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

Intraoperative rupture of an aneurysm can lead to disastrous results when the rupture occurs at the neck. The authors have encountered eight cases (5%) of intraoperative rupture in a series of 155 patients. All patients were operated on in the acute stage by one of the authors of this paper (T.Y.). In six cases, the aneurysm ruptured at the dome and in two, at the neck. We report these two patients with intraoperative rupture at the neck. The first case, a 50-year-old female, developed SAH, but a 4-vessel study failed to show an aneurysm. The second series of angiograms obtained ten days later showed a broad-based, left proximal A1 aneurysm. It was decided to employ a right pterional approach. The aneurysm was arising from the right A1 segment just proximal to the anterior communicating artery. The neck was wide, with thin walls. Thus, it seemed better to apply a clip parallel to the A1 segment axis than to apply it from a direction perpendicular to the A1 segment axis. However, the right pterional approach precluded a parallel clipping, so the blades of a clip were applied perpendicularly. The clip seemed not to be completely across the neck of the aneurysm. After applying a temporary clip to the A1 segment proximal to the aneurysm, the clip blades were opened and advanced just when bursting of the sac at the base occurred and microvascular suture repair was required to control the bleeding. The second case, a 57-year-old female, underwent clipping of a right IC-PC aneurysm. However, two years postoperatively, the patient again suffered SAH. Cerebral angiography at this time revealed a relatively large recurrent IC-PC aneurysm in which the old clip was situated on the dome of the aneurysm. Aneurysmal clipping was performed on the day of rupture. Tough granular tissue was removed from the ICA, PcomA, aneurysmal neck, and the old clip. After the true neck was identified, a straight clip was applied to the neck parallel to the ICA. Soon after the clipping, arterial bleeding occurred near the neck. The ruptured aneurysm was trapped using two temporary clips. A curved clip was applied to the ruptured neck, including the wall of the ICA, to control the bleeding. This clipping caused a substantial stenosis of the ICA. Both patients demonstrated postoperative neurological deficits due to ischemia caused by temporary clipping. These encounters dramatically demonstrated that a very thin-walled aneurysm or a recurrent aneurysm has a fragile neck. In surgical treatment of these unusual aneurysms, a clip should be placed on the neck parallel to the parent artery. Furthermore, temporary clipping is advisable when dissecting the neck or applying the clip to the neck to reduce the damage to the neck.
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PMID:[Intraoperative aneurysmal rupture at the neck]. 905 36

The mechanisms underlying the loss of consciousness following the SAH can be only hypothesized at present time. The more convincing hypothesis appears to be the role of a cerebral circulatory insufficiency. Such an hypothesis stems from the following chain of events: 1) immediate increase of the intracranial pressure; 2) simultaneous constriction of the arteries of the poligone of Willis (early vasospasm); 3) decrease of the cerebral perfusion pressure; 4) cerebral ischemia. Different cerebral regions can be affected by the ischemia according to the prevalent location of the SAH, as for instance brain stem or telencephalon; consequently, different pathophysiological modalities can be responsible for the consciousness impairment. The entity of the SAH and of the consequent events responsible for the cerebral ischemia, influence the severity and reversibility of the loss of consciousness.
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PMID:[Physiopathology of non-traumatic subarachnoid hemorrhage: loss of consciousness]. 977 36

Medical treatment of subarachnoid haemorrhage, is focused on the prevention of rebleeding and vasospasm, of damages of oxitading products, and on the improvement of general conditions of the patient. Some authors consider use of antifibrinolytic usefull to reduce the risk of rebleeding, but the percentage of hydrocephalus and ischemia are increased. In our Centre combination of nimodipine-cloricromene and hemodilution is used for the prevention of vasospasm. We report conclusions about 216 patients in I-II-III grade of Hunt-Hess scale, treated before 48 hours from SAH. We obtained only 8% postspasm ischemias, with no neurological deficit, and only 23% of increased cerebral blood flow revealed by transcranial Doppler. Cloricromene is used only after aneurysm is occlused. It presents different action mechanisms. It is an inhibitor of platelet activation and aggregation, of cyclooxygenase and lipooxygenase activity, so reducing thromboxanes ratio. Phospholipase A2 inhibition it's possible but not demonstrated. It also interferes with phosphoinositoles path and so with proteinkinase C activity, and reduces hemostatic thrombotic balance activation and leukocyte endothelial adhesion and activation. It reduces, finally, the release of free radicals, cytokines inflammation amplyfing. The reduced damage to the endothelium allows the releasing of vasodilatatory agents like NO.
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PMID:[Pharmacologic therapy of subarachnoid hemorrhage]. 977 63

Syndromes of intracranial hemorrhage, and particularly subarachnoidal, i.e., intracerebral hemorrhage (SAH and IH) present clinical entities that are the most severe conditions in neurology. Timely recognition, diagnosis and adequate therapy are imperative. The most important factor that aggravates an already difficult prognosis of those entities is cerebral vasospasm. Upon the presented facts, the aim of this investigation was to establish the value and role of administration of selective calcium channel blocker--nimodipine in patients with SAH and IH compared to the degree of neurological and functional impairment, as well as the recovery of the function of consciousness compared to the patients with those syndromes from an earlier period, who were not treated with this medicament. Investigation comprised 30 patients who received nimodipine and 20 patients without this agent in therapeutic program. Results of the investigation confirmed significant difference concerning the neurological recovery, improvement of functional capability and recovery or consciousness disturbances, respectively, in patients who received nimodipine compared to the group without this agent. It can be concluded that nimodipine as calcium channel blocker with multitopic pharmacological effects on mechanism of SAH or IH development, respectively, as well as on the development of complications of those syndromes, particularly to the development of vasospasm and reactive ischemia, with the improvement of hemorrheologic disorders deserves to be included as the unavoidable segment of therapeutic program of SAH and IH syndrome immediately after clinical phenomenology is revealed.
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PMID:[Role of nimodipine in the therapy of subarachnoid and intracerebral hemorrhage]. 1070 8

Vasopasm is a dreadful complication of SAH associated with an important mortality and morbidity. Therapy begins with adequate monitoring and lines, and prevention of secondary brain injuries. 3-H therapy (hypervolemia--hypertension--hemodilution--hyperdynamism) aims to increase perfusion in ischemia areas. 3-H therapy is associated with systemic complication precluding it's prophylactic use. Calcium antagonists, in particular nimodipine, improve outcome and parenteral route is better than oral administration. Tirilazad seems to improve outcome of severe grades. Numerous experiments are performed with drugs interfering with the biochemical cascade leading to vasospasm, but up to today no drug is used in current clinical practice. Intraaortic balloon is still considered as experimental and may have a role in patients presenting with concomitant cardiac failure. Invasive radiology must be considered in vasospasm not improving with standard therapies. Vasopasm is a dire complication after SAH. Support and specific therapies allow a 3-fold reduction in morbidity associated with vasospasm. Vasospasm is a vital emergency, and intervention has to be quick and aggressive.
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PMID:[Vasospasm treatment in intensive care]. 1085 75

Experiments were designed to study the extent, duration and severity of the impairment of cerebrocortical microciroflow during acute ischemia following experimental SAH in the rat. Twenty five male, adult anesthetized and mechanically ventilated Wistar rats were used. SAH was induced by perforation of the middle cerebral artery (MCA) using intravascular filament. Cerebrocortical microflow (LDF) was recorded bilaterally in the territory supplied by the MCA at normocapnia before SAH and up to 180 min thereafter. Reactivity of microcirculation to CO2 was also studied. In order to further explain mechanisms of post-SAH microcirculatory changes, L-arginine--a precursor of NO and 17-octadecynoic acid (17-ODYA)--an inhibitor of the enzymes of cytochrome P-450 family were administered. SAH resulted in acute decrease of microflow on both sides although during the first 20 min this effect was much better pronounced on the side ipsilateral to ruptured MCA (p < 0.05). Pretreatment with L-arginine or 17-ODYA didn't improve microflow after SAH. On the contrary, in rats pretreated with 17-ODYA LDF on the side ipsilateral to bleeding significantly deteriorated (p < 0.05 vs. control group at all times beginning 10 min after SAH). Following SAH the impairment of CO2 reactivity was also observed.
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PMID:Acute decrease of cerebrocortical microflow and lack of carbon dioxide reactivity following subarachnoid haemorrhage in the rat. 1475 89

Even with rapid development of other neuroimaging modalities such as MR imaging and CT, PET is the only technique that provides accurate, quantitative measurements of regional hemodynamics and metabolism in human subjects. Through the use of these combined measurements, we have greatly expanded our knowledge of the pathophysiology of cerebrovascular disease of different types. It has been possible to document the compensatory responses of the brain to reductions in perfusion pressure and to directly relate these responses to prognosis. PET measurements of OEF identify a subgroup of patients who have carotid occlusion and who are at increased risk for recurrent stroke who cannot be identified by any other clinical or arteriographic means. These measurements of OEF are being used to identify high-risk patients for inclusion in a clinical trial to assess the efficacy of surgical revascularization in reducing the subsequence of ipsilateral ischemic stroke. In acute ischemic stroke, attempts have been made to define the "ischemic penumbra" and to predict tissue viability and clinical outcome, although the reliability of PET markers of ischemia in distinguishing viable from irreversibly damaged tissue needs to be confirmed with independent data sets. Much work has been devoted to the investigation of the metabolic effects of infarcts and hemorrhages on remote areas of the brain; the clinical importance of such findings appears to be minimal. Early studies of recovery from stroke suggested functional reorganization of the brain, but further investigations with more rigorous experimental design need to be performed. Given the case of performing such studies with functional MR imaging, it is likely that this technology will supplant PET for this specific indication. The importance of ischemia as a secondary mechanism of brain injury has been addressed in ICH and SAH. PET demonstrated that hematomas exert a primary depression of metabolism rather than inducing ischemia in the surrounding tissue. It also documented the integrity of autoregulation and provided clinically useful information regarding the safety of blood pressure reduction after ICH. Studies in SAH have differentiated the primary effects of the hemorrhage on cerebral hemodynamics and metabolism from those of vasospasm. PET studies are time-consuming, expensive, and require extensive facilities and technical support. In the field of cerebrovascular disease, PET has served as a specialized research tool at a few centers to help elucidate the pathophysiology of stroke. Up until now, however, PET scans in individual patients have not been demonstrated to be necessary for making patient care decisions. Whether the role of PET expands to impact the management of individual patients will depend on the results of investigations like the Carotid Occlusion Surgery Study that directly assess the ability of PET to influence patient outcome.
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PMID:The use of positron emission tomography in cerebrovascular disease. 1502 58

The main consequence of subarachnoid hemorrhage, for those who survive bleeding, is delayed, persistent vasospasm of intracranial conduit arteries which occurs between the third and seventh day after the insult and results in symptomatic brain ischemia in about 40% of cases. This vasospasm is considered to be a major cause of disability of post-SAH patients. Despite extensive experimental and clinical research, mechanisms of vasospasm are not fully understood. Dysfunction of the endothelium resulting in enhanced production of vasoconstrictors, phenotypic changes of the receptors in endothelium and smooth muscle cells, increased sensitivity of vascular smooth muscle cells to vasoconstrictors, release of spasmogens from lysed blood clot and inflammatory response of the vascular wall have been demonstrated and discussed as pathological mechanisms participating in the development of spasm. In recent years more attention is paid to the functional and structural changes in microcirculation and a concept of microvascular spasm is evolving. Our experimental studies in rat model of SAH strongly suggest that microcirculatory dysfunction and delayed vasospasm are related to the severity of acute, transient ischemia caused by critical decrease of perfusion pressure and active vasoconstriction immediately after the bleeding.
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PMID:Mechanisms of vascular dysfunction after subarachnoid hemorrhage. 1724 46

The causes of postoperative cardiovascular disturbances in neurosurgical patients include direct cardiac neurogenic effects, clinical situations where brain tissue is underperfused, and hyperdynamic states. EKG and echographic abnormalities are common in subarachnoid hemorrhage where cardiac troponin I is the most useful predictor of cardiac risk after SAH. Neurogenic pulmonary edema is short lived and often resolves with resolution of the neurologic problem. In traumatic brain injury, where areas of ischemia co-exist with luxury perfusion, advanced hemodynamic monitoring and prevention of jugular venous desaturation best avoid secondary brain injury and achieve optimal neurologic outcome. Induced hypertension improves blood flow through vessels compromised by cerebral stenting, angioplasty, microcatheters, thrombolysis, carotid clamping, intracranial bypass and cerebral vasospasm. Hyperdynamic lesions include vascular breakthrough after elimination of cerebral arteriovenous malformations, but also emergence hypertension and hyperemia. Pharmacologic agents and adjunctive measures are effective in controlling both the systemic and the cerebral circulation.
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PMID:Cardiovascular therapy of neurosurgical patients. 1828 33

Crossed aphasia (CA) refers to aphasia occurring after right brain damage in right handers. In the literature, numerous CA cases following cerebral ischemia have been reported, but few met the criteria for a prompt diagnosis. The authors present the case of a 52-year-old woman with SAH caused by a right middle cerebral artery (MCA) saccular aneurysm who developed non-fluent aphasia characterized by reduced verbal output, word-finding disturbances and phonemic paraphasias in both oral and written language. 99mTc-HMPAO SPECT was also consistent with right parieto-temporal and frontoparietal ischemia with crossed cerebellar diaschisis on the right cerebellum. A diagnosis of CA was made. One year follow-up showed improvement in communication skills but persistent right fronto-temporo-parietal ischemia. Cerebral vasospasm after aneurysmal SAH symptomatology may vary from motor and sensory disturbances to cognitive disabilities. Aphasia developing after cerebral ischemia of the right hemisphere in a right-hand dominant patient following vasospasm may be a misleading symptom for the localization of the insult. Keeping a high index of suspicion may help in making the correct diagnosis. The changes in the perfusion patterns of cerebellum as assessed by SPECT study during the acute and recovery phases suggests the involvement of cerebellum in language functions.
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PMID:Crossed Wernicke's aphasia after aneurysmal subarachnoid hemorrhage: a case report. 1926 59


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