the risk of developing vasospasm was at its lowest (42%) for depositions only in the frontal interhemispheric fissure and was at its highest (79%) for depositions in multiple cisterns. The site of cisternal deposition corresponded closely to the area of ischemia on later CT. The persistence of subarachnoid blood more than 72 hours after hemorrhage probably increases the risk of vasospasm, although our data are not conclusive. The definition of a CT scan "at risk" for vasospasm--based on the previous findings--gives practical advantages: proper selection of patients in regard to timing of operation, closer observation and the possibility of prophylactic treatment in patients "at risk," and more adequate evaluation of different therapeutic modalities for vasospasm. With regard to the last point, the incidence of vasospasm was not statistically different between two groups of patients uniformly "at risk": the first group submitted to early operation and the second awaiting operation.
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PMID:Role of computed tomography in the management of vasospasm after subarachnoid hemorrhage. 648 49

Seventy-eight EEGs from 44 premature infants with CT- or autopsy-verified intraventricular hemorrhage (IVH) were reviewed retrospectively. The patient's most abnormal EEG was a reliable predictor of outcome, independent of the estimated gestational age, 1- and 5-minute Apgar scores, and IVH grade. Nine of 12 infants who had all normal or mildly abnormal EEGs had favorable outcomes. The nine infants whose worst EEGs were moderately abnormal experienced mixed outcomes, ranging from normal survival to death. All 23 infants with one or more markedly abnormal EEGs suffered unfavorable outcomes. Positive rolandic sharp waves, a highly specific EEG pattern for IVH in premature infants, occurred in only 29.5% of the patients. The degree of EEG abnormality correlated significantly with the patient's mental status, but not with the IVH grade. Subarachnoid hemorrhage, hypoxia-ischemia, and focal parenchymal lesions caused electrographic seizures in 14 patients, 12 of whom died (85.7%). This study suggests that EEG has limited value in the diagnosis of IVH. However, it may play an important role in the neurologic assessment of the premature infant with established IVH by confirming clinically suspected seizures and providing reliable prognostic information.
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PMID:EEG in premature infants with intraventricular hemorrhage. 653 51


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