Subarachnoid hemorrhage
From Wikipedia, the free encyclopedia
| Subarachnoid hemorrhage Classification and external resources |
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|---|---|
| CT scan of the brain showing subarachnoid hemorrhage as a white area in the center | |
| ICD-10 | I60., S06.6 |
| ICD-9 | 430, 852.0-852.1 |
| OMIM | 105800 |
| DiseasesDB | 12602 |
| MedlinePlus | 000701 |
| eMedicine | med/2883 neuro/357 emerg/559 |
| MeSH | D013345 |
Subarachnoid hemorrhage (SAH, pronounced /sʌbərəknuːd heɪmɔrhɛgɛ/), 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. Treatment is made with close observation and prompt neurosurgical investigations, medications and other treatment methods to help prevent recurrence 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. Half of all SAH cases are fatal, with 10–15% dying before arriving at a hospital.[1] Subarachnoid hemorrhage is considered a form of stroke and causes between 1 and 7% of all strokes.[2]
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[edit] Signs and symptoms
The classic symptom of subarachnoid hemorrhage is thunderclap headache (a headache described as the "worst ever" developing over seconds to minutes). This headache is often described like being "kicked in the head".[3] Thunderclap headache is a symptom in only about a third of all SAH patients and one in ten people who attend for medical care with this symptom are diagnosed with a subarachnoid hemorrhage. Patients may also present with vomiting and 1 in 14 have seizures. Neck stiffness and other signs of meningism may be present, as may confusion, decreased level of consciousness or coma. Intraocular hemorrhage (bleeding into the eyeball) may occur in response to the raised pressure around the brain.[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.[4]
In a patient with thunderclap headache, none of the signs mentioned are helpful in confirming or ruling out hemorrhage, although seizures are more common if the bleeding is the result of a ruptured aneurysm as opposed to other causes. Oculomotor nerve abnormalities (affected eye looking downward and outward, inability to lift the eyelid on the same side but normal pupillary reflexes) may indicate bleeding from the posterior communicating artery. Isolated dilation of a pupil may also reflect brain herniation as a result of rising intracranial pressure (pressure inside the skull).[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 patients) may occur rapidly after the onset of hemorrhage.[1][5]
Subarachnoid hemorrhage may also occur in people who have suffered a head injury. Symptoms may include headache, decreased level of consciousness or hemiparesis (paralysis of one side of the body). It is regarded as a severe complication of head injury, especially if it is associated with lower Glasgow Coma Scale levels.[6]
[edit] Diagnosis
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. Only 10–25% of patients admitted to the emergency department with a thunderclap headache are suffering from an SAH; therefore other possible causes are usually considered simultaneously, such as meningitis, migraine, and cerebral venous sinus thrombosis.[3] Intracerebral hemorrhage, which is twice as common as SAH, is often misdiagnosed as the latter.[7]
The diagnosis of subarachnoid hemorrhage cannot 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 haemorrhage 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] The CSF sample is examined for xanthochromia — the yellow appearance of centrifugated fluid, or using spectrophotometry (measuring the absorption of particular wavelengths of light) for bilirubin, a breakdown product of hemoglobin in the CSF.[1][8]
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.[9]
After a subarachnoid hemorrhage is confirmed, its origin needs to be determined. CT angiography (visualizing blood vessels with radiocontrast on a CT scan) to identify aneurysms is generally the first step since invasive angiography (injecting radiocontrast through a [[catheter] to the brain arteries) has a higher risk of complications. The latter is useful if there are plans to obliterate the source of bleeding, such as an aneurysm, at the same time.[1]
[edit] 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 it's branches. While most cases of SAH are due to bleeding from small aneurysms, larger aneurysms (which are more uncommon) are more likely to rupture.[1]
In 15–20% of cases of spontaneous SAH, no aneurysm is detected from the first angiogram.[10] Non-aneurysmal perimesencephalic hemorrhage, in which the blood is limited to the area of the midbrain, causes another 10% of SAH cases. In these, no aneurysms are generally found. The remaining 5% of cases are due to vasculitic damage to arteries, other disorders affecting the vessels, disorders of the spinal cord blood vessels 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.[10] Most traumatic SAHs occur near a skull fracture or intracerebral contusion.[10]
[edit] 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.[11]
The first scale of severity was described by Hunt and Hess in 1968:[12]
| 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.[13] This scale has been modified by Claassen and coworkers, reflecting the additive risk from SAH size and accompanying intraventricular hemorrhage.[14]
| 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.[15]
| 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.[16] 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.
[edit] Treatment
The management of subarachnoid hemorrhage consists of general measures to stabilize the patient whilst conducting specific measures to prevent rebleeding by obliterating the bleeding source, prevention of a phenomenon known as vasospasm, and prevention and treatment of complications.[1]
[edit] 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]
[edit] Prevention of rebleeding
Patients with 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. After the first 24 hours, rebleeding risk remains at around 40% over the subsequent four weeks, suggesting that interventions should be aimed at reducing this risk.[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[17] and coiling.[18] 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 lead to the formation of a blood clot in the aneurysm and leads to obliteration. 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] Rebleeding is hard to predict yet it may happen at any time and carries a dismal prognosis. Interventions to prevent rebleeding are therefore performed as early as possible.[1]
There is little direct scientific evidence available to guide the decision between clipping and coiling other than technical experience. 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.[19] The only situation where a randomized controlled trial has been conducted is 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.[19][20] This trial, the International Subarachnoid Aneurysm Trial (ISAT), showed that in this group of patients the likelihood of death or dependency was reduced (23.5% in relative terms and 7.4% in absolute terms) if endovascular coiling was used as opposed to surgery.[19] 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, patients 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.[21] Other trials have also found a higher rate of recurrence necessitating further treatments.[22][23]
[edit] 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 and permanent brain damage, and can be fatal if severe. This condition, which can be verified by transcranial doppler or cerebral angiography, is detected in about one third of all people admitted with subarachnoid hemorrhage, and causes permanent damage in half those people.[24] It is possible to screen for the development of vasospasm with transcranial doppler every 24–48 hours. A blood flow velocity of >120 cm/second is suggestive of vasospasm.[25]
Nimodipine, an oral calcium channel blocker, has been shown in clinical trials to reduce the chance of a bad outcome, even if it does not significantly reduce the amount of vasospasm detected on angiography.[26] 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.[24] In traumatic subarachnoid hemorrhage, nimodipine does not affect long-term outcome, and is not recommended.[27]
A protocol referred to as "triple H" is often used as a measure to treat vasospasm; 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).[28] Evidence for this approach is inconclusive and no sufficiently large randomized controlled trials have been undertaken to demonstrate its benefits.[29][30]
If symptomatic vasospasm is resistant to 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.[25]
[edit] 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, surgical drainage of the excess fluid (for instance with a shunt) is occasionally necessary.[1][25]
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. They are managed symptomatically.[1]
Seizures occur in about a third of all cases.[25] Since seizures are common following SAH, many health professionals believe that some patients might benefit from prevention with antiepileptic drugs. Although this is widely practiced in some areas and centers,[31] it is a controversial practice not based on good evidence.[32][33] 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.[34][35]
[edit] Prognosis
[edit] Early morbidity and mortality
SAH is often associated with a poor outcome.[2] The mortality rate for SAH is between 40 and 50%,[7] although 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.[19] Delay in diagnosis of minor SAH without coma (or mistaking the sudden headache for migraine) contributes to poor outcome.[9]
Numerous other factors are associated with poorer outcome; many of them are not modifiable risk factors. On admission, risk factors include higher age, poorer neurological grade, more blood and larger aneurysm on the initial CT scan, location of an aneurysm in the posterior circulation, systolic hypertension, and a previous diagnosis of heart attack, hypertension, liver disease or a previous SAH.[34] During the hospital stay, 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 carry a worse prognosis.[34]
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.[10] Perimesencephalic SAH (bleeding around the mesencephalon part of the brain), however, has a very low rate of rebleeding or delayed ischemia, and the prognosis of this subtype is excellent.[36]
There is also modest evidence that genetic factors influence the prognosis in SAH. For example, those carrying two particular copies the gene encoding apolipoprotein E (those with Apo E4, which also plays a role in Alzheimer's disease) seem to be at a higher risk for delayed ischemia (lack of blood flow) and a worse outcome.[37]
[edit] 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. As many as 46% of people who suffer SAH have cognitive impairment that affects their quality of life.[25] Over 60% report frequent headaches.[38]
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 deficiencies in one or more of the hypothalamic-pituitary hormones (a state known as hypopituitarism) such as growth hormone, prolactin or thyroid-stimulating hormone.[39]
[edit] Epidemiology
According to a review of 51 studies from 21 countries, the incidence of subarachnoid hemorrhage is on average 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.[40]
The group of people at risk for SAH is younger than the population usually affected by stroke,[2] 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.[40] The risk continues to rise with age and is 60% higher in the very elderly (over 85) than in those between 45 and 55.[40] Risk of SAH is about 25% higher in women above 55, probably reflecting the hormonal changes that result from the menopause and possibly the lack of estrogen.[40]
Genetics may play a role in a person's disposition to SAH, since close relatives have a 3-5 fold increase chance of SAH.[3] However, lifestyle choices are more important.[2] Lifestyle risk factors for subarachnoid hemorrhage are smoking, hypertension (high blood pressure) and excessive alcohol intake.[7] Having smoked in the past confers a doubled risk of SAH compared to those who have never smoked.[2] Some protection of uncertain significance is conferred by Caucasian ethnicity, hormone replacement therapy, higher than normal levels of cholesterol and diabetes mellitus.[2]
[edit] Screening and prevention
Prevention of subarachnoid hemorrhage depends on the detection of cerebral aneurysms, and safety and expected benefit from treatment for aneurysms detected in this way. Due to the relative rarity of cerebral aneurysms, screening is not performed for reasons of cost-effectiveness. An exception may be people who have two or more first-degree relatives who have suffered an aneurysmal subarachnoid hemorrhage.[1][41]
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.[42]
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.[43] 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 have a high likelihood of rupturing.[41]
[edit] History
While the clinical picture of subarachnoid hemorrhage may have been recognized by Hippocrates,[44] 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.[45] 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".[44][46][47] Symonds also described the use of lumbar puncture and xanthochromia in diagnosis.[48]
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, and was an early pioneer in the use of angiograms.[47] American neurosurgeon Dr Walter Dandy, working in Baltimore, was the first to introduce clips.[17] Microsurgery was applied to aneurysm treatment in 1972 in order to further improve outcomes.[49] The 1980s saw the introduction of 3H therapy[28] as a treatment for delayed ischemia due to vasospasm, and trials with nimodipine[26] in the attempt of trying to prevent this complication. The Italian neurosurgeon Dr Guido Guiglielmi introduced his endovascular coil treatment in 1991.[18][50]
[edit] See also
[edit] References
- ^ a b c d e f g h i j k l m n o p q r s t van Gijn J, Kerr RS, Rinkel GJ (2007). "Subarachnoid haemorrhage". Lancet 369 (9558): 306–18. doi:. PMID 17258671.
- ^ a b c d e f Feigin VL, Rinkel GJ, Lawes CM, et al (2005). "Risk factors for subarachnoid hemorrhage: an updated systematic review of epidemiological studies". Stroke 36 (12): 2773–80. doi:. PMID 16282541.
- ^ a b c Longmore, Murray; Ian Wilkinson, Tom Turmezei, Chee Kay Cheung (2007). Oxford Handbook of Clinicial Medicine, 7th edition. Oxford, 841. ISBN 0-19-856837-1.
- ^ McCarron MO, Alberts MJ, McCarron P (2004). "A systematic review of Terson's syndrome: frequency and prognosis after subarachnoid haemorrhage". J. Neurol. Neurosurg. Psychiatr. 75 (3): 491–3. doi:. PMID 14966173.
- ^ Banki NM, Kopelnik A, Dae MW, et al (2005). "Acute neurocardiogenic injury after subarachnoid hemorrhage". Circulation 112 (21): 3314–9. doi:. PMID 16286583.
- ^ Servadei F, Murray GD, Teasdale GM, et al (February 2002). "Traumatic subarachnoid hemorrhage: demographic and clinical study of 750 patients from the European brain injury consortium survey of head injuries". Neurosurgery 50 (2): 261–7; discussion 267–9. doi:. PMID 11844260.
- ^ a b c Teunissen LL, Rinkel GJ, Algra A, van Gijn J (1996). "Risk factors for subarachnoid hemorrhage: a systematic review". Stroke 27 (3): 544–9. PMID 8610327.
- ^ Chalmers AH, Kiley M (1998). "Detection of xanthochromia in cerebrospinal fluid". Clin. Chem. 44 (8 Pt 1): 1740–2. PMID 9702963.
- ^ a b Kowalski RG, Claassen J, Kreiter KT, et al (February 2004). "Initial misdiagnosis and outcome after subarachnoid hemorrhage". JAMA 291 (7): 866–9. doi:. PMID 14970066.
- ^ a b c d Rinkel GJ, van Gijn J, Wijdicks EF (1993). "Subarachnoid hemorrhage without detectable aneurysm. A review of the causes" (PDF). Stroke 24 (9): 1403–9. PMID 8362440.
- ^ Rosen D, Macdonald R (2005). "Subarachnoid hemorrhage grading scales: A systematic review". Neurocritical Care 2 (2): 110–8. doi:. PMID 16159052.
- ^ Hunt W, Hess R (1968). "Surgical risk as related to time of intervention in the repair of intracranial aneurysms". Journal of Neurosurgery 28 (1): 14–20. PMID 5635959.
- ^ Fisher C, Kistler J, Davis J (1980). "Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning". Neurosurgery 6 (1): 1–9. doi:. PMID 7354892.
- ^ Claassen J, Bernardini GL, Kreiter K, et al (September 2001). "Effect of cisternal and ventricular blood on risk of delayed cerebral ischemia after subarachnoid hemorrhage: the Fisher scale revisited". Stroke 32 (9): 2012–20. PMID 11546890.
- ^ Teasdale G, Drake C, Hunt W, Kassell N, Sano K, Pertuiset B, De Villiers J (1988). "A universal subarachnoid hemorrhage scale: Report of a committee of the World Federation of Neurosurgical Societies". J Neurol Neurosurg Psychiatry 51 (11): 1457. PMID 3236024. Full text at PMC: 1032822
- ^ Ogilvy CS, Carter BS (May 1998). "A proposed comprehensive grading system to predict outcome for surgical management of intracranial aneurysms". Neurosurgery 42 (5): 959–68; discussion 968–70. doi:. PMID 9588539.
- ^ a b Dandy WE (1938). "Intracranial aneurysm of the internal carotid artery: Cured by operation". Ann. Surg. 107 (5): 654–9. doi:. PMID 17857170. Full text at PMC: 1386933
- ^ a b Guglielmi G, Viñuela F, Dion J, Duckwiler G (1991). "Electrothrombosis of saccular aneurysms via endovascular approach. Part 2: Preliminary clinical experience". J. Neurosurg. 75 (1): 8–14. PMID 2045924.
- ^ a b c d Molyneux AJ, Kerr RS, Yu LM, et al (2005). "International subarachnoid aneurysm trial (ISAT) of neurosurgical clipping versus endovascular coiling in 2143 patients with ruptured intracranial aneurysms: a randomised comparison of effects on survival, dependency, seizures, rebleeding, subgroups, and aneurysm occlusion". Lancet 366 (9488): 809–17. doi:. PMID 16139655.
- ^ van der Schaaf I, Algra A, Wermer M, et al (2005). "Endovascular coiling versus neurosurgical clipping for patients with aneurysmal subarachnoid haemorrhage". Cochrane Database Syst Rev (4): CD003085. doi:. PMID 16235314.
- ^ Campi A, Ramzi N, Molyneux AJ, et al (2007). "Retreatment of ruptured cerebral aneurysms in patients randomized by coiling or clipping in the International Subarachnoid Aneurysm Trial (ISAT)". Stroke 38 (5): 1538–44. doi:. PMID 17395870.
- ^ Piotin M, Spelle L, Mounayer C, et al (2007). "Intracranial aneurysms: Treatment with bare platinum coils—aneurysm packing, complex coils, and angiographic recurrence". Radiology 243 (2): 500–8. doi:. PMID 17293572.
- ^ Raymond J, Guilbert F, Weill A, et al (2003). "Long-term angiographic recurrences after selective endovascular treatment of aneurysms with detachable coils". Stroke 34 (6): 1398–403. doi:. PMID 12775880.
- ^ a b Dorhout Mees S, Rinkel G, Feigin V, et al (2007). "Calcium antagonists for aneurysmal subarachnoid haemorrhage". Cochrane database of systematic reviews (Online) (3): CD000277. doi:. PMID 17636626.
- ^ a b c d e Suarez JI, Tarr RW, Selman WR (January 2006). "Aneurysmal subarachnoid hemorrhage". N. Engl. J. Med. 354 (4): 387–96. doi:. PMID 16436770.
- ^ a b Allen GS, Ahn HS, Preziosi TJ, et al (1983). "Cerebral arterial spasm: A controlled trial of nimodipine in patients with subarachnoid hemorrhage". New England Journal of Medicine 308 (11): 619–24. PMID 6338383.
- ^ Vergouwen MD, Vermeulen M, Roos YB (December 2006). "Effect of nimodipine on outcome in patients with traumatic subarachnoid haemorrhage: a systematic review". Lancet Neurol 5 (12): 1029–32. doi:. PMID 17110283.
- ^ a b Kassell NF, Peerless SJ, Durward QJ, Beck DW, Drake CG, Adams HP (September 1982). "Treatment of ischemic deficits from vasospasm with intravascular volume expansion and induced arterial hypertension". Neurosurgery 11 (3): 337–43. doi:. PMID 7133349.
- ^ Sen J, Belli A, Albon H, Morgan L, Petzold A, Kitchen N (October 2003). "Triple-H therapy in the management of aneurysmal subarachnoid haemorrhage". Lancet Neurol 2 (10): 614–21. doi:. PMID 14505583.
- ^ Rinkel GJ, Feigin VL, Algra A, van Gijn J (2004). "Circulatory volume expansion therapy for aneurysmal subarachnoid haemorrhage". Cochrane Database Syst Rev (4): CD000483. doi:. PMID 15494997.
- ^ Rosengart AJ, Huo JD, Tolentino J, et al (August 2007). "Outcome in patients with subarachnoid hemorrhage treated with antiepileptic drugs". J. Neurosurg. 107 (2): 253–60. doi:. PMID 17695377.
- ^ Naval NS, Stevens RD, Mirski MA, Bhardwaj A (February 2006). "Controversies in the management of aneurysmal subarachnoid hemorrhage". Crit. Care Med. 34 (2): 511–24. PMID 16424735.
- ^ Liu KC, Bhardwaj A (2007). "Use of prophylactic anticonvulsants in neurologic critical care: a critical appraisal". Neurocrit Care 7 (2): 175–84. doi:. PMID 17763834.
- ^ a b c Rosengart AJ, Schultheiss KE, Tolentino J, Macdonald RL (August 2007). "Prognostic factors for outcome in patients with aneurysmal subarachnoid hemorrhage". Stroke 38 (8): 2315–21. doi:. PMID 17569871.
- ^ Naidech AM, Kreiter KT, Janjua N, et al (March 2005). "Phenytoin exposure is associated with functional and cognitive disability after subarachnoid hemorrhage". Stroke 36 (3): 583–7. doi:. PMID 15662039.
- ^ Greebe P, Rinkel GJ (April 2007). "Life expectancy after perimesencephalic subarachnoid hemorrhage". Stroke 38 (4): 1222–4. doi:. PMID 17332451.
- ^ Lanterna LA, Ruigrok Y, Alexander S, et al (August 2007). "Meta-analysis of APOE genotype and subarachnoid hemorrhage: clinical outcome and delayed ischemia". Neurology 69 (8): 766–75. doi:. PMID 17709709.
- ^ Powell J, Kitchen N, Heslin J, Greenwood R (June 2002). "Psychosocial outcomes at three and nine months after good neurological recovery from aneurysmal subarachnoid haemorrhage: predictors and prognosis". J. Neurol. Neurosurg. Psychiatr. 72 (6): 772–81. doi:. PMID 12023423.
- ^ Schneider HJ, Kreitschmann-Andermahr I, Ghigo E, Stalla GK, Agha A (September 2007). "Hypothalamopituitary dysfunction following traumatic brain injury and aneurysmal subarachnoid hemorrhage: a systematic review". JAMA 298 (12): 1429–38. doi:. PMID 17895459.
- ^ a b c d de Rooij NK, Linn FH, van der Plas JA, Algra A, Rinkel GJ (December 2007). "Incidence of subarachnoid haemorrhage: a systematic review with emphasis on region, age, gender and time trends". J. Neurol. Neurosurg. Psychiatr. 78 (12): 1365–72. doi:. PMID 17470467.
- ^ a b White PM, Wardlaw JM (December 2003). "Unruptured intracranial aneurysms". J Neuroradiol 30 (5): 336–50. PMID 14752379.
- ^ Gibbs GF, Huston J, Qian Q, et al (May 2004). "Follow-up of intracranial aneurysms in autosomal-dominant polycystic kidney disease". Kidney Int. 65 (5): 1621–7. doi:. PMID 15086900.
- ^ International Study of Unruptured Intracranial Aneurysms Investigators (December 1998). "Unruptured intracranial aneurysms--risk of rupture and risks of surgical intervention". N. Engl. J. Med. 339 (24): 1725–33. doi:. PMID 9867550.
- ^ a b Longstreth WT, Koepsell TD, Yerby MS, van Belle G (1985). "Risk factors for subarachnoid hemorrhage". Stroke 16 (3): 377–85. PMID 3890278.
- ^ Bramwell B (1886). "Spontaneous meningeal haemorrhage". Edin Med J 32: 101.
- ^ Symonds CP (1924). "Spontaneous subarachnoid hemorrhage". Q J Med 18: 93–122.
- ^ a b Todd NV, Howie JE, Miller JD (June 1990). "Norman Dott's contribution to aneurysm surgery". J. Neurol. Neurosurg. Psychiatr. 53 (6): 455–8. PMID 2199609. Full text at PMC: 1014202
- ^ Symonds CP (1924). "Spontaneous sub-arachnoid hæmorrhage". Proc Roy Soc Med 17: 39–52. Full text at PMC: 2201441
- ^ Krayenbühl HA, Yaşargil MG, Flamm ES, Tew JM (December 1972). "Microsurgical treatment of intracranial saccular aneurysms". J. Neurosurg. 37 (6): 678–86. PMID 4654697.
- ^ Strother CM (May 2001). "Historical perspective. Electrothrombosis of saccular aneurysms via endovascular approach: part 1 and part 2". AJNR Am J Neuroradiol 22 (5): 1010–2. PMID 11337350.
[edit] External links
- Neuroland SAH page
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