eMedicine Specialties > Neurology > Neuro-vascular Diseases

Cerebral Aneurysms

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

Updated: Mar 10, 2009

Introduction

Background

Cerebral aneurysms are pathologic focal dilatations of the cerebrovasculature that are prone to rupture. These vascular abnormalities are classified by presumed pathogenesis. Saccular, berry, or congenital aneurysms constitute 90% of all cerebral aneurysms and are located at the major branch points of large arteries. Dolichoectatic, fusiform, or arteriosclerotic aneurysms are elongated outpouchings of proximal arteries that account for 7% of all cerebral aneurysms. Infectious or mycotic aneurysms are situated peripherally and comprise 0.5% of all cerebral aneurysms. Other peripheral lesions include neoplastic aneurysms, rare sequelae of embolized tumor fragments, and traumatic aneurysms. Traumatic injury also may result in dissecting aneurysms in proximal vessels. Microaneurysms of small perforating vessels may result from hypertension.

Saccular aneurysms are situated in the anterior circulation in 85-95% of cases, whereas dolichoectatic aneurysms affect predominantly the vertebrobasilar system. The location of saccular aneurysms at specific arterial segments varies in frequency because of differences in reported study populations. Multiple saccular aneurysms are noted in 20-30% of patients with cerebral aneurysms.

Saccular aneurysms frequently rupture into the subarachnoid space, accounting for 70-80% of spontaneous subarachnoid hemorrhages (SAH). Aneurysmal rupture also may result in intraparenchymal, intraventricular, or subdural hemorrhage. Giant saccular aneurysms, defined as greater than 25 mm in diameter, represent 3-5% of all intracranial aneurysms. Although giant aneurysms may cause SAH, these lesions frequently produce mass effects and result in distal thromboembolism.

Aneurysmal SAH is a catastrophic condition, affecting 30,000 individuals in the United States every year. Most of these individuals (60%) either die or suffer permanent disability; 50% of survivors with favorable outcomes experience considerable neuropsychological dysfunction. Cerebral vasospasm (ie, narrowing of proximal arterial segments) complicates 20-50% of cases and is the major cause of death and disability associated with aneurysmal SAH.

Pathophysiology

The pathogenesis of cerebral aneurysms is related inherently to structural aberrations of the cerebrovasculature, although the etiology of these abnormalities may be diverse. The integrity of the internal elastic lamina is compromised, with associated elastic defects in the adjacent layers of the tunica media and adventitia. Muscular defects of the tunica media and minimal support of adjacent brain parenchyma augment the pathologic potential of chronic hemodynamic stress on the arterial wall. Focal turbulence and discontinuity of the normal architecture at vessel bifurcations may account for the propensity of saccular aneurysm formation at these locations. Distal aneurysms may be smaller compared with proximal sites, yet the risk of rupture may be dissimilar due to the relatively thinner parent artery wall thickness.

The development of cerebral aneurysms remains a controversial topic. A multifactorial etiology is most likely, reflecting the interaction of environmental factors, such as atherosclerosis or hypertension, and a congenital predisposition associated with various vascular abnormalities. Abnormalities of the internal elastic lamina may be congenital or degenerative. Multiple conditions have been associated with cerebral aneurysms; they include the following:

• Autosomal dominant inherited polycystic kidney disease
• Fibromuscular dysplasia
• Arteriovenous malformations
• Osler-Weber-Rendu syndrome
• Coarctation of the aorta
• Other vascular anomalies
• Moyamoya syndrome
• Marfan syndrome
• Ehlers-Danlos syndrome, type IV
• Other collagen type III disorders
• Pseudoxanthoma elasticum
• Alpha1-antitrypsin deficiency
• Systemic lupus erythematosus
• Sickle cell anemia
• Bacterial endocarditis
• Fungal infections
• Neurofibromatosis type 1
• Tuberous sclerosis

Environmental stressors, such as hypertension, have been associated with the presence of multiple aneurysms. A familial inheritance pattern has been noted in fewer than 2% of intracranial aneurysms.

Dolichoectatic aneurysms of proximal vessels most likely have an arteriosclerotic etiology. These tortuous, elongated dilatations devoid of a true aneurysmal neck frequently contain laminated thrombus. Although aneurysmal SAH may occur, these lesions typically exert mass effects on adjacent parenchyma, with brainstem compression and cranial neuropathies, or result in obstruction of cerebrospinal fluid (CSF) outflow or distal thromboembolic sequelae.

Infectious aneurysms typically are situated in distal branches of the middle cerebral artery (MCA; 75-80% of cases), reflecting the embolic origin of these lesions. Cardioembolism of septic material complicates the course of 4% of patients with subacute bacterial endocarditis and may affect other patients with congenital heart disease and right-to-left shunts. Direct extension from lumen to adventitia of septic emboli containing Streptococcus viridans or Staphylococcus aureus (ie, the most common pathogens) may lead to degradation and aneurysm formation. Alternatively, diffuse infiltration from the periphery to the lumen may occur in the setting of meningitis, exemplified by aneurysms of the basal circulation associated with fungal infections. Infectious aneurysms are frequently multiple (20%) and have a greater propensity to bleed than other aneurysms.

Traumatic aneurysms may be located in peripheral cortical branches secondary to contact with the falcine edge or skull fractures associated with penetrating or closed head injury. Traumatic dissecting aneurysms due to expansion of intramural hematomas are noted most commonly at the skull base. These false aneurysms, devoid of all layers of the vessel wall, may compress cranial nerves or lead to distal embolization. Rupture of the internal carotid artery (ICA) may produce a carotid-cavernous fistula.

Distal embolization of tumor fragments from a cardiac myxoma or choriocarcinoma may lead to neoplastic aneurysm formation.

Vein of Galen aneurysms or malformations may cause hydrocephalus associated with aqueductal compromise or congestive heart failure in infants.

Aneurysmal rupture typically results in SAH, with diffuse or focal forms of vasospasm that may lead to ischemia and infarction. Recent animal data suggest therapeutic benefit of nitrite infusions to enhance cerebral perfusion in the setting of aneurysmal SAH. This delayed complication of vasospasm is of unclear pathogenesis but most likely is due to the presence of blood and the formation of multiple substances in the subarachnoid space. Spontaneous thrombosis of an aneurysm and subsequent recurrence have been reported in a few cases.

Frequency

United States

The frequency of cerebral aneurysms is difficult to ascertain because of variation in the definitions of the size of aneurysm and modes of detection. Autopsy series cite prevalences of 0.2-7.9%. Prevalence ranges from 5-10%, with unruptured aneurysms accounting for 50% of all aneurysms. Pediatric aneurysms account for only 2% of all cerebral aneurysms. In the United States, the incidence of ruptured aneurysms is approximately 12 per 100,000 individuals or 30,000 annual cases of aneurysmal SAH. The frequency of cerebral aneurysms has not declined in recent years.

International

Incidence of aneurysmal SAH varies widely depending on geographic location, ranging from 3.9-19.4 per 100,000 individuals, with the highest reported rates in Finland and Japan. Overall, the incidence has been estimated at 10.5 per 100,000 individuals.

Mortality/Morbidity

• Aneurysmal SAH has devastating consequences. About 10% of individuals with aneurysmal SAH die before reaching medical attention, 25% die within 24 hours, and 40-49% die within 3 months. Mortality rate has been estimated to be as high as 65%, with most deaths occurring early in the clinical course.
• Early surgical treatment is associated with higher operative morbidity and mortality rates; however, overall morbidity and mortality rates are lower in patients who undergo surgery. Intraoperative aneurysmal rupture has a combined morbidity and mortality rate of 30-35%.
• Aneurysmal SAH during pregnancy has a mortality rate of 35%, accounting for one of the leading causes of maternal mortality during pregnancy.

Race

The racial predilection of cerebral aneurysms is largely unknown, although a higher incidence has been noted in African Americans, with an odds ratio of 2.1.

Sex

Cerebral aneurysms affect equal numbers of women and men younger than 40 years, although women are affected more frequently in older age groups. Overall, the female-to-male ratio has been estimated at 1.6:1.

• Saccular aneurysms are most common in the anterior communicating artery (ACoA) or anterior cerebral artery (ACA) in men, whereas the junction of the ICA with the posterior communicating artery (PCoA) is the most common site for saccular aneurysms in women.
• Giant aneurysms are 3 times more common in women than men.
• The prognosis of aneurysmal SAH is worse for women than men.

Age

• Cerebral aneurysms are rarely apparent in infants and children. Clinical manifestations increase with age, reaching a peak in people aged 55-60 years.
• Carotid artery is affected most commonly in individuals younger than 18 years.
• The prognosis of aneurysmal SAH worsens with increasing age.

Clinical

History

• The clinical presentation of cerebral aneurysms includes symptoms associated with major aneurysmal rupture (eg, SAH), minor aneurysmal hemorrhage (eg, warning leak or sentinel bleed), nonhemorrhagic manifestations (eg, mass effects or cerebral ischemia), and asymptomatic scenarios (eg, incidental aneurysm detection or identification through screening¹ ).
• Although aneurysmal SAH has characteristic historical features, the constellation of symptoms may vary with location, size, shape, and direction of the aneurysm.
• Aneurysmal rupture also may present with intraparenchymal hemorrhage (more common with distal aneurysms), intraventricular hemorrhage (13-28%), or subdural hematoma (2-5%).
• Minor aneurysmal hemorrhage may precede rupture with a wide variation in latency, although these warning leaks also may be clinically silent.
• Giant aneurysms may compress brain parenchyma, resulting in focal neurological complaints.
• Aneurysmal expansion may produce pain or herald new neurological manifestations.
• Traumatic aneurysms may have a delayed presentation, with intracranial hemorrhage or recurrent epistaxis.
• Symptoms associated with cerebral aneurysms and SAH are as follows:
  • Headache: This is characterized by the acute onset of severe pain, which patients often describe as "the worst headache of my life." Aneurysmal expansion, thrombosis, or intramural hemorrhage may cause a subacute, unilateral, periorbital headache. Headache does not always accompany aneurysmal SAH.
  • Facial pain: Cavernous-carotid aneurysms may produce facial pain.
  • Alterations in consciousness: The sudden elevation of intracranial pressure associated with aneurysmal rupture may lead to a precipitous decline in cerebral perfusion pressure, causing syncope (50% of cases). Confusion or mild impairment in alertness also may be noted.
  • Seizures: Focal or generalized seizures are present in 25% of aneurysmal SAH cases, with most events occurring within 24 hours of onset.
  • Manifestations of meningeal irritation: Neck pain or stiffness, photophobia, sonophobia, or other hyperesthesia may be noted with SAH.
  • Autonomic disturbances: Subarachnoid accumulation of products of blood degradation may elicit fever. Nausea or vomiting, sweating, chills, and cardiac arrhythmias also may be present.
  • Focal neurological complaints: Hemorrhage or ischemia may manifest with focal deficits including weakness, hemisensory loss, language disturbances, neglect, memory loss, or olfactory disturbances. Focal symptoms are more common with giant aneurysms.
  • Visual symptoms: Blurring of vision, diplopia, or visual field defects may be present.
  • Respiratory dysfunction or cardiovascular instability: These are ominous signs of brainstem compression.
  • Hormonal dysfunction: Intrasellar aneurysms may interfere with pituitary function.
  • Epistaxis: This is noted occasionally with traumatic aneurysms.

Physical

• The general examination occasionally reveals manifestations of associated conditions such as subacute bacterial endocarditis, trauma, or collagen-vascular disease.
• Specific physical examination findings may include prominent scalp veins, signs of congestive heart failure (eg, vein of Galen aneurysms), or orbital bruits (eg, cavernous carotid aneurysms).
• Neurologic findings exhibit considerable variability, depending on aneurysm characteristics.
  • Aneurysmal SAH may be accompanied by nuchal rigidity, decreased level of consciousness, subhyaloid hemorrhages, pupillary abnormalities (ie, typically dilated), ophthalmoplegia, cranial neuropathies, and other focal deficits.
  • Giant aneurysms or dolichoectatic aneurysms may cause mass effects or distal thromboembolism with prominent focal deficits, optic atrophy or other cranial neuropathies, or brainstem compression.
• Specific syndromes have been associated with particular aneurysmal locations.
  • Anterior communicating artery: This is the most common site of aneurysmal SAH (34%). Usually, ACoA aneurysms are silent until they rupture. Suprachiasmatic pressure may cause altitudinal visual field deficits, abulia or akinetic mutism, amnestic syndromes, or hypothalamic dysfunction. Neurological deficits in aneurysmal rupture may reflect intraventricular hemorrhage (79%), intraparenchymal hemorrhage (63%), acute hydrocephalus (25%), or frontal lobe strokes (20%).
  • Anterior cerebral artery: Aneurysms of this vessel, excluding ACoA, account for about 5% of all cerebral aneurysms. Most are asymptomatic until they rupture, although frontal lobe syndromes, anosmia, or motor deficits may be noted.
  • Middle cerebral artery: Aneurysms of the middle cerebral artery (see Media files 1-2) account for about 20% of aneurysms, typically at first or second division in the sylvian fissure. Aphasia, hemiparesis, hemisensory loss, anosognosia, or visual field defects may be noted.
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    Cerebral aneurysms. CT angiography of a right middle cerebral artery aneurysm.

    
    
  • Posterior communicating artery: Aneurysms present at the junction of the termination of the ICA and PCoA account for 23% of cerebral aneurysms; they are directed laterally, posteriorly, and inferiorly. Pupillary dilatation, ophthalmoplegia, ptosis, mydriasis, and hemiparesis may result.
  • Internal carotid artery: Besides PCoA aneurysms, aneurysms of the ICA (see Media file 3) account for about 4% of all cerebral aneurysms. Supraclinoid aneurysms may cause ophthalmoplegia due to compression of cranial nerve (CN) III or variable visual defects and optic atrophy due to compression of the optic nerve. Chiasmal compression may produce bilateral temporal hemianopsia. Hypopituitarism or anosmia may be seen with giant aneurysms. Cavernous-carotid aneurysms exert mass effects within the cavernous sinus, producing ophthalmoplegia and facial sensory loss. Rupture of these aneurysms typically produces a carotid-cavernous fistula, SAH, or epistaxis.
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    Cerebral aneurysms. Sagittal multiplanar reformatted view of a left internal carotid artery aneurysm.

    
    
  • Basilar artery: Basilar tip aneurysms (see Media files 4-5) are the most common in the posterior circulation, accounting for 5% of all aneurysms. Clinical findings usually are those associated with SAH, although bitemporal hemianopsia or an oculomotor palsy may occur. Dolichoectatic aneurysms may cause bulbar dysfunction, respiratory difficulties, or neurogenic pulmonary edema.
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    Cerebral aneurysms. Basilar tip aneurysm illustrated on CT scan (left) and T2-weighted MRI (right).

    
    
  • Vertebral artery or posterior inferior cerebellar artery: Aneurysms at these arterial segments typically result in ataxia, bulbar dysfunction, or spinal involvement.
  • False localizing signs: False localization may be associated with CN III palsy and hemiparesis in uncal herniation, CN VI palsy with elevated intracranial pressure, homonymous hemianopsia due to posterior cerebral artery compression along the tentorial edge, brainstem dysfunction associated with tonsillar herniation, and vasospasm in remote vessels.

Causes

• Congenital or familial inheritance
• Atherosclerosis
• Hypertension
• Autosomal dominant inherited polycystic kidney disease
• Vasculopathies
• Arteriovenous malformations (see Media file 6)
  
  

  

  Cerebral aneurysms. Aneurysm associated with an arteriovenous malformation (AVM) shown on T1-weighted MRI (left), 3D-time-of-flight MRI (middle), and conventional angiography (right).

  
  
• Connective tissue disorders
• Sickle cell anemia
• Infections
• Trauma
• Neoplasms
• Cigarette smoking
• Illicit drug use
• Alcohol

Differential Diagnoses

Other Problems to Be Considered

Increased intracranial pressure
Neuroimaging of vascular malformations and hematomas of the brain
Hypertension and stroke

Workup

Laboratory Studies

• CBC with platelets: Monitor for infection, evaluate anemia, and identify bleeding risk.
• Prothrombin time (PT)/activated partial thromboplastin time (aPTT): Identify a coagulopathy that increases bleeding risk.
• Serum chemistries, including electrolytes and osmolarity: Obtain baseline studies to monitor hyponatremia, address arrhythmogenic abnormalities, assess blood glucose, and monitor hyperosmolar therapy for elevated intracranial pressure.
• Liver function tests: Identify hepatic dysfunction that may complicate clinical course.
• Arterial blood gases: Assess blood oxygenation.

Imaging Studies

• Advances in neuroimaging techniques have altered the diagnosis of cerebral aneurysms dramatically. Noninvasive angiographic methods, such as computed tomographic angiography (CTA) and magnetic resonance angiography (MRA), allow for detection and characterization of aneurysms, further enhanced by postprocessing techniques that enable 3-dimensional evaluation of aneurysm morphology. Contemporaneous parenchymal imaging with CT scan or MRI yields a wealth of information that may assist surgical planning. However, minor aneurysmal hemorrhage may not be detected with noninvasive methods.
• CT
  • Aneurysmal SAH may be detected in 90-95% of cases. If CT scan result is negative and SAH is suspected, perform lumbar puncture (LP).
  • Noncontrast CT scan should be performed, as contrast may obscure detection of SAH.
  • Curvilinear calcification, aneurysmal thrombosis, or bone erosion may be characterized; however, bone structures also may produce artifacts.
  • Surrounding edema and an inflammatory reaction may be appreciated with contrast administration following the noncontrast study.
  • CTA may detect aneurysms greater than 3 mm, providing detailed evaluation of morphology such as relationship to the parent vessel and neck width.
  • CTA can detect more than 95% of aneurysms identified on conventional angiography. CTA may be superior to MRA because of shorter acquisition times, diminished motion artifacts, and detailed demonstration of other landmarks. However, bone and venous structures may complicate analysis.
  • Increasing use of CT perfusion in combination with CTA allows for reconstruction of multiphase CT angiographic images, potentially providing greater definition beyond standard CTA.²
• MRI
  • Fluid-attenuated inversion recovery (FLAIR) sequences are very sensitive for SAH, although the comparison of CT scan and MRI in detection of SAH is controversial.
  • MRI may be impractical for patients in unstable condition. Flow voids may be seen extending from the parent vessel into the aneurysm.
  • Heterogeneous signal intensity adjacent to the aneurysm wall may be seen with thrombus of varying ages, although MRI is relatively insensitive to the presence of calcium.
  • Dolichoectatic and giant aneurysms are identified readily with MRI. Pulsation artifacts and the presence of turbulence may help to differentiate these aneurysms from other mass lesions, but slow and turbulent flow may preclude visualization on MRA.
  • MRA may reliably provide 3-dimensional imaging of aneurysms 4 mm or larger.
  • Phase-contrast techniques may facilitate detection of flow patterns and slow flow. Although phase-contrast MRA is preferable for large aneurysms, 3-dimensional time-of-flight techniques are preferable for small aneurysms. Source images should be inspected routinely in conjunction with the reconstructed views.
• Angiography
  • Conventional angiography is the definitive procedure for the detection and characterization of cerebral aneurysms. Aneurysm location, size, and morphology may be evaluated in the acute or chronic setting with this modality.
  • Digital subtraction angiography with biplanar magnification views provides details that may be helpful in identifying an acutely ruptured aneurysm.
  • Aneurysmal irregularity, the presence of a daughter loculus, or focal spasm may be noted with acute rupture. Vasospasm may be depicted reliably and the collateral circulation may be demonstrated.
  • Perform 4-vessel angiography to identify remote vasospasm and the presence of multiple aneurysms. Acute angiography occasionally yields negative results (eg, due to thrombosis or vasospasm), in which case angiography should be repeated 1-3 weeks later. However, the risk and expense of this procedure may not be appropriate for screening of high-risk individuals.
  • A junctional dilatation of the terminal carotid artery at the origin of the PCoA may be noted in about 5-10% of patients. These infundibula or conical enlargements of less than 3 mm are unlikely to enlarge or rupture. However, overt aneurysms at the juncture of the terminal carotid artery with a persistent PCoA configuration may be more prone to rupture.
  • Further refinements in the characterization of cerebral aneurysms are expected following the recent introduction of 3-dimensional rotational angiography. Recent work has demonstrated that this technique may offer superior resolution and increased sensitivity for detection of small aneurysms.³
• Transcranial Doppler ultrasonography: TCD facilitates the diagnosis of vasospasm and serial monitoring of cerebral blood flow at the bedside. TCD has exhibited close correlation with angiography in the setting of vasospasm, typically manifesting 3-21 days following aneurysmal SAH.
• Single-photon emission computed tomography (SPECT), positron emission tomography (PET), xenon-CT (XeCT): With these techniques, cerebral blood flow studies may depict ischemia associated with vasospasm, although these modalities are not employed routinely.
• Cervical spine imaging: Radiographic assessment of the cervical spine should be performed in all comatose patients with an unwitnessed loss of consciousness.

Other Tests

• ECG: Cardiac arrhythmias and myocardial ischemia may be evident. Aneurysmal SAH may be associated with several ECG changes, including peaked P waves, prolonged QT interval, and tall T waves.
• Echocardiography: Cardiac sources of embolism, including endocarditis and myxomas, may be visualized in cases of infectious or neoplastic aneurysms.
• Evoked potentials and EEG: These functional neurophysiologic studies may be used to monitor cerebral aneurysm surgery or patients critically ill with aneurysmal SAH.

Procedures

• Lumbar puncture
  • LP may help to establish the diagnosis of SAH in the absence of focal signs of mass effects. Aneurysmal SAH demonstrates hemorrhagic CSF with a xanthochromic supernatant, although these findings may be absent within the first few hours following aneurysmal rupture.
  • The opening pressure may be elevated.
  • WBC count may increase after a delay, reflecting a meningeal inflammatory reaction.
  • The protein may be elevated with normal or decreased glucose.
  • Cultures may reveal an infectious etiology.
• Ventriculostomy: External drainage of CSF may assist in the management of hydrocephalus and cases with poor clinical grades.

Histologic Findings

Gross pathologic examination may reveal brownish pigmentation and fibrous adhesions of surrounding brain parenchyma. Aneurysm size may be diminished on postmortem examination, although a multilobular shape may be appreciated. A ruptured fundus may be visualized with calcifications of the aneurysm wall and intraluminal thrombus.

• Microscopic examination reveals defects in the normal architecture of the vessel wall. The tunica media and internal elastic lamina may be absent or degenerated, with hemosiderin-laden phagocytes and lymphocytic infiltration.
• Infectious aneurysms may exhibit an infected embolus adherent to a necrotic arterial wall. The intima and internal elastic lamina may be destroyed with an inflammatory infiltrate consisting of polymorphonuclear cells, lymphocytes, and macrophages.
• Myofilament fragmentation and sarcolemmal destruction may be seen with vasospastic vessels.

Staging

Table 1. Clinical Condition at Presentation

Table 2. World Federation of Neurological Surgeons Scale

Treatment

Medical Care

• Prehospital care should include assessment of vital signs and neurological status. Airway, breathing, and circulation should be addressed with endotracheal intubation, if necessary, and establishment of intravenous access.
• Medical therapy of cerebral aneurysms involves general supportive measures and prevention of complications for individuals who are in the periprocedural period or are poor surgical candidates. Treatment decisions should be based on the clinical status of the patient, vascular anatomy of the aneurysm, and surgical or endovascular considerations.
  • Medical management of aneurysmal SAH is orchestrated in the ICU, with cardiac monitoring and placement of an arterial line.
  • Prior to definitive aneurysm treatment, medical approaches involve control of hypertension, administration of calcium channel blockers, and prevention of seizures.
  • Following surgical or endovascular aneurysm treatment, blood pressure is maintained at higher levels to diminish complications associated with vasospasm. Vasospasm usually occurs between days 3 and 21, presenting with headache, decreased level of consciousness, and variable neurological deficits. Serial TCD may be employed to detect trends in cerebral blood flow during this period.
  • Induced hypertension, hypervolemia, and hemodilution (ie, "triple-H therapy") aims to maintain adequate cerebral perfusion pressure in the setting of impaired cerebrovascular autoregulation.
  • Intraarterial papaverine or endovascular balloon angioplasty may be used to treat vasospasm in select patients.
• Infectious aneurysms are friable, with an increased propensity for hemorrhage. Anticoagulation is avoided in this setting. As these lesions resolve with antibiotic therapy, surgical approaches usually are deferred. Regression or evolution of these aneurysms is monitored with serial angiography.
• The management of unruptured intracranial aneurysms is highly controversial. The International Study of Unruptured Intracranial Aneurysms (ISUIA) indicated a relatively low risk of rupture in small aneurysms without history of SAH. Aneurysms less than 10 mm in size had an annual rupture rate of approximately 0.05%. For posterior communicating, vertebrobasilar/posterior cerebral, or basilar tip aneurysms less than 10 mm, the risk of rupture over 7.5 years approximated 2%, with all other locations harboring a risk of almost 0%. Recent guidelines and an evidence-based systematic review of the literature have formulated recommendations for the care of patients with unruptured intracranial aneurysms, principally based on age, history, and aneurysm size.
  • The anatomical characterization and morphology of unruptured aneurysms are not readily standardized, however. Some investigators have advocated endovascular or surgical treatment of all aneurysms less than 10 mm if age is less than 50 years, in the absence of contraindications. The presence of cigarette smoking, family history of aneurysms, polycystic kidney disease, or systemic lupus erythematosus may elevate the risk of rupture and should be considered. Asymptomatic aneurysms greater than 10 mm should also be considered for treatment, accounting for age, coexisting medical conditions, and relative risks for treatment.
  • Considerable surgical mortality and morbidity rates at 1 year (as high as 3.8% and 15.7%, respectively) have been demonstrated in preventive treatment of unruptured aneurysms. The surgeon's experience may be a significant and highly variable factor in operative morbidity rate and functional outcome. More recently, application of diffusion-weighted MRI has demonstrated silent thromboembolic events associated with endovascular treatment of unruptured cerebral aneurysms. Quality-of-life issues, including the psychological morbidity of living with an unruptured intracranial aneurysm, also must be addressed.
  • Therapeutic decision making must balance endovascular or surgical morbidity and mortality rates with the risk of hemorrhage and other considerations on an individual basis. Future studies in the management of unruptured intracranial aneurysms may systematically account for the evolving technology of advanced endovascular approaches, detailed aneurysm morphology, novel neuroimaging correlates, ethnic and geographical variation, neurocognitive impairment following endovascular or surgical treatment, and quality-of-life issues.

Surgical Care

• Microsurgical techniques focus on exclusion of the aneurysm from the cerebral circulation and reduction of mass effects on adjacent structures. Various approaches have been developed and tailored to the anatomy and location of the aneurysm. A surgical clip usually is placed across the aneurysm neck with preservation of the parent vessel, eliminating any aneurysmal rests that may redevelop subsequently. Alternative surgical techniques involve proximal or Hunterian ligation, wrapping of the aneurysm, or trapping (ie, a combination of proximal and distal vessel occlusion).
• Adjunctive measures have been developed to reduce operative morbidity and to provide cerebral protection. Aneurysmal rupture, the principal surgical complication, may be avoided with induced hypotension, CSF drainage, diuretics, hyperventilation, and use of minimal brain retraction. Hypothermia, with or without circulatory arrest, and systemic hypotension are used commonly. A large recent study of mild intraoperative hypothermia, however, failed to demonstrate benefit of this adjunctive technique. Lumbar spinal drainage allows for relaxation of brain parenchyma and provides a clean surgical field. Postoperative angiography is performed routinely to check for major vessel occlusion or persistence of an aneurysmal rest. Operative morbidity rate increases with aneurysm size (2.3% for <5 mm; 6.8% for 6-15 mm, 14% for 16-25 mm) and varies by location.
• Optimal timing of aneurysm surgery depends on the clinical status of the patient and associated factors. Early surgery (ie, <48-96 h after SAH) is favored for candidates in good condition or those with unstable blood pressure, seizures, mass effect from thrombus, large amounts of blood, or evidence of aneurysm growth or rebleeding. Early surgery carries an increased operative morbidity, although the risks of vasospasm and rebleeding are reduced considerably. Delayed surgery (ie, 10-14 d after SAH) may be considered for large aneurysms in difficult locations or for candidates in poor clinical condition. Surgery is indicated for ruptured or symptomatic aneurysms in patients without extenuating contraindications or considerably advanced age. Surgery generally is precluded if the clinical status is poor, corresponding to Hunt and Hess grade 4 or 5.
• Advances in endovascular techniques have provided novel therapeutic alternatives that may be employed even in the setting of acute aneurysmal SAH. These techniques allow for parent vessel preservation and may be combined with surgical approaches. Electrolytically detachable platinum coils (eg, Guglielmi detachable coils [GDC]) may be deployed strategically within the aneurysm, promoting thrombosis and eventual obliteration. Wide-neck aneurysms may be more difficult to occlude with these devices. Other materials, such as balloons or glue, also may be used. Complications include vessel perforation, hemorrhage, or distal thromboembolism.
• Endovascular therapy or coiling of cerebral aneurysms has proliferated during the last several years. The respective roles of coiling versus surgical clipping of particular cerebral aneurysms are likely influenced by numerous factors. The International Subarachnoid Aneurysm Trial (ISAT) demonstrated the superiority of coiling with improved clinical outcomes. Seizures were also less common in patients with endovascular treatment, yet late rebleeding was also more common. Selection bias may also have influenced ISAT and, therefore, treatment for a given individual must still be tailored to each case.
• Progressive refinement in endovascular techniques and devices tailored for the cerebrovasculature have expanded therapeutic options available for definitive treatment of cerebral aneurysms. More pliable, low profile stents may be used for stent-assisted coiling for obliteration of wide-necked aneurysms.
  • Self-expanding or balloon-expandable covered stents may be used for treatment of selected carotid or vertebral artery pseudoaneurysms.⁴
  • Large or giant intracranial aneurysms may be treated with a combination of devices, such as stent-assisted coil placement.⁵ However, the requirement of dual antiplatelet therapy in stent-assisted coiling may increase the risk of intracranial hemorrhage.⁶
  • Refinement of endovascular techniques for very small intracranial aneurysms has expanded treatment options, yet complications may also increase in this particular subset.⁷

Consultations

A multidisciplinary approach to the treatment of cerebral aneurysms is recommended. The following specialists should be a part of the multidisciplinary team:

• Neurosurgeon
• Interventional neuroradiologist
• Neurologist
• Rehabilitation specialist

Diet

• Restrict possible surgical candidates to taking nothing by mouth (NPO).
• Employ nasogastric feedings for individuals with a decreased level of consciousness.
• Recommend a soft, high-fiber diet to alert patients; patients should avoid caffeine.

Activity

• Advise bed rest in a quiet dark environment during the initial week following aneurysmal SAH.
• Perform passive range of motion exercises and frequent turning.
• Assist patients with self-care activities, followed by slow advancement in activity as tolerated.

Medication

Nimodipine has been demonstrated to improve outcome and decrease the incidence of delayed neurological deficits when administered for the first 21 days after aneurysmal SAH. Although the prophylactic role of antiepileptic medications in aneurysmal SAH is controversial, seizures may be treated with these medications. Antihypertensive medications may be needed to control blood pressure. After aneurysmal occlusion, these medications are held typically for 2 weeks. Sedatives and pain control may be needed for aneurysmal SAH. Antiemetics, antacids, and stool softeners also are used routinely.

Calcium channel blockers

These agents are administered to minimize sequelae of cerebral vasospasm.

Nimodipine (Nimotop)

For improvement of neurological impairments resulting from spasms following SAH caused by ruptured congenital intracranial aneurysm in patients in good postictal neurological condition.
While studies show benefit in severity of neurological deficits caused by cerebral vasospasm following SAH, no evidence shows that the drug either prevents or relieves spasm of cerebral arteries. Actual mechanism of action unknown but may involve protection of brain against ischemia.
Therapy should start within 96 h of SAH. If capsule cannot be swallowed because patient undergoing surgery or unconscious, a hole can be made at both ends of capsule with 18-gauge needle, and contents extracted into a syringe. Contents then can be emptied into patient's nasogastric tube in situ and washed down tube with 30 mL isotonic saline.

Dosing

Adult

60 mg PO q4h for 21 d

Pediatric

Not established

Interactions

Although advantageous in some patients, beta-blockers may result in increased adverse effects due to depressant effects on myocardial contractility or AV conduction; fentanyl may cause severe hypotension; may increase fluid volume requirements; cimetidine may increase blood levels

Contraindications

Documented hypersensitivity; systolic blood pressure <90 mm Hg; sick sinus syndrome; second- or third-degree AV block except when using pacemaker

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Rare cases of elevated levels of LDH, alkaline phosphatase, and ALT may occur

Antiepileptics

These agents are administered for treatment and prevention of seizures.

Fosphenytoin (Cerebyx)

Diphosphate ester salt of phenytoin that acts as water-soluble prodrug of phenytoin. Following administration, plasma esterases convert fosphenytoin to phosphate, formaldehyde, and phenytoin. Phenytoin, in turn, stabilizes neuronal membranes and decreases seizure activity.
To avoid need to perform molecular weight-based adjustments when converting between fosphenytoin and phenytoin sodium doses, express dose as phenytoin sodium equivalents (PE). Although can be administered IV and IM, IV is route of choice and should be used in emergency situations.
Concomitant administration of IV benzodiazepine usually necessary to control status epilepticus. Full antiepileptic effect of phenytoin, whether given as fosphenytoin or parenteral phenytoin, not immediate.

Dosing

Adult

Loading dose: 15-20 mg PE/kg IV/IM, 100-150 mg PE/min
Maintenance dose: 4-6 mg PE/kg/d IV/IM, 150 mg PE/min to minimize risk of hypotension

Pediatric

Loading dose: 15-20 mg PE/kg IV/IM
Initial dose: 5 mg PE/kg/d IV/IM
Maintenance dose: 4-8 mg PE/kg IV/IM
>6 years: May require minimum adult dose (300 mg PE/d); not to exceed 300 mg PE/d

Interactions

Amiodarone, benzodiazepines, chloramphenicol, cimetidine, disulfiram, ethanol (acute ingestion), omeprazole, phenacemide, phenylbutazone, succinimides, fluconazole, isoniazid, metronidazole, miconazole, sulfonamides, trimethoprim, and valproic acid may increase toxicity
Barbiturates, carbamazepine, theophylline, diazoxide, ethanol (chronic ingestion), rifampin, antacids, charcoal, or sucralfate may decrease effects
May decrease effects of acetaminophen, corticosteroids, dicumarol, disopyramide, doxycycline, estrogens, haloperidol, amiodarone, carbamazepine, cardiac glycosides, methadone, metyrapone, mexiletine, oral contraceptives, quinidine, theophylline, valproic acid

Contraindications

Documented hypersensitivity; sino-atrial block; second- and third-degree AV block; Adams-Stokes syndrome

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Death from cardiac arrest has occurred after too-rapid IV administration, preceded sometimes by marked QRS widening
Blood dyscrasias have occurred; therefore, perform blood counts and urinalyses when therapy initiated and at monthly intervals for several mo thereafter; discontinue use if skin rash appears—if rash is exfoliative, bullous, or purpuric do not resume use; use caution in acute intermittent porphyria and diabetes (may raise blood glucose levels); discontinue drug if hepatic dysfunction occurs

Antihypertensives

These agents help in controlling systemic blood pressure.

Labetalol (Normodyne, Trandate)

Blocks beta1-, alpha-, and beta2-adrenergic receptor sites, thereby decreasing blood pressure.

Dosing

Adult

20-30 mg IV over 2 min, followed by 40-80 mg at 10-min intervals; not to exceed 300 mg/dose

Pediatric

Not established; suggested dose is 0.4-1 mg/kg/h IV; not to exceed 3 mg/kg/h

Interactions

Decreases effect of diuretics and increases toxicity of methotrexate, lithium, and salicylates; may diminish reflex tachycardia resulting from nitroglycerin use without interfering with hypotensive effects; cimetidine may increase blood levels; glutethimide may decrease effects by inducing microsomal enzymes

Contraindications

Documented hypersensitivity; cardiogenic shock; pulmonary edema; bradycardia; atrioventricular block; uncompensated congestive heart failure; reactive airway disease; severe bradycardia

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Use caution in impaired hepatic function (discontinue therapy if signs of liver dysfunction) and in elderly patients (lower response rate and higher incidence of toxicity may be observed)

Hydralazine (Apresoline)

Decreases systemic resistance through direct vasodilation of arterioles.

Dosing

Adult

10-20 mg/dose PO q4-6h prn initially; increase to 40 mg/dose if necessary; change to PO as soon as possible

Pediatric

Not established

Interactions

MAOIs and beta-blockers may increase toxicity; indomethacin may decrease pharmacologic effects

Contraindications

Documented hypersensitivity; mitral valve rheumatic heart disease

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Has been implicated in myocardial infarction; caution in suspected coronary artery disease

Analgesics

These agents help in pain relief.

Morphine sulfate (MSIR, Duramorph, Astramorph, MS Contin)

Drug of choice for analgesia because of reliable and predictable effects, safety profile, and ease of reversibility with naloxone.
Various IV doses used; commonly titrated until desired effect obtained.

Dosing

Adult

Starting dose: 0.1 mg/kg IV/IM/SC
Maintenance dose: 5-20 mg/70 kg IV/IM/SC q4h
Relatively hypovolemic patients: Start with 2 mg IV/IM/SC; reassess hemodynamic effects of dose

Pediatric

Infants and children: 0.1-0.2 mg/kg dose IV/IM/SC q2-4h prn; not to exceed 15 mg/dose; can initiate at 0.05 mg/kg/dose

Interactions

Phenothiazines may antagonize analgesic effects; tricyclic antidepressants, MAOIs, and other CNS depressants may potentiate adverse effects

Contraindications

Documented hypersensitivity; hypotension; potentially compromised airway in which establishing rapid airway control would be difficult

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid in hypotension, respiratory depression, nausea, emesis, constipation, and urinary retention; use caution in atrial flutter and other supraventricular tachycardias; has vagolytic action and may increase ventricular response rate

Antiemetics

These agents help in minimizing nausea and vomiting.

Prochlorperazine (Compazine)

May relieve nausea and vomiting by blocking postsynaptic mesolimbic dopamine receptors through anticholinergic effects and depressing reticular activating system. In addition to antiemetic effects, has advantage of augmenting hypoxic ventilatory response, acting as respiratory stimulant at high altitude.

Dosing

Adult

5-10 mg PO/IM tid/qid; not to exceed 40 mg/d
2.5-10 mg IV q3-4h prn; not to exceed 10 mg/dose or 40 mg/d
Alternatively, 25 mg PR bid

Pediatric

2.5 mg PO/PR q8h or 5 mg q12h prn; not to exceed 15 mg/d; IV dosing not recommended for children
0.1-0.15 mg/kg/dose IM and change to PO as soon as possible

Interactions

CNS depressants or anticonvulsants may cause additive effects; may cause hypotension with epinephrine

Contraindications

Documented hypersensitivity; bone marrow suppression; narrow-angle glaucoma; severe liver or cardiac disease

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Drug-induced Parkinson syndrome or pseudoparkinsonism occurs quite frequently; akathisia is most common extrapyramidal reaction in elderly patients; lowers seizure threshold; use caution in patients with history of seizures

Antacids

These agents help in relieving gastrointestinal acid reflux.

Ranitidine (Zantac)

Inhibits stimulation of H2 receptor in gastric parietal cells, which in turn reduces gastric acid secretion, gastric volume, and hydrogen-ion concentration.

Dosing

Adult

150 mg PO bid; not to exceed 600 mg/d
Alternatively, 50 mg/dose IV/IM q6-8h

Pediatric

<12 years: Not established
>12 years: 1.25-2.5 mg/kg/dose PO q12h; not to exceed 300 mg/d
0.75-1.5 mg/kg/dose IV/IM q6-8h; not to exceed 400 mg/d

Interactions

May decrease effects of ketoconazole and itraconazole; may alter serum levels of ferrous sulfate, diazepam, nondepolarizing muscle relaxants, and oxaprozin

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Use caution in renal or liver impairment—if changes in renal function occur during therapy, consider adjusting dose or discontinuing treatment

Stool softeners

These agents help in softening stools and minimizing straining.

Docusate sodium (Colace, Dialox, Surfak, Regulax, Sulfalax)

For patients who should avoid straining during defecation; allows incorporation of water and fat into stool, causing stool to soften.

Dosing

Adult

50-500 mg/d PO qd or divided qid

Pediatric

3-6 years: 20-60 mg/d PO qd or divided qid
6-12 years: 40-150 mg/d qd or divided qid

Interactions

Decreases effects of warfarin and increases effects of phenolphthalein

Contraindications

Documented hypersensitivity; nausea, vomiting, or acute abdominal pain

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Prolonged use may result in electrolyte imbalance

Follow-up

Further Inpatient Care

Following neurosurgical or endovascular intervention, continued care in the ICU generally includes the following:

• Serial neurologic examinations
• Avoidance of hypotension or hypertension (mean arterial pressure [MAP] should be in the range of 70-130 mm Hg)
• Use of isotonic solutions, such as normal saline, to minimize cerebral edema
• Treatment or prophylaxis of seizures
• Treatment of urinary tract infections
• Prevention of venous thrombosis
• Prophylaxis for gastric ulcers
• Physical, occupational, and speech therapy
• Repeat CT scan in case of clinical deterioration

Further Outpatient Care

• After hospital discharge, continue physical, occupational, and speech therapy.
• Administer medications for vasospasm and to prevent complications such as seizures, urinary tract infections, or venous thromboses.
• Following definitive treatment of a cerebral aneurysm with either endovascular or surgical obliteration, serial imaging studies should be obtained as an outpatient. Various imaging modalities, including CTA, 1.5 or 3T MRA, and conventional angiography may be used. The use of noninvasive angiographic techniques for serial evaluation has grown in recent years.⁸

Inpatient & Outpatient Medications

• Nimodipine for vasospasm
• Phenytoin for prevention or treatment of seizures

Transfer

Immediately after prehospital evaluation and emergent stabilization, transfer patients with aneurysmal SAH to a center with neurosurgical expertise.

Deterrence/Prevention

• Prevention of neurological injury necessitates definitive treatment of a diagnosed cerebral aneurysm.
• Patient education regarding symptoms of aneurysmal rupture may be important, as 10% of individuals die before reaching medical attention.
• Noninvasive screening with CTA or MRA is important in patients with medical conditions associated with cerebral aneurysms or a family history of SAH or aneurysms.
• Recent data showing superior functional outcomes and reduced complications for those on statins prior to aneurysmal SAH may promote the use of statins.

Complications

• Vasospasm
• Recurrent hemorrhage
• Seizures
• Hydrocephalus
• Hyponatremia
• Cardiac arrhythmia, myocardial infarction, or congestive heart failure
• Neurogenic pulmonary edema, pneumonia, or atelectasis
• Gastrointestinal bleeding
• Anemia
• Venous thromboembolism

Prognosis

• Prognosis of aneurysmal SAH has been associated with the following:
  • Age
  • Neurological status on admission
  • Aneurysm location
  • Number of days after SAH of admission (ie, delay from SAH to hospital admission)
  • Presence of hypertension and other medical illnesses
  • Degree of vasospasm
  • Degree of SAH
  • Extent of intraparenchymal or intraventricular hemorrhage
• Outcome assessments following aneurysmal SAH may not be properly evaluated with the use of a single scale or measure. Cognitive dysfunction and subjective experience of recovery should also be considered.

Patient Education

• Educate regarding the warning signs and symptoms of SAH.
• Educate regarding potential risk factors for aneurysmal SAH, including the following:
  • Hypertension
  • Cigarette smoking
  • Illicit drug use
  • Alcohol
• For excellent patient education resources, visit eMedicine's Headache Center. Also, see eMedicine's patient education article, Aneurysm, Brain.

Miscellaneous

Medicolegal Pitfalls

• Failure to consider the diagnosis of aneurysmal SAH
• Failure to order a CT scan for a severe headache that is atypical for the patient
• Failure to perform an LP if aneurysmal SAH is suspected and CT scan is negative
• Failure to recognize signs and symptoms of cerebral vasospasm or rebleeding

Special Concerns

• Aneurysmal SAH accounts for about 7% of maternal deaths during pregnancy. For women who are pregnant, the fetus should be shielded during CT scan and angiography.
• The teratogenic potential of nimodipine is unknown; therefore, use caution in pregnant women.
• Because of the risk of rebleeding, surgical or endovascular treatment of the aneurysm is recommended.
• Ischemic lesions on follow-up CT after aneurysmal SAH may be predicted by the severity of bleeding, delayed cerebral ischemia, excess weight, duration of temporary artery occlusion, and occurrence of nocturnal aneurysm rupture.

Multimedia

Media file 1: Cerebral aneurysms. Volume-rendered CT angiography of a left middle cerebral artery aneurysm.

Video available at http://img.medscape.com/pi/emed/ckb/neurology/1134815-1159751-1161518-1161653.flv.

Media file 2: Cerebral aneurysms. CT angiography of a right middle cerebral artery aneurysm.

Media file 3: Cerebral aneurysms. Sagittal multiplanar reformatted view of a left internal carotid artery aneurysm.

Media file 4: Cerebral aneurysms. Basilar tip aneurysm illustrated on CT scan (left) and T2-weighted MRI (right).

Media file 5: Cerebral aneurysms. Volume-rendered CT angiography of a basilar tip aneurysm.

Video available at http://img.medscape.com/pi/emed/ckb/neurology/1134815-1159751-1161518-1161657.swf.

Media file 6: Cerebral aneurysms. Aneurysm associated with an arteriovenous malformation (AVM) shown on T1-weighted MRI (left), 3D-time-of-flight MRI (middle), and conventional angiography (right).

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Keywords

intracranial aneurysm, intracerebral aneurysm, saccular aneurysm, berry aneurysm, giant aneurysm, fusiform aneurysm, dolichoectasia, infectious aneurysm, mycotic aneurysm

Contributor Information and Disclosures

Author

David S Liebeskind, MD, Associate Professor of Neurology, Program Director, Vascular Neurology Residency Program, University of California at Los Angeles; 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.

Medical Editor

Draga Jichici, MD, FRCP, Associate Clinical Professor, Department of Medicine, Division of Neurology and Critical Care Medicine, McMaster University, Canada
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

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: Boehringer Ingelheim Honoraria Speaking and teaching; BMS/Sanofi Honoraria Speaking and teaching; Novartis Honoraria Speaking and teaching

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health & Science University; 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; Talecris Consulting fee Review panel membership; AGA Medical Consulting fee Review panel membership; Boehringer Ingelheim Honoraria Speaking and teaching; Concentric Medical Consulting fee Review panel membership; Abbott Consulting fee Consulting; Sanofi  Consulting

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