Disease relevance of Subarachnoid Hemorrhage

• We conclude that nimodipine should be given to patients who are neurologically normal after subarachnoid hemorrhage in order to reduce the occurrence of severe neurologic deficits due to cerebral arterial spasm [1].
• Serious bleeding complications, including massive upper gastrointestinal hemorrhage, epistaxes, or subarachnoid hemorrhage confirmed at autopsy, occurred in five of the 19 patients and only during treatment with aspirin and dipyridamole [2].
• Phosphorus-31 magnetic resonance spectra reveal prolonged intracellular acidosis in the brain following subarachnoid hemorrhage [3].
• Tranexamic acid is valuable in the treatment of subarachnoid hemorrhage caused by ruptured intracranial aneurysms [4].
• Acute toxicity included a flu-like syndrome in all patients, increased serum transaminase levels in five, seizures in three (two cases temporally related to fever and one to a thrombocytopenic subarachnoid hemorrhage), and prolonged activated partial thromboplastin times in seven [5].

Psychiatry related information on Subarachnoid Hemorrhage

• Selectivity for the cerebrovascular bed makes nimodipine potentially useful in the treatment of subarachnoid hemorrhage, migraine headache, dementia, and stroke [6].
• A consecutive series of 100 individuals with aneurysmal subarachnoid hemorrhage were subjected to early aneurysm operation followed by subsequent intravenous administration of the calcium antagonist nimodipine during the critical period for symptomatic vasospasm [7].
• With deferoxamine treatment, only a minor increase in latency periods (4.5%) was detected after subarachnoid hemorrhage [8].
• Cerebral amyloid angiopathy can remain symptom-free, but can also give a broad spectrum of clinical and radiological manifestations, including (vascular) dementia, cerebellar and cerebral hemorrhage, subarachnoid hemorrhage, and leukoencephalopathy [9].
• 5. Systolic blood pressure attenuated the effect of alcohol consumption in all subtypes of stroke, whereas HDL cholesterol strengthened the effect of alcohol in subarachnoid hemorrhage and cerebral infarction but attenuated the effect in intracerebral hemorrhage [10].

High impact information on Subarachnoid Hemorrhage

• We conclude that until some method can be found to minimize ischemic complications, tranexamic acid is of no benefit in patients with subarachnoid hemorrhage [11].
• Cerebral arterial spasm--a controlled trial of nimodipine in patients with subarachnoid hemorrhage [1].
• Functional recovery did not depend on age but was to some degree related to the cause of coma (subarachnoid hemorrhage and other cerebrovascular disease having the worst recovery; hypoxia-ischemia, intermediate; and hepatic and miscellaneous causes, best) and especially to early clinical signs of brain dysfunction [12].
• Beneficial effects of systemic administration of recombinant human erythropoietin in rabbits subjected to subarachnoid hemorrhage [13].
• Here we report that increased levels of 3-aminopropanal-modified protein levels in humans after aneurysmal subarachnoid hemorrhage correlate with the degree of cerebral injury as measured by admission Hunt/Hess grade [14].

Chemical compound and disease context of Subarachnoid Hemorrhage

• Endothelium-dependent relaxations are inhibited during chronic vasospasm after subarachnoid hemorrhage in the canine basilar artery, although the luminal release of endothelium-derived relaxing factor (EDRF) is maintained [15].
• The resting levels of cGMP in rings with endothelium (reflecting the effect of spontaneous release of EDRF) and those evoked by bradykinin in rings with endothelium and by nitric oxide in rings without endothelium were diminished in the subarachnoid hemorrhage group [15].
• Relaxations evoked by M&B22,948 (an inhibitor of cGMP phosphodiesterases) were smaller, but those evoked by the lipophilic cGMP analogue 8-bromo-cGMP were potentiated slightly in the subarachnoid hemorrhage group [15].
• The patient received phenytoin prophylactically for 2 1/2 months after an uncomplicated subarachnoid hemorrhage and was in good health when the treatment was started [16].
• Elevations of the CSF lactate concentration with concomitantly negative Gram's stains and cultures were found in patients with infections at anatomic sites other than the CNS, accidental or neurosurgical head trauma, subarachnoid hemorrhage, and seizures due to alcoholism [17].

Biological context of Subarachnoid Hemorrhage

• Prevention of impairment of cerebral blood flow autoregulation during acute stage of subarachnoid hemorrhage by gene transfer of Cu/Zn SOD-1 to cerebral vessels [18].
• Hemodynamic and metabolic effects of flunarizine in experimental subarachnoid hemorrhage in dogs [19].
• 17beta-estradiol reduces cell death after global and focal ischemia and subarachnoid hemorrhage in rodents [20].
• In a prospective clinical investigation on neurochemical intensive care monitoring, the authors' aim was to elucidate the temporal profile of nitric oxide metabolite concentrations-that is, nitrite and nitrate (NO(x))--and compounds related to energy-metabolism in the cerebral interstitium of patients after aneurysmal subarachnoid hemorrhage (SAH) [21].
• The ability of the nonglucocorticoid 21-aminosteroid U74006F, a potent inhibitor of iron-dependent lipid peroxidation, to antagonize acute progressive cerebral hypoperfusion following experimental subarachnoid hemorrhage (SAH) was examined in chloralose-anesthetized cats [22].

Anatomical context of Subarachnoid Hemorrhage

• Clinical studies have demonstrated elevated levels of both arachidonic acid and prostaglandins in the cerebrospinal fluid of humans after ischemic stroke and subarachnoid hemorrhage [23].
• This study was designed to determine the effect of subarachnoid hemorrhage (SAH) on potassium (K+) channels involved in relaxations of cerebral arteries to nitrovasodilators [24].
• From 2 hours to 23 days following experimental subarachnoid hemorrhage, the accumulation of indium-111-labeled platelets on the intimal surface of the middle cerebral artery was studied in 23 cats [25].
• We conclude that damage to membrane lipids by peroxidative and/or lipolytic processes is involved in the subarachnoid hemorrhage-induced blood-brain barrier opening and that U-74006F protects the blood-brain barrier against the effects of subarachnoid hemorrhage by preventing or limiting these pathologic membrane lipid changes [26].
• The second patient had systemic lupus erythematosus and presented with a subarachnoid hemorrhage attributed to an intracranial vertebral artery dissection by the demonstration of an extracranial dissection [27].

Gene context of Subarachnoid Hemorrhage

• Endothelin (ET) receptor antagonists are of great potential clinical interest for the treatment pathological conditions associated with vasospasm, such as subarachnoid hemorrhage (SAH) [28].
• Subarachnoid hemorrhage (SAH) leads to the development of vasospasm in which endothelin-1 plays a very important role [29].
• To begin to examine HO activity following subarachnoid hemorrhage (SAH), the expression of HO-1 and HO-2 was investigated after experimental SAH in adult rats [30].
• Cerebrospinal fluid interleukin-1 receptor antagonist and tumor necrosis factor-alpha following subarachnoid hemorrhage [31].
• Serum von Willebrand factor, matrix metalloproteinase-9, and vascular endothelial growth factor levels predict the onset of cerebral vasospasm after aneurysmal subarachnoid hemorrhage [32].

Analytical, diagnostic and therapeutic context of Subarachnoid Hemorrhage

• However, the endothelium-independent response to sodium nitroprusside of the subarachnoid hemorrhage group did not differ from that of the control group [33].
• However, with the exception of nimodipine in the management of subarachnoid hemorrhage, clinical trials have yielded results that are not so promising as one could expect from those obtained in experimental research [34].
• Tranexamic acid in subarachnoid hemorrhage. A double-blind study [35].
• A patient developed signs, symptoms, and radiologic findings compatible with acute subarachnoid hemorrhage after receiving a large dose of heparin and intravascular contrast medium for coronary angiography and stent placement [36].
• CONCLUSIONS: Bacterial meningitis, which may be associated with severe vasculopathy of the basilar artery and lead to cerebral infarction, aneurysm formation, and subarachnoid hemorrhage, should be considered in the differential diagnosis of these conditions [37].

References