available. in contrast to the tablets and solution formulations of nimodipine which require an administration every 4hrs for a total of 21 days, the sustained formulation, eg-1962, needs to be administered once directly into the ventricles. the csf concentrations from eg-1962, however, were at least 2 orders of magnitude higher than those with oral nimodipine. these results supported a phase 3 study that demonstrated a favorable safety profile for eg-1962 but yielded inconclusive efficacy results due to notable differences in clinical outcome based on baseline disease severity. some older studies have suggested that statin therapy might reduce vasospasm, but a subsequent meta-analysis including further trials did not demonstrate benefit on either vasospasm or outcomes. while corticosteroids with mineralocorticoid activity may help prevent vasospasm their use does not appear to change outcomes. a protocol referred to as "triple h" is often used as a measure to treat vasospasm when it causes symptoms; this is the use of intravenous fluids to achieve a state of hypertension (high blood pressure), hypervolemia (excess fluid in the circulation), and hemodilution (mild dilution of the blood). evidence for this approach is inconclusive; no randomized controlled trials have been undertaken to demonstrate its effect. if the symptoms of delayed ischemia do not improve with medical treatment, angiography may be attempted to identify the sites of vasospasms and administer vasodilator medication (drugs that relax the blood vessel wall) directly into the artery. angioplasty (opening the constricted area with a balloon) may also be performed. other complications hydrocephalus (obstruction of the flow of cerebrospinal fluid) may complicate sah in both the short and long term. it is detected on ct scanning, on which there is enlargement of the lateral ventricles. if the level of consciousness is decreased, drainage of the excess fluid is performed by therapeutic lumbar puncture, extraventricular drain (a temporary device inserted into one of the ventricles), or occasionally a permanent shunt. relief of hydrocephalus can lead to an enormous improvement in a person's condition. fluctuations in blood pressure and electrolyte imbalance, as well as pneumonia and cardiac decompensation occur in about half the hospitalized persons with sah and may worsen prognosis. seizures occur during the hospital stay in about a third of cases. people have often been treated with preventative antiepileptic medications. this is controversial and not based on good evidence. in some studies, use of these medications was associated with a worse prognosis; although it is unclear whether this might be because the drugs themselves actually cause harm, or because they are used more often in persons with a poorer prognosis. there is a possibility of a gastric hemorrhage due to stress ulcers. prognosis short-term outcomes sah is often associated with a poor outcome. the death rate (mortality) for sah is between 40 and 50 percent, but trends for survival are improving. of those that survive hospitalization, more than a quarter have significant restrictions in their lifestyle, and less than a fifth have no residual symptoms whatsoever. delay in diagnosis of minor sah (mistaking the sudden headache for migraine) contributes to poor outcome. factors found on admission that are associated with poorer outcome include poorer neurological grade; systolic hypertension; a previous diagnosis of heart attack or sah; liver disease; more blood and larger aneurysm on the initial ct scan; location of an aneurysm in the posterior circulation; and higher age. factors that carry a worse prognosis during the hospital stay include occurrence of delayed ischemia resulting from vasospasm, development of intracerebral hematoma, or intraventricular hemorrhage (bleeding into the ventricles of the brain) and presence of fever on the eighth day of admission. so-called "angiogram-negative subarachnoid hemorrhage", sah that does not show an aneurysm with four-vessel angiography, carries a better prognosis than sah with aneurysm, but it is still associated with a risk of ischemia, rebleeding, and hydrocephalus. perimesencephalic sah (bleeding around the mesencephalon in the brain), however, has a very low rate of rebleeding or delayed ischemia, and the prognosis of this subtype is excellent. the prognosis of head trauma is thought to be influenced in part by the location and amount of subarachnoid bleeding. it is difficult to isolate the effects of sah from those of other aspects of traumatic brain injury; it is unknown whether the presence of subarachnoid blood actually worsens the prognosis or whether it is merely a sign that a significant trauma has occurred. people with moderate and severe traumatic brain injury who have sah when admitted to a hospital have as much as twice the risk of dying as those who do not. they also have a higher risk of severe disability and persistent vegetative state, and traumatic sah has been correlated with other markers of poor outcome such as post traumatic epilepsy, hydrocephalus, and longer stays in the intensive care unit. more than 90 percent of people with traumatic subarachnoid bleeding and a glasgow coma score over 12 have a good outcome. there is also modest evidence that genetic factors influence the prognosis in sah. for example, having two copies of apoe4 (a variant of the gene encoding apolipoprotein e that also plays a role in alzheimer's disease) seems to increase risk for delayed ischemia and a worse outcome. the occurrence of hyperglycemia (high blood sugars) after an episode of sah confers a higher risk of poor outcome. long-term outcomes autopsy of a case with subarachnoid hemorrhage. the arachnoid mater is left in place on the exterior surface, containing extensive hemorrhage that also fills the sulci, as detailed in magnified image. neurocognitive symptoms, such as fatigue, mood disturbances, and other related symptoms, are common sequelae. even in those who have made good neurological recovery, anxiety, depression, posttraumatic stress disorder, and cognitive impairment are common; 46 percent of people who have had a subarachnoid hemorrhage have cognitive impairment that affects their quality of life. over 60 percent report frequent headaches. aneurysmal subarachnoid hemorrhage may lead to damage of the hypothalamus and the pituitary gland, two areas of the brain that play a central role in hormonal regulation and production. more than a quarter of people with a previous sah may develop hypopituitarism (deficiencies in one or more of the hypothalamic–pituitary hormones such as growth hormone, luteinizing hormone, or follicle-stimulating hormone). sah is also associated with siadh and cerebral salt wasting, and is the most common cause of the latter. epidemiology average number of people with sah per 100,000 person-years, broken down by age according to a review of 51 studies from 21 countries, the average incidence of subarachnoid hemorrhage is 9.1 per 100,000 annually. studies from japan and finland show higher rates in those countries (22.7 and 19.7, respectively), for reasons that are not entirely understood. south and central america, in contrast, have a rate of 4.2 per 100,000 on average. although the group of people at risk for sah is younger than the population usually affected by stroke, the risk still increases with age. young people are much less likely than middle-age people (risk ratio 0.1, or 10 percent) to have a subarachnoid hemorrhage. the risk continues to rise with age and is 60 percent higher in the very elderly (over 85) than in those between 45 and 55. risk of sah is about 25 percent higher in women over 55 compared to men the same age, probably reflecting the hormonal changes that result from the menopause, such as a decrease in estrogen levels. genetics may play a role in a person's disposition to sah; risk is increased three- to fivefold in first-degree relatives of people having had a subarachnoid hemorrhage. but lifestyle factors are more important in determining overall risk. these risk factors are smoking, hypertension (high blood pressure), and excessive alcohol consumption. having smoked in the past confers a doubled risk of sah compared to those who have never smoked. some protection of uncertain significance is conferred by caucasian ethnicity, hormone replacement therapy, and diabetes mellitus. there is likely an inverse relationship between total serum cholesterol and the risk of non-traumatic sah, though confirmation of this association is hindered by a lack of studies. approximately 4 percent of aneurysmal bleeds occur after sexual intercourse and 10 percent of people with sah are bending over or lifting heavy objects at the onset of their symptoms. overall, about 1 percent of all people have one or more cerebral aneurysms. most of these are small and unlikely to rupture. history while the clinical picture of subarachnoid hemorrhage may have been recognized by hippocrates, the existence of cerebral aneurysms and the fact that they could rupture was not established until the 18th century. the associated symptoms were described in more detail in 1886 by edinburgh physician dr byrom bramwell. in 1924, london neurologist sir charles p. symonds (1890–1978) gave a complete account of all major symptoms of subarachnoid hemorrhage, and he coined the term "spontaneous subarachnoid hemorrhage". symonds also described the use of lumbar puncture and xanthochromia in diagnosis. the first surgical intervention was performed by norman dott, who was a pupil of harvey cushing then working in edinburgh. he introduced the wrapping of aneurysms in the 1930s, and was an early pioneer in the use of angiograms. american neurosurgeon dr walter dandy, working in baltimore, was the first to introduce clips in 1938. microsurgery was applied to aneurysm treatment in 1972 in order to further improve outcomes. the 1980s saw the introduction of triple h therapy as a treatment for delayed ischemia due to vasospasm, and trials with nimodipine in an attempt to prevent this complication. in 1983, the russian neurosurgeon zubkov and colleagues reported the first use of transluminal balloon angioplasty for vasospasm after aneurysmal sah. the italian neurosurgeon dr guido guglielmi introduced his endovascular coil treatment in 1991.