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In 15–20% of cases of spontaneous SAH, no aneurysm is detected on the first [[angiogram]].<ref name="Rinkel93">{{cite journal |author=Rinkel GJ, van Gijn J, Wijdicks EF |title=Subarachnoid hemorrhage without detectable aneurysm. A review of the causes |journal=Stroke |volume=24 |issue=9 |pages=1403–9 |year=1993 |pmid=8362440 | url=http://stroke.ahajournals.org/cgi/reprint/24/9/1403 | format=PDF}}</ref> About half of these are attributed to ''non-aneurysmal perimesencephalic hemorrhage'', in which the blood is limited to the subarachnoid spaces around the [[midbrain]]. In these, no aneurysms are generally found and the origin of the blood is uncertain.<ref name=vanGijn/> The remainder are due to other disorders affecting the blood vessels (such as [[Cerebral arteriovenous malformation|arteriovenous malformations]]), disorders of the blood vessels in the [[spinal cord]], and bleeding into various [[tumor]]s.<ref name=vanGijn/> [[Cocaine]] abuse and [[sickle cell anemia]] (usually in children) and, rarely, [[anticoagulant]] therapy and [[coagulopathy|problems with blood clotting]] can also result in SAH.<ref name="Rinkel93"/>
In 15–20% of cases of spontaneous SAH, no aneurysm is detected on the first [[angiogram]].<ref name="Rinkel93">{{cite journal |author=Rinkel GJ, van Gijn J, Wijdicks EF |title=Subarachnoid hemorrhage without detectable aneurysm. A review of the causes |journal=Stroke |volume=24 |issue=9 |pages=1403–9 |year=1993 |pmid=8362440 | url=http://stroke.ahajournals.org/cgi/reprint/24/9/1403 | format=PDF}}</ref> About half of these are attributed to ''non-aneurysmal perimesencephalic hemorrhage'', in which the blood is limited to the subarachnoid spaces around the [[midbrain]]. In these, no aneurysms are generally found and the origin of the blood is uncertain.<ref name=vanGijn/> The remainder are due to other disorders affecting the blood vessels (such as [[Cerebral arteriovenous malformation|arteriovenous malformations]]), disorders of the blood vessels in the [[spinal cord]], and bleeding into various [[tumor]]s.<ref name=vanGijn/> [[Cocaine]] abuse and [[sickle cell anemia]] (usually in children) and, rarely, [[anticoagulant]] therapy and [[coagulopathy|problems with blood clotting]] can also result in SAH.<ref name="Rinkel93"/>


Traumatic SAH (tSAH) usually occurs near the site of a [[skull fracture]] or [[intracerebral contusion]].<ref name="Rinkel93"/> It usually happens in the setting of other [[traumatic brain injury]] and has been linked with a poorer prognosis. It is unclear, however, if this is a direct result of the SAH or whether the presence of subarachnoid blood is simply an indicator of severity of the head injury and the prognosis is determined by other associated mechanisms.<ref>{{cite journal |author=Armin SS, Colohan AR, Zhang JH |title=Traumatic subarachnoid hemorrhage: our current understanding and its evolution over the past half century |journal=Neurol. Res. |volume=28 |issue=4 |pages=445–52 |year=2006 |month=June |pmid=16759448 |doi=10.1179/016164106X115053}}</ref>
Traumatic SAH (tSAH) usually occurs near the site of a [[skull fracture]] or [[intracerebral contusion]].<ref name="Rinkel93"/> It usually happens in the setting of other [[traumatic brain injury]] and has been linked with a poorer prognosis. It is unclear, however, if this is a direct result of the SAH or whether the presence of subarachnoid blood is simply an indicator of severity of the head injury and the prognosis is determined by other associated mechanisms.<ref name="Armin06">{{cite journal |author=Armin SS, Colohan AR, Zhang JH |title=Traumatic subarachnoid hemorrhage: Our current understanding and its evolution over the past half century |journal=Neurol. Res. |volume=28 |issue=4 |pages=445–52 |year=2006 |month=June |pmid=16759448 |doi=10.1179/016164106X115053}}</ref> SAH has been detected on CT scanning in as many as 60% of people with TBI.<ref name="Armin06"/>


==Classification==
==Classification==

Revision as of 22:44, 22 June 2008

Subarachnoid hemorrhage
SpecialtyEmergency medicine, neurology, neurosurgery Edit this on Wikidata

Subarachnoid hemorrhage (SAH, Template:Pron-en), or subarachnoid haemorrhage in British English, is bleeding into the subarachnoid space — the area between the arachnoid membrane and the pia mater surrounding the brain. This may occur spontaneously, usually from a cerebral aneurysm, or may result from trauma. Symptoms include an intense headache with a rapid onset ("thunderclap headache"), vomiting, and an altered level of consciousness.[1] Diagnosis is generally made with computed tomography (CT scanning) or occasionally by lumbar puncture. SAH is treated with close observation and prompt neurosurgical investigations, medications and other treatment methods to help prevent recurrence of the bleeding and complications.[1]

SAH is a medical emergency and can lead to death or severe disability — even when recognized and treated at an early stage. Up to half of all SAH cases are fatal, with 10–15% dying before arriving at a hospital,[1] and those who survive often have neurological or cognitive impairment.[2] Subarachnoid hemorrhage is considered a form of stroke and causes between 1 and 7% of all strokes.[3] Surgery for aneurysms was introduced in the 1930s, but since the 1990s many aneurysms are treated by a procedure called "coiling", which is carried out from within the blood vessels.[1]

Signs and symptoms

The classic symptom of subarachnoid hemorrhage is thunderclap headache (a headache described as "like being kicked in the head",[4] or the "worst ever", developing over seconds to minutes). About a third of all people with SAH have no symptoms apart from the characteristic headache, and about one in ten people who seek medical care with this symptom are later diagnosed with a subarachnoid hemorrhage.[1]

Vomiting may also be a presenting symptom, and 1 in 14 have seizures.[1] Neck stiffness and other signs of meningism may be present, as may confusion, decreased level of consciousness or coma.[1] Isolated dilation of a pupil and loss of the pupillary light reflex may reflect brain herniation as a result of rising intracranial pressure (pressure inside the skull).[1] Intraocular hemorrhage (bleeding into the eyeball) may occur in response to the raised pressure.[1] Subhyaloid (the hyaloid membrane envelopes the vitreous body of the eye) and vitreous hemorrhage may be visible on fundoscopy. This is known as Terson syndrome (occurring in 3–13% of cases) and is more common in more severe SAH.[5]

Oculomotor nerve abnormalities (affected eye looking downward and outward and inability to lift the eyelid on the same side) may indicate bleeding from the posterior communicating artery.[1] Seizures make hemorrhage from an aneurysm more likely; it is otherwise difficult to predict the site and origin of the hemorrhage from the symptoms.[1]

As a result of the bleeding, the body releases large amounts of adrenaline and similar hormones. This leads to a sharp increase in the blood pressure; the heart comes under substantial strain, and neurogenic pulmonary edema (accumulation of fluid in the lungs), cardiac arrhythmias (irregularities in the heart rate and rhythm), electrocardiographic changes (with occasional giant inverted "cerebral" T waves) and cardiac arrest (in 3% of cases) may occur rapidly after the onset of hemorrhage.[1][6]

Subarachnoid hemorrhage may also occur in people who have suffered a head injury. Symptoms may include headache, decreased level of consciousness and hemiparesis (weakness of one side of the body). SAH is a frequent ocurence in traumatic brain injury, and carries a poor prognosis if it is associated with deterioration in the level of consciousness.[7]

Diagnosis

CT scanning is the imaging method of choice for early suspicion of SAH.

The initial steps for evaluating a person with a suspected subarachnoid hemorrhage are obtaining a medical history and performing a physical examination; these are aimed at assessing the likelihood that the symptoms are due to SAH and identifying other potential causes. The diagnosis of subarachnoid hemorrhage can however not be made on clinical grounds alone; therefore medical imaging is generally required to confirm or exclude bleeding. The modality of choice is computed tomography (CT scan) of the brain. This has a high sensitivity (it will correctly identify over 95% of the cases), especially on the first day after the onset of bleeding. Magnetic resonance imaging (MRI scan) may be more sensitive after several days, compared to CT. In people with normal CT or MRI scans, lumbar puncture, in which cerebrospinal fluid (CSF) is removed with a needle from the lumbar sac, shows evidence of hemorrhage in 3% of the group in whom the CT was found to be normal; lumbar puncture is therefore regarded as mandatory if imaging is negative.[1] Several bottles of CSF are collected. If an elevated number of red blood cells are present in equal numbers in all bottles, this indicates a subarachnoid hemorrhage. If the number of cells decreases per bottle, it is more likely that it is due to damage to a small blood vessel during the procedure.[2] The CSF sample is also examined for xanthochromia — the yellow appearance of centrifugated fluid. More sensitive is spectrophotometry (measuring the absorption of particular wavelengths of light) for detection of bilirubin (a breakdown product of hemoglobin from red blood cells).[1][8] Xanthochromia and spectrophotometry remain reliable tests several days after the onset of headache.[8]

As only 10% of people admitted to the emergency department with a thunderclap headache are suffering from an SAH, other possible causes are usually considered simultaneously, such as meningitis, migraine, and cerebral venous sinus thrombosis.[4] Intracerebral hemorrhage, which is twice as common as SAH, is often misdiagnosed as the latter.[9] It is not unusual for SAH to be initially misdiagnosed as a migraine or tension headache, which can lead to a delay in obtaining a CT scan. In a 2004 study, this occurred in 12% of all cases and was more likely in people who had smaller hemorrhages and no impairment in their mental status. The delay in diagnosis led to a worse outcome.[10]

After a subarachnoid hemorrhage is confirmed, its origin needs to be determined. If the bleeding is likely to have originated from an aneurysm (as determined by the CT scan appearance), the choice is between cerebral angiography (injecting radiocontrast through a catheter to the brain arteries) and CT angiography (visualizing blood vessels with radiocontrast on a CT scan) to identify aneurysms. Catheter angiography also offers the possibility of coiling an aneurysm (see below).[1][2]

Causes

Spontaneous SAH is most often due to rupture of cerebral aneurysms (85%) — weaknesses in the walls of arteries in the brain that become enlarged. They tend to be located in the circle of Willis and its branches. While most cases of SAH are due to bleeding from small aneurysms, larger aneurysms (which are less common) are more likely to rupture.[1]

In 15–20% of cases of spontaneous SAH, no aneurysm is detected on the first angiogram.[11] About half of these are attributed to non-aneurysmal perimesencephalic hemorrhage, in which the blood is limited to the subarachnoid spaces around the midbrain. In these, no aneurysms are generally found and the origin of the blood is uncertain.[1] The remainder are due to other disorders affecting the blood vessels (such as arteriovenous malformations), disorders of the blood vessels in the spinal cord, and bleeding into various tumors.[1] Cocaine abuse and sickle cell anemia (usually in children) and, rarely, anticoagulant therapy and problems with blood clotting can also result in SAH.[11]

Traumatic SAH (tSAH) usually occurs near the site of a skull fracture or intracerebral contusion.[11] It usually happens in the setting of other traumatic brain injury and has been linked with a poorer prognosis. It is unclear, however, if this is a direct result of the SAH or whether the presence of subarachnoid blood is simply an indicator of severity of the head injury and the prognosis is determined by other associated mechanisms.[12] SAH has been detected on CT scanning in as many as 60% of people with TBI.[12]

Classification

There are several grading scales available for SAH. These have been derived by retrospectively matching characteristics of patients with their outcomes. In addition to the ubiquitously used Glasgow Coma Scale, three other specialized scores are in use. In all scores, a higher number is associated with a worse outcome.[13]

The first scale of severity was described by Hunt and Hess in 1968:[14]

Grade Signs and symptoms Survival
1 Asymptomatic or minimal headache and slight neck stiffness 70%
2 Moderate to severe headache; neck stiffness; no neurologic deficit except cranial nerve palsy 60%
3 Drowsy; minimal neurologic deficit 50%
4 Stuporous; moderate to severe hemiparesis; possibly early decerebrate rigidity and vegetative disturbances 20%
5 Deep coma; decerebrate rigidity; moribund 10%

The Fisher Grade classifies the appearance of subarachnoid hemorrhage on CT scan.[15] This scale has been modified by Claassen and coworkers, reflecting the additive risk from SAH size and accompanying intraventricular hemorrhage.[16]

Grade Appearance of hemorrhage
1 None evident
2 Less than 1 mm thick
3 More than 1 mm thick
4 Any thickness with intraventricular hemorrhage or parenchymal extension

The World Federation of Neurosurgeons classification uses Glasgow coma score (GCS) and focal neurological deficit to gauge severity of symptoms.[17]

Grade GCS Focal neurological deficit
1 15 Absent
2 13–14 Absent
3 13–14 Present
4 7–12 Present or absent
5 <7 Present or absent

A comprehensive classification scheme has been suggested by Ogilvy and Carter to predict outcome and gauge therapy.[18] The system consists of five grades and it assigns one point for the presence or absence of each of five factors: age greater than 50; Hunt and Hess grade 4 or 5; Fischer scale 3 or 4; aneurysm size greater than 10 mm; and posterior circulation aneurysm 25 mm or more.[18]

Treatment

The management of subarachnoid hemorrhage consists of general measures to stabilize the patient whilst using specific investigations and treatments to prevent rebleeding by obliterating the bleeding source, prevention of a phenomenon known as vasospasm, and prevention and treatment of complications.[1]

General measures

Stabilizing the patient is the first priority. Those with a depressed level of consciousness may need to be intubated and mechanically ventilated. Blood pressure, pulse, respiratory rate and Glasgow Coma Scale are monitored frequently. Once the diagnosis is confirmed, admission to an intensive care unit may be preferable — especially given that 15% have a further episode (rebleeding) soon after admission. Nutrition is an early priority, with oral or nasogastric tube feeding being preferable over parenteral routes. Analgesia (pain control) is generally restricted to non-sedating agents such as codeine, as sedation may impact on the mental status and thus interfere with the ability to monitor the level of consciousness. Deep vein thrombosis is prevented with compression stockings, intermittent pneumatic compression of the calves or both.[1]

Prevention of rebleeding

The arteries of the brain, viewed from underneath. Image originally from Gray's Anatomy, 1918.

People whose CT scan shows a large hematoma, depressed level of consciousness or focal neurological symptoms may be candidates for urgent surgical removal of the blood or occlusion of the bleeding site. The remainder are stabilized more extensively and undergo an transfemoral angiogram or CT angiogram later. It is hard to predict who will suffer a rebleed, yet it may happen at any time and carries a dismal prognosis. After the first 24 hours have passed, rebleeding risk remains at around 40% over the subsequent four weeks, suggesting that interventions should be aimed at reducing this risk as soon as possible.[1]

If a cerebral aneurysm is identified on angiography, two measures are available to reduce the risk of further bleeding from the same aneurysm: clipping[19] and coiling.[20] Clipping requires a craniotomy (opening of the skull) to locate the aneurysm, followed by the placement of clips around the neck of the aneurysm. Coiling is performed through the large blood vessels: a catheter is inserted into the femoral artery in the groin and advanced through the aorta to the arteries (both carotid arteries and both vertebral arteries) that supply the brain. When the aneurysm has been located, platinum coils are deployed that cause a blood clot to form in the aneurysm, obliterating it. The decision as to which treatment is undertaken is typically made by a multidisciplinary team consisting of a neurosurgeon, neuroradiologist and often other health professionals.[1]

Generally, the decision between clipping and coiling is made on the basis of the location of the aneurysm, its size and the condition of the patient. On the whole, aneurysms of the middle cerebral artery and its related vessels are hard to reach with angiography and tend to be amenable to clipping, whilst those of the basilar artery and posterior cerebral artery are hard to reach surgically and are more accessible for endovascular management.[21] These approaches are based on general experience, and the only randomized controlled trial directly comparing the different modalities was performed in relatively well patients with small (less than 10 mm) aneurysms of the anterior cerebral artery and anterior communicating artery (together the "anterior circulation"), who constitute about 20% of all patients with aneurysmal SAH.[21][22] This trial, the International Subarachnoid Aneurysm Trial (ISAT), showed that in this group the likelihood of death or being dependent on others for activities of daily living was reduced (23.5% in relative terms and 7.4% in absolute terms) if endovascular coiling was used as opposed to surgery.[21] The main drawback of coiling is the possibility that the aneurysm will reoccur; this risk is extremely small in the surgical approach. In ISAT, 8.3% needed further treatment in the longer term. Hence, people who have undergone coiling are typically followed up for many years afterwards with angiography or other measures to ensure recurrence of aneurysms is identified early.[23] Other trials have also found a higher rate of recurrence necessitating further treatments.[24][25]

Vasospasm

Vasospasm, in which the blood vessels constrict and thus restrict blood flow, is a serious complication of SAH. It can cause ischemic brain injury (referred to as "delayed ischemia") and permanent brain damage due to lack of oxygen in parts of the brain. It can be fatal if severe. Delayed ischemia is characterized by new neurological symptoms; it can be confirmed by transcranial doppler or cerebral angiography. Delayed ischemia is detected in about one third of all people admitted with subarachnoid hemorrhage, and half of those suffer permanent damage as a result.[26] It is possible to screen for the development of vasospasm with transcranial doppler every 24–48 hours. A blood flow velocity of more than 120 centimeters per second is suggestive of vasospasm.[2]

Nimodipine, an oral calcium channel blocker, has been shown in clinical trials to reduce the chance of a bad outcome if administered between the fourth and twenty-first day after the hemorrhage, even if it does not significantly reduce the amount of vasospasm detected on angiography.[27] In traumatic subarachnoid hemorrhage, nimodipine does not affect long-term outcome, and is not recommended.[28] Other calcium channel blockers and magnesium sulfate have been studied, but are not presently recommended; neither is there any evidence that shows benefit if nimodipine is given intravenously.[26]

A protocol referred to as "triple H" is often used as a measure to treat vasospam 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).[29] Evidence for this approach is inconclusive and no sufficiently large randomized controlled trials have been undertaken to demonstrate its benefits.[30][31]

If the symptoms of delayed ischemia don't 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.[2]

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, an extraventricular drain (a temporary device inserted into the one of the ventricles) and occasionally a permanent shunt.[1][2]

Fluctuations in blood pressure and electrolyte disturbances, as well as pneumonia and cardiac decompensation occur in about half the hospitalized persons with SAH and may worsen prognosis.[1]

Seizures occur in about a third of all cases during their hospital stay.[2] Many believe that patients might benefit from prevention with antiepileptic drugs.[2] Although this is widely practiced,[32] it is a controversial practice not based on good evidence.[33][34] In some studies, use of these drugs was associated with a worse prognosis; this might be because they actually cause harm, or because they are used more often in persons with a poorer prognosis.[35][36]

Prognosis

Early morbidity and mortality

SAH is often associated with a poor outcome.[3] The mortality rate for SAH is between 40 and 50%,[9] but trends for survival are improving.[1] Of those who survive initial hospitalization, treatment and complications, more than a quarter have significant restrictions in their lifestyle, and less than a fifth have no residual symptoms whatsoever.[21] Delay in diagnosis of minor SAH without coma (or mistaking the sudden headache for migraine) contributes to poor outcome.[10]

Poorer outcome is associated with numerous other factors, many of which are not modifiable risk factors. On admission, risk factors include higher age; 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; and location of an aneurysm in the posterior circulation.[35] 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.[35]

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; however, it is still associated with a risk of ischemia, rebleeding and hydrocephalus.[11] 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.[37]

There is also modest evidence that genetic factors influence the prognosis in SAH. For example, those carrying two copies of ApoE4 (a variant of the gene encoding apolipoprotein E that also plays a role in Alzheimer's disease) seem to be at a higher risk for delayed ischemia and a worse outcome.[38]

Long-term outcomes

Neurocognitive symptoms, such as fatigue, mood disturbances, and other related symptoms are common in people who have suffered a subarachnoid hemorrhage. Even in those who have made good neurological recovery, anxiety, depression, posttraumatic stress disorder and cognitive impairment are common. 46% of people who have suffered a SAH have cognitive impairment that affects their quality of life.[2] Over 60% report frequent headaches.[39]

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. A 2007 study showed that 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, prolactin or thyroid-stimulating hormone.[40]

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.[41]

The group of people at risk for SAH is younger than the population usually affected by stroke,[3] but the risk still increases with age. Young people are much much less likely than middle-aged people (risk ratio 0.1, or 10%) to suffer a subarachnoid hemorrhage.[41] The risk continues to rise with age and is 60% higher in the very elderly (over 85) than in those between 45 and 55.[41] Risk of SAH is about 25% higher in women above 55 compared to men the same age, probably reflecting the hormonal changes that result from the menopause and possibly the lack of estrogen.[41]

Genetics may play a role in a person's disposition to SAH, since risk of SAH is increased three- to fivefold in first-degree relatives of people who have suffered a subarachnoid hemorrhage.[4] However, lifestyle factors are more important in determining overall risk.[3] These risk factors are are smoking, hypertension (high blood pressure) and excessive alcohol intake.[9] Having smoked in the past confers a doubled risk of SAH compared to those who have never smoked.[3] Some protection of uncertain significance is conferred by Caucasian ethnicity, hormone replacement therapy, diabetes mellitus and higher than normal levels of cholesterol.[3]

Overall, about 1% of all people have one or more cerebral aneurysms. Most of these, however, are small in size and unlikely to rupture.[42]

Screening and prevention

Screening for aneurysms is not performed on a population level, because they are relatively rare, and would not be cost-effective. If someone has two or more first-degree relatives who have suffered an aneurysmal subarachnoid hemorrhage, screening may be worthwhile.[1][43]

Autosomal dominant polycystic kidney disease (ADPKD), a hereditary kidney condition, is known to be associated with cerebral aneurysms in 8%, but most of these are small and therefore unlikely to rupture. As a result, screening is only recommended in families with ADPKD where one family member has suffered a ruptured aneurysm.[44]

The incidental detection of an aneurysm (e.g. when someone undergoes an MRI scan of the brain for a different reason) presents a conundrum, as all treatments for cerebral aneurysms are associated with potential complications. The International Study of Unruptured Intracranial Aneurysms (ISUIA) provided prognostic data both in people who had previously suffered a subarachnoid hemorrhage and people who had aneurysms detected by other means. Those who had previously suffered SAH were more likely to bleed from other aneurysms. In contrast, those who had never bled and had small aneurysms (<10 mm) were very unlikely to suffer SAH and were likely to sustain harm from attempts to repair these aneurysms.[42] On the basis of the ISUIA and other studies, it is now recommended that people are only considered for preventative treatment if they have a reasonable life expectancy and have aneurysms that are highly likely to rupture.[43]

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.[45] The associated symptoms were described in more detail in 1886 by Edinburgh physician Dr Byrom Bramwell.[46] In 1924, London neurologist Sir Dr Charles P. Symonds (1890–1978) gave a complete account of all major symptoms of subarachnoid hemorrhage, and he coined the term "spontaneous subarachnoid hemorrhage".[45][47][48] Symonds also described the use of lumbar puncture and xanthochromia in diagnosis.[49]

The first surgical intervention was performed by Mr Norman Dott, who was a pupil of Dr 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.[48] American neurosurgeon Dr Walter Dandy, working in Baltimore, was the first to introduce clips in 1938.[19] Microsurgery was applied to aneurysm treatment in 1972 in order to further improve outcomes.[50] The 1980s saw the introduction of 3H therapy[29] as a treatment for delayed ischemia due to vasospasm, and trials with nimodipine[27] in an attempt to prevent this complication. The Italian neurosurgeon Dr Guido Guiglielmi introduced his endovascular coil treatment in 1991.[20][51]

References

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