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[Clinical, neuroradiologic and developmental aspects of idiopathic benign subarachnoid hemorrhage (subarachnoid hemorrhage of unknown cause). Retrospective study of 65 cases].

Sixty-five patients with a mean age of 50.2 +/- 10.9 were admitted with a subarachnoid hemorrhage and a subsequent normal cerebral panangiography. On admission, 69% of the patients were graded I or II on the Hunt and Hess scale, versus 14% of them admitted on grade IV or V. Fifty-one patients (78%) were submitted to a second angiography between day 10 and day 132 after their hemorrhage (average day 29). A third angiography was performed on twenty-six patients (40%). Angiographic vasospasm was present on 52% of the first angiograms and affected predominantly the vertebro-basilar arterial system. On the second angiography, the vasospasm was still present on 26 out of 32 angiograms performed before day 30, and was only noted on 2 out of 19 angiograms performed later. No rebleeding was recorded in this group of patients who were followed-up for an average of 49 +/- 23 months. Complication as acute hydrocephalus affected 17% of the patients. In two patients (3%), symptomatic vasospasm was judged responsible of a delayed neurological deficit with concomitant hypodensity on the CT scan. Angiographic explorations were complicated by a transient ischemic deficit in 3 cases and by a fatal stroke in one case (4 cases out of 65 procedures, or 6%). As another patient died with bronchopneumonia during the hospitalization, the initial mortality rate was 3%. During the period of follow-up, two patients died from medical causes unrelated to their initial hemorrhage. Finally, 92% of the patients were alive and in an excellent or good clinical condition.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

Experimental subarachnoid hemorrhage: subarachnoid blood volume, mortality rate, neuronal death, cerebral blood flow, and perfusion pressure in three different rat models.

OBJECTIVE: To investigate which of three subarachnoid hemorrhage (SAH) models is the most suitable for studies of pathological and pathophysiological processes after SAH. METHODS: SAH was induced in rats via intracranial endovascular perforation (perforation model), blood injection into the cisterna magna (300 microl), or blood injection into the prechiasmatic cistern (200 microl). The subarachnoid blood volume was quantitatively measured. Cerebral blood flow (CBF) (as assessed with laser Doppler flowmetry), intracranial pressure, and mean arterial blood pressure were recorded for 90 minutes after SAH. Mortality was recorded, and neuronal death was assessed in animals that survived 7 days after SAH. RESULTS: The subarachnoid blood volume was close to the injected amount after prechiasmatic SAH. In the other models, the volume varied between 40 and 480 microl. The mortality rates were 44% in the perforation SAH group, 25% in the prechiasmatic SAH group, and 0% in the cisterna magna SAH group; the corresponding values for neuronal death were 11, 44, and 28%. Cerebral perfusion pressure approached baseline values within 5 minutes after SAH in all three models. CBF decreased to approximately 35% of baseline values immediately after SAH in all groups; it gradually increased to normal values 15 minutes after SAH in the cisterna magna SAH group and to 60 and 89% of baseline values 90 minutes post-SAH in the perforation and prechiasmatic SAH groups. CBF was significantly correlated with the subarachnoid blood volume. CONCLUSION: The prechiasmatic SAH model seems to be the most suitable for study of the sequelae after SAH; it produces a significant decrease in CBF, an acceptable mortality rate, and substantial pathological lesions, with high reproducibility. The CBF reduction is predominantly dependent on the amount of subarachnoid blood.

Animals↗

Comparison between perimesencephalic nonaneurysmal subarachnoid hemorrhage and subarachnoid hemorrhage caused by posterior circulation aneurysms.

OBJECT: Some authors have questioned the need to perform cerebral angiography in patients presenting with a benign clinical picture and a perimesencephalic pattern of subarachnoid hemorrhage (SAH) on initial computerized tomography (CT) scans, because the low probability of finding an aneurysm does not justify exposing patients to the risks of angiography. It has been stated, however, that ruptured posterior circulation aneurysms may present with a perimesencephalic SAH pattern in up to 10% of cases. The aim of the present study was twofold: to define the frequency of the perimesencephalic SAH pattern in the setting of ruptured posterior fossa aneurysms, and to determine whether this clinical syndrome and pattern of bleeding could be reliably and definitely distinguished from that of aneurysmal SAH. METHODS: Twenty-eight patients with ruptured posterior circulation aneurysms and 44 with nonaneurysmal perimesencephalic SAH were selected from a series of 408 consecutive patients with spontaneous SAH admitted to the authors' institution. The admission unenhanced CT scans were evaluated by a neuroradiologist in a blinded fashion and classified as revealing a perimesencephalic SAH or a nonperimesencephalic pattern of bleeding. Of the 28 patients with posterior circulation aneurysms, five whose grade was I according to the World Federation of Neurosurgical Societies scale were classified as having a perimesencephalic SAH pattern on the initial CT scan. The data show that the likelihood of finding an aneurysm on angiographic studies obtained in a patient with a perimesencephalic SAH pattern is 8.9%. Conversely, ruptured aneurysms of the posterior circulation present with an early perimesencephalic SAH pattern in 16.6% of cases. CONCLUSIONS: This study supports the impression that there is no completely sensitive and specific CT pattern for a nonaneurysmal SAH. In addition, the authors believe that there is no specific clinical syndrome that can differentiate patients who have a perimesencephalic SAH pattern caused by an aneurysm from those without aneurysms. Digital subtraction angiography continues to be the gold standard for the diagnosis of cerebral aneurysms and should be performed even in patients who have the characteristic perimesencephalic SAH pattern on admission CT scans.

Adult↗

Enhanced reactivity to vasopressin in rat basilar arteries during vasospasm after subarachnoid hemorrhage.

Subarachnoid hemorrhage increases the plasma level of vasopressin, a well-known vasoconstrictor. We examined the sensitivity to vasopressin in rat basilar artery after subarachnoid hemorrhage using a rat subarachnoid hemorrhage model. Vasospasm was observed 1-2 days after subarachnoid hemorrhage induction, and the contractile response to vasopressin in rat basilar arteries was assessed. The concentration-response curve for vasopressin in subarachnoid hemorrhage (1 day) rats shifted leftward compared with that of control rats. The concentration-response curve for vasopressin V(1) receptor agonist also shifted leftward and upward compared with that of control rats. The concentration-response curve for vasopressin was inhibited not by vasopressin V(2) receptor antagonist but by vasopressin V(1) receptor antagonist. Thus, it was demonstrated that the vasoconstricting effect of vasopressin was significantly enhanced in the vasospasm phase after subarachnoid hemorrhage.

Animals↗

Comparison of blood pressure-associated risk of intracerebral hemorrhage and subarachnoid hemorrhage: Korea Medical Insurance Corporation study.

Intracerebral hemorrhage and subarachnoid hemorrhage have different pathogeneses and risk factor profiles. However, little information is available on the difference between intracerebral and subarachnoid hemorrhages in relation to blood pressure. We prospectively investigated the relationships between blood pressure and risks of stroke subtypes. We measured blood pressure and other cardiovascular risk factors in 100,147 men and 59,558 women 35 to 59 years of age in 1990 and 1992. Outcomes were fatal and nonfatal events of stroke and its subtypes from 1993 to 2002. Independent relationships between baseline blood pressure and stroke subtypes were assessed using Cox's proportional hazard models. During the 10 years, 1714 ischemic and 1159 hemorrhagic strokes (742 intracerebral and 308 subarachnoid hemorrhages) occurred. Blood pressure was related more closely with hemorrhagic stroke than ischemic stroke, and the difference was more prominent in women. Among the subtypes of hemorrhagic stroke, intracerebral hemorrhage was more closely related with blood pressure than subarachnoid hemorrhage. For each 20 mm Hg increase in systolic blood pressure, adjusted relative risks of ischemic stroke, intracerebral hemorrhage, and subarachnoid hemorrhage were 1.79 (95% confidence interval, 1.68 to 1.90), 2.48 (2.30 to 2.68), and 1.65 (1.38 to 1.97) in men, and 1.64 (1.42 to 1.89), 3.15 (2.61 to 3.80), and 2.29 (1.82 to 2.89) in women, respectively. In conclusion, blood pressure is more closely related with intracerebral hemorrhage than subarachnoid hemorrhage, thus proportion of intracerebral hemorrhage in hemorrhagic stroke may affect the association between blood pressure and hemorrhagic stroke. Our data also emphasize the importance of blood pressure control for the prevention of stroke, especially in countries with a high incidence of intracerebral hemorrhage.

Adult↗

Effect of methemoglobin formation on the MR appearance of subarachnoid hemorrhage.

Subarachnoid hemorrhage has a much higher intensity in magnetic resonance (MR) images with the passage of time. Acute subarachnoid hemorrhage is difficult to see; within 1 week its appearance has become intensified on T1-weighted images. Different concentrations of blood and lysed red blood cells in cerebrospinal fluid (CSF) were examined spectroscopically but did not significantly alter T1 and T2 relaxation of CSF acutely. Ultraviolet visible spectroscopy of bloody CSF stored hypoxically for 3 days showed the presence of methemoglobin. The iron in methemoglobin is paramagnetic; in combination with water this facilitates T1 relaxation. It is concluded that methemoglobin formation with T1 shortening at least partially accounts for the increasing intensity of the MR appearance of subarachnoid hemorrhage over time in the central nervous system and may also explain the intense appearance of subacute hemorrhage in MR images elsewhere in the body.

Acute Disease↗

Outcome following intracerebral hemorrhage and subarachnoid hemorrhage.

Intracerebral hemorrhage and subarachnoid hemorrhage account for almost 20% of all stroke cases. Both forms of stroke are associated with a high morbidity and mortality rate. The incidence of intracerebral hemorrhage increases with the age and certain ethnical groups are more affected. Subarachnoid hemorrhage tends to occur in a much younger population than other types of strokes. Outcome predictors for intracerebral and subarachnoid hemorrhage have been extensively discussed in the literature. Based on the current literature, we review the morbidity and mortality rates and predictors of outcome for these two life-threatening diseases. Initial Glasgow Coma Scale (GCS) score, hematoma volume, and presence of ventricular blood are the most prominent predictors of outcome following intracerebral hemorrhage. Age and initial severity of neurologic deficits on presentation, measured by GCS, Hunt and Hess Scale or the World Federation of Neurological Surgeons Scale, are the most important predictors of outcome following subarachnoid hemorrhage.

Cerebral Hemorrhage↗

Treatment of aneurysmal subarachnoid hemorrhage.

Subarachnoid hemorrhage is a formidable and common health care problem. Early diagnosis and management are crucial to reduce the morbidity form this complex and multifaceted disease. Open surgery and endovascular techniques both aim at eliminating the source of hemorrhage. The choice of therapy can be made rationally based on an understanding of the merits, risks, and limitations of each therapy. The care of pregnant patients with subarachnoid hemorrhage and patients who harbor both aneurysms and AVMs can be approached rationally with an understanding of the complex pathophysiology behind these clinical scenarios. Familiarity with the signs of mild SAH, and advances in familial screening, noninvasive imaging, and therapies for vasospasm will continue to lessen the toll of this dramatic illness on the public well-being.

Aneurysm, Ruptured↗

17-beta estradiol can reduce secondary ischemic damage and mortality of subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) is a unique disorder commonly occurring when an aneurysm ruptures, leading to bleeding and clot formation, with a higher incidence in females. To evaluate the influence of 17-beta estradiol (E2) in the outcome of subarachnoid hemorrhage, SAH was induced by endovascular puncture of the intracranial segment of internal carotid artery in 15 intact females (INT), 19 ovariectomized females (OVX), and 13 ovariectomized female rats with E2 replacement (OVX + E2). Cerebral blood flow was recorded before and after SAH. All animals were decapitated immediately after death or 24 hours after SAH for clot area analysis. Brains were sliced and stained with 2,3,5-triphenyltetrazolium chloride (TTC) for secondary ischemic lesion analysis. The cortical cerebral blood flow (CBF), which was measured by a laser-Doppler flowmeter, decreased to 29.6%+/-17.7%, 22.8%+/-8.3%, and 43.5%+/-22.9% on the ipsilateral side (P = 0.01), and decreased to 63.4%+/-14.1%, 57.4%+/-11.0%, and 66.6%+/-17.9% on the contralateral side (P = 0.26) in INT, OVX, and OVX + E2, respectively. The subcortical CBF, which were measured by the H2 clearance method, were 7.77+/-12.03, 7.80+/-8.65, and 20.58+/-8.96 mL 100 g(-1) min(-1) on the ipsilateral side (P < 0.01), and 21.53+/-2.94, 25.13+/-3.01, and 25.30+/-3.23 mL 100 g(-1) min(-1) on the contralateral side in INT, OVX, and OVX + E2, respectively. The mortality was 53.3%, 68.4%, and 15.4% in INT, OVX, and OVX + E2, respectively (P = 0.01), whereas no significant difference in clot area was noted among the groups. The secondary ischemic lesion volume was 9.3%+/-8.4%, 24.3%+/-16.3%. and 7.0%+/-6.4% in INT, OVX, and OVX + E2, respectively (P < 0.01). This study demonstrated that E2 can reduce the mortality and secondary ischemic damage in a SAH model without affecting the clot volume.

Animals↗

Pharmacologic management of subarachnoid hemorrhage.

Subarachnoid hemorrhage, following rupture of an intracranial aneurysm, affects about 25 000 people in the U.S. each year. Less than half the patients who survive until hospital admission have an overall favorable outcome. This high morbidity and mortality rate is a result of serious complications following the initial subarachnoid hemorrhage, the most significant of these being rebleeding and cerebral ischemia secondary to vasospasm. While surgical clipping of the aneurysm is the most definitive therapy, this procedure may be postponed for a week or two after the initial hemorrhage, depending on the patient's clinical condition. Pharmacological therapy is a critical part of the preoperative care of these patients and of the postoperative management of complications. This article discusses the syndromes of rebleeding and vasospasm and reviews the current pharmacologic therapy for each.

Adrenergic beta-Agonists↗

Electrocardiographic abnormalities in patients with subarachnoid hemorrhage.

Subarachnoid hemorrhage is a serious neurological disorder that is often complicated by the occurrence of electrocardiographic abnormalities unexplained by preexisting cardiac conditions. These morphological waveform changes and arrhythmias often are unrecognized or misinterpreted, potentially placing patients at risk for inappropriate management. Many previous investigations were retrospective and relied on data collected in an unsystematic manner. More recent studies that included use of serial electrocardiograms and Holter recordings have provided new insight into the high prevalence of electrocardiographic changes in subarachnoid hemorrhage. Research on the prevalence, duration, and clinical significance of these electrocardiographic abnormalities and on associated factors and etiological theories is reviewed.

Electrocardiography↗

Phosphorus-31 magnetic resonance spectra reveal prolonged intracellular acidosis in the brain following subarachnoid hemorrhage.

Subarachnoid hemorrhage may be complicated by cerebral ischemia which, though reversible initially, can progress to an irreversible neurological deficit. 31P magnetic resonance spectroscopy, which can determine intracellular pH and thus detect areas of ischemia noninvasively, was applied to 10 patients on 30 occasions, at various times after subarachnoid hemorrhage. In 5 of them, there were focal areas of the brain in which the intracellular pH was reduced to < 6.8 compared with the normal range of 7.05 +/- 0.05. Consciousness was impaired in 4 of these patients. Repeat studies in these 4 patients showed that intracellular pH remained abnormally low for several days but eventually returned toward normal. The return of intracellular pH to normal paralleled an improvement in clinical condition in each case. In the fifth patient with lowered regions of intracellular pH, there had been an impaired level of consciousness and a transient focal deficit prior to the single study. In the other 5 patients there were no areas of reduced pHi even though in 3 of them there was intraventricular or cisternal blood shown on brain computerized tomography. In 2 of these 3 patients there were no abnormal neurological signs at the time of the magnetic resonance study. The third patient had a dense and persistent hemiparesis. The remaining two patients had no abnormal neurological signs at any stage. We suggest that the areas of acidosis may reflect ischemia which is potentially reversible. Since the technique is noninvasive, sequential 31P magnetic resonance spectroscopy of the brain offers a method of detecting cerebral ischemia and, more importantly, of assessing methods of treatment.

Acidosis↗

Cytokine levels in cerebrospinal fluid and delayed ischemic deficits in patients with aneurysmal subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) induces an inflammatory reaction and may lead to ischemic brain damage. The pathogenesis of brain dysfunction and delayed ischemic symptoms remain difficult to understand despite extensive surveys of such reactions. Cytokine production in the central nervous system following SAH and its relation with clinical outcome have hardly been studied. This study was aimed to determine whether the levels of IL-1 beta, IL-6 and TNF-alpha in the initial cerebrospinal fluid would increase following aneurysmal SAH, and be related with development of delayed ischemic deficit and clinical outcome. Nineteen patients suffering from aneurysmal SAH and 12 control volunteers were the subjects in this study. Cerebrospinal fluid samples were obtained on admission and the levels of each cytokine were determined with enzyme-linked immunosorbent assay. Patients with aneurysmal subarachnoid hemorrhage showed elevated levels of IL-1 beta, and TNF-alpha on admission. The patients with poor neurological status showed high levels of IL-1 beta, and IL-6. The patients who developed delayed ischemic deficit had high level of IL-6. We suggest that elevated level of IL-6 in cerebrospinal fluid of patients with aneurysmal SAH on admission can predict the high risk of delayed ischemic deficit.

Adult↗

Inflammatory cytokine cascade released by leukocytes in cerebrospinal fluid after subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) elicits an inflammatory response in the subarachnoid space, which is mediated by the release of various cytokines. To assess their involvement in post-hemorrhagic complications, we determined the source and time-course of the release of inflammatory cytokines and acute-phase proteins in cerebrospinal fluid (CSF) following SAH. Concentrations of interleukin (IL)- 1beta, IL-6, transforming growth factor-beta1 (TGF-beta1) and C-reactive protein (CRP) in CSF of 36 patients with SAH were measured by enzyme-linked immunoabsorbent assay (ELISA). Floating cells collected from the CSF were centrifuged four to six days after SAH, and examined immunohistochemically. Intracellular IL-1beta and IL-6 were examined by flow cytometric analysis. The molecular weight of TGF-beta1 in CSF of 30 patients was examined by Western blot analysis. The TGF-beta1 levels of patients who had undergone ventriculoperitoneal (VP) shunt (n = 19) was significantly higher than nonshunt group (n = 16). The CRP levels of VP shunt group was significantly higher than nonshunt group. IL-6 concentration was maximal within day 0-1 and it was secreted by neutrophils and monocytes. ELISA showed consistently low levels of IL-1beta, whereas a proportion of monocytes and lymphcytes were IL- 1beta-positive by flow cytometric analysis. TGF-beta1 levels were also maximal on day 0-1 according to ELISA, although it tended to be in the inactive form derived from platelets. A 25 kDa band of TGF-1 was detectable for at least 13 days after SAH, which may have been secreted in part by neutrophils and monocytes. CRP levels in CSF peaked on day 2-3. The present results suggest that leukocytes induced by SAH play an important role in post-hemorrhagic inflammation in the subarachnoid space by releasing IL-6 and TGF-beta1. The CRP and TGF-beta1 levels in CSF are strongly concerned with communicating hydrocephalus after SAH.

Adult↗

Hypervolemic hemodilution: a new approach to subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) refers to the sudden accumulation of blood in the subarachnoid space or in the ventricular system. The hemorrhage may occur with cerebral anomalies, tumors, or trauma. The presence of SAH has been associated with decreases in cerebral blood flow (CBF), which may be attributed in part to increased blood viscosity and hematocrit. Hypervolemic hemodilution is a new therapy that is used in the patient with decreased CBF. The therapy is designed to decrease the hematocrit and the viscosity of blood, subsequently increasing CBF. The patient must have a documented SAH and have a baseline neurologic status compatible with aggressive intervention to qualify for the therapy. The infusion technique is begun with 5% albumin and continued for 3 to 7 days. The dosage is gradually tapered before discontinuation. Effectiveness of the therapy is measured through improvement in neurologic function and regional CBF measurements. The critical care nurse plays a vital role in administering and monitoring the therapy and in educating the family about the disease process and interventions.

Albumins↗

Perioperative and intensive care unit care of patients with aneurysmal subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) is a complex pathophysiological event that results in a number of intracranial and systemic alterations. The effective management of SAH has its foundation in the prevention, early diagnosis, and correction of complications. Successful outcome in these compromised patients requires close monitoring and intensive care. This article will review the pathophysiology of SAH, identify the most common medical and neurological events that complicate SAH, examine the impact of secondary cerebral insults after aneurysm rupture, and outline current ICU care for SAH.

Cerebrovascular Circulation↗

Pseudoaneurysm of the anterior spinal artery in a patient with Moyamoya: an unusual cause of subarachnoid hemorrhage.

Subarachnoid hemorrhage (SAH) is a recognized presentation of Moyamoya disease in adults. Because there are extensive collateral networks and potential complications that develop, a thorough investigation of the intracranial and extracranial circulation is necessary to exclude a treatable cause when these patients present with SAH. We present a case of SAH due to a ruptured pseudoaneurysm of the anterior spinal artery arising from the supreme intercostal artery, which was the sole source of blood supply to the intracranial circulation.

Aneurysm, False↗