Hemorrhagic Stroke in Emergency Medicine Treatment & Management

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

Approach Considerations

The treatment and management of patients with acute stroke depends on the cause and severity of the bleeding. Basic life support as well as control of bleeding, seizures, blood pressure (BP), and intracranial pressure are critical.

For more information, see Acute Stroke Management.

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Medical Treatment

Medications used in the treatment of acute stroke include anticonvulsants to prevent seizure recurrence, antihypertensive agents to reduce BP and other risk factors of heart disease, and osmotic diuretics to decrease intracranial pressure in the subarachnoid space.

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Stabilization of vital signs

Perform endotracheal intubation for patients with a decreased level of consciousness and poor airway protection. Intubate and hyperventilate if intracranial pressure is increased, and initiate administration of mannitol for further control. Rapidly stabilize vital signs, and simultaneously acquire emergent CT scan.

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Management of seizures

Early seizure activity occurs in 4-28% of patients with intracerebral hemorrhage, and these seizures are often nonconvulsive seizures.[23, 21] Seizure activity should be rapidly controlled with a benzodiazepine, such as lorazepam or diazepam, accompanied by either phenytoin or fosphenytoin loading. Prophylactic anticonvulsant therapy is recommended in patients with lobar hemorrhages to reduce the risk of early seizures.[1, 23] However, the use of prophylactic anticonvulsant therapy in all cases of intracerebral hemorrhage is controversial, as no prospective controlled trials have demonstrated a clear benefit.

According to the AHA/ASA 2010 guidelines for management of spontaneous ICH, patients with a change in mental status and whose EEG shows electrographic seizures should receive antiepileptic drugs.[22]

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Blood pressure control

No controlled studies define optimum BP levels, but greatly elevated BP is thought to lead to rebleeding and hematoma expansion. Patients who have had a stroke may lose their cerebral autoregulation of cerebral perfusion pressure. Rapid or aggressive BP lowering may compromise cerebral perfusion. Nicardipine, labetalol, esmolol, and hydralazine are agents that may be used when necessary for BP control. Avoid nitroprusside because it may raise intracranial pressure.

The American Heart Association guidelines for treating elevated BP are as follows[1] :

  • If systolic BP is >200 mm Hg or mean arterial pressure (MAP) is >150 mm Hg, then consider aggressive reduction of BP with continuous IV infusion with frequent BP (every 5 min) checks.
  • If systolic BP is >180 mm Hg or MAP is >130 mm Hg and there is evidence or suspicion of elevated intracranial pressure, then consider monitoring of intracranial pressure and reducing BP using intermittent or continuous IV medications to maintain cerebral perfusion pressure >60-80 mm Hg.
  • If systolic BP is >180 or MAP is >130 mm Hg and there is NOT evidence or suspicion of elevated intracranial pressure, then consider modest reduction of BP (target MAP of 110 mm Hg or target BP of 160/90 mm Hg) with BP checks every 15 minutes.

One prospective study found a hazard ratio of 1.89 for the risk of poor outcome for each 10% decrease in systolic BP in the first 24 hours of an acute stroke.[24] Another study found that the use of calcium channel blockers acutely lowered diastolic BP and was associated with worse outcomes.[25]

Current recommendations include avoiding more than 10% reduction of BP within the first 24 hours, unless values exceed certain thresholds. These values, which are not based on any specific randomized studies, are 220 mm Hg systolic (some recommend 200 mm Hg systolic) and 115 mm Hg diastolic. Suggested agents for use in the acute setting are beta-blockers (eg, labetalol) and angiotensin-converting enzyme inhibitors (ACEIs) (eg, enalapril). For more refractory hypertension, agents such as nicardipine, nitroprusside, and hydralazine are used.

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Medical treatment of increased intracranial pressure

Elevated intracranial pressure may result from the hematoma itself, surrounding edema, or both. The frequency of increased intracranial pressure in patients with intracerebral hemorrhage is not known.

Elevate the head of the bed to 30 degrees. This improves jugular venous outflow and lowers intracranial pressure. The head should be midline and not turned to the side. Provide analgesia and sedation as needed.

More aggressive therapies such as osmotic therapy (mannitol, hypertonic saline), barbiturate anesthesia, and neuromuscular blockage generally require concomitant monitoring of intracranial pressure and BP with an intracranial pressure monitor to maintain adequate cerebral perfusion pressure (CPP) greater than 70 mm Hg. A randomized controlled study of mannitol in intracerebral hemorrhage failed to demonstrate any difference in disability or death at 3 months.[26]

Hyperventilation (partial pressure of carbon dioxide [PaCO2] of 25 to 30-35 mm Hg) is not recommended, because its effect is transient, it decreases CBF, and it may result in rebound elevated intracranial pressure.[1] Glucocorticoids are not effective and result in higher rates of complications with poorer outcomes.

Antacids are used to prevent gastric ulcers associated with intracerebral hemorrhage.

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Ventriculostomy

Ventriculostomy (CSF drainage by intraventricular catheter drainage) is often used in the setting of obstructive hydrocephalus, which is a common complication of thalamic hemorrhage with third ventricle compression and of cerebellar hemorrhage with fourth ventricle compression. Ventriculostomies are associated with high rates of complications, including bacterial meningitis.

Endoscopic hematoma evacuation

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

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Hemostatic therapy

Much interest has been generated to determine if treatment with hemostatic therapy to stop ongoing hemorrhage or prevent hematoma expansion may be effective.

A preliminary study of treatment with recombinant factor VIIa (rFVIIa) demonstrated reduced mortality and improved functional outcomes. Unfortunately, the results of the larger randomized trial revealed no overall benefit of treatment. Hemostatic therapy with rFVIIa reduced growth of the hematoma but did not improve survival or functional outcome.[27]

Diringer et al found that higher doses of rFVIIa in a high-risk population are associated with a small increased risk of what are usually minor cardiac events.[28] Their study randomized the use of 20 or 80 mcg/kg rFVIIa or placebo in 841 patients who presented less than 3 hours after spontaneous intracerebral hemorrhage.[28] Although venous events were similar among the groups, arterial events were associated with receiving 80 mcg/kg dose of rFVIIa, cardiac or cerebral ischemia at presentation , advanced age, or antiplatelet use.[28] The investigators concluded that additional research is needed to measure the benefit of hemorrhage control in patients with cerebral hemorrhage with the risk for arterial thromboembolic events.

Continued findings fail to offer support for off-label use of rFVIIa.[29, 30, 31]

Currently, no effective targeted therapy for hemorrhagic stroke exists. Further studies are necessary to develop other potential treatment options.

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Treatment of anticoagulation-associated intracranial hemorrhage

Patients on warfarin have an increased incidence of hemorrhagic stroke. Morbidity and mortality for warfarin-associated bleeding is high: over one half of patients die within 30 days. Most episodes occur with a therapeutic international normalized ratio (INR), but overanticoagulation is further associated with an increased risk of bleeding. Reversal of warfarin anticoagulation is a true medical emergency and must be accomplished as quickly as possible to prevent further hematoma expansion.

Warfarin reversal options include IV vitamin K, fresh frozen plasma (FFP), prothrombin complex concentrates (PCC), and rFVIIa. Because vitamin K requires more than 6 hours to normalize the INR, it should be administered with either FFP or PCC. FFP needs to be given 15-20 mL/kg and therefore requires a large volume infusion. PCC contains high levels of vitamin K-dependent cofactors, with a smaller volume of infusion than FFP, resulting in more rapid administration. If available, PCC is preferable over FFP as a reversal agent.[32, 33] Based upon the available medical evidence, the use of FVIIa is currently not recommended over other agents.

Patients on heparin (either unfractionated or low molecular weight heparin [LMWH]) who develop a hemorrhagic stroke should immediately have anticoagulation reversed with protamine.[1] The dose of protamine is dependent upon the dose of heparin that was given and the time elapsed since that dose.

For more information, see the article on Reperfusion Injury in Stroke.

The 2010 AHA/ASA guideline for management of spontaneous ICH recommends factor replacement therapy for patients with spontaneous ICH and a severe coagulation factor deficiency.[22]

Reversal of antiplatelet therapy and platelet dysfunction

Patients on antiplatelet medications including aspirin, aspirin/dipyridamole (Aggrenox), and clopidogrel should be given desmopressin (DDAVP) and platelet transfusion. Patients with renal failure and platelet dysfunction may also benefit from the administration of desmopressin (DDAVP).

The 2010 AHA/ASA guideline for management of spontaneous ICH recommends platelet therapy for patients with spontaneous ICH and severe thrombocytopenia.[22]

Management of glucose

The 2010 AHA/ASA guideline for spontaneous ICH states that glucose levels should be monitored, with normoglycemia recommended.[22]

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Surgical Intervention

Craniotomy and clot evacuation

A potential treatment of hemorrhagic stroke is surgical evacuation of the hematoma. The role of surgical treatment for supratentorial intracranial hemorrhage remains controversial. Outcomes in published studies are conflicting. A published meta-analysis of studies suggested some promise for early surgical intervention. However, one study comparing early surgery versus initial conservative treatment failed to demonstrate a benefit with surgery.[34]

Surgical intervention for cerebellar hematoma has been shown to improve outcome. It can be lifesaving in the prevention of brainstem compression.

Endovascular treatment of aneurysms

Endovascular therapy using coil embolization has been increasingly used in recent years with great success as an alternative to surgical clipping (see the following images), although controversy still exists over which treatment is ultimately superior.

A cerebral angiogram was performed in a 57-year-olA 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 aFollow-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 International Subarachnoid Aneurysm Trial (ISAT) of neurosurgical clipping versus endovascular coiling reported that independent survival was higher at 1 year with endovascular coiling and that the survival benefit continued for at least 7 years.[35] This randomized, multicenter trial was conducted mainly in the United Kingdom and Europe and was the largest of its type, with 2143 patients. The investigators also noted that the small risk of late rebleeding found in both groups was higher in the endovascular coiling group, reconfirming the higher long-term anatomic cure rate of surgery.[35, 36]

Endovascular treatment of aneurysms may be favored over surgical clipping when the aneurysm is in a location that is difficult to access surgically, such as cavernous ICA or basilar terminus; when the aneurysms are small-necked and located in the posterior fossa; when the patients are elderly; and when the patients have a poor clinical grade.[37]

Factors mitigating against endovascular treatment include wide-based aneurysms or those without an identifiable neck; aneurysms with a vessel extending off the aneurysm dome; and patients with severely atherosclerotic or tortuous vessels that limit the endovascular approach.

Vasospasm may be treated with intra-arterial pharmaceutical agents, such as verapamil or nicardipine, or with balloon angioplasty for opening larger vessels (see the images below). The combination of the 2 treatments appears to provide safe and long-lasting therapy of severe clinical significant vasospasm.[38]

Frontal view from a cerebral angiogram in a 41-yeaFrontal 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 (imAngiographic 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.

For more information, see Mechanical Thrombolysis in Acute Stroke and Cerebral Revascularization.

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Prevention of Hemorrhagic Stroke

Exercise

A Finnish study showed that the likelihood of stroke in men with the lowest degree of physical fitness (maximal oxygen uptake [VO2max] < 25.2 mL/kg/min) was more than 3 times greater than in men with the highest degree of physical fitness (VO2max >35.3 mL/kg/min).[39]

In this analysis, level of physical fitness was a more powerful risk factor than LDL cholesterol level, body mass index, and smoking, and it was nearly comparable to hypertension as a risk factor.

The 2011 AHA/ASA guidelines for the primary prevention of stroke address both hemorrhagic and ischemic stroke. They emphasize exercise and other lifestyle modifications, endorsing the 2008 Physical Activity Guidelines for Americans, which include a recommendation at least 150 minutes per week of moderate intensity aerobic physical activity.[40]

Antihypertensives

The 2010 AHA/ASA guideline for spontaneous ICH recommends that after acute ICH, patients without medical contraindications should have blood pressure well controlled, especially for ICH in typical hypertensive vasculopathy locations.[22]

The 2011 AHA/ASA primary stroke prevention guidelines strongly recommend maintenance of blood pressure less than 140/90 mm Hg to prevent a first stroke. Patients with hypertension as well as diabetes or renal disease should be treated to less than 130/80 mm Hg.[40]

BP-lowering medications include thiazide diuretics, ACEIs, and angiotensin receptor blockers (ARBs). For patients with diabetes, the use of ACEIs and ARBs to treat hypertension is a class I-A recommendation (strongest and best-documented) according to the 2011 AHA/ASA primary prevention guidelines. Statin therapy is also recommended (class I-A recommendation), especially if other risk factors are present. Adding a fibrate to statin therapy for patients with diabetes is not recommended, although fibrate monotherapy may be considered in these patients.[40]

In the Heart Outcomes Prevention Evaluation (HOPE) study, the addition of the ACE inhibitor ramipril to all other medical therapy, including antiplatelet agents, reduced the relative risk of stroke, death, and myocardial infarction by 32% compared with placebo.[41] Only 40% of the efficacy of ramipril could be attributed to its BP-lowering effects. Postulated mechanisms included endothelial protection.

In the Perindopril Protection Against Recurrent Stroke Study (PROGRESS), a regimen based on perindopril, an ACEI, was superior to placebo.[42] However, perindopril alone was not superior to placebo, but the combination of perindopril with indapamide (a thiazide diuretic) substantially reduced the recurrence of stroke.[42] Much of the effect in reducing stroke recurrence was due to the lowering of BP, in contrast to findings from the HOPE study.

The Antihypertensive and Lipid-Lowering Treatment to Prevent Heart Attack Trial (ALLHAT) showed slight superiority of chlorthalidone (a thiazide diuretic) compared with lisinopril (an ACEI) in terms of stroke occurrence.[43]

The Losartan Intervention for Endpoint Reduction in Hypertension Study (LIFE) demonstrated that an ARB (losartan) was superior to a beta-blocker (atenolol) in reducing the occurrence of stroke.[44]

The Morbidity and Mortality after Stroke, Eprosartan Compared with Nitrendipine for Secondary Prevention (MOSES) study found that the ARB eprosartan was superior in the secondary prevention of stroke and TIA compared with the calcium channel blocker nitrendipine.[45] This was true despite comparable BP reductions.[45] The absolute annual difference in stroke and TIA risk was approximately 4%. The study was relatively small, and most events were TIAs.

Whether the beneficial effect of ramipril represents a class effect of ACEIs or whether it is a property unique to ramipril is unclear. Adverse effects of ACEIs include cough (10%), which is less common with ARBs.

At this time, first-line agents for the treatment of hypertension in stroke include thiazide diuretics, calcium channel blockers, ACEIs, and ARBs. Beta-blockers are considered second-line agents given their inferiority in preventing events despite similar reductions in blood pressure.

Lifestyle interventions

Smoking cessation, BP control, diabetes control, a low-fat diet (eg, Dietary Approaches to Stop Hypertension [DASH] or Mediterranean diets), weight loss, and regular exercise should be encouraged as strongly as the medications described above. The 2011 AHA/ASA guidelines for primary stroke prevention also recommends reducing sodium intake and increasing consumption of foods high in potassium to reduce blood pressure.[40] Written prescriptions for exercise and medications for smoking cessation (nicotine patch, bupropion, varenicline) increase the likelihood of success with these interventions.

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Consultations

Emergent neurosurgical or neurologic consultation is often indicated; local referral patterns may vary.

Need for invasive intracranial pressure monitoring and for emergent cerebral angiography should be assessed by the neurosurgeon. Patients with no clear cause of the hemorrhage and who would otherwise be candidates for surgery should be considered for angiographic evaluation.

Also see Stroke Team Creation and Primary Stroke Center Certification.

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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

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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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