Hemorragia Subaracnoidea No Aneurismatica

Nonaneurysmal subarachnoid hemorrhage

Authors Farhan Siddiq, MD David G Brock, MD, CIP Section Editor Jose Biller, MD, FACP, FAAN, FAHA Deputy Editor Janet L Wilterdink, MD Last literature review version 16.2: May 2008 | This Topic Last Updated: June 13, 2008 (More) INTRODUCTION — Subarachnoid hemorrhage (SAH) refers to bleeding within the subarachnoid space, which lies between the arachnoid and pia mater and is normally filled with cerebrospinal fluid. Most cases of subarachnoid hemorrhage are caused by rupture of an intracranial aneurysm. Approximately 15 to 20 percent of patients presenting with SAH do not have a vascular lesion on initial four-vessel cerebral angiography [1,2] . The causes of these nonaneurysmal SAH (NASAH) are potentially diverse, and the mechanism of bleeding in these cases is often not identified. This topic discusses nonaneurysmal subarachnoid hemorrhage. Aneurysmal SAH and perimesencephalic SAH are discussed separately. (See "Etiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid hemorrhage" and see "Treatment of aneurysmal subarachnoid hemorrhage" and see "Perimesencephalic nonaneurysmal subarachnoid hemorrhage"). ETIOLOGIES

Perimesencephalic nonaneurysmal subarachnoid hemorrhage — A subtype of NASAH, socalled perimesencephalic nonaneurysmal SAH is characterized by a specific pattern of localized blood on computed tomography (CT), normal cerebral angiography, and a benign course that distinguishes these patients not only from aneurysmal SAH, but also from other patients with nonaneurysmal SAH [2-5] . In some case series, this makes up the majority, up to two-thirds, of patients with NASAH [1] . The CT findings that define perimesencephalic NASAH (PM-NASAH) include blood isolated to the perimesencephalic cisterns anterior to the brainstem; there may be extension into the ambient cisterns or basal parts of the sylvian fissures, but not into the lateral sylvian fissure, anterior interhemispheric fissure, or lateral ventricles [1,5] . Perimesencephalic nonaneurysmal subarachnoid hemorrhage is discussed separately. (See "Perimesencephalic nonaneurysmal subarachnoid hemorrhage").

Occult aneurysm — Up to 24 percent of all SAH patients with initial negative angiography have an aneurysm found on repeat angiography [6-10] . This may increase to as much as 49 percent if patients with perimesencephalic SAH and patients with normal CT scans are excluded [7] . Reasons for an initial false-negative angiogram include technical or reading errors, small aneurysm size, and obscuration of the aneurysm because of vasospasm, hematoma, or thrombosis within the aneurysm [1,2,6,7] . Even two negative angiograms do not exclude an aneurysmal source of bleeding. In some cases, another angiogram or surgical exploration have revealed an aneurysmal bleeding source, even after two negative angiograms [2,6,11,12] . Other case series suggest that the similarities in rebleeding and other complication rates among patients with aneurysmal SAH and patients with SAH and no identified bleeding source suggest that an occult aneurysm is likely in these patients as well [2,4,7,13,14] . Vascular malformations — Less than 10 percent of SAH are caused by vascular malformations [6,13] . These can be intracranial or spinal in location. Intracranial — Intracranial vascular malformations include both acquired and congenital lesions; the latter are more common. These typically exist within the brain parenchyma and produce intracerebral hemorrhage. However, depending on the location of the vascular lesion, bleeding can be primarily or exclusively in the subarachnoid space [6,8,15-17] . Rebleeding occurs in more than half of patients. Rebleeding from arteriovenous malformations is less likely to be acute than with aneurysmal SAH; however, dural arteriovenous fistulae, particularly those with cortical venous drainage, appear to be at higher risk for early rebleeding [16,18] . Most brain vascular malformations that produce SAH are either arteriovenous malformations or dural arteriovenous fistulae. These are usually visualized on cerebral angiography [10,15,19] . Catheterization of the external carotid artery may be required to image intracranial dural arteriovenous malformations. Angiographically occult vascular malformations such as some cavernous malformations, venous angiomas, and capillary telangiectasias are visualized on brain MRI, but are less likely to be a source of SAH. Vascular malformations associated with bleeding are usually managed surgically and/or with endovascular interventions [20] . (See "Brain arteriovenous malformations" and see "Vascular malformations of the central nervous system"). Spinal — Spinal vascular malformations can also be a source of NASAH. Up to 10 percent of spinal vascular malformations present with SAH [8,21,22] . Dural arteriovenous fistulae are the most common type of spinal vascular malformation [23] . Those that cause SAH are usually, but not always, located in the cervical cord or craniocervical junction [24] . Prominent back or neck pain or myelopathic signs at presentation can indicate this source, but these are often absent and the clinical appearance can mimic that of intracranial aneurysm rupture [24-27] . Vascular malformations in the spine can be difficult to visualize on neuroimaging modalities [8,24,25] . Proximal vertebral artery angiography may reveal more rostral lesions. Often the diagnosis is delayed until the patient presents with recurrent SAH. These lesions are generally

managed by neurosurgical and/or endovascular interventions. (See "Disorders affecting the spinal cord", section on Vascular malformations). Intracranial arterial dissection — Dissection of an intracranial artery can produce SAH; in one case series, this accounted for 4.5 percent of SAH cases, but this high proportion likely reflects referral or case-ascertainment bias [28] . Dissection of an intracranial artery is usually initiated by a tear in the media producing an intramural hemorrhage that dissects longitudinally between the adventitia and media [29] . When the tear extends through (or is initiated in) the intima, a second, so-called false, lumen is created. Usually, this leads to narrowing of the lumen, thrombus formation, and thromboembolic stroke. However, if the dissection tears through the adventitia, a SAH occurs. The latter scenario is more common with vertebrobasilar dissections. If SAH occurs, bleeding is massive and often devastating [28,30,31] . If patients survive the initial event, rebleeding occurs in 40 to 60 percent, often within the first 24 hours. Many intracranial dissections are believed to occur in the setting of sudden or unusual stretching of arteries, but such a history is often lacking. While connective tissue diseases such as Ehler-Danlos syndrome and fibromuscular dysplasia are associated with intracranial arterial dissection, most patients with dissection do not have these conditions [8,28,29] . Migraine and hypertension may be risk factors. Most cases of intracranial arterial dissection in the setting of SAH are diagnosed by conventional cerebral angiography [2,29,30] . Magnetic resonance imaging (MRI) with fat saturation is also a sensitive test, demonstrating intramural blood on cross-sectional images [29] . Vertebrobasilar dissections are generally treated surgically or with endovascular intervention [30,31] . Management is individualized according to location and other anatomic features, and can include ligation of the vertebral artery, trapping or wrapping of the pseudoaneurysm, bypass, and stenting. These are complicated procedures that can incur additional morbidity in these very sick patients. Other causes: Cerebral venous thrombosis can rarely present with subarachnoid hemorrhage as its primary manifestation [6,32-36] . Usually the presentation is somewhat less abrupt than with aneurysmal rupture and the bleeding is localized and superficial. The thrombosis may be visualized on venous phase of digital subtraction angiography and/or on MRI. (See "Etiology; clinical features; and diagnosis of cerebral venous thrombosis"). Sickle cell disease can be complicated by subarachnoid as well as intracerebral hemorrhage [1,8,37] . Most reported cases occur in children with an established diagnosis. These children are often found to have one or more aneurysms; in some cases SAH is believed to result from fragile collateral blood vessels. Recent transfusion and treatment with corticosteroid therapy may be risk factors. Case fatality rate was as high as 34 percent in one report [37] . Survivors appear to have a low rate of recurrence. (See "Cerebrovascular disease in sickle cell disease", section on Subarachnoid hemorrhage). Bleeding disorders and anticoagulant therapy can be complicated by SAH, but this is a somewhat rare complication; intracerebral and subdural hemorrhages are

more common [4,8,38-40] . Systemic bleeding usually accompanies the SAH if this is the primary cause; if it does not, the patient should be assumed to have an underlying aneurysm or other vascular lesion until proven otherwise. Pituitary apoplexy often presents with sudden onset of headache and vomiting, and there can be prominent subarachnoid blood on CT scan, which may distract from or obscure the pituitary adenoma [41-44] . Pituitary apoplexy is usually heralded by vision change and is accompanied by extraocular nerve palsy. If not visualized on the initial CT scan, MRI will demonstrate the tumor [45,46] . Neurosurgical decompression is indicated for visual loss. Patients also require endocrine evaluation for potentially life-threatening, acute hypopituitarism. (See "Causes of hypopituitarism", section on Pituitary apoplexy). Traumatic SAH is usually identified by the clinical setting. However, if a clinical history is unavailable, radiologic clues of a traumatic origin include localized bleeding in superficial sulci, adjacent skull fracture, and cerebral contusion as well as external evidence of traumatic injury [8,40] . Cocaine abuse has been associated with both aneurysmal and nonaneurysmal SAH [6,8,47,48] . The mechanism of bleeding in the latter is not known, but may be related to acute blood pressure surges and/or an underlying hypertensive or toxic vasculopathy [8,49] . Patients with SAH and cocaine abuse should be assumed to have an underlying aneurysm or other vascular lesion until proven otherwise. Rare causes of SAH include spinal aneurysms that can produce subarachnoid hemorrhage, usually with prominent neck or back pain and myeloradicular symptoms [50,51] . Brain or cervical tumors have been reported to produce SAH as the presenting manifestation [6,52] . Moyamoya disease is associated with cerebral aneurysms which can rupture and produce SAH; rarely SAH occurs due to rupture of the fragile transdural anastomotic vessels [53] . (See "Moyamoya disease"). DIAGNOSTIC EVALUATION — Subarachnoid hemorrhage (SAH) should be considered in any patient complaining of a severe headache of sudden onset. Emergent computed tomography (CT) of the head should immediately follow consideration of the diagnosis [40] . If the suspicion is high and the CT scan fails to show blood in subarachnoid space, a lumbar must be obtained. (See "Etiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid hemorrhage", section on Diagnosis). Patients with SAH should undergo basic laboratory testing including complete blood count, serum chemistries, coagulation studies, and toxicology screen. A baseline electrocardiogram should also be obtained. Cerebral angiography — Most vascular lesions responsible for SAH are identified using conventional digital subtraction cerebral angiography (DSA) that includes injections of the external carotid circulation and deep cervical branches, which may supply a cryptic dural arteriovenous fistula. Angiographic demonstration of key branch points, including the proximal posterior circulation, is essential to definitively rule out aneurysm. Proximal vertebral artery angiography may reveal a vascular malformation in the cervical spine or cranio-cervical junction. (See "Etiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid hemorrhage"). The utility of CT angiography (CTA) is continuously improving [54] . A major advantage of CTA over conventional angiography is the speed and ease by which it can be obtained, often immediately after the diagnosis of SAH is made by head CT when the patient is still in the

scanner. CTA is increasingly used as a first test in many patients with SAH, avoiding the need for conventional angiography in some patients [55-57] . In this setting, CTA is a more practical approach to acute diagnosis than magnetic resonance angiography (MRA), given the constraints of acute patient management. CTA has imperfect sensitivity for the detection of cerebral aneurysms, particularly small aneurysms [57] . Even when an aneurysm is identified by other technologies, DSA is often advocated to exclude multiple aneurysms and to better plan surgical intervention [58] . Repeat angiography — Up to 24 percent of all SAH patients with initial negative angiography have an aneurysm found on repeat angiography [1,6-8,10,12,59] . This may increase to as much as 49 percent if patients with perimesencephalic SAH and patients with normal CT scans are excluded [1,7,9] . Repeat studies may also reveal an arterial dissection or a vascular malformation not identified on the initial study [24,25,60] . Therefore, it is critical to repeat DSA if the initial angiogram is negative. The appropriate timing of this study is unclear and probably should be individualized according to the patient's condition and presence of other complications. In reported case series, the repeat DSA has been performed between four days and four weeks [1,6-10,61-63] . Repeat DSA may not be necessary in patients who have an identified nonaneurysmal etiology of SAH and possibly perimesencephalic SAH [3,7] . (See "Perimesencephalic nonaneurysmal subarachnoid hemorrhage", section on Repeated testing). A third angiogram at a period of two to three months is advocated by some, but is probably not necessary in most patients [2,6,8,59,60] . If the prior studies are technically inadequate, or if rebleeding occurs, repeat angiography, if not surgical exploration, is warranted [2] . (See "Further diagnostic study" below). Magnetic resonance imaging — MRI may demonstrate angiographically occult vascular lesions that can cause SAH. Such lesions include some vascular malformations in the brain or spinal cord, tumors, including pituitary adenoma, and arterial wall hematoma suggesting arterial dissection [27,64] . All patients with SAH and negative angiography should have gadoliniumenhanced MRI of the brain and spinal cord [6,23] . Further diagnostic study — Surgical exploration is not a routine aspect of the diagnostic evaluation, but is reported to lead to a diagnosis of ruptured aneurysm, even after two or more negative angiograms [2,6,11] . While in some cases this intervention was prompted by an episode of rebleeding or a suspicious but not diagnostic finding on angiography, it is not always certain in other cases why surgical exploration was performed. Spinal angiography is also undertaken for diagnosis in some cases [24-27] . Usually this is prompted by a specific clinical suspicion for a spinal vascular anomaly such as prominent back or neck pain, radicular or myelopathic features on examination, or an abnormal, but not diagnostic finding on other neuroimaging studies, such as MRI. COMPLICATIONS — Common complications of SAH are: Rebleeding Vasospasm and cerebral ischemia Hydrocephalus Increased intracranial pressure Seizures Hyponatremia Cardiac abnormalities Hypothalamic dysfunction and pituitary insufficiency [60]

There is little specific information about the incidence or severity of these complications in NASAH in comparison to aneurysmal SAH. Rebleeding risk is likely specific to the origin of SAH; this is discussed above under the individual etiologies. Other complications, however, may be expected to be somewhat similar across etiology. The pathogenesis and clinical features of these complications are discussed separately. (See "Etiology, clinical manifestations, and diagnosis of aneurysmal subarachnoid hemorrhage", section on Complications). TREATMENT — The general care of patients with NASAH should be the same as aneurysmal SAH patients. Patients are admitted to an intensive care setting for constant hemodynamic and cardiac monitoring, given stool softeners, kept at bedrest, and given analgesia to diminish hemodynamic fluctuations and lower the risk of rebleeding. Pneumatic compression stockings to limit risk of deep vein thrombosis should be utilized while patients are immobile. (See "Treatment of aneurysmal subarachnoid hemorrhage", section on General management). Patients should receive other interventions to monitor, prevent, and treat complications of SAH. These are discussed separately. (See "Treatment of aneurysmal subarachnoid hemorrhage", sections on General management, Prevention of vasospasm, and Management of complications). Patients with perimesencephalic SAH may be managed somewhat differently once aneurysmal SAH has been excluded. (See "Perimesencephalic nonaneurysmal subarachnoid hemorrhage"). Interventions to prevent rebleeding and other etiologic-specific complications are individualized to the underlying etiology. (See "Etiologies" above as well as other topic reviews). SUMMARY AND RECOMMENDATIONS — An estimated 15 to 20 percent of patients with subarachnoid hemorrhage (SAH) are nonaneurysmal. The causes of nonaneurysmal SAH (NASAH) are potentially diverse, and the mechanism of bleeding in these cases is often not identified. Perimesencephalic NASAH make up the majority of NASAH in some case series. These have a distinctive appearance on computed tomography and a benign course. (See "Perimesencephalic nonaneurysmal subarachnoid hemorrhage"). Other causes of NASAH include occult aneurysm, intracranial or spinal vascular malformations, and intracranial arterial dissection. Less common etiologies include sickle cell disease, pituitary apoplexy, cocaine abuse, cerebral venous thrombosis, and bleeding disorders. (See "Etiologies" above). The diagnosis of SAH is usually made by computed tomography (CT) of the brain, which should always be performed emergently in a patient with an abrupt onset of headache. A lumbar puncture should follow a negative CT scan if the clinical suspicion is high. (See "Diagnostic evaluation" above). All patients with SAH should be evaluated with basic laboratory testing including complete blood count, serum chemistries, and coagulation studies and toxicology screen. A baseline electrocardiogram should also be obtained. (See "Diagnostic evaluation" above). We recommend that conventional digital subtraction cerebral angiography (DSA) be performed in all patients with SAH, unless CT and/or CT angiography adequately defines the pathogenesis. (See "Cerebral angiography" above). We recommend repeating DSA within 4 to 14 days after an initial negative study, because of the risk of a false negative. (See "Repeat

angiography" above). Patients with negative angiography should undergo gadoliniumenhanced magnetic resonance imaging (MRI) of brain and spinal cord. (See "Magnetic resonance imaging" above). Some patients will not have an etiologic diagnosis after DSA and MRI. If rebleeding occurs in such patients, further diagnostic interventions may include further angiographic study of the brain and/or spinal cord, and/or surgical exploration. (See "Further diagnostic study" above). Complications of aneurysmal SAH, hydrocephalus, vasospasm and cerebral ischemia, seizures, hyponatremia, and cardiac abnormalities also occur in NASAH. In this regard, patients with NASAH should be managed similarly to aneurysmal SAH. (See "Treatment of aneurysmal subarachnoid hemorrhage"). Patients may also require interventions that are etiology-specific. (See "Etiologies" above, as well as other topic reviews). Bibliografia Schwartz, TH, Solomon, RA. Perimesencephalic nonaneurysmal subarachnoid hemorrhage: review of the literature. Neurosurgery 1996; 39:433. Rinkel, GJ, Wijdicks, EF, Hasan, D, Kienstra, GE, et al. Outcome in patients with subarachnoid haemorrhage and negative angiography according to pattern of haemorrhage on computed tomography. Lancet 1991; 338:964. van Gijn, J, van Dongen, KJ, Vermeulen, M, Hijdra, A. Perimesencephalic hemorrhage: a nonaneurysmal and benign form of subarachnoid hemorrhage. Neurology 1985; 35:493. Canhao, P, Ferro, JM, Pinto, AN, et al. Perimesencephalic and nonperimesencephalic subarachnoid haemorrhages with negative angiograms. Acta Neurochir (Wien) 1995; 132:14. Rinkel, GJ, Wijdicks, EF, Vermeulen, M, et al. Nonaneurysmal perimesencephalic subarachnoid hemorrhage: CT and MR patterns that differ from aneurysmal rupture. AJNR Am J Neuroradiol 1991; 12:829. Tatter, SB, Crowell, RM, Ogilvy, CS. Aneurysmal and microaneurysmal "angiogram-negative" subarachnoid hemorrhage. Neurosurgery 1995; 37:48. Jung, JY, Kim, YB, Lee, JW, et al. Spontaneous subarachnoid haemorrhage with negative initial angiography: A review of 143 cases. J Clin Neurosci 2006; 13:1011. Rinkel, GJ, van Gijn, J, Wijdicks, EF. Subarachnoid hemorrhage without detectable aneurysm. A review of the causes. Stroke 1993; 24:1403. Urbach, H, Zentner, J, Solymosi, L. The need for repeat angiography in subarachnoid haemorrhage. Neuroradiology 1998; 40:6. du Mesnil, de Rochemont R, Heindel, W, Wesselmann, C, et al. Nontraumatic subarachnoid hemorrhage: value of repeat angiography. Radiology 1997; 202:798. Di Lorenzo, N, Guidetti, G. Anterior communicating aneurysm missed at angiography: report of two cases treated surgically. Neurosurgery 1988; 23:494. Suzuki, S, Kayama, T, Sakurai, Y, et al. Subarachnoid hemorrhage of unknown cause. Neurosurgery 1987; 21:310. Ildan, F, Tuna, M, Erman, T, et al. Prognosis and prognostic factors in nonaneurysmal perimesencephalic hemorrhage: a follow-up study in 29 patients. Surg Neurol 2002; 57:160. Ruigrok, YM, Rinkel, GJ, Van Gijn, J. CT patterns and long-term outcome in patients with an aneurysmal type of subarachnoid hemorrhage and repeatedly negative angiograms. Cerebrovasc Dis 2002; 14:221. Cordonnier, C, Al-Shahi Salman, R, Bhattacharya, JJ, et al. Differences between intracranial vascular malformation types in the characteristics of their presenting haemorrhages: prospective, population-based study. J Neurol Neurosurg Psychiatry 2008; 79:47. Halbach, VV, Higashida, RT, Hieshima, GB, et al. Dural fistulas involving the transverse and sigmoid sinuses: results of treatment in 28 patients. Radiology 1987; 163:443. Bikmaz, K, Erdem, E, Krisht, A. Arteriovenous fistula originating from proximal part of the anterior cerebral artery. Clin Neurol Neurosurg 2007; 109:589. Duffau, H, Lopes, M, Janosevic, V, et al. Early rebleeding from intracranial dural arteriovenous fistulas: report of 20 cases and

review of the literature. J Neurosurg 1999; 90:78. Brown, RD Jr, Wiebers, DO, Torner, JC, O'Fallon, WM. Frequency of intracranial hemorrhage as a presenting symptom and subtype analysis: a population-based study of intracranial vascular malformations in Olmsted Country, Minnesota. J Neurosurg 1996; 85:29. van Rooij, WJ, Sluzewski, M, Beute, GN. Dural arteriovenous fistulas with cortical venous drainage: incidence, clinical presentation, and treatment. AJNR Am J Neuroradiol 2007; 28:651. Caroscio, JT, Brannan, T, Budabin, M, et al. Subarachnoid hemorrhage secondary to spinal arteriovenous malformation and aneurysm. Report of a case and review of the literature. Arch Neurol 1980; 37:101. Kandel, EI. Complete excision of arteriovenous malformations of the cervical cord. Surg Neurol 1980; 13:135. Koch, C. Spinal dural arteriovenous fistula. Curr Opin Neurol 2006; 19:69. van Beijnum, J, Straver, DC, Rinkel, GJ, Klijn, CJ. Spinal arteriovenous shunts presenting as intracranial subarachnoid haemorrhage. J Neurol 2007; 254:1044. Aviv, RI, Shad, A, Tomlinson, G, et al. Cervical dural arteriovenous fistulae manifesting as subarachnoid hemorrhage: report of two cases and literature review. AJNR Am J Neuroradiol 2004; 25:854. Kinouchi, H, Mizoi, K, Takahashi, A, et al. Dural arteriovenous shunts at the craniocervical junction. J Neurosurg 1998; 89:755. Rogg, JM, Smeaton, S, Doberstein, C, et al. Assessment of the value of MR imaging for examining patients with angiographically negative subarachnoid hemorrhage. AJR Am J Roentgenol 1999; 172:201. Sasaki, O, Ogawa, H, Koike, T, et al. A clinicopathological study of dissecting aneurysms of the intracranial vertebral artery. J Neurosurg 1991; 75:874. Caplan, LR. Dissections of brain-supplying arteries. Nat Clin Pract Neurol 2008; 4:34. Santos-Franco, JA, Zenteno, M, Lee, A. Dissecting aneurysms of the vertebrobasilar system. A comprehensive review on natural history and treatment options. Neurosurg Rev 2008; 31:131. Zhao, WY, Krings, T, Alvarez, H, et al. Management of spontaneous haemorrhagic intracranial vertebrobasilar dissection: review of 21 consecutive cases. Acta Neurochir (Wien) 2007; 149:585. Adaletli, I, Sirikci, A, Kara, B, et al. Cerebral venous sinus thrombosis presenting with excessive subarachnoid hemorrhage in a 14-year-old boy. Emerg Radiol 2005; 12:57. Oppenheim, C, Domigo, V, Gauvrit, JY, et al. Subarachnoid hemorrhage as the initial presentation of dural sinus thrombosis. AJNR Am J Neuroradiol 2005; 26:614. Chang, R, Friedman, DP. Isolated cortical venous thrombosis presenting as subarachnoid hemorrhage: a report of three cases. AJNR Am J Neuroradiol 2004; 25:1676. Sztajzel, R. Subarachnoid hemorrhage: a rare presentation of cerebral venous thrombosis. Headache 2001; 41:889. Kurosu, A, Suzukawa, K, Amo, M, et al. Perimesencephalic non-aneurysmal subarachnoid hemorrhage caused by cavernous sinus thrombosis: case report. Neurol Med Chir (Tokyo) 2007; 47:258. Strouse, JJ. Primary hemorrhagic stroke in children with sickle cell disease is associated with recent transfusion and use of corticosteroids. Pediatrics 2006; 118:1916. Rogers, LR. Cerebrovascular complications in cancer patients. Neurol Clin 2003; 21:167. Schwartzman, RJ, Hill, JB. Neurologic complications of disseminated intravascular coagulation. Neurology 1982; 32:791. van Gijn, J. Subarachnoid haemorrhage: diagnosis, causes and management. Brain 2001; 124:249. Bjerre, P, Videbaek, H, Lindholm, J. Subarachnoid hemorrhage with normal cerebral angiography: a prospective study on sellar abnormalities and pituitary function. Neurosurgery 1986; 19:1012. Wohaibi, MA, Russell, NA, Ferayan, AA, et al. Pituitary apoplexy presenting as massive subarachnoid hemorrhage. J Neurol Neurosurg Psychiatry 2000; 69:700. Sergides, IG, Minhas, PS, Anotun, N, Pickard, JD. Pituitary apoplexy can mimic subarachnoid haemorrhage clinically and radiologically. Emerg Med J 2007; 24:308. Satyarthee, GD, Mahapatra, AK. Pituitary apoplexy in a child presenting with massive

subarachnoid and intraventricular hemorrhage. J Clin Neurosci 2005; 12:94. Inamasu, J, Hori, S, Sekine, K, Aikawa, N. Pituitary apoplexy without ocular/visual symptoms. Am J Emerg Med 2001; 19:88. Hernandez, A, Angeles Del, Real M, Aguirre, M, et al. Pituitary apoplexy: a transient benign presentation mimicking mild subarachnoid hemorrhage with negative angiography. Eur J Neurol 1998; 5:499. Levine, SR, Brust, JC, Futrell, N, et al. A comparative study of the cerebrovascular complications of cocaine: alkaloidal versus hydrochloride--a review. Neurology 1991; 41:1173. Nolte, KB, Brass, LM, Fletterick, CF. Intracranial hemorrhage associated with cocaine abuse: a prospective autopsy study. Neurology 1996; 46:1291. Storen, EC, Wijdicks, EF, Crum, BA, Schultz, G. Moyamoya-like vasculopathy from cocaine dependency. AJNR Am J Neuroradiol 2000; 21:1008. Gonzalez, LF, Zabramski, JM, Tabrizi, P, et al. Spontaneous spinal subarachnoid hemorrhage secondary to spinal aneurysms: diagnosis and treatment paradigm. Neurosurgery 2005; 57:1127. Massand, MG, Wallace, RC, Gonzalez, LF, et al. Subarachnoid hemorrhage due to isolated spinal artery aneurysm in four patients. AJNR Am J Neuroradiol 2005; 26:2415. Scotti, G, Filizzolo, F, Scialfa, G, et al. Repeated subarachnoid hemorrhages from a cervical meningioma. Case report. J Neurosurg 1987; 66:779. Marushima, A, Yanaka, K, Matsuki, T, et al. Subarachnoid hemorrhage not due to ruptured aneurysm in moyamoya disease. J Clin Neurosci 2006; 13:146. Brilstra, EH, Hop, JW, Rinkel, GJ. Quality of life after perimesencephalic haemorrhage. J Neurol Neurosurg Psychiatry 1997; 63:382. Madureira, S, Canhao, P, Guerreiro, M, Ferro, JM. Cognitive and emotional consequences of perimesencephalic subarachnoid hemorrhage. J Neurol 2000; 247:862. Marquardt, G, Niebauer, T, Schick, U, Lorenz, R. Long term follow up after perimesencephalic subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry 2000; 69:127. Colen, TW, Wang, LC, Ghodke, BV, et al. Effectiveness of MDCT angiography for the detection of intracranial aneurysms in patients with nontraumatic subarchnoid hemorrhage. AJR Am J Roentgenol 2007; 189:898. Hashimoto, Y, Kin, S, Haraguchi, K, Niwa, J. Pitfalls in the preoperative evaluation of subarachnoid hemorrhage without digital subtraction angiography: report on 2 cases. Surg Neurol 2007; 68:344. Topcuoglu, MA, Ogilvy, CS, Carter, BS, et al. Subarachnoid hemorrhage without evident cause on initial angiography studies: diagnostic yield of subsequent angiography and other neuroimaging tests. J Neurosurg 2003; 98:1235. Hashimoto, H, Iida, J, Hironaka, Y, et al. Use of spiral computerized tomography angiography in patients with subarachnoid hemorrhage in whom subtraction angiography did not reveal cerebral aneurysms. J Neurosurg 2000; 92:278. Bradac, GB, Bergui, M, Ferrio, MF, et al. False-negative angiograms in subarachnoid haemorrhage due to intracranial aneurysms. Neuroradiology 1997; 39:772. Duong, H, Melancon, D, Tampieri, D, Ethier, R. The negative angiogram in subarachnoid haemorrhage. Neuroradiology 1996; 38:15. Inamasu, J, Nakamura, Y, Saito, R, et al. "Occult" ruptured cerebral aneurysms revealed by repeat angiography: result from a large retrospective study. Clin Neurol Neurosurg 2003; 106:33. Wijdicks, EF, Schievink, WI, Miller, GM. MR imaging in pretruncal nonaneurysmal subarachnoid hemorrhage: is it worthwhile?. Stroke 1998; 29:2514.

© 2008 UpToDate,

ANGIOGRAFIA CEREBRAL

MI POLIGONO DE WILLIS Y MIS IMPRESIONANTES COLATERALES

RESONANCIA CERVICAL 1

RESONANCIA CERVICAL 2

ANGIORESONANCIA DORSOLUMBAR 1

ANGIORESONANCIA DORSOLUMBAR 2

ANGIORESONANCIA DORSAL