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Hemorrhagic Stroke Medication

  • Author: David S Liebeskind, MD; Chief Editor: Robert E O'Connor, MD, MPH  more...
 
Updated: Jan 08, 2015
 

Medication Summary

Medications used in the treatment of acute stroke include anticonvulsants such as diazepam, to prevent seizure recurrence; antihypertensive agents such as labetalol, to reduce blood pressure (BP) and other risk factors for heart disease; and osmotic diuretics such as mannitol, to decrease intracranial pressure in the subarachnoid space.

As previously mentioned, the treatment and management of patients with acute intracerebral hemorrhage depends on the cause and severity of the bleeding. However, there is currently no effective targeted therapy for hemorrhagic stroke.

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Anticonvulsants, Other

Class Summary

Benzodiazepines are commonly used to control seizure activity and recurrence. Agents such as lorazepam and diazepam are often used acutely, in combination with either phenytoin or fosphenytoin loading.

Diazepam (Diastat, Diazemuls, Valium)

 

Diazepam controls active seizures by modulating the postsynaptic effects of gamma-aminobutyric acid type A (GABA-A) transmission, resulting in an increase in presynaptic inhibition. It appears to act on part of the limbic system, the thalamus, and hypothalamus, to induce a calming effect. It also acts as an effective adjunct for the relief of skeletal muscle spasm caused by upper motor neuron disorders.

Diazepam should be augmented by longer-acting anticonvulsants, such as phenytoin or phenobarbital, because it rapidly distributes to other body fat stores.

Lorazepam (Ativan)

 

Lorazepam is a short-acting acting benzodiazepine with a moderately long half-life. It has become the drug of choice in many centers for treating active seizures.

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Anticonvulsants, Hydantoins

Class Summary

Anticonvulsants prevent seizure recurrence and terminate clinical and electrical seizure activity. These agents are used routinely to avoid seizures that may be induced by cortical damage.

According to the American Heart Association/American Stroke Association (AHA/ASA) 2010 guidelines for management of spontaneous intracranial hemorrhage, treatment with antiepileptic drugs is indicated for those patients with clinical seizures or with electroencephalographic (EEG) seizure activity accompanied by a change in mental status.[3] Prophylactic use of anticonvulsants is controversial and should be used judiciously, if at all.

Phenytoin (Dilantin)

 

Phenytoin may act in the motor cortex, where it may inhibit spread of seizure activity, as well as in the brainstem centers responsible for the tonic phase of grand mal seizures. All doses should be individualized. The antiepileptic effect of phenytoin is not immediate. Concomitant administration of an intravenous benzodiazepine will usually be necessary to control status epilepticus. In addition, a larger dose before retiring should be administered if the dose cannot be divided equally.

Fosphenytoin (Cerebyx)

 

Fosphenytoin is a diphosphate ester salt of phenytoin that acts as water-soluble prodrug of phenytoin. Phenytoin, in turn, stabilizes neuronal membranes and decreases seizure activity.

To avoid the need to perform molecular-weight-based adjustments when converting between fosphenytoin and phenytoin sodium doses, express the dose as phenytoin sodium equivalents. Although fosphenytoin can be administered intravenously or intramuscularly, the intravenous route is the route of choice and should be used in emergency situations.

The antiepileptic effect of phenytoin, whether given as fosphenytoin or parenteral phenytoin, is not immediate. Concomitant administration of an intravenous benzodiazepine will usually be necessary to control status epilepticus.

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Beta Blockers, Alpha Activity

Class Summary

Beta blockers are used to reduce BP and risk factors for heart disease. They are first-line agents for acute BP reduction in hemorrhagic stroke, but they are second-line agents for stroke prevention. Selective beta blockers obstruct access to beta-1 receptors more than they do to beta-2 receptors; nonselective beta blockers obstruct access to beta-1 and beta-2 receptors.

Labetalol (Trandate)

 

Labetalol blocks beta1-, alpha-, and beta2-adrenergic receptor sites to decrease BP. It is administered as a 5-20 mg intravenous bolus over 2 minutes, then as a continuous infusion at 2 mg/min (not to exceed 300 mg/dose).

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Beta Blockers, Beta-1 Selective

Class Summary

Beta blockers are used to reduce BP and risk factors for heart disease. They are first-line agents for acute BP reduction in hemorrhagic stroke, but they are second-line agents for stroke prevention. Selective beta blockers obstruct access to beta-1 receptors more than they do to beta-2 receptors; nonselective beta blockers obstruct access to beta-1 and beta-2 receptors.

Esmolol (Brevibloc)

 

Esmolol is an ultra-short-acting agent that selectively blocks beta-1 receptors with little or no effect on beta-2 receptor types. This drug is particularly useful in patients with elevated arterial pressure, especially if surgery is planned, and its short half-life of 8 minutes allows for titration and quick discontinuation, if necessary.

Esmolol is also useful in patients at risk for experiencing complications from beta blockade, particularly those with reactive airway disease, mild to moderate left-ventricular dysfunction, and/or peripheral vascular disease.

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Vasodilators

Class Summary

Vasodilators lower BP through direct vasodilation and relaxation of the vascular smooth muscle. They are used more for BP lowering in refractory situations.

Hydralazine (Apresoline)

 

Hydralazine decreases systemic resistance through direct vasodilation of arterioles and is used to treat hypertensive emergencies. The use of a vasodilator will reduce the stroke volume ratio (SVR), which, in turn, may allow forward flow, improving cardiac output. Hydralazine is typically not a first-line agent, because of its side-effect profile.

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Calcium Channel Blockers

Class Summary

Calcium channel blockers are used to lower BP by relaxing the blood vessels and increasing the amount of blood and oxygen that is delivered to the heart, while reducing the heart’s workload. In acute situations, intravenous calcium channel blockers are frequently used to control BP. These are first-line agents for long-term BP control in stroke patients (along with thiazides, ACEIs, and angiotensin receptor blockers [ARBs]).

Nicardipine (Cardene, Cardene IV, Cardene SR)

 

Nicardipine relaxes coronary smooth muscle and produces coronary vasodilation, which, in turn, improves myocardial oxygen delivery and reduces myocardial oxygen consumption.

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Angiotensin-converting Enzyme Inhibitors

Class Summary

ACEIs prevent the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion. These are first-line agents for emergent and long-term BP control in hemorrhagic stroke patients.

Enalapril (Vasotec)

 

Enalapril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion. It helps to control BP and proteinuria.

Ramipril (Altace)

 

Ramipril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in increased levels of plasma renin and a reduction in aldosterone secretion.

Lisinopril (Zestril)

 

Lisinopril prevents the conversion of angiotensin I to angiotensin II, a potent vasoconstrictor, resulting in lower aldosterone secretion.

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Angiotensin Receptor Blockers

Class Summary

ARBs may be used as an alternative to ACEIs in patients who develop adverse effects, such as a persistent cough.

Losartan (Cozaar)

 

Losartan blocks the vasoconstrictor and aldosterone-secreting effects of angiotensin II. It may induce a more complete inhibition of the renin-angiotensin system than ACEIs do. In addition, it does not affect the response to bradykinin and is less likely to be associated with cough and angioedema.

Candesartan (Atacand)

 

Candesartan blocks vasoconstriction and the aldosterone-secreting effects of angiotensin II. It may induce a more complete inhibition of the renin-angiotensin system than ACEIs do. In addition, it does not affect response to bradykinin and is less likely to be associated with cough and angioedema.

Valsartan (Diovan)

 

Valsartan produces direct antagonism of angiotensin II receptors. It displaces angiotensin II from the AT1 receptor and may lower BP by antagonizing AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake, and hypertrophic responses.

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Diuretics, Thiazide

Class Summary

Thiazide diuretics inhibit sodium and chloride reabsorption in the distal tubules of the kidney, resulting in increased urinary excretion of sodium and water.

Hydrochlorothiazide (Microzide)

 

Hydrochlorothiazide inhibits the reabsorption of sodium in distal tubules, causing increased excretion of sodium and water, as well as potassium and hydrogen ions.

Chlorthalidone (Diuril)

 

Chlorthalidone inhibits the reabsorption of sodium in distal tubules, causing increased excretion of sodium and water, as well as potassium and hydrogen ions.

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Diuretics, Osmotic Agents

Class Summary

Osmotic diuretics, such as mannitol, may be used to decrease intracranial pressure in the subarachnoid space. As water diffuses from the subarachnoid space into the intravascular compartment, pressure in the subarachnoid compartment may decrease.

Mannitol (Osmitrol)

 

Mannitol reduces cerebral edema with the help of osmotic forces. It also decreases blood viscosity, resulting in reflex vasoconstriction and lowering of intracranial pressure.

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Analgesics, Other

Class Summary

Because hyperthermia may exacerbate neurologic injury, these agents may be given to reduce fever and relieve pain.

Acetaminophen (Tylenol, FeverAll, Aspirin Free Anacin)

 

Acetaminophen reduces fever, maintains normothermia, and reduces headache.

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Hemostatics

Class Summary

Vitamin K is used to promote the formation of clotting factors. Phytonadione can overcome the competitive block produced by warfarin and other related anticoagulants. A fresh frozen plasma (FFP) infusion followed by oral vitamin K should be given without delay in the emergency department to manage warfarin-related intracranial hemorrhage.

Vitamin K1 (phytonadione; vitamin K, Mephyton, AquaMephyton)

 

Phytonadione can overcome the competitive block produced by warfarin and other related anticoagulants. Vitamin K3 (menadione) is not effective for this purpose. There is a delay of the clinical effect for several hours while liver synthesis of the clotting factors is initiated and plasma levels of clotting factors II, VII, IX, and X are gradually restored.

Phytonadione should not be administered prophylactically and is used only if evidence of anticoagulation exists. The required dose varies with the clinical situation, including the dose and duration of action of the anticoagulant ingested. Intravenous phytonadione is recommended for life-threatening bleeding, including intracerebral hemorrhage complicating warfarin therapy, although it carries a small risk of anaphylaxis.

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Blood Components

Class Summary

These agents are indicated for the correction of abnormal hemostatic parameters.

Fresh frozen plasma

 

Plasma, the fluid component of blood, contains the blood's soluble clotting factors. FFP is created by separating plasma from a unit of blood and freezing it for use in patients with blood-product deficiencies.

Platelets

 

Platelets are fragments of large bone marrow cells found in the blood that play a role in blood coagulation. A single random donor unit of platelets per 10 kg is administered in adults when the platelet count drops below 50,000/µL.

Prothrombin complex concentrate (Bebulin VH, Profilnine SD)

 

Prothrombin complex concentrate (PCC) is a mixture of vitamin K-dependent clotting factors found in normal plasma that replaces deficient clotting factors, provides an increase in plasma levels of factor IX, and can temporarily correct a coagulation defect in patients with factor IX deficiency. PCC is usually reserved for situations in which volume overload is a concern.

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Antidotes, Other

Class Summary

Protamine is used to neutralize the effects of anticoagulants.

Protamine

 

Protamine sulfate forms a salt with heparin and neutralizes its effects. The dosage administered is dependent on the amount of time that has passed since heparin was given.

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Vasopressin-Related

Class Summary

These agents improve bleeding time and hemostasis.

Desmopressin acetate (DDAVP, Stimate)

 

Desmopressin releases von Willebrand protein from endothelial cells. It improves bleeding time and hemostasis in patients with mild and moderate von Willebrand disease without abnormal molecular forms of von Willebrand protein. It is effective in uremic bleeding. Tachyphylaxis usually develops after 48 hours, but the drug can be effective again after several days.

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Contributor Information and Disclosures
Author

David S Liebeskind, MD 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, Stroke Council of the American Heart Association, American Heart Association, American Medical Association, American Society of Neuroimaging, American Society of Neuroradiology, National Stroke Association

Disclosure: Nothing to disclose.

Chief Editor

Robert E O'Connor, MD, MPH Professor and Chair, Department of Emergency Medicine, University of Virginia Health System

Robert E O'Connor, MD, MPH is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American Association for Physician Leadership, American Heart Association, Medical Society of Delaware, Society for Academic Emergency Medicine, Wilderness Medical Society, American Medical Association, National Association of EMS Physicians

Disclosure: Nothing to disclose.

Acknowledgements

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.

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.

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.

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

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

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

References
  1. Flint AC, Conell C, Rao VA, et al. Effect of statin use during hospitalization for intracerebral hemorrhage on mortality and discharge disposition. JAMA Neurol. 2014 Sep 22. [Medline]. [Full Text].

  2. Anderson P. In-hospital statins linked to better outcome in ICH. Medscape Medical News. September 22, 2014. [Full Text].

  3. [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. 2010 Sep. 41(9):2108-29. [Medline].

  4. 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. 2003 Jan. 2(1):43-53. [Medline].

  5. [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. 2007 Oct 16. 116(16):e391-413. [Medline].

  6. 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. 2011 Aug. 58(2):156-63. [Medline].

  7. 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. 2005 May. 26(5):1050-5. [Medline].

  8. Roger VL, Go AS, Lloyd-Jones DM, Benjamin EJ, Berry JD, Borden WB, et al. Heart disease and stroke statistics--2012 update: a report from the American Heart Association. Circulation. 2012 Jan 3. 125(1):e2-e220. [Medline].

  9. 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. 1993 Jan. 24(1):35-41. [Medline].

  10. 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. 2001 Aug. 32(8):1732-8. [Medline].

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

  12. 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. 2005 Oct. 26(9):2207-12. [Medline].

  13. 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. 2002 Mar. 33(3):735-42. [Medline].

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

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

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

  17. International Warfarin Pharmacogenetics Consortium, Klein TE, Altman RB, et al. Estimation of the warfarin dose with clinical and pharmacogenetic data. N Engl J Med. 2009 Feb 19. 360(8):753-64. [Medline]. [Full Text].

  18. Chapman AB, Rubinstein D, Hughes R, Stears JC, Earnest MP, Johnson AM, et al. Intracranial aneurysms in autosomal dominant polycystic kidney disease. N Engl J Med. 1992 Sep 24. 327(13):916-20. [Medline].

  19. Regalado E, Medrek S, Tran-Fadulu V, et al. Autosomal dominant inheritance of a predisposition to thoracic aortic aneurysms and dissections and intracranial saccular aneurysms. Am J Med Genet A. 2011 Sep. 155A(9):2125-30. [Medline].

  20. 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. 2001 Apr. 11(2):184-8. [Medline].

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

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

  23. 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. 2004 Sep. 126(3 Suppl):483S-512S. [Medline].

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

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

  26. Flaherty ML, Woo D, Haverbusch M, Sekar P, Khoury J, Sauerbeck L, et al. Racial variations in location and risk of intracerebral hemorrhage. Stroke. 2005 May. 36(5):934-7. [Medline].

  27. Global Burden of Stroke. The Atlas of Heart Disease and Stroke. MacKay J, Mensah GA. World Health Organization. [Full Text].

  28. Sacco S, Marini C, Toni D, Olivieri L, Carolei A. Incidence and 10-year survival of intracerebral hemorrhage in a population-based registry. Stroke. 2009. 40:394–399.

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

  30. Hemphill JC 3rd, Bonovich DC, Besmertis L, Manley GT, Johnston SC. The ICH score: a simple, reliable grading scale for intracerebral hemorrhage. Stroke. 2001 Apr. 32(4):891-7. [Medline]. [Full Text].

  31. Zhu XL, Chan MS, Poon WS. Spontaneous intracranial hemorrhage: which patients need diagnostic cerebral angiography? A prospective study of 206 cases and review of the literature. Stroke. 1997 Jul. 28(7):1406-9. [Medline].

  32. Hughes S. BP Control More Important in ICH Patients on Antithrombotics. Medscape Medical News. May 15 2014. Available at http://www.medscape.com/viewarticle/825206. Accessed: May 20 2014.

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

  34. 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. 2003 May 13. 60(9):1441-6. [Medline].

  35. Connolly ES Jr, Rabinstein AA, Carhuapoma JR, Derdeyn CP, Dion J, Higashida RT, et al. Guidelines for the management of aneurysmal subarachnoid hemorrhage: a guideline for healthcare professionals from the American Heart Association/american Stroke Association. Stroke. 2012 Jun. 43(6):1711-37. [Medline]. [Full Text].

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

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

  38. 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. 2011 Apr 19. 154(8):529-40. [Medline].

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

  40. 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. 2008 May 15. 358(20):2127-37. [Medline].

  41. 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. 2010 Jan. 41(1):48-53. [Medline].

  42. Sarode R, Matevosyan K, Bhagat R, Rutherford C, Madden C, Beshay JE. Rapid warfarin reversal: a 3-factor prothrombin complex concentrate and recombinant factor VIIa cocktail for intracerebral hemorrhage. J Neurosurg. 2012 Mar. 116(3):491-7. [Medline].

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

  44. 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. 2006 Jun. 37(6):1465-70. [Medline].

  45. Steiner T, Freiberger A, Griebe M, Hüsing J, Ivandic B, Kollmar R, et al. International normalised ratio normalisation in patients with coumarin-related intracranial haemorrhages--the INCH trial: a randomised controlled multicentre trial to compare safety and preliminary efficacy of fresh frozen plasma and prothrombin complex--study design and protocol. Int J Stroke. 2011 Jun. 6(3):271-7. [Medline].

  46. 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. 2005 Jan 29-Feb 4. 365(9457):387-97. [Medline].

  47. Gregson BA, Broderick JP, Auer LM, Batjer H, Chen XC, Juvela S, et al. Individual patient data subgroup meta-analysis of surgery for spontaneous supratentorial intracerebral hemorrhage. Stroke. 2012 Jun. 43(6):1496-504. [Medline]. [Full Text].

  48. Steiner T, Vincent C, Morris S, Davis S, Vallejo-Torres L, Christensen MC. Neurosurgical outcomes after intracerebral hemorrhage: results of the Factor Seven for Acute Hemorrhagic Stroke Trial (FAST). J Stroke Cerebrovasc Dis. 2011 Jul-Aug. 20(4):287-94. [Medline].

  49. Mendelow AD, Gregson BA, Mitchell PM, Murray GD, Rowan EN, Gholkar AR. Surgical trial in lobar intracerebral haemorrhage (STICH II) protocol. Trials. 2011 May 17. 12:124. [Medline]. [Full Text].

  50. 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. 2005 Sep 3-9. 366(9488):809-17. [Medline].

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

  52. McDougall CG, Spetzler RF, Zabramski JM, Partovi S, Hills NK, Nakaji P, et al. The Barrow Ruptured Aneurysm Trial. J Neurosurg. 2012 Jan. 116(1):135-44. [Medline].

  53. Lanzino G. The Barrow Ruptured Aneurysm Trial. J Neurosurg. 2012 Jan. 116(1):133-4; discussion 134. [Medline].

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

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

  56. [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. 2011 Feb. 42(2):517-84. [Medline]. [Full Text].

  57. McKinney JS, Kostis WJ. Statin therapy and the risk of intracerebral hemorrhage: a meta-analysis of 31 randomized controlled trials. Stroke. 2012 Aug. 43(8):2149-56. [Medline].

  58. 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. 2000 Jan 20. 342(3):145-53. [Medline].

  59. 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. 2001 Sep 29. 358(9287):1033-41. [Medline].

  60. 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. 2002 Dec 18. 288(23):2981-97. [Medline].

  61. 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. 2002 Mar 23. 359(9311):995-1003. [Medline].

  62. 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. 2005 Jun. 36(6):1218-26. [Medline].

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

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

  65. 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. 2009 Feb. 36(2):294-301. [Medline].

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

  67. 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. 2003 Jun-Jul. 24(6):1117-22. [Medline].

  68. 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. 2008 Aug. 29(7):1409-13. [Medline].

  69. 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. 1989 Nov-Dec. 10(6):1215-22. [Medline].

  70. 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. 1989 Sep. 236(6):340-2. [Medline].

  71. 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. 1989 Jul. 20(7):864-70. [Medline].

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

  73. 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. 1998 Sep. 171(3):791-5. [Medline].

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

  75. Chandra VR, Pandav R, Laxminarayan R, et al. Neurologic Disorders. 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.

  76. 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. 2009 May. 251(2):493-502. [Medline].

  77. 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. 1997 Jul. 11(4):374-7. [Medline].

  78. 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.

  79. 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. 2002 Jan. 222(1):227-36. [Medline].

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

  81. 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].

  82. 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. 1999 Jan. 210(1):155-62. [Medline].

  83. 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. 2003 Nov. 229(2):340-6. [Medline].

  84. 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. 2000 Jan. 214(1):247-52. [Medline].

  85. 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. 2001 Jan. 22(1):103-11. [Medline].

  86. 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. 2002 Jul. 33(7):1786-91. [Medline].

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

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

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

  90. 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. 2010 Apr. 74(1):104-9. [Medline].

  91. 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. 1992 Jan. 42(1):235-40. [Medline].

  92. 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. 1999 Oct. 213(1):141-9. [Medline].

  93. 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].

  94. 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. 1997 Jun. 39(6):406-10. [Medline].

  95. 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. 2003 Oct 28. 61(8):1047-51. [Medline].

  96. 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. 2000 Aug. 42(8):602-7. [Medline].

  97. 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. 1985 Dec. 5(4):600-8. [Medline].

  98. 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.

  99. 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. 2003 May. 24(5):878-85. [Medline].

  100. 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. 2004 Jun-Jul. 25(6):951-7. [Medline].

  101. 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. 2006 Jan. 27(1):20-5. [Medline].

  102. 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. 2004 Jul. 35(7):1652-8. [Medline].

  103. 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].

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

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

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

  107. 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. 2008 Apr. 39(4):1205-12. [Medline].

  108. 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.

  109. 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. 1996 May. 199(2):391-401. [Medline].

  110. Steiner T, Freiberger A, Griebe M, Hüsing J, Ivandic B, Kollmar R, et al. International normalised ratio normalisation in patients with coumarin-related intracranial haemorrhages--the INCH trial: a randomised controlled multicentre trial to compare safety and preliminary efficacy of fresh frozen plasma and prothrombin complex--study design and protocol. Int J Stroke. 2011 Jun. 6(3):271-7. [Medline].

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

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

  113. 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. 2008 Jun. 29(6):1111-7. [Medline].

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

  115. 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. 1990 Sep. 176(3):801-6. [Medline].

  116. 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. 1994 Jan. 15(1):9-15; discussion 16-8. [Medline].

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

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

  119. 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].

  120. Wong GK, Siu DY, Ahuja AT, King AD, Yu SC, Zhu XL, et al. Comparisons of DSA and MR angiography with digital subtraction angiography in 151 patients with subacute spontaneous intracerebral hemorrhage. J Clin Neurosci. 2010 May. 17(5):601-5. [Medline].

  121. 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. 2001 Oct. 22(9):1698-703. [Medline].

  122. 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. 2009 Nov. 40(11):3567-73. [Medline].

 
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Axial noncontrast computed tomography scan of the brain of a 60-year-old man with a history of acute onset of left-sided weakness. Two areas of intracerebral hemorrhage are seen 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 imaging scan (middle image) again demonstrates 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 in a 75-year-old man who was admitted for stroke 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 man 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 and in the basilar cisterns, as well as in the dependent portions of the ventricles. FLAIR is highly sensitive to acute subarachnoid hemorrhage; the suppression of high cerebrospinal fluid signal aids in making subarachnoid hemorrhage more conspicuous than do conventional magnetic resonance imaging sequences.
Computed tomographic angiography examination and subsequent cerebral angiography were performed in 71-year-old man who presented with acute onset of severe headache and underwent rapid neurologic deterioration. 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 as arising 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: (1) the A1 segment extends from the internal carotid artery (ICA) bifurcation to the anterior communicating artery, (2) A2 extends to the junction of the rostrum and genu of the corpus callosum, (3) A3 extends into the bend of the genu of the corpus callosum, and (4) 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-man who presented 7 days earlier with subarachnoid hemorrhage from a ruptured anterior communicating artery (ACA) aneurysm (which was 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 a 41-year-man who presented 7 days earlier with subarachnoid hemorrhage from a ruptured anterior communicating artery (ACA) aneurysm (which was treated with surgical clipping). Superimposed road map image demonstrates placement of a wire across the left M1 segment and balloon angioplasty. The left proximal ACA and supraclinoid internal carotid artery (ICA) were also angioplastied, and intra-arterial 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 man 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 after coil embolization in a 57-year-old man with a left distal internal carotid artery aneurysm. 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.
 
 
 
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