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

The physiological mechanisms of known importance in the control of cerebral blood flow (CBF) and smooth muscle contraction and relaxation are reviewed. The pathophysiology of vasospasm following subarachnoid hemorrhage (SAH) is correlated with an alteration of these mechanisms. It is emphasized that smooth muscle relaxation is an energy-dependent process and that vasodilators require a functional smooth muscle membrane that may be severely impaired in ischemia or subarachnoid hemorrhage. The temporal profile of ischemia from spasm is correlated with the pathophysiology of altered metabolism of smooth muscle. The relevance of this complication to the timing of aneurysm surgery in 337 cases operated by one surgeon is considered along with various drug regimens suggested for its management.
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PMID:Physiological considerations important for the management of vasospasm. 32 8

Scanning electron microscopy of feline basilar arterial endothelium 4 hours, and 1, 3,5, and 7 days after subarachnoid hemorrhage (SAH) showed longitudinal furrows that correlated with angiographically demonstrated vasospasm. These ridges persisted after fixation at physiological pressure, and probably reflected medial contraction with undulation of the underlying elastic lamina. No change in endothelial cell morphology or thrombogenesis was observed as long as 7 days after SAH. There is no evidence from this study to suggest that ischemia from vasospasm is a product of thromboembolism from damaged endothelial surfaces.
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PMID:Ultrastructural changes in feline arterial endothelium following subarachnoid hemorrhage. 61 24

From a larger series of autopsies with subarachnoid hemorrhage (SAH), 20 cases were selected for the known complication of cerebral vasospasm. Evidence for vasospasm was radiological and pathological in 17 cases and pathological alone in three. A systematic histological examination of the large arteries in places known formerly to have been in spasm showed that, in the 12 early cases (death before 3 weeks), there were relevant changes in all the layers of the arterial wall, the most significant being evidence of necrosis in the tunica media. In the eight late cases (death after 3 weeks), in addition to the sequelae of the earlier acute changes, there was marked concentric intimal thickening by subendothelial fibrosis, again located in the segments of arteries formerly in spasm. Changes were also found in the small arteries, capillaries, and veins, both in the early and late cases but these changes, although striking, were thought to be caused by the ischemia due to the vasospasm; similar changes were also seen in the control cases with ischemia from arterial occlusion.
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PMID:Cerebral artery spasm. A histological study at necropsy of the blood vessels in cases of subarachnoid hemorrhage. 63 76

We analyzed the management of 310 patients with acute subarachnoid hemorrhage from a ruptured intracranial aneurysm, 280 of whom survived to operation, according to preoperative neurologic function, location and size of the aneurysm and timing of operation. Severe initial bleeding, rebleeding (usually within two weeks) and delayed ischemia were major preoperative problems; 10 per cent died, and 13 per cent deteriorated before operation. Operative mortality was 5 per cent, ranging from 1.6 per cent of patients with normal preoperative neurologic function to 35 per cent of severely disabled patients. Intraoperative complications (5 per cent of cases) related chiefly to the size and location of the aneurysm, but postoperative delayed ischemia (minor and reversible in 10 per cent and severe in 5 per cent) related to timing of operation and occurred primarily in patients afflicted within the previous 10 days. The results of surgical treatment, including preoperative deaths, were better than the natural history of the illness, the difference being apparent after one month's observation.
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PMID:Subarachnoid hemorrhage from intracranial aneurysms. Surgical management and natural history of disease. 66 71

A group of 20 necropsies of subarachnoid hemorrhage (SAH) were selected because of the known complication of cerebral vasospasm. Evidence for vasospasm was radiological and pathological in 17 cases and pathological alone in 3 cases. A histological examination of the large arteries in areas known formerly to be in spasm showed that in the 13 early cases (death before 3 weeks) there were relevant changes in all layers of the arterial wall, the most significant being a degeneration of the media and elastica. In the 7 late cases (death after 3 weeks), in addition to the sequelae of the acute changes, there was marked concentric intimal thickening; and the localization was again in the particular segments of arteries formerly in spasm. Changes found in the small arteries, capillaries, and veins in the early and the late cases were thought to be caused by the ischemia due to the vasospasm. These changes were also seen in control material.
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PMID:Cerebral artery spasm: histological changes in necropsies of cases of subarachnoid hemorrhage. 67 16

The authors have analyzed a total of 96 consecutive cases in which vasospasm followed subarachnoid hemorrhage (SAH). The SAH was caused by ruptured intracranial aneurysm or developed after aneurysm surgery. Usually at least 4 days elapsed between SAH and the onset of vasospasm. Vasospasm subsided an average of 2 weeks after onset. Of 68 patients with preoperative vasospasm, eight died due to cerebral edema resulting from ischemia, and 49% of survivors had neurological deficits. Preoperative vasospasm was not aggravated by surgical intervention when operations were carried out more than 7 days after the onset of vasospasm. Postoperative vasospasm was found in 25 of 52 patients who underwent operation within 1 week after SAH (excluding cases in Grade V). Five of these patients died, all of whom underwent surgery between the fourth and seventh day after SAH (the day of SAH was counted as the first day). There were no deaths among 20 patients operated on within the first 3 days after SAH. Postoperative vasospasm was always mild in these cases, when it occurred, probably because blood clot or blood-stained cerebrospinal fluid was removed by operative procedures. In all cases, 4 to 11 days elapsed between the last SAH and the onset of postoperative vasospasm regardless of the timing of surgery.
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PMID:Significance of vasospasm in the treatment of ruptured intracranial aneurysms. 89 45

The author reviews a form of management for patients deteriorating preoperatively or postoperatively from apparent ischemia attributed to progressive vasospasm after a subarachnoid hemorrhage. The clinical picture and relative frequency of this complication are considered in relationship to the status (grade) of the patient, location of the aneurysm, and ultimate neurological recovery. Experience suggests that the drug regimen reported is useful when instituted early after the onset of symptoms and is safe with proper monitoring techniques. The data do not justify early operative intervention after a subarachnoid hemorrhage, operation when there is angiographic evidence of severe spasm, or expectation of a dramatic effect in patients with a profound deficit or a fixed deficit several hours old.
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PMID:Management of ischemic complications after subarachnoid hemorrhage. 115 79

We investigated the function of monoaminergic neuron in the brainstem by measuring its metabolites using in vivo microdialysis following experimental subarachnoid hemorrhage in rats. Dialysis probe was implanted into the nucleus tractus solitarius (NTS) and continuous perfusion was then started. The perfusates were collected every 10-20 minutes and assayed by high-performance liquid chromatography (HPLC) with electrochemical detection (ECD). The main monoamine metabolites in extracellular space measured in NTS were 3,4-dihydroxy-phenylacetic acid (DOPAC), homovanillic acid (HVA), and 5-hydroxyindoleacetic acid (5-HIAA). The extracellular content of DOPAC was abruptly increased after cisternal autologous blood (0.3ml) injection, reached a peak at 20-40 minutes, and then decreased over 120 minutes. The content of HVA and 5-HIAA changed as well as DOPAC. These results showed non-specific response for ischemia of the brainstem, because the similar changes were seen after cisternal saline injection. The disappearance rate of monoamine metabolites after pargyline administration (75 mg/kg, i.p.) at various time periods after cisternal blood injection was most rapid at 2 days after SAH and recovered gradually. In particular the decline curve of DOPAC consisted of two compartments and early compartment was disturbed more severely than late compartment. These results indicate that the functional disturbance of nerve terminals is more severe than nerve cell body in adrenergic neurons.
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PMID:[Changes in monoamine metabolites measured by in vivo microdialysis of the brainstem following experimental subarachnoid hemorrhage in rats]. 137 47

Cerebral vasospasm is a major determinant of outcome after subarachnoid hemorrhage (SAH). Brain SPECT with 99mTc-HMPAO was obtained before and after cerebral angioplasty in 10 patients with delayed ischemia due to vasospasm. Eight patients had clinically evident neurologic improvement after the procedure. Visual interpretation and an internal-reference (cerebellum), manual, semi-quantitative region of interest (ROI) analysis revealed improvement of regional cerebral blood flow (rCBF) in 9 out of 10. There were disagreements between the visual and ROI analysis in the two that did not improve clinically. For all 10, the average increase per anterior circulation vessel dilated (n = 17) was 8.8% by comparison of the corticocerebellar ratios. For the eight that improved, the average increase was 10.5%. Brain SPECT is valuable for evaluating delayed cerebral ischemia caused by vasospasm after SAH and is useful to document the changes in rCBF induced by angioplasty. It is possible that SPECT may be useful to detect critical reductions in perfusion before clinical deficits develop, thereby offering the potential to identify candidates for early treatment with angioplasty.
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PMID:Brain SPECT and the effect of cerebral angioplasty in delayed ischemia due to vasospasm. 140 46

Internal carotid artery dissection is a major cause of ischemic stroke in the young. Pain is the leading symptom and is associated with other focal signs such as Horner's syndrome and painful tinnitus or with signs of cerebral or retinal ischemia. We report two patients with angiographically confirmed extracranial internal carotid artery dissection presenting with cephalic pain as the only manifestation. The first patient had a diffuse headache and a latero-cervical pain lasting for 12 days, reminiscent of carotidynia. The second patient experienced an exploding headache suggestive of subarachnoid hemorrhage, which was ruled out by computed tomography of the head and cerebrospinal fluid study. These patients demonstrate that recognition of carotid artery dissection as a cause of carotidynia and headache suggestive of subarachnoid hemorrhage may permit an earlier diagnosis and possibly the prevention of a stroke through the use of anticoagulation.
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PMID:Pain as the only manifestation of internal carotid artery dissection. 142 63


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