J Korean Soc Radiol.  2016 Jun;74(6):380-388. 10.3348/jksr.2016.74.6.380.

Isolated Acute Nontraumatic Cortical Subarachnoid Hemorrhage: Etiologies Based on MRI Findings

Affiliations
  • 1Department of Radiology, Dong-A University Medical Center, Busan, Korea. sgeisilver@gmail.com

Abstract

PURPOSE
The purpose of this study was to identify common underlying etiologies that may be responsible for isolated acute nontraumatic cortical subarachnoid hemorrhage (cSAH) by analysis of magnetic resonance imaging (MRI) findings of the brain.
MATERIALS AND METHODS
From August 2005 to February 2014, 15 cSAH patients were admitted to our institution. All patients with cSAH underwent brain MRI and magnetic resonance angiography as a part of their initial evaluation. An analysis of the patients' medical history, clinical presentations, and brain MRI findings was retrospectively performed.
RESULTS
Among the combined pathologies that were suspected causes of cSAH, 11 patients showed acute or subacute cerebral infarctions at the ipsilateral hemisphere of cSAH on the diffusion-weighted images. Four of 11 patients had only cerebral infarction, but the other 7 had combined vasculopathy of extra- and intracranial arteries. Four of 15 patients who did not have cerebral infarction, had intracranial artery stenosis, or showed possible cerebral amyloid angiopathy, or no abnormal findings on the brain MRI.
CONCLUSION
Ischemic stroke, such as cerebral infarction or vasculopathy of the extraand intracranial arteries is regarded as a common underlying etiology of the cSAH based on MRI findings.


MeSH Terms

Arteries
Brain
Cerebral Amyloid Angiopathy
Cerebral Cortex
Cerebral Infarction
Constriction, Pathologic
Humans
Magnetic Resonance Angiography
Magnetic Resonance Imaging*
Pathology
Retrospective Studies
Stroke
Subarachnoid Hemorrhage*

Figure

  • Fig. 1 74-year-old man with isolated acute nontraumatic cortical subarachnoid hemorrhage (cSAH) and acute cerebral infarction. A. FLAIR image shows a cSAH in the right central sulcus (arrowheads). The adjacent right parietal cortex exhibits a hyperintense signal in this image (black arrows). B. DWI shows a patchy hyperintense signal in the same area, suggesting acute cerebral infarction (white arrows). The cSAH is represented by a hypointense signal along the right central sulcus on the DWI. DWI = diffusion-weighted image, FLAIR = fluid-attenuated inversion recovery

  • Fig. 2 52-year-old woman with cSAH and acute cerebral infarction and intracranial arterial stenosis. A. FLAIR image shows cSAH in the sulci of left frontal area. B. DWI shows focal acute infarction in the left frontal cortical area (arrowhead). C. Magnetic resonance angiographic (MRA) image shows the stenosis of the left middle cerebral artery M1 portion (arrow). cSAH = cortical subarachnoid hemorrhage, DWI = diffusion-weighted image, FLAIR = fluid-attenuated inversion recovery

  • Fig. 3 66-year-old man with cSAH and acute cerebral infarction and extracranial arterial stenosis. A. Pre-enhanced brain CT image shows localized high density along left central sulcus, suggesting cSAH. B. FLAIR image shows the localized high-signal intensity in the left central sulcus. C, D. DWI (D) shows multiple small hyperintense foci in the left parietal cortex departing from the cSAH, suggesting acute cerebral infarction. The cSAH is represented by a hypointense signal along the right central sulcus on the DWI (C). E. MRA image shows the stenosis of the petrous segment of the left internal carotid artery (arrow). cSAH = cortical subarachnoid hemorrhage, DWI = diffusion-weighted image, FLAIR = fluid-attenuated inversion recovery, MRA = magnetic resonance angiographic

  • Fig. 4 78-year-old woman with cSAH and intracranial arterial stenosis. A. Pre-enhanced brain CT image shows a localized high density along the left central sulcus (arrowheads). B. FLAIR image shows cSAH in the left central sulcus (white arrows). C, D. DWI (C) shows a strong linear signal along the left central sulcus (the same area), indicating a cSAH (black arrows). However, the apparent diffusion coefficient map (D) shows no evidence of diffusion restriction; thus, there is no evidence of acute cerebral infarction. E. However, the MRA image shows the stenosis of the left middle cerebral artery M1 portion (arrow). cSAH = cortical subarachnoid hemorrhage, DWI = diffusion-weighted image, FLAIR = fluid-attenuated inversion recovery, MRA = magnetic resonance angiographic


Reference

1. Kumar S, Goddeau RP Jr, Selim MH, Thomas A, Schlaug G, Alhazzani A, et al. Atraumatic convexal subarachnoid hemorrhage: clinical presentation, imaging patterns, and etiologies. Neurology. 2010; 74:893–899.
2. Cuvinciuc V, Viguier A, Calviere L, Raposo N, Larrue V, Cognard C, et al. Isolated acute nontraumatic cortical subarachnoid hemorrhage. AJNR Am J Neuroradiol. 2010; 31:1355–1362.
3. Oppenheim C, Domigo V, Gauvrit JY, Lamy C, Mackowiak-Cordoliani MA, Pruvo JP, et al. Subarachnoid hemorrhage as the initial presentation of dural sinus thrombosis. AJNR Am J Neuroradiol. 2005; 26:614–617.
4. Benabu Y, Mark L, Daniel S, Glikstein R. Cerebral venous thrombosis presenting with subarachnoid hemorrhage. Case report and review. Am J Emerg Med. 2009; 27:96–106.
5. Ducros A, Boukobza M, Porcher R, Sarov M, Valade D, Bousser MG. The clinical and radiological spectrum of reversible cerebral vasoconstriction syndrome. A prospective series of 67 patients. Brain. 2007; 130(Pt 12):3091–3101.
6. Kumar R, Wijdicks EF, Brown RD Jr, Parisi JE, Hammond CA. Isolated angiitis of the CNS presenting as subarachnoid haemorrhage. J Neurol Neurosurg Psychiatry. 1997; 62:649–651.
7. Jain R, Deveikis J, Hickenbottom S, Mukherji SK. Varicellazoster vasculitis presenting with intracranial hemorrhage. AJNR Am J Neuroradiol. 2003; 24:971–974.
8. Kannoth S, Iyer R, Thomas SV, Furtado SV, Rajesh BJ, Kesavadas C, et al. Intracranial infectious aneurysm: presentation, management and outcome. J Neurol Sci. 2007; 256:3–9.
9. Osanai T, Kuroda S, Nakayama N, Yamauchi T, Houkin K, Iwasaki Y. Moyamoya disease presenting with subarachnoid hemorrhage localized over the frontal cortex: case report. Surg Neurol. 2008; 69:197–200.
10. Shah AK. Non-aneurysmal primary subarachnoid hemorrhage in pregnancy-induced hypertension and eclampsia. Neurology. 2003; 61:117–120.
11. Karabatsou K, Lecky BR, Rainov NG, Broome JC, White RP. Cerebral amyloid angiopathy with symptomatic or occult subarachnoid haemorrhage. Eur Neurol. 2007; 57:103–105.
12. Vilela P, Saraiva P, Goulão A. Intracranial angiolipoma as cause of subarachnoid haemorrhage. Case report and review of the literature. Neuroradiology. 2005; 47:91–99.
13. Hentschel S, Toyota B. Intracranial malignant glioma presenting as subarachnoid hemorrhage. Can J Neurol Sci. 2003; 30:63–66.
14. Raposo N, Viguier A, Cuvinciuc V, Calviere L, Cognard C, Bonneville F, et al. Cortical subarachnoid haemorrhage in the elderly: a recurrent event probably related to cerebral amyloid angiopathy. Eur J Neurol. 2011; 18:597–603.
15. Beitzke M, Gattringer T, Enzinger C, Wagner G, Niederkorn K, Fazekas F. Clinical presentation, etiology, and long-term prognosis in patients with nontraumatic convexal subarachnoid hemorrhage. Stroke. 2011; 42:3055–3060.
16. Knudsen KA, Rosand J, Karluk D, Greenberg SM. Clinical diagnosis of cerebral amyloid angiopathy: validation of the Boston criteria. Neurology. 2001; 56:537–539.
17. Vinters HV, Gilbert JJ. Cerebral amyloid angiopathy: incidence and complications in the aging brain II The distribution of amyloid vascular changes. Stroke. 1983; 14:924–928.
18. Thal DR, Ghebremedhin E, Orantes M, Wiestler OD. Vascular pathology in Alzheimer disease: correlation of cerebral amyloid angiopathy and arteriosclerosis/lipohyalinosis with cognitive decline. J Neuropathol Exp Neurol. 2003; 62:1287–1301.
19. Spitzer C, Mull M, Rohde V, Kosinski CM. Non-traumatic cortical subarachnoid haemorrhage: diagnostic work-up and aetiological background. Neuroradiology. 2005; 47:525–531.
20. Refai D, Botros JA, Strom RG, Derdeyn CP, Sharma A, Zipfel GJ. Spontaneous isolated convexity subarachnoid hemorrhage: presentation, radiological findings, differential diagnosis, and clinical course. J Neurosurg. 2008; 109:1034–1041.
21. Geraldes R, Santos C, Canhão P. Atraumatic localized convexity subarachnoid hemorrhage associated with acute carotid artery occlusion. Eur J Neurol. 2011; 18:e28–e29.
22. Kleinig TJ, Kimber TE, Thompson PD. Convexity subarachnoid haemorrhage associated with bilateral internal carotid artery stenoses. J Neurol. 2009; 256:669–671.
23. Chandra RV, Leslie-Mazwi TM, Oh D, Mehta B, Yoo AJ. Extracranial internal carotid artery stenosis as a cause of cortical subarachnoid hemorrhage. AJNR Am J Neuroradiol. 2011; 32:E51–E52.
24. Jin X, Liu J, Yang Y, Liu KJ, Yang Y, Liu W. Spatiotemporal evolution of blood brain barrier damage and tissue infarction within the first 3h after ischemia onset. Neurobiol Dis. 2012; 48:309–316.
25. Ivens S, Gabriel S, Greenberg G, Friedman A, Shelef I. Bloodbrain barrier breakdown as a novel mechanism underlying cerebral hyperperfusion syndrome. J Neurol. 2010; 257:615–620.
26. Hjort N, Wu O, Ashkanian M, Sølling C, Mouridsen K, Christensen S, et al. MRI detection of early blood-brain barrier disruption: parenchymal enhancement predicts focal hemorrhagic transformation after thrombolysis. Stroke. 2008; 39:1025–1028.
27. Topakian R, Barrick TR, Howe FA, Markus HS. Blood-brain barrier permeability is increased in normal-appearing white matter in patients with lacunar stroke and leucoaraiosis. J Neurol Neurosurg Psychiatry. 2010; 81:192–197.
28. Yang Y, Rosenberg GA. Blood-brain barrier breakdown in acute and chronic cerebrovascular disease. Stroke. 2011; 42:3323–3328.
29. Wardlaw JM, Farrall A, Armitage PA, Carpenter T, Chappell F, Doubal F, et al. Changes in background blood-brain barrier integrity between lacunar and cortical ischemic stroke subtypes. Stroke. 2008; 39:1327–1332.
30. Rosenberg GA. Neurological diseases in relation to the blood-brain barrier. J Cereb Blood Flow Metab. 2012; 32:1139–1151.
31. Henning EC, Latour LL, Warach S. Verification of enhancement of the CSF space, not parenchyma, in acute stroke patients with early blood-brain barrier disruption. J Cereb Blood Flow Metab. 2008; 28:882–886.
32. Brott T, Broderick J, Kothari R, Barsan W, Tomsick T, Sauerbeck L, et al. Early hemorrhage growth in patients with intracerebral hemorrhage. Stroke. 1997; 28:1–5.
33. Montaner J, Alvarez-Sabín J, Molina CA, Anglés A, Abilleira S, Arenillas J, et al. Matrix metalloproteinase expression is related to hemorrhagic transformation after cardioembolic stroke. Stroke. 2001; 32:2762–2767.
34. White H, Boden-Albala B, Wang C, Elkind MS, Rundek T, Wright CB, et al. Ischemic stroke subtype incidence among whites, blacks, and Hispanics: the Northern Manhattan Study. Circulation. 2005; 111:1327–1331.
35. Jung KH, Lee SH, Kim BJ, Yu KH, Hong KS, Lee BC, et al. Secular trends in ischemic stroke characteristics in a rapidly developed country: results from the Korean Stroke Registry Study (secular trends in Korean stroke). Circ Cardiovasc Qual Outcomes. 2012; 5:327–334.
Full Text Links
  • JKSR
Actions
Cited
CITED
export Copy
Close
Share
  • Twitter
  • Facebook
Similar articles
Copyright © 2024 by Korean Association of Medical Journal Editors. All rights reserved.     E-mail: koreamed@kamje.or.kr