eMedicine Specialties > Neurology > Critical Care Neurology

Epidural Hematoma

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

Epidural hematoma (ie, accumulation of blood in the potential space between dura and bone) may be intracranial (EDH) or spinal (SEDH). Intracranial epidural hematoma occurs in approximately 2% of patients with head injuries and 5-15% of patients with fatal head injuries. Intracranial epidural hematoma is considered to be the most serious complication of head injury, requiring immediate diagnosis and surgical intervention. Intracranial epidural hematoma may be acute (58%), subacute (31%), or chronic (11%). Spinal epidural hematoma may also be traumatic, though it may occur spontaneously.

This MRI demonstrates spinal epidural hematoma.

Pathophysiology

Epidural hematoma usually results from a brief linear contact force to the calvaria that causes separation of the periosteal dura from bone and disruption of interposed vessels due to shearing stress. Skull fractures occur in 85-95% of adult cases, but they are much less common in children because of the plasticity of the immature calvaria. Arterial or venous structures may be compromised, causing rapid expansion of the hematoma; however, chronic or delayed manifestations may occur when venous sources are involved. Extension of the hematoma usually is limited by suture lines owing to the tight attachment of the dura at these locations. Recent analyses have revealed that epidural hematomas may actually traverse suture lines in a minority of cases.¹

The temporoparietal region and the middle meningeal artery are involved most commonly (66%), although the anterior ethmoidal artery may be involved in frontal injuries, the transverse or sigmoid sinus in occipital injuries, and the superior sagittal sinus in trauma to the vertex. Bilateral epidural hematomas account for 2-10% of all acute epidural hematomas in adults but are exceedingly rare in children. Posterior fossa epidural hematomas represent 5% of all cases of epidural hematomas.

Spinal epidural hematoma may be spontaneous or may follow minor trauma, such as lumbar puncture or epidural anesthesia. Spontaneous spinal epidural hematoma may be associated with anticoagulation, thrombolysis, blood dyscrasias, coagulopathies, thrombocytopenia, neoplasms, or vascular malformations. The peridural venous plexus usually is involved, though arterial sources of hemorrhage also occur. The dorsal aspect of the thoracic or lumbar region is involved most commonly, with expansion limited to a few vertebral levels.

Frequency

United States

Epidural hematoma complicates 2% of cases of head trauma (approximately 40,000 cases per year). Spinal epidural hematoma affects 1 per 1,000,000 people annually. Alcohol and other forms of intoxication have been associated with a higher incidence of epidural hematoma.

International

International frequency is unknown, though it is likely to parallel the frequency in the United States.

Mortality/Morbidity

Mortality rate associated with epidural hematoma has been estimated to be 5-50%.

• The level of consciousness prior to surgery has been correlated with mortality rate: 0% for awake patients, 9% for obtunded patients, and 20% for comatose patients.
• Bilateral intracranial epidural hematoma has a mortality rate of 15-20%.
• Posterior fossa epidural hematoma has a mortality rate of 26%.

Race

No racial predilection has been reported.

Sex

Intracranial and spinal epidural hematomas are more frequent in men, with a male-to-female ratio of 4:1.

Age

• Intracranial epidural hematoma is rare in individuals younger than 2 years.
• Intracranial epidural hematoma is also rare in individuals older than 60 years because the dura is tightly adherent to the calvaria.
• Spinal epidural hematoma has a bimodal distribution with peaks during childhood and during the fifth and sixth decades of life. Increasing age has been noted as a risk factor for postoperative spinal epidural hematoma.

Clinical

History

Epidural hematoma should be suspected in any individual who sustains head trauma. Although classically associated with a lucid interval between the initial loss of consciousness at the time of impact and a delayed decline in mental status (10-33% of cases), alterations in the level of consciousness may have a variable presentation. Posterior fossa epidural hematoma may exhibit a rapid and delayed progression from minimal symptoms to even death within minutes.

• Symptoms of epidural hematoma include the following:
  • Headache
  • Nausea/vomiting
  • Seizures
  • Focal neurologic deficits (eg, visual field cuts, aphasia, weakness, numbness)
• Spinal epidural hematoma typically causes severe localized back pain with delayed radicular radiation that may mimic disk herniation. Associated symptoms may include the following:
  • Weakness
  • Numbness
  • Urinary incontinence
  • Fecal incontinence

Physical

• The physical examination should include a thorough evaluation for evidence of traumatic sequelae and associated neurological deficits, including the following:
  • Bradycardia and/or hypertension indicative of elevated intracranial pressure
  • Skull fractures, hematomas, or lacerations
  • Cerebrospinal fluid (CSF) otorrhea or rhinorrhea resulting from skull fracture with disruption of the dura
  • Hemotympanum
  • Instability of the vertebral column
  • Alteration in level of consciousness (ie, Glasgow Coma Scale score)
  • Anisocoria (eg, ipsilateral dilation of the pupil due to uncal herniation with compression of the oculomotor nerve)
  • Facial nerve injury
  • Weakness (eg, contralateral hemiparesis due to compression of the cerebral peduncle)
  • Other focal neurological deficits (eg, aphasia, visual field defects, numbness, ataxia)
• Spinal epidural hematoma may have variable findings on physical examination, determined by the level of the lesion. The findings include the following:
  • Weakness (unilateral or bilateral)
  • Sensory deficits with radicular paresthesias (unilateral or bilateral)
  • Various alterations in reflexes
  • Alterations of bladder or anal sphincter tone

Causes

• Trauma
• Anticoagulation
• Thrombolysis
• Lumbar puncture
• Epidural anesthesia
• Coagulopathy or bleeding diathesis
• Hepatic disease with portal hypertension
• Cancer
• Vascular malformation
• Disk herniation
• Paget disease of bone
• Valsalva maneuver
• Hypertension
• Chiropractic manipulation²

Differential Diagnoses

Other Problems to Be Considered

Back pain
Spinal Cord Disease

Workup

Laboratory Studies

• Complete blood count (CBC) with platelets - To monitor for infection and assess hematocrit and platelets for further hemorrhagic risk.
• Prothrombin time (PT)/activated partial thromboplastin time (aPTT) - To identify bleeding diathesis.
• Serum chemistries, including electrolytes, blood urea nitrogen (BUN), creatinine, and glucose - To characterize metabolic derangements that may complicate clinical course.
• Toxicology screen and serum alcohol level - To identify associated causes of head trauma and establish need for surveillance with regard to withdrawal symptoms.
• Type and hold an appropriate amount of blood - To prepare for necessary transfusions needed because of blood loss or anemia.

Imaging Studies

• Plain radiography of the head (skull radiography) may reveal skull fractures, though CT scanning has largely replaced the use of skull radiography because the diagnostic information is so much greater with CT. Cervical spine radiographs with anteroposterior, lateral, and odontoid views are useful to identify associated traumatic fractures. Plain radiographs of the vertebral column may identify a cavernous angioma.
• Myelography outlines the epidural space and may illustrate a space-occupying mass. CT myelography may be used when MRI is unavailable or if the patient cannot tolerate MRI.
• Noncontrast CT scanning of the head not only visualizes skull fractures but also directly images an epidural hematoma.
  • Acute epidural hematoma may appear as a hyperdense lenticular-shaped mass situated between the brain and the skull, though regions of hypodensity may be seen with serum or fresh blood. On rare occasion, an acute epidural may appear completely isointense with respect to brain. Planoconvex or crescent-shaped epidural hematoma must be differentiated from subdural hemorrhage. Subacute lesions are homogenously hyperdense.
  • Chronic epidural hematoma may have a heterogeneous appearance due to neovascularization and granulation, with peripheral enhancement on contrast administration.
  • CT scanning may also depict air collections and displacement of brain parenchyma.
  • Clinical deterioration should prompt repeat imaging with CT scanning.
• MRI also demonstrates the evolution of an epidural hematoma, though this imaging modality may not be appropriate for patients in unstable condition.
  • Spinal MRI may delineate the location of an epidural hematoma and identify an associated vascular malformation.
  • Spinal cord enhancement may be apparent and should be distinguished from inflammation or neoplasia.
  • Diffusion-weighted imaging with the use of periodically rotated overlapping parallel lines with enhanced reconstruction (PROPELLER) MRI may be used for improved detection of acute spinal epidural hematoma.³
  • Gadolinium-enhanced magnetic resonance arteriography (MRA) may further define the extent of an arteriovenous malformation.
• Conventional angiography may be required to demonstrate definitively the presence of a vascular malformation.

Other Tests

Functional studies of the spinal cord, such as somatosensory evoked potentials, may be used for intraoperative monitoring or for prognostication following surgery.

Procedures

• Emergent decompression with placement of a burr hole may be necessary when neurosurgical consultation is unavailable. For patients showing rapid deterioration with clinical signs of impending herniation, place a burr hole on the side of the dilating pupil. In the absence of a CT scan, place the burr hole 2 finger widths anterior to the tragus of the ear and 3 finger widths above the tragus of the ear.⁴
• Lumbar puncture provides little additional information and may exacerbate neurologic damage.

Treatment

Medical Care

Initial resuscitation efforts should include assessment and stabilization of airway patency, breathing, and circulation. A thorough trauma evaluation is mandatory, including inspection for skull fractures and appreciation of the force and location of impact. Immobilization of the spine should be followed by emergent transfer of the patient to the nearest level I trauma center supported with neurosurgical consultation.

• Triage and initial management of a patient with epidural hematoma may be tailored to the degree of neurological impairment at presentation. Alert patients may be evaluated with a CT scan following a brief neurologic examination.
• A patient with a small epidural hematoma may be treated conservatively, though close observation is advised, as delayed, yet sudden, neurological deterioration may occur.
• Trauma patients may require diagnostic peritoneal lavage and radiographs of the chest, pelvis, and cervical spine.
• While neurosurgical consultation is requested, administer intravenous fluids to maintain euvolemia and to provide adequate cerebral perfusion pressure.
• Patients with elevated intracranial pressure may be treated with osmotic diuretics and hyperventilation, with elevation of the head of the bed at an angle of 30 degrees. Patients who are intubated may be hyperventilated with intermittent mandatory ventilation at a rate of 16-20 breaths per minute and tidal volume of 10-12 mL/kg. A carbon dioxide partial pressure of 28-32 mm Hg is ideal, as severe hypocapnia (<25 mm Hg) may induce cerebral vasoconstriction and ischemia.
• Coagulopathy or persistent bleeding may require administration of vitamin K, protamine sulfate, fresh frozen plasma, platelet transfusions, or clotting factor concentrates.

Surgical Care

Although several recent reports have described successful conservative management of epidural hematoma, surgical evacuation constitutes definitive treatment of this condition. Craniotomy or laminectomy is followed by evacuation of the hematoma, coagulation of bleeding sites, and inspection of the dura. The dura is then tented to the bone and, occasionally, epidural drains are employed for as long as 24 hours.

• Minimally invasive surgical procedures, including the use of burr holes and negative pressure drainage, may be used in selected cases.
• Novel therapeutic approaches
  • Endovascular embolization to minimize bleeding during the acute stage
  • Thrombolytic evacuation using closed suction drain

CT scanning performed before and after surgical evacuation of an intracranial epidural hematoma.

Consultations

• Neurosurgeon (for potential emergent evacuation of the hematoma)
• Neurologist
• Rehabilitation specialist

Diet

The hypermetabolic and catabolic phenomena associated with severe head injury necessitate caloric supplementation. Initiate enteral feedings as soon as possible.

Activity

Patients who are treated conservatively should undergo close observation and should avoid strenuous activity. Inpatients should remain on bedrest during the initial phase; this can be followed by a progressive increase in activity.

Medication

Osmotic diuretics, such as mannitol or hypertonic saline, may be used to diminish intracranial pressure. As hyperthermia may exacerbate neurological injury, acetaminophen may be given to reduce fevers. Anticonvulsants are used routinely to avoid seizures that may be induced by cortical damage. Patients with spinal epidural hematoma may require high-dose methylprednisolone when spinal cord compression is involved. Immobilized patients may require heparin for prevention of venous thrombosis, whereas vitamin K and protamine may be administered to restore normal coagulation parameters. Antacids are used to prevent gastric ulcers associated with traumatic brain injury and spinal cord damage.

Osmotic diuretics

These agents reverse the pressure gradient across the blood-brain barrier, reducing intracranial pressure.

Mannitol (Osmitrol, Resectisol)

Reduces cerebral edema by osmotic forces and decreases blood viscosity, resulting in reflex vasoconstriction and lowering of intracranial pressure.

Dosing

Adult

0.75-1 g/kg IV, followed by 0.25-0.5 g/kg IV q3-5h to maintain serum hyperosmolarity (approximately 320 mOsm/L)

Pediatric

Not established; dose is dependent on weight, clinical condition, and laboratory results

Interactions

May decrease serum lithium levels

Contraindications

Documented hypersensitivity; anuria; severe pulmonary congestion or frank pulmonary edema; active intracranial bleeding; severe dehydration; progressive renal or cardiac failure

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

Perform periodic clinical evaluation and laboratory assessment to monitor changes in serum osmolarity, fluids, and electrolytes; persistently elevated serum osmolarity may result in rebound intracranial hypertension
Caution in renal dysfunction, hypervolemia, urinary tract obstruction, or cardiovascular instability

Antipyretic agents

These agents are helpful in relieving the fever associated with the condition.

Acetaminophen (Tylenol, Feverall, Aspirin Free Anacin)

Reduces fever and maintains normothermia. DOC for pain in patients with documented hypersensitivity to aspirin or NSAIDs, with upper GI disease, or who are taking oral anticoagulants.

Dosing

Adult

650 mg PO/PR q4-6h; not to exceed maximum daily dosage of 4 g

Pediatric

<12 years: 10-15 mg/kg/dose PO/PR q4-6h prn; not to exceed 2.6 g/d
>12 years: 325-650 mg PO/PR q4h; not to exceed 5 doses (2.6 g) in 24 h

Interactions

Rifampin can reduce analgesic effects; barbiturates, carbamazepine, hydantoins, and isoniazid may increase hepatotoxicity

Contraindications

Documented hypersensitivity; known G-6-P deficiency; hepatic dysfunction

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

Hepatotoxicity possible in patients with chronic alcoholism following various dose levels; severe or recurrent pain or high or continued fever may indicate serious illness; acetaminophen contained in many OTC products and combined use with these products may result in cumulative doses exceeding recommended maximum dose

Anticonvulsants

These agents reduce frequency of early posttraumatic seizures from 14% to 4%, but they do not prevent later seizures. If seizures are not experienced for 7-10 d, the drug may be discontinued.

Fosphenytoin (Cerebyx)

Converted to phenytoin, which modulates neuronal voltage-dependent sodium channels.

Dosing

Adult

15-20 mg/kg IV loading dose, followed by 300 mg IV q24h

Pediatric

Not established; weight-adjusted dosage similar to that in adults

Interactions

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

Contraindications

Documented hypersensitivity; sinus bradycardia; sinoatrial 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

Avoid rapid administration to reduce risks of hypotension and cardiac arrhythmias; monitor for blood dyscrasias with serial blood tests; discontinue use if skin rash appears and do not resume use if rash is exfoliative, bullous, or purpuric; use caution in patients with acute intermittent porphyria, diabetes, or hepatic dysfunction

Corticosteroids

Anti-inflammatory properties mitigate tissue damage in spinal cord compression.

Methylprednisolone (Adlone, Medrol, Solu-Medrol)

Reduces injury associated with spinal cord compression. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability.

Dosing

Adult

30 mg/kg IV bolus, followed by 4 mg/kg IV infusion over next 23 h

Pediatric

Administer as in adults

Interactions

Inhibits metabolism of cyclosporine; inducers of hepatic enzymes (eg, phenobarbital, phenytoin, rifampin) increase clearance; troleandomycin and ketoconazole inhibit metabolism; variable interaction with aspirin and oral anticoagulants

Contraindications

Documented hypersensitivity; systemic fungal infection

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

Caution in ulcerative colitis, peptic ulcer disease, renal insufficiency, hypertension, osteoporosis, myasthenia gravis, hypothyroidism, cirrhosis, and ocular herpes simplex; reductions in dosage should be gradual; psychic derangements may occur

Antidotes

These agents reverse some coagulopathies or bleeding diatheses.

Phytonadione; vitamin K (AquaMEPHYTON, Konakion, Mephyton)

Promotes hepatic synthesis of clotting factors that inhibit warfarin effects.

Dosing

Adult

2.5-10 mg IM/SC; repeat administration q6-8h until PT normalized

Pediatric

Not established; suggested dose is as in adults

Interactions

Antagonizes effects of warfarin sodium and dicumarol

Contraindications

Documented hypersensitivity

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

Ineffective in hereditary hypoprothrombinemia

Protamine sulfate

Neutralizes effects of heparin.

Dosing

Adult

Dosage adjusted to time interval since discontinuation of IV heparin
Immediately: 1-1.5 mg/100 U heparin
30-60 min from discontinuation of heparin: 0.5-0.75 mg/100 U heparin
>60 min from discontinuation of heparin: 0.25-0.375 mg/100 U heparin
If SC heparin used, give 1-1.5 mg/100 U heparin; not to exceed 50 mg IV over 10 min

Pediatric

Not established; suggested dose is as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

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

Anticoagulant effects may occur if maximum dose exceeded

Antacids

These agents provide prophylaxis of gastric ulcers.

Famotidine (Pepcid)

Competitively inhibits histamine at H2 receptor of gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and hydrogen concentrations. Minimizes development of gastric ulcers.

Dosing

Adult

20 mg IV/PO bid

Pediatric

Not established; suggested dose is as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

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

Precautions

Adjust dosage in patients with renal insufficiency

Anticoagulants

These agents reduce risk of venous complications in immobilized patients.

Heparin

Augments activity of antithrombin III and prevents conversion of fibrinogen to fibrin. Does not actively lyse but is able to inhibit further thrombogenesis. Prevents re-accumulation of clot after spontaneous fibrinolysis. Used for prophylaxis of deep venous thrombosis.

Dosing

Adult

5000 U SC bid

Pediatric

Weight-adjusted dosage

Interactions

Antiplatelet agents may exacerbate hemorrhagic risk associated with heparin; digitalis, tetracyclines, nicotine, and antihistamines may interfere with heparin; precipitates may form when used in conjunction with doxorubicin, droperidol, ciprofloxacin, or mitoxantrone

Contraindications

Documented hypersensitivity; subacute bacterial endocarditis; active bleeding; history of heparin-induced thrombocytopenia

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

In neonates, preservative-free heparin recommended to avoid possible toxicity (ie, gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock; monitor for bleeding in peptic ulcer disease, menstruation, increased capillary permeability, and when giving IM injections; discontinue use if thrombocytopenia develops

Follow-up

Further Inpatient Care

Following initial management in the emergency department, the patient may be sent for emergent neurosurgical evacuation of the hematoma or may be transferred to the ICU for further care. Subsequent care generally includes the following:

• Serial neurologic examinations
• Treatment of elevated intracranial pressure
• Avoidance of hypotension or hypertension (ie, maintain mean arterial pressure [MAP] between 70-130 mm Hg)
• Use of isotonic solutions, such as normal saline, to minimize cerebral edema
• Avoidance of hyperthermia
• Treatment or prevention of posttraumatic seizures
• Observation and potential repair of CSF leaks
• Treatment of urinary tract infections
• Prevention of venous thrombosis
• Prophylaxis for gastric ulcers
• Physical, occupational, and speech therapy
• Repeat CT scan for clinical deterioration

Further Outpatient Care

After hospital discharge, continued physical, occupational, and speech therapy may be required.

Inpatient & Outpatient Medications

• Mannitol or other osmotic diuretics for elevated intracranial pressure
• Steroids for spinal cord compression
• Acetaminophen for fever
• Subcutaneous heparin for prevention of venous complications
• Famotidine or other antacids for gastric ulcer prophylaxis
• Fosphenytoin or other anticonvulsants for posttraumatic seizures
• Anticholinergics for bladder complications
• Baclofen, diazepam, or tizanidine for spasticity due to spinal cord damage
• Amitriptyline, carbamazepine, or gabapentin for neuropathic pain

Transfer

Although emergent decompression of an epidural hematoma should not be delayed, trauma patients should be transferred to centers with neurosurgical expertise.

Deterrence/Prevention

• Educate the public regarding traumatic brain injury, including appropriate use of safety equipment, precautions, and measures that may reduce the incidence of head injury.
• Avoid lumbar puncture or epidural anesthesia in individuals on anticoagulation, following thrombolysis, or when a bleeding diathesis is suspected.

Complications

• Neurological deficits or death may occur.
• Posttraumatic seizures due to cortical damage may develop 1-3 months after the initial injury, with decreasing frequency over time. Alcoholism increases the risk of posttraumatic seizures.
• Delayed effects of an epidural hematoma include the postconcussion syndrome, which is characterized by headaches, dizziness, vertigo, restlessness, emotional lability, inability to concentrate, and fatigue.
• Spinal epidural hematoma may cause spasticity, neuropathic pain, and urinary complications.

Prognosis

• Declines with advancing age
• Deteriorates when associated with other intracranial injuries
• Depends on the initial Glasgow Coma Scale score (0% mortality for awake patients, 40% mortality for comatose individuals)
• Worsens with delays between injury and surgical intervention
• In spinal epidural hematoma, the MRI appearance of T2-hyperintensity within the spinal cord may portend a poor clinical outcome.⁵

Patient Education

Educate patients regarding prevention of traumatic brain injury, with particular emphasis on sports injuries, use of safety precautions, and proper use of safety equipment.

Miscellaneous

Medicolegal Pitfalls

• Consider epidural hematoma in all patients who have experienced head injury.
• Alteration in the level of consciousness may be highly variable and unreliable as a clinical predictor.
• Obtain CT scan whenever possible.
• Skull fractures are not always present, particularly in children.
• Delayed transfer and triage may be the principal determinant of death.
• Close observation requires frequent neurologic evaluations.

Multimedia

Media file 1: CT scanning performed before and after surgical evacuation of an intracranial epidural hematoma.

Media file 2: This MRI demonstrates spinal epidural hematoma.

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Keywords

epidural hemorrhage, extradural hematoma, extradural hemorrhage, cerebral epidural hematoma, spinal epidural hematoma, EDH, SEDH, head injury, intracranial epidural hematoma

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

Edward L Hogan, MD, Professor, Department of Neurology, Medical College of Georgia; Emeritus Professor and Chair, Department of Neurology, Medical University of South Carolina
Edward L Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, American Neurological Association, American Society for Biochemistry and Molecular Biology, Phi Beta Kappa, Sigma Xi, Society for Neuroscience, and Southern Clinical Neurological Society
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

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

CME Editor

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, University of South Florida School of Medicine, Tampa General Hospital
Selim R Benbadis, MD is a member of the following medical societies: American Academy of Neurology, American Academy of Sleep Medicine, American Clinical Neurophysiology Society, American Epilepsy Society, and American Medical Association
Disclosure: Nothing to disclose.

Chief Editor

Helmi L Lutsep, MD, Professor, Department of Neurology, Oregon Health and 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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