Hemorrhagic Stroke in Emergency Medicine 

  • Author: David S Liebeskind, MD; Chief Editor: Rick Kulkarni, MD   more...
 
Updated: Aug 17, 2011
 

Background

The terms intracerebral hemorrhage (ICH) and hemorrhagic stroke are used interchangeably in this discussion and are regarded as separate entities from hemorrhagic transformation of ischemic stroke. Intracerebral hemorrhage accounts for 10-15% of all strokes and is associated with higher mortality rates than cerebral infarctions.[1]

Acute ischemic stroke refers to stroke caused by thrombosis or embolism and is more common than hemorrhagic stroke. Previous literature indicates that only 8-18% of strokes were hemorrhagic. (See Etiology.)

Although a 2010 retrospective review from a stroke center found that 40.9% of 757 strokes were hemorrhagic,[2] nonetheless, the authors stated that the increased percentage of hemorrhagic stroke may be due to improvement of computed tomography (CT) scanning availability and implementation, unmasking a previous underestimation of the actual percentage (see Workup), or it may be due to an increase in therapeutic use of antiplatelet agents and warfarin causing an increase in the incidence of hemorrhage (see Treatment and Management).[2]

Patients with hemorrhagic stroke present with similar focal neurologic deficits but tend to be more ill than patients with ischemic stroke. Patients with intracerebral bleeds are more likely to have headache, altered mental status, seizures, nausea and vomiting, and/or marked hypertension; however, none of these findings reliably distinguishes between hemorrhagic stroke and ischemic stroke. Though stroke is less common in children, the clinical presentation is similar (See Clinical Presentation).[3]

An intracerebral hemorrhage is shown in the CT scan below.

Axial noncontrast computed tomography scan of the Axial noncontrast computed tomography scan of the brain in a 60-year-old male with history of acute onset of left-sided weakness demonstrates 2 areas of intracerebral hemorrhage in the right lentiform nucleus with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral ventricle with intraventricular extension of the hemorrhage.
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Anatomy

Knowledge of cerebrovascular arterial anatomy and the territories supplied by each is useful in determining which vessels are involved in acute stroke. Atypical patterns that do not conform to a vascular distribution may indicate another diagnosis, such as venous infarction. The cerebral hemispheres are supplied by 3 paired major arteries, the anterior, middle, and posterior cerebral arteries. The anterior and middle cerebral arteries comprise the anterior circulation and arise from the supraclinoid internal carotid arteries. The posterior cerebral arteries arise from the basilar artery and form the posterior circulation, which also supplies the thalami, brainstem, and cerebellum.

The angiograms in the images below demonstrate some of the circulation involved in hemorrhagic strokes.

Frontal view of a cerebral angiogram with selectivFrontal view of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation. The anterior cerebral artery consists of the A1 segment proximal to the anterior communicating artery with the A2 segment distal to it. The middle cerebral artery can be divided into 4 segments: the M1 (horizontal segment) extends to the limen insulae and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches), and M4 (distal cortical branches on the lateral hemispheric convexities). Lateral view of a cerebral angiogram illustrates tLateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery (ACA) and Sylvian triangle. The pericallosal artery has been described to arise distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery; A2 extends to the junction of the rostrum and genu of the corpus callosum; A3 extends into the bend of the genu of the corpus callosum; A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The Sylvian triangle overlies the opercular branches of the middle cerebral artery, with the apex representing the Sylvian point. Frontal projection from a right vertebral artery aFrontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICA) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICA) arise from the proximal basilar artery. The superior cerebellar arteries (SCA) arise distally from the basilar artery before its bifurcation into the posterior cerebral arteries.

The image below shows the supratentorial vascular territories of the major cerebral arteries.

The supratentorial vascular territories of the majThe supratentorial vascular territories of the major cerebral arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images through the level of the basal ganglia and thalami. The middle cerebral artery (red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal, and anterior temporal lobes, insula, and basal ganglia. The anterior cerebral artery (blue) supplies the medial frontal and parietal lobes. The posterior cerebral artery (green) supplies the thalami and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal capsule and part of the hippocampus extending to the anterior and superior surface of the occipital horn of the lateral ventricle.
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Pathophysiology

In intracerebral hemorrhage, bleeding occurs directly into the brain parenchyma. The usual mechanism is thought to be leakage from small intracerebral arteries damaged by chronic hypertension. Other mechanisms include bleeding diatheses, iatrogenic anticoagulation, cerebral amyloidosis, and cocaine abuse.

Intracerebral hemorrhage has a predilection for certain sites in the brain, including the thalamus, putamen, cerebellum, and brainstem. In addition to the area of the brain injured by the hemorrhage, the surrounding brain can be damaged by pressure produced by the mass effect of the hematoma. A general increase in intracranial pressure may occur.

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Etiology

The etiologies of stroke are varied, but they can be broadly categorized into ischemic or hemorrhagic infarctions. Approximately 80-87% of strokes are from ischemic infarction due to thrombotic or embolic cerebrovascular occlusion. Hemorrhagic infarctions comprise most of the remainder of strokes, with a smaller number due to aneurysmal subarachnoid hemorrhage.[4, 5, 6, 7] Furthermore, 20-40% of patients with ischemic infarction may develop hemorrhagic transformation within 1 week after ictus.[8, 9] Differentiating between these different types of stroke is an essential part of the initial workup of these patients, as the subsequent management of each will be vastly different.

Risk factors

The risk of stroke is increased with the following factors:

  • Advanced age
  • Hypertension (up to 60% of cases)
  • Previous history of stroke
  • Alcohol and illicit drug use, such as cocaine and other sympathomimetic drugs

Causes of hemorrhagic stroke include the following:

  • Cerebral amyloidosis (affects people who are elderly and may cause up to 10% of intracerebral hemorrhages)
  • Coagulopathies (eg, due to underlying systemic disorders such as bleeding diathesis or liver disease)
  • Anticoagulant therapy
  • Thrombolytic therapy for acute myocardial infarction (MI) and acute ischemic stroke (can cause iatrogenic hemorrhagic transformation)
  • Arteriovenous malformation
  • Intracranial aneurysm
  • Vasculitis
  • Intracranial neoplasm

To see complete information on Genetic and Inflammatory Mechanisms in Stroke, please go to the main article by clicking here. To see complete information on Blood Dyscrasias and Stroke, please go to the main article by clicking here. In addition, complete information on the following metabolic disease and stroke can be found in the main articles:

Hypertension

The most common etiology of primary hemorrhagic stroke (intracerebral hemorrhage) is hypertension, with at least two thirds of patients with primary intraparenchymal hemorrhage reported to have preexisting or newly diagnosed hypertension. Hypertensive small-vessel disease results from tiny lipohyalinotic aneurysms that subsequently rupture and result in intraparenchymal hemorrhage. Typical locations include the basal ganglia, thalami, cerebellum, and pons.

Axial noncontrast computed tomography scan of the Axial noncontrast computed tomography scan of the brain in a 60-year-old male with history of acute onset of left-sided weakness demonstrates 2 areas of intracerebral hemorrhage in the right lentiform nucleus with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral ventricle with intraventricular extension of the hemorrhage. Noncontrast computed tomography scan of the brain Noncontrast computed tomography scan of the brain (left) demonstrates an acute hemorrhage in the left gangliocapsular region with surrounding white matter hypodensity consistent with vasogenic edema. T2-weighted axial magnetic resonance image (middle image) redemonstrates the hemorrhage with surrounding high-signal edema. The coronal gradient-echo image (right) demonstrates susceptibility related to the hematoma with markedly low signal adjacent the left caudate head. Gradient-echo images are highly sensitive for blood products.

Aneurysms and subarachnoid hemorrhage

The most common cause of atraumatic hemorrhage into the subarachnoid space is rupture of an intracranial aneurysm. Aneurysms are focal dilatations of arteries, with the most frequently encountered intracranial type being the berry aneurysm or saccular aneurysms. Aneurysms may less commonly be related to altered hemodynamics associated with arteriovenous malformations, collagen vascular disease, polycystic kidney disease, septic emboli, and neoplasms.

Nonaneurysmal perimesencephalic subarachnoid hemorrhage may also be seen and is thought to arise from capillary or venous rupture. It has a less severe clinical course and, in general, better prognosis.

Berry aneurysms are most commonly isolated lesions that form due to a combination of hemodynamic stresses and acquired or congenital weakness in the vessel wall. Saccular aneurysms typically occur at vascular bifurcations, with more than 90% occurring in the anterior circulation. These include the junction of the anterior communication arteries and anterior cerebral arteries—most commonly, the MCA bifurcation—the supraclinoid internal carotid artery at the origin of the posterior communicating artery, and the bifurcation of the internal carotid artery (ICA).

The pathologic effects of subarachnoid hemorrhage (SAH) on the brain are multifocal. SAH results in elevated intracranial pressure and impairs cerebral autoregulation. This, in combination with acute vasoconstriction, microvascular platelet aggregation, and loss of microvascular perfusion are also seen, resulting in profound reduction in blood flow and cerebral ischemia.[10] See the images below.

Noncontrast computed tomography (CT) scanning was Noncontrast computed tomography (CT) scanning was performed emergently in a 71-year-old male who presented with acute onset of severe headache and underwent rapid neurologic deterioration requiring intubation. The noncontrast CT scan (left image) demonstrates diffuse, high-density subarachnoid hemorrhage in the basilar cisterns and both Sylvian fissures. There is diffuse loss of gray-white differentiation. The fluid-attenuated inversion-recovery (FLAIR) image (right) demonstrates high signal throughout the cortical sulci, basilar cisterns and in the dependent portions of the ventricles. FLAIR is highly sensitive to acute subarachnoid hemorrhage, owing to the suppression of high cerebrospinal fluid signal lending to greater conspicuity of subarachnoid hemorrhage compared with conventional magnetic resonance image sequences. The patient above subsequently underwent a computeThe patient above subsequently underwent a computed tomographic angiography examination and subsequent cerebral angiography. Multiple aneurysms were identified, including a 9-mm aneurysm at the junction of the anterior cerebral and posterior communicating arteries seen on this lateral view of an internal carotid artery injection. Balloon-assisted coil embolization was performed. Lateral view of a selective injection of the left Lateral view of a selective injection of the left internal carotid artery demonstrates a microcatheter passing distal to the aneurysm neck. This lateral view from an angiogram performed during balloon-assisted coil embolization demonstrates significantly diminished filling of the aneurysm.

Hemorrhagic transformation of ischemic stroke

Hemorrhagic transformation represents the conversion of a bland infarction into an area of hemorrhage. Proposed mechanisms for hemorrhagic transformation include reperfusion of ischemically injured tissue, either from recanalization of an occluded vessel or from collateral blood supply to the ischemic territory or disruption of the blood-brain barrier. With disruption of the blood-brain barrier, red blood cells extravasate from the weakened capillary bed, producing petechial hemorrhage or more frank intraparenchymal hematoma.[7, 8, 11]

To see complete information on Reperfusion Injury in Stroke, please go to the main article by clicking here.

Hemorrhagic transformation of an ischemic infarct occurs within 2-14 days post ictus, usually within the first week. It is more commonly seen following cardioembolic strokes and is more likely with larger infarct size.[7, 9, 12] Hemorrhagic transformation is also more likely following administration of tissue plasminogen activator (tPA) and with noncontrast CT scans demonstrating areas of hypodensity.[13, 14, 11] See the image below.

Noncontrast computed tomography scan (left) obtainNoncontrast computed tomography scan (left) obtained after a 75-year-old male was admitted for cerebrovascular accident demonstrates a large right middle cerebral artery distribution infarction with linear areas of developing hemorrhage. These become more confluent on day 2 of hospitalization (middle image), with increased mass effect and midline shift. There is massive hemorrhagic transformation by day 6 (right) with increased leftward midline shift and subfalcine herniation. Obstructive hydrocephalus is also noted with dilatation of the lateral ventricles, likely due to compression of the foramen of Monroe. Intraventricular hemorrhage is also noted layering in the left occipital horn. Larger infarctions are more likely to undergo hemorrhagic transformation and are one contraindication to thrombolytic therapy.

Vascular malformations and amyloid angiography

The remaining cases of spontaneous intraparenchymal hemorrhage may be secondary to vascular malformations (eg, arteriovenous malformations and cavernous malformations) or amyloid angiopathy.[7, 8, 15, 16, 17]

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Epidemiology

United States statistics

Each year in the United States, approximately 795,000 people experience new or recurrent stroke. Of these, approximately 610,000 represent initial attacks, and 185,000 represent recurrent strokes. Approximately 87% of strokes in the United States are ischemic, 10% are secondary to intracerebral hemorrhage, and another 3% may be secondary to subarachnoid hemorrhage.[4, 18]

The incidence of stroke varies depending on age, sex, ethnicity, and socioeconomic status. For example, American Heart Association (AHA) researchers found that black persons had a 3-fold higher multivariate-adjusted risk ratio of lacunar stroke than white individuals.[4]

International statistics

The global incidence of stroke has at least a modest variation from nation to nation, suggesting the importance of genetics and environmental factors, such as disparities in access to health care for developing countries. According to the World Health Organization (WHO), 15 million people suffer stroke worldwide each year. The age-adjusted incidence of total strokes per 1000 person-years for people 55 years or older has been reported in the range of 4.2 to 6.5. The highest incidences have been reported in Russia, Ukraine, and Japan.

Overall, the incidence of acute stroke has demonstrated a constant decline over the past several decades, most notably during the 1970s-1990s, although in recent years this trend has begun to plateau. However, the increased survival among stroke victims will place an increased demand on healthcare systems globally.[7, 19]

Stroke subtypes also vary greatly in different parts of the world and between different races. For example, the proportion of hemorrhagic strokes may be even higher in certain populations, such as the Chinese population, in which it has been reported to be up to 39.4%, and the Japanese, in which it is reportedly up to 38.7%.[19, 20] Also, an increased proportion of intracerebral hemorrhage and lacunar infarcts have been reported in Asia.

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Prognosis

The prognosis of hemorrhagic stroke varies depending on the severity of stroke and the location and the size of the hemorrhage. Lower Glasgow Coma Scale scores are associated with poorer prognosis and higher mortality rate. A larger volume of blood at presentation is associated with a poorer prognosis. Growth of the hematoma volume is associated with a poorer functional outcome and increased mortality rate.

Nonaneurysmal perimesencephalic has a less severe clinical course and, in general, a better prognosis.

The presence of blood in the ventricles is associated with a higher mortality rate. In one study, the presence of intraventricular blood at presentation was associated with more than a 2-fold increase in death. Patients with oral anticoagulation-associated intracerebral hemorrhage have higher mortality rates and poorer functional outcomes.

Endoscopic hematoma evacuation may be a promising ultra-early stage treatment for intracerebral hemorrhage that improves long-term prognosis (see Treatment and Management).[21]

The 2010 guideline for management of spontaneous ICH from the American Heart Association (AHA) and American Stroke Association (ASA) notes that in studies, withdrawal of medical support or issuance of DNR orders within the first day of hospitalization are predictors of poor outcome independent of clinical factors. The writing committee has concern that current methods of early prognostication do not account for the effects of limiting care after a pessimistic estimate of prognosis. Therefore, initial therapy should probably be aggressive, and new DNR orders should probably be postponed until at least the second full day of hospitalization. Patients with DNRs should be given all other medical and surgical treatment, unless the DNR explicitly says otherwise.[22]

For more information, see Motor Recovery in Stroke.

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Patient Education

For excellent patient education resources, visit eMedicine's Stroke Center. Also, see eMedicine's patient education article Stroke.

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Contributor Information and Disclosures
Author

David S Liebeskind, MD  Associate Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California, Los Angeles, David Geffen School of Medicine; Neurology Director, Stroke Imaging Program, Co-Medical Director, Cerebral Blood Flow Laboratory, Associate Neurology Director, UCLA Stroke Center

David S Liebeskind, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Society of Neuroimaging, American Society of Neuroradiology, National Stroke Association, and Stroke Council of the American Heart Association

Disclosure: Nothing to disclose.

Coauthor(s)

Howard S Kirshner, MD  Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neurorehabilitation, National Stroke Association, Phi Beta Kappa, and Tennessee Medical Association

Disclosure: Nothing to disclose.

Denise Nassisi, MD  Assistant Professor, Department of Emergency Medicine, Mount Sinai Medical Center

Denise Nassisi, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, American Heart Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Jeffrey L Saver, MD, FAHA, FAAN  Professor of Neurology, Director, UCLA Stroke Center, University of California, Los Angeles, David Geffen School of Medicine

Jeffrey L Saver, MD, FAHA, FAAN is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Neurological Association, and National Stroke Association

Disclosure: University of California The University of California Regents receive funds for consulting services on clinical trial design provided to Telecris, Ev3, and CoAxia. Consulting

Specialty Editor Board

Richard S Krause, MD  Senior Clinical Faculty/Clinical Assistant Professor, Department of Emergency Medicine, University of Buffalo State University of New York School of Medicine and Biomedical Sciences

Richard S Krause, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

J Stephen Huff, MD  Associate Professor of Emergency Medicine and Neurology, Department of Emergency Medicine, University of Virginia School of Medicine

J Stephen Huff, MD is a member of the following medical societies: American Academy of Emergency Medicine, American Academy of Neurology, American College of Emergency Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Helmi L Lutsep, MD  Professor, Department of Neurology, Oregon Health and Science University School of Medicine; Associate Director, Oregon Stroke Center

Helmi L Lutsep, MD is a member of the following medical societies: American Academy of Neurology and American Stroke Association

Disclosure: Co-Axia Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Concentric Medical Consulting fee Review panel membership

Chief Editor

Rick Kulkarni, MD  Attending Physician, Department of Emergency Medicine, Cambridge Health Alliance, Division of Emergency Medicine, Harvard Medical School

Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine

Disclosure: WebMD Salary Employment

References

  1. [Guideline] Broderick J, Connolly S, Feldmann E, Hanley D, Kase C, Krieger D, et al. Guidelines for the management of spontaneous intracerebral hemorrhage in adults: 2007 update: a guideline from the American Heart Association/American Stroke Association Stroke Council, High Blood Pressure Research Council, and the Quality of Care and Outcomes in Research Interdisciplinary Working Group. Circulation. Oct 16 2007;116(16):e391-413. [Medline].

  2. Shiber JR, Fontane E, Adewale A. Stroke registry: hemorrhagic vs ischemic strokes. Am J Emerg Med. Mar 2010;28(3):331-3. [Medline].

  3. Yock-Corrales A, Mackay MT, Mosley I, Maixner W, Babl FE. Acute childhood arterial ischemic and hemorrhagic stroke in the emergency department. Ann Emerg Med. Aug 2011;58(2):156-63. [Medline].

  4. Lloyd-Jones D, Adams R, Carnethon M, De Simone G, Ferguson TB, Flegal K, et al. Heart disease and stroke statistics--2009 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. Jan 27 2009;119(3):480-6. [Medline].

  5. Adams HP Jr, Bendixen BH, Kappelle LJ, Biller J, Love BB, Gordon DL, et al. Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment. Stroke. Jan 1993;24(1):35-41. [Medline].

  6. Thrift AG, Dewey HM, Macdonell RA, McNeil JJ, Donnan GA. Incidence of the major stroke subtypes: initial findings from the North East Melbourne stroke incidence study (NEMESIS). Stroke. Aug 2001;32(8):1732-8. [Medline].

  7. Donnan GA, Fisher M, Macleod M, Davis SM. Stroke. Lancet. May 10 2008;371(9624):1612-23. [Medline].

  8. Mullins ME, Lev MH, Schellingerhout D, Gonzalez RG, Schaefer PW. Intracranial hemorrhage complicating acute stroke: how common is hemorrhagic stroke on initial head CT scan and how often is initial clinical diagnosis of acute stroke eventually confirmed?. AJNR Am J Neuroradiol. Oct 2005;26(9):2207-12. [Medline].

  9. Nighoghossian N, Hermier M, Adeleine P, Blanc-Lasserre K, Derex L, Honnorat J, et al. Old microbleeds are a potential risk factor for cerebral bleeding after ischemic stroke: a gradient-echo T2*-weighted brain MRI study. Stroke. Mar 2002;33(3):735-42. [Medline].

  10. Kim EY, Na DG, Kim SS, Lee KH, Ryoo JW, Kim HK. Prediction of hemorrhagic transformation in acute ischemic stroke: role of diffusion-weighted imaging and early parenchymal enhancement. AJNR Am J Neuroradiol. May 2005;26(5):1050-5. [Medline].

  11. Dubey N, Bakshi R, Wasay M, Dmochowski J. Early computed tomography hypodensity predicts hemorrhage after intravenous tissue plasminogen activator in acute ischemic stroke. J Neuroimaging. Apr 2001;11(2):184-8. [Medline].

  12. Tissue plasminogen activator for acute ischemic stroke. The National Institute of Neurological Disorders and Stroke rt-PA Stroke Study Group. N Engl J Med. Dec 14 1995;333(24):1581-7. [Medline].

  13. González RG. Imaging-guided acute ischemic stroke therapy: From "time is brain" to "physiology is brain". AJNR Am J Neuroradiol. Apr 2006;27(4):728-35. [Medline].

  14. Albers GW, Amarenco P, Easton JD, Sacco RL, Teal P. Antithrombotic and thrombolytic therapy for ischemic stroke: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy. Chest. Sep 2004;126(3 Suppl):483S-512S. [Medline].

  15. Auer RN, Sutherland GR. Primary intracerebral hemorrhage: pathophysiology. Can J Neurol Sci. Dec 2005;32 Suppl 2:S3-12. [Medline].

  16. Thrift AG, Donnan GA, McNeil JJ. Epidemiology of intracerebral hemorrhage. Epidemiol Rev. 1995;17(2):361-81. [Medline].

  17. Gokaslan ZL, Narayan RK. Intracranial hemorrhage in the hypertensive patient. Neuroimaging Clin N Am. 1992;Vol. 2:171-86.

  18. Murray CJ, Lopez AD. Mortality by cause for eight regions of the world: Global Burden of Disease Study. Lancet. May 3 1997;349(9061):1269-76. [Medline].

  19. Centers for Disease Control and Prevention (CDC. Prevalence of stroke--United States, 2005. MMWR Morb Mortal Wkly Rep. May 18 2007;56(19):469-74. [Medline].

  20. Feigin VL, Lawes CM, Bennett DA, Anderson CS. Stroke epidemiology: a review of population-based studies of incidence, prevalence, and case-fatality in the late 20th century. Lancet Neurol. Jan 2003;2(1):43-53. [Medline].

  21. Vespa PM, O'Phelan K, Shah M, Mirabelli J, Starkman S, Kidwell C, et al. Acute seizures after intracerebral hemorrhage: a factor in progressive midline shift and outcome. Neurology. May 13 2003;60(9):1441-6. [Medline].

  22. [Guideline] Morgenstern LB, Hemphill JC 3rd, Anderson C, Becker K, Broderick JP, Connolly ES Jr, et al. Guidelines for the management of spontaneous intracerebral hemorrhage: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. Sep 2010;41(9):2108-29. [Medline].

  23. Passero S, Rocchi R, Rossi S, Ulivelli M, Vatti G. Seizures after spontaneous supratentorial intracerebral hemorrhage. Epilepsia. Oct 2002;43(10):1175-80. [Medline].

  24. Oliveira-Filho J, Silva SC, Trabuco CC, Pedreira BB, Sousa EU, Bacellar A. Detrimental effect of blood pressure reduction in the first 24 hours of acute stroke onset. Neurology. Oct 28 2003;61(8):1047-51. [Medline].

  25. Ahmed N, Näsman P, Wahlgren NG. Effect of intravenous nimodipine on blood pressure and outcome after acute stroke. Stroke. Jun 2000;31(6):1250-5. [Medline]. [Full Text].

  26. Misra UK, Kalita J, Ranjan P, Mandal SK. Mannitol in intracerebral hemorrhage: a randomized controlled study. J Neurol Sci. Jul 15 2005;234(1-2):41-5. [Medline].

  27. Mayer SA, Brun NC, Begtrup K, Broderick J, Davis S, Diringer MN, et al. Efficacy and safety of recombinant activated factor VII for acute intracerebral hemorrhage. N Engl J Med. May 15 2008;358(20):2127-37. [Medline].

  28. [Best Evidence] Diringer MN, Skolnick BE, Mayer SA, Steiner T, Davis SM, Brun NC, et al. Thromboembolic events with recombinant activated factor VII in spontaneous intracerebral hemorrhage: results from the Factor Seven for Acute Hemorrhagic Stroke (FAST) trial. Stroke. Jan 2010;41(1):48-53. [Medline].

  29. Avorn J, Kesselheim A. A hemorrhage of off-label use. Ann Intern Med. Apr 19 2011;154(8):566-7. [Medline].

  30. Yank V, Tuohy CV, Logan AC, et al. Systematic Review: Benefits and Harms of In-Hospital Use of Recombinant Factor VIIa for Off-Label Indications. Ann Intern Med. Apr 19 2011;154(8):529-40. [Medline].

  31. Logan AC, Yank V, Stafford RS. Off-Label Use of Recombinant Factor VIIa in U.S. Hospitals: Analysis of Hospital Records. Ann Intern Med. Apr 19 2011;154(8):516-22. [Medline].

  32. Lankiewicz MW, Hays J, Friedman KD, Tinkoff G, Blatt PM. Urgent reversal of warfarin with prothrombin complex concentrate. J Thromb Haemost. May 2006;4(5):967-70. [Medline].

  33. Huttner HB, Schellinger PD, Hartmann M, Köhrmann M, Juettler E, Wikner J, et al. Hematoma growth and outcome in treated neurocritical care patients with intracerebral hemorrhage related to oral anticoagulant therapy: comparison of acute treatment strategies using vitamin K, fresh frozen plasma, and prothrombin complex concentrates. Stroke. Jun 2006;37(6):1465-70. [Medline].

  34. [Best Evidence] Mendelow AD, Gregson BA, Fernandes HM, Murray GD, Teasdale GM, Hope DT, et al. Early surgery versus initial conservative treatment in patients with spontaneous supratentorial intracerebral haematomas in the International Surgical Trial in Intracerebral Haemorrhage (STICH): a randomised trial. Lancet. Jan 29-Feb 4 2005;365(9457):387-97. [Medline].

  35. Molyneux AJ, Kerr RS, Yu LM, Clarke M, Sneade M, Yarnold JA, et al. 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. Sep 3-9 2005;366(9488):809-17. [Medline].

  36. Byrne JV. The aneurysm "clip or coil" debate. Acta Neurochir (Wien). Feb 2006;148(2):115-20. [Medline].

  37. Hunt WE, Hess RM. Surgical risk as related to time of intervention in the repair of intracranial aneurysms. J Neurosurg. Jan 1968;28(1):14-20. [Medline].

  38. Fisher CM, Kistler JP, Davis JM. Relation of cerebral vasospasm to subarachnoid hemorrhage visualized by computerized tomographic scanning. Neurosurgery. Jan 1980;6(1):1-9. [Medline].

  39. Kurl S, Laukkanen JA, Rauramaa R, Lakka TA, Sivenius J, Salonen JT. Cardiorespiratory fitness and the risk for stroke in men. Arch Intern Med. Jul 28 2003;163(14):1682-8. [Medline].

  40. [Guideline] Goldstein LB, Bushnell CD, Adams RJ, Appel LJ, Braun LT, Chaturvedi S, et al. Guidelines for the primary prevention of stroke: a guideline for healthcare professionals from the American Heart Association/American Stroke Association. Stroke. Feb 2011;42(2):517-84. [Medline]. [Full Text].

  41. Yusuf S, Sleight P, Pogue J, Bosch J, Davies R, Dagenais G. Effects of an angiotensin-converting-enzyme inhibitor, ramipril, on cardiovascular events in high-risk patients. The Heart Outcomes Prevention Evaluation Study Investigators. N Engl J Med. Jan 20 2000;342(3):145-53. [Medline].

  42. PROGRESS Collaborative Group. Randomised trial of a perindopril-based blood-pressure-lowering regimen among 6,105 individuals with previous stroke or transient ischaemic attack. Lancet. Sep 29 2001;358(9287):1033-41. [Medline].

  43. ALLHAT Officers and Coordinators for the ALLHAT Collaborative Research Group. Major outcomes in high-risk hypertensive patients randomized to angiotensin-converting enzyme inhibitor or calcium channel blocker vs diuretic: The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT). JAMA. Dec 18 2002;288(23):2981-97. [Medline].

  44. Dahlöf B, Devereux RB, Kjeldsen SE, Julius S, Beevers G, de Faire U, et al. Cardiovascular morbidity and mortality in the Losartan Intervention For Endpoint reduction in hypertension study (LIFE): a randomised trial against atenolol. Lancet. Mar 23 2002;359(9311):995-1003. [Medline].

  45. Schrader J, Lüders S, Kulschewski A, Hammersen F, Plate K, Berger J, et al. Morbidity and Mortality After Stroke, Eprosartan Compared with Nitrendipine for Secondary Prevention: principal results of a prospective randomized controlled study (MOSES). Stroke. Jun 2005;36(6):1218-26. [Medline].

  46. Aso K, Ogasawara K, Sasaki M, Kobayashi M, Suga Y, Chida K, et al. Preoperative cerebrovascular reactivity to acetazolamide measured by brain perfusion SPECT predicts development of cerebral ischemic lesions caused by microemboli during carotid endarterectomy. Eur J Nucl Med Mol Imaging. Feb 2009;36(2):294-301. [Medline].

  47. Becker H, Desch H, Hacker H, Pencz A. CT fogging effect with ischemic cerebral infarcts. Neuroradiology. Oct 31 1979;18(4):185-92. [Medline].

  48. Borisch I, Horn M, Butz B, Zorger N, Draganski B, Hoelscher T, et al. Preoperative evaluation of carotid artery stenosis: comparison of contrast-enhanced MR angiography and duplex sonography with digital subtraction angiography. AJNR Am J Neuroradiol. Jun-Jul 2003;24(6):1117-22. [Medline].

  49. Bose A, Henkes H, Alfke K, Reith W, Mayer TE, Berlis A, et al. The Penumbra System: a mechanical device for the treatment of acute stroke due to thromboembolism. AJNR Am J Neuroradiol. Aug 2008;29(7):1409-13. [Medline].

  50. Bozzao L, Bastianello S, Fantozzi LM, Angeloni U, Argentino C, Fieschi C. Correlation of angiographic and sequential CT findings in patients with evolving cerebral infarction. AJNR Am J Neuroradiol. Nov-Dec 1989;10(6):1215-22. [Medline].

  51. Bozzao L, Fantozzi LM, Bastianello S, Bozzao A, Argentino C, Lenzi GL, et al. Ischaemic supratentorial stroke: angiographic findings in patients examined in the very early phase. J Neurol. Sep 1989;236(6):340-2. [Medline].

  52. Brott T, Adams HP Jr, Olinger CP, Marler JR, Barsan WG, Biller J, et al. Measurements of acute cerebral infarction: a clinical examination scale. Stroke. Jul 1989;20(7):864-70. [Medline].

  53. Brown PB, Zwiebel WJ, Call GK. Degree of cervical carotid artery stenosis and hemispheric stroke: duplex US findings. Radiology. Feb 1989;170(2):541-3. [Medline].

  54. Burdette JH, Ricci PE, Petitti N, Elster AD. Cerebral infarction: time course of signal intensity changes on diffusion-weighted MR images. AJR Am J Roentgenol. Sep 1998;171(3):791-5. [Medline].

  55. Carroll BA. Duplex sonography in patients with hemispheric symptoms. J Ultrasound Med. Oct 1989;8(10):535-40. [Medline].

  56. Chandra VR, Pandav R, Laxminarayan R, et al. Neurologic Disorders. In: Jamison DT, Measham AR, Breman JB, et al, eds. Disease Control Priorities in Developing Countries. 2nd ed. New York, NY: Oxford University Press and The World Bank; 2006:627-43.

  57. Chappell FM, Wardlaw JM, Young GR, Gillard JH, Roditi GH, Yip B, et al. Carotid artery stenosis: accuracy of noninvasive tests--individual patient data meta-analysis. Radiology. May 2009;251(2):493-502. [Medline].

  58. de Virgilio C, Toosie K, Arnell T, Lewis RJ, Donayre CE, Baker JD, et al. Asymptomatic carotid artery stenosis screening in patients with lower extremity atherosclerosis: a prospective study. Ann Vasc Surg. Jul 1997;11(4):374-7. [Medline].

  59. Delgado AL, Jahromi B, Muller N, Farhat H, Salame J, Zauner A. Endovascular therapy of cerebral vasospasm: two year experience with angioplasty and/or intraarterial administration of nicardipine and verapamil. Acta Neurochir Suppl. 2008;104:347-51.

  60. Eastwood JD, Lev MH, Azhari T, Lee TY, Barboriak DP, Delong DM, et al. CT perfusion scanning with deconvolution analysis: pilot study in patients with acute middle cerebral artery stroke. Radiology. Jan 2002;222(1):227-36. [Medline].

  61. Elster AD, Moody DM. Early cerebral infarction: gadopentetate dimeglumine enhancement. Radiology. Dec 1990;177(3):627-32. [Medline].

  62. Goldenberg G, Reisner T. Angiographic findings in relation to clinical course and results of computed tomography in cerebrovascular disease. Eur Neurol. 1983;22(2):124-30. [Medline].

  63. González RG, Schaefer PW, Buonanno FS, Schwamm LH, Budzik RF, Rordorf G, et al. Diffusion-weighted MR imaging: diagnostic accuracy in patients imaged within 6 hours of stroke symptom onset. Radiology. Jan 1999;210(1):155-62. [Medline].

  64. Grant EG, Benson CB, Moneta GL, Alexandrov AV, Baker JD, Bluth EI, et al. Carotid artery stenosis: gray-scale and Doppler US diagnosis--Society of Radiologists in Ultrasound Consensus Conference. Radiology. Nov 2003;229(2):340-6. [Medline].

  65. Grant EG, Duerinckx AJ, El Saden SM, Melany ML, Hathout GM, Zimmerman PT, et al. Ability to use duplex US to quantify internal carotid arterial stenoses: fact or fiction?. Radiology. Jan 2000;214(1):247-52. [Medline].

  66. Karonen JO, Partanen PL, Vanninen RL, Vainio PA, Aronen HJ. Evolution of MR contrast enhancement patterns during the first week after acute ischemic stroke. AJNR Am J Neuroradiol. Jan 2001;22(1):103-11. [Medline].

  67. Kucinski T, Väterlein O, Glauche V, Fiehler J, Klotz E, Eckert B, et al. Correlation of apparent diffusion coefficient and computed tomography density in acute ischemic stroke. Stroke. Jul 2002;33(7):1786-91. [Medline].

  68. Lyden PD, Zivin JA. Hemorrhagic transformation after cerebral ischemia: mechanisms and incidence. Cerebrovasc Brain Metab Rev. Spring 1993;5(1):1-16. [Medline].

  69. Marks MP. CT in ischemic stroke. Neuroimaging Clin N Am. Aug 1998;8(3):515-23. [Medline].

  70. Martin PJ, Enevoldson TP, Humphrey PR. Causes of ischaemic stroke in the young. Postgrad Med J. Jan 1997;73(855):8-16. [Medline]. [Full Text].

  71. Meerwaldt R, Slart RH, van Dam GM, Luijckx GJ, Tio RA, Zeebregts CJ. PET/SPECT imaging: from carotid vulnerability to brain viability. Eur J Radiol. Apr 2010;74(1):104-9. [Medline].

  72. Minematsu K, Li L, Fisher M, Sotak CH, Davis MA, Fiandaca MS. Diffusion-weighted magnetic resonance imaging: rapid and quantitative detection of focal brain ischemia. Neurology. Jan 1992;42(1):235-40. [Medline].

  73. Nabavi DG, Cenic A, Craen RA, Gelb AW, Bennett JD, Kozak R, et al. CT assessment of cerebral perfusion: experimental validation and initial clinical experience. Radiology. Oct 1999;213(1):141-9. [Medline].

  74. Nishihara T, Nagata K, Tanaka S, Suzuki Y, Izumi M, Mochizuki Y, et al. Newly developed endoscopic instruments for the removal of intracerebral hematoma. Neurocrit Care. 2005;2(1):67-74. [Medline].

  75. Noguchi K, Ogawa T, Inugami A, Fujita H, Hatazawa J, Shimosegawa E, et al. MRI of acute cerebral infarction: a comparison of FLAIR and T2-weighted fast spin-echo imaging. Neuroradiology. Jun 1997;39(6):406-10. [Medline].

  76. Oppenheim C, Logak M, Dormont D, Lehéricy S, Manaï R, Samson Y, et al. Diagnosis of acute ischaemic stroke with fluid-attenuated inversion recovery and diffusion-weighted sequences. Neuroradiology. Aug 2000;42(8):602-7. [Medline].

  77. Powers WJ, Grubb RL Jr, Darriet D, Raichle ME. Cerebral blood flow and cerebral metabolic rate of oxygen requirements for cerebral function and viability in humans. J Cereb Blood Flow Metab. Dec 1985;5(4):600-8. [Medline].

  78. Pressman BD, Tourje EJ, Thompson JR. An early sign of ischemic infarction: increased density in a cerebral artery. AJR Am J Roentgenol. 1987;149(3):583-6.

  79. Saur D, Kucinski T, Grzyska U, Eckert B, Eggers C, Niesen W, et al. Sensitivity and interrater agreement of CT and diffusion-weighted MR imaging in hyperacute stroke. AJNR Am J Neuroradiol. May 2003;24(5):878-85. [Medline].

  80. Schaefer PW, Hassankhani A, Putman C, Sorensen AG, Schwamm L, Koroshetz W, et al. Characterization and evolution of diffusion MR imaging abnormalities in stroke patients undergoing intra-arterial thrombolysis. AJNR Am J Neuroradiol. Jun-Jul 2004;25(6):951-7. [Medline].

  81. Schaefer PW, Roccatagliata L, Ledezma C, Hoh B, Schwamm LH, Koroshetz W, et al. First-pass quantitative CT perfusion identifies thresholds for salvageable penumbra in acute stroke patients treated with intra-arterial therapy. AJNR Am J Neuroradiol. Jan 2006;27(1):20-5. [Medline].

  82. Schramm P, Schellinger PD, Klotz E, Kallenberg K, Fiebach JB, Külkens S, et al. Comparison of perfusion computed tomography and computed tomography angiography source images with perfusion-weighted imaging and diffusion-weighted imaging in patients with acute stroke of less than 6 hours' duration. Stroke. Jul 2004;35(7):1652-8. [Medline].

  83. Schuierer G, Huk W. The unilateral hyperdense middle cerebral artery: an early CT-sign of embolism or thrombosis. Neuroradiology. 1988;30(2):120-2. [Medline].

  84. Shetty SK, Lev MH. CT perfusion in acute stroke. Neuroimaging Clin N Am. Aug 2005;15(3):481-501, ix. [Medline].

  85. Skriver EB, Olsen TS. Transient disappearance of cerebral infarcts on CT scan, the so-called fogging effect. Neuroradiology. 1981;22(2):61-5. [Medline].

  86. Smith TP, Enterline DS. Endovascular treatment of cerebral vasospasm. J Vasc Interv Radiol. May 2000;11(5):547-59. [Medline].

  87. Smith WS, Sung G, Saver J, Budzik R, Duckwiler G, Liebeskind DS, et al. Mechanical thrombectomy for acute ischemic stroke: final results of the Multi MERCI trial. Stroke. Apr 2008;39(4):1205-12. [Medline].

  88. Sorensen A, Copen W, Ostergaard L, Vainio PA, Aronen HJ. Hyperacute stroke: simultaneous measurement of relative cerebral blood volume, relative cerebral blood flow and mean tissue transit time. Radiology. 1999;210 (2):519-27.

  89. Sorensen AG, Buonanno FS, Gonzalez RG, Schwamm LH, Lev MH, Huang-Hellinger FR, et al. Hyperacute stroke: evaluation with combined multisection diffusion-weighted and hemodynamically weighted echo-planar MR imaging. Radiology. May 1996;199(2):391-401. [Medline].

  90. Sunshine JL, Tarr RW, Lanzieri CF, Landis DM, Selman WR, Lewin JS. Hyperacute stroke: ultrafast MR imaging to triage patients prior to therapy. Radiology. Aug 1999;212(2):325-32. [Medline].

  91. Tomura N, Uemura K, Inugami A, Fujita H, Higano S, Shishido F. Early CT finding in cerebral infarction: obscuration of the lentiform nucleus. Radiology. Aug 1988;168(2):463-7. [Medline].

  92. Torres-Mozqueda F, He J, Yeh IB, Schwamm LH, Lev MH, Schaefer PW, et al. An acute ischemic stroke classification instrument that includes CT or MR angiography: the Boston Acute Stroke Imaging Scale. AJNR Am J Neuroradiol. Jun 2008;29(6):1111-7. [Medline].

  93. Toyoda K, Ida M, Fukuda K. Fluid-attenuated inversion recovery intraarterial signal: an early sign of hyperacute cerebral ischemia. AJNR Am J Neuroradiol. Jun-Jul 2001;22(6):1021-9. [Medline].

  94. Truwit CL, Barkovich AJ, Gean-Marton A, Hibri N, Norman D. Loss of the insular ribbon: another early CT sign of acute middle cerebral artery infarction. Radiology. Sep 1990;176(3):801-6. [Medline].

  95. von Kummer R, Meyding-Lamadé U, Forsting M, Rosin L, Rieke K, Hacke W, et al. Sensitivity and prognostic value of early CT in occlusion of the middle cerebral artery trunk. AJNR Am J Neuroradiol. Jan 1994;15(1):9-15; discussion 16-8. [Medline].

  96. Wetzel SG. Cerebral arteries and veins. In: Rubin GD, Rofsky NM, eds. CT and MR Angiography: Comprehensive Vascular Assessment. Philadelphia, Pa: Lippincott Williams & Wilkins; 2009:381-441.

  97. Williams LS, Yilmaz EY, Lopez-Yunez AM. Retrospective assessment of initial stroke severity with the NIH Stroke Scale. Stroke. Apr 2000;31(4):858-62. [Medline].

  98. Wintermark M, Maeder P, Thiran JP, Schnyder P, Meuli R. Quantitative assessment of regional cerebral blood flows by perfusion CT studies at low injection rates: a critical review of the underlying theoretical models. Eur Radiol. 2001;11(7):1220-30. [Medline].

  99. Woodcock RJ Jr, Short J, Do HM, Jensen ME, Kallmes DF. Imaging of acute subarachnoid hemorrhage with a fluid-attenuated inversion recovery sequence in an animal model: comparison with non-contrast-enhanced CT. AJNR Am J Neuroradiol. Oct 2001;22(9):1698-703. [Medline].

  100. Zia E, Engström G, Svensson PJ, Norrving B, Pessah-Rasmussen H. Three-year survival and stroke recurrence rates in patients with primary intracerebral hemorrhage. Stroke. Nov 2009;40(11):3567-73. [Medline].

 
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Axial noncontrast computed tomography scan of the brain in a 60-year-old male with history of acute onset of left-sided weakness demonstrates 2 areas of intracerebral hemorrhage in the right lentiform nucleus with surrounding edema and effacement of the adjacent cortical sulci and right sylvian fissure. Mass effect is present upon the frontal horn of the right lateral ventricle with intraventricular extension of the hemorrhage.
Noncontrast computed tomography scan of the brain (left) demonstrates an acute hemorrhage in the left gangliocapsular region with surrounding white matter hypodensity consistent with vasogenic edema. T2-weighted axial magnetic resonance image (middle image) redemonstrates the hemorrhage with surrounding high-signal edema. The coronal gradient-echo image (right) demonstrates susceptibility related to the hematoma with markedly low signal adjacent the left caudate head. Gradient-echo images are highly sensitive for blood products.
Noncontrast computed tomography scan (left) obtained after a 75-year-old male was admitted for cerebrovascular accident demonstrates a large right middle cerebral artery distribution infarction with linear areas of developing hemorrhage. These become more confluent on day 2 of hospitalization (middle image), with increased mass effect and midline shift. There is massive hemorrhagic transformation by day 6 (right) with increased leftward midline shift and subfalcine herniation. Obstructive hydrocephalus is also noted with dilatation of the lateral ventricles, likely due to compression of the foramen of Monroe. Intraventricular hemorrhage is also noted layering in the left occipital horn. Larger infarctions are more likely to undergo hemorrhagic transformation and are one contraindication to thrombolytic therapy.
Noncontrast computed tomography (CT) scanning was performed emergently in a 71-year-old male who presented with acute onset of severe headache and underwent rapid neurologic deterioration requiring intubation. The noncontrast CT scan (left image) demonstrates diffuse, high-density subarachnoid hemorrhage in the basilar cisterns and both Sylvian fissures. There is diffuse loss of gray-white differentiation. The fluid-attenuated inversion-recovery (FLAIR) image (right) demonstrates high signal throughout the cortical sulci, basilar cisterns and in the dependent portions of the ventricles. FLAIR is highly sensitive to acute subarachnoid hemorrhage, owing to the suppression of high cerebrospinal fluid signal lending to greater conspicuity of subarachnoid hemorrhage compared with conventional magnetic resonance image sequences.
The patient above subsequently underwent a computed tomographic angiography examination and subsequent cerebral angiography. Multiple aneurysms were identified, including a 9-mm aneurysm at the junction of the anterior cerebral and posterior communicating arteries seen on this lateral view of an internal carotid artery injection. Balloon-assisted coil embolization was performed.
Lateral view of a selective injection of the left internal carotid artery demonstrates a microcatheter passing distal to the aneurysm neck. This lateral view from an angiogram performed during balloon-assisted coil embolization demonstrates significantly diminished filling of the aneurysm.
Lateral view of a cerebral angiogram illustrates the branches of the anterior cerebral artery (ACA) and Sylvian triangle. The pericallosal artery has been described to arise distal to the anterior communicating artery or distal to the origin of the callosomarginal branch of the ACA. The segmental anatomy of the ACA has been described as follows: the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery; A2 extends to the junction of the rostrum and genu of the corpus callosum; A3 extends into the bend of the genu of the corpus callosum; A4 and A5 extend posteriorly above the callosal body and superior portion of the splenium. The Sylvian triangle overlies the opercular branches of the middle cerebral artery, with the apex representing the Sylvian point.
Frontal projection from a right vertebral artery angiogram illustrates the posterior circulation. The vertebral arteries join to form the basilar artery. The posterior inferior cerebellar arteries (PICA) arise from the distal vertebral arteries. The anterior inferior cerebellar arteries (AICA) arise from the proximal basilar artery. The superior cerebellar arteries (SCA) arise distally from the basilar artery before its bifurcation into the posterior cerebral arteries.
Frontal view of a cerebral angiogram with selective injection of the left internal carotid artery illustrates the anterior circulation. The anterior cerebral artery consists of the A1 segment proximal to the anterior communicating artery with the A2 segment distal to it. The middle cerebral artery can be divided into 4 segments: the M1 (horizontal segment) extends to the limen insulae and gives off lateral lenticulostriate branches, the M2 (insular segment), M3 (opercular branches), and M4 (distal cortical branches on the lateral hemispheric convexities).
Frontal view from a cerebral angiogram in a 41-year-male who presented 7 days before with subarachnoid hemorrhage from a ruptured anterior communicating artery (ACA) aneurysm treated with surgical clipping. There is significant narrowing of the proximal left ACA, left M1 segment and left supraclinoid internal carotid artery indicating vasospasm.
Angiographic view in the same patient as above (image on left) with superimposed road map image to demonstrate placement of a wire across the left M1 segment and balloon angioplasty. The left proximal anterior communicating artery (ACA) and supraclinoid internal carotid artery (ICA) were also angioplastied and intraarterial verapamil was administered. Follow-up image on the right after treatment demonstrates resolution of the left M1 segment and distal ICA, which are now widely patent. Residual narrowing is seen in the left proximal ACA.
A cerebral angiogram was performed in a 57-year-old male with a family history of subarachnoid hemorrhage and who was found on previous imaging to have a left distal internal carotid artery (ICA) aneurysm. The lateral projection from this angiogram demonstrates a narrow-necked aneurysm arising off the posterior aspect of the distal supraclinoid left ICA, with an additional nipplelike projection off the inferior aspect of the dome of the aneurysm. There is also a mild, lobulated dilatation of the cavernous left ICA.
Follow-up cerebral angiogram in the same patient as above following coil embolization. Multiple coils were placed with sequential occlusion of the aneurysm, including the nipple at its inferior aspect. A small amount of residual filling is noted at the proximal neck of the aneurysm, which may thrombose over time.
The supratentorial vascular territories of the major cerebral arteries are demonstrated superimposed on axial (left) and coronal (right) T2-weighted images through the level of the basal ganglia and thalami. The middle cerebral artery (red) supplies the lateral aspects of the hemispheres, including the lateral frontal, parietal, and anterior temporal lobes, insula, and basal ganglia. The anterior cerebral artery (blue) supplies the medial frontal and parietal lobes. The posterior cerebral artery (green) supplies the thalami and occipital and inferior temporal lobes. The anterior choroidal artery (yellow) supplies the posterior limb of the internal capsule and part of the hippocampus extending to the anterior and superior surface of the occipital horn of the lateral ventricle.
 
 
 
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