الفهرس 
Anatomical and Physiological Considerations of Cerebral CirculationOnly 14 pages are availabe for public view
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Abstract
Spontaneous subarachnoid hemorrhage is a bleeding into the subarachnoid space without trauma. Aneurysms are the underlying cause in 80% of the cases. Among other causes are arteriovenous malformations, anticoagulation, vasculitis and brain tumor. Spontaneous subarachnoid hemorrhage is a serious disease where up to half of the patients die. Of those who survive, only half return to work and many have a reduced quality of life.
Spontaneous subarachnoid hemorrhage is presented by severe headache with rapid onset, vomiting, confusion or disturbed consciousness, neck stiffness and sometimes seizures and complicated by cerebral vasospasm, obstructive hydrocephalus, hyponatremia, neurogenic pulmonary oedema, cardiac dysfunction and terson’s syndrome.
Delayed cerebral ischemia (DCI) is a common complication of aneurysmal SAH and remains the single most important cause of morbidity and mortality in those patients who survive the initial bleed. Cerebral vaspospasm is considered the main culprit of DCI.
DCI was defined as symptomatic vasospasm or the appearance of new infarction on computerized tomography (CT) or magnetic resonance (MR) when the cause was felt to be attributable to vasospasm.
Clinical diagnosis of delayed ischemic neurological deficit (DIND) is made when other possible causes of neurological deterioration such as rebleeding, hydrocephalus, seizures and electrolyte abnormalities have been excluded.
The presence and the amount of oxyhemoglobin and other by-product of red cell lysis(eg,bilirubin and methemoglobin) in the subarachnoid cisterns is believed to be the major trigger of the phenomena that ultimately cause smooth muscle spasm, narrowing of the arterial lumen,revrsible vasculopathy, impaired blood flow autoregulation and hypovolemia that lead to the reduction of cerebral perfusion and finally ischemia. Various mediators of cerebral vasospasm, such as endothelium-derived, vascular smooth muscle-derived, proinflammatory mediators, cytokines and adhesion molecules, stress induced gene activation, and platelet-derived growth factors have been identified.
Conventional angiography has been conceived as the most accurate and reliable modality of detecting vasospasm, but it is sometimes invasive.Fluid-attenuated inversion recovery (FLAIR) is the most sensitive imaging pulse sequence for the detection of subarachnoid hemorrhage.
Besides hemodynamic treatment, various pharmacological treatments have been tested. Nimodipine is the currently recommended drug given due to its relatively modest effects.
Systemic pharmacological therapy includes: Endolthelin-1 antagonist e.g., clazosentan, intravenous magnesium sulphate from the day of admission, nitric oxide donors, high doses of statins, erythropoietin and fasudil. Other potential systemic drug therapies e.g., dantrolene, sildenafil and complementary chinese herbs.Local pharmacological therapies, in terms of direct intrathecal application are promising; e.g., intrathecal nicardipine pellets, magnesium and thrombolytics. However, there is a risk of infection and the need of a surgical access.Other measures include: endovascular therapy concepts, lumbar drainage, addressing cortical depression depolarization and kinetic therapy.
Both severity of disability and length of rehabilitation after SAH are linked to the extent of the initial injury. SAH takes a tremendous physical and emotional toll on patients and their families.