eMedicine Specialties > Neurology > Introductory Topics

Cauda Equina and Conus Medullaris Syndromes: Treatment & Medication

Author: Segun T Dawodu, MD, JD, MBA, FAAPMR, FAANEM, CIME, DipMI(RCSed), Former Clinical Instructor, Mount Sinai Medical School; Current Director, Pain and Injuries Rehabilitation Services, PMRehab Pain and Sports Medicine Associates
Coauthor(s): Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Contributor Information and Disclosures

Updated: Feb 10, 2009

Treatment

Medical Care

Specific treatment is directed at the primary cause; these are discussed in other articles. As discussed below, the general treatment goals are to minimize the extent of injury and to treat ensuing general complications.

  • Acute care: In an acute setting, treatment options entail minimizing possible inflammation and preventing further trauma that might cause worsening of the injury. This is of even greater importance if the cause is trauma.
    • Maintenance of adequate airway, cardiopulmonary resuscitation, fluid management, and initial immobilization (using a molded thoracolumbosacral orthosis) are necessary to limit further damage.
    • Methylprednisolone should be administered as indicated in Medication. This treatment must be started within 8 hours of injury. No evidence exists of any benefit if it is started more than 8 hours after injury; on the contrary, late treatment may have detrimental effects.
    • Administration of GM1 ganglioside sodium salt beginning within 72 hours of injury may be beneficial; the dose is 100 mg IV qd for 18-32 days.
    • Tirilazad mesylate (a nonglucocorticoid 21-aminosteroid) has been proven to be of benefit in animals and is currently under investigation. It inhibits lipid peroxidation and hydrolysis in the same manner as glucocorticoids.
  • Any specific causal factor should be treated as soon as it has been identified.
  • Treatment/prevention of possible complications should begin immediately, including the following:
    • Deep venous thrombosis/pulmonary embolism: Patients should use antiembolic compression stockings and subcutaneous heparin for 3 months as prophylaxis. Low-molecular-weight heparin also has been approved for prophylaxis. Ultrasound of the lower extremities may need to be done as an initial screening test with follow-up later.
    • Neurogenic bladder: Patients may require bladder catheterization.
    • Pressure ulcers: These may be prevented by eliminating pressure, optimizing wound-healing environment, and debriding if necessary.
    • Impotence: Use of sildenafil (Viagra) is becoming popular. Other drugs include yohimbine, papaverine, and alprostadil. Methods to promote coitus and/or ejaculation could also be used; these include implantable penile prostheses or vibrator stimulation.
    • Fecal incontinence: Patients may require use of stool softener or manual evacuation.
    • Heterotopic ossification: Heterotropic ossification (HO) can be confirmed by a triple-bone scan with associated elevated alkaline phosphatase and phosphate, especially in the early stage. Treatment includes stretching exercises, disodium etidronate (20 mg/kg qd x 2 wk, then 10 mg/kg for as long as 12 wk), radiation, and surgical excision. Surgery is done only when the HO has matured or stabilized, which is evident by stable plain x-ray, normal alkaline phosphatase level, and decline in triple-phase bone scan activity.
    • Pain: Pain should be treated appropriately based on its origin; treatment may include narcotics in the acute setting and tricyclic antidepressants later. Patient education, biofeedback, and relaxation techniques may also be used.
    • Spasticity: Use of orthoses is advised to prevent contractures. Use of antispasticity medications also is encouraged. Other medications include dantrolene, diazepam, clonidine, and tizanidine. Nerve blocks also could be done to relieve spasticity; appropriate agents include phenol, botulinum toxin, or local anesthetics.

Surgical Care

In acute compression of the conus medullaris or cauda equina, surgical decompression as soon as possible (preferably within 6 h of injury) becomes mandatory. In a more chronic presentation with less severe symptoms, decompression could be performed when medically feasible and should be delayed to optimize the patient's medical condition; with this precaution, decompression is less likely to lead to irreversible neurological damage.

  • Surgical treatment may be necessary for decompression or tumor removal, especially if the patient presents with acute onset of symptoms. Surgical treatment may include any of the following:
    • Laminectomy and instrumentation/fusion for stabilization
    • Discectomy
  • Other surgical care may entail wound care, eg, debridement, skin graft, and skin flap/myocutaneous flap.

Consultations

Consultations to different specialties are needed for acute care and follow-up care.

  • Urgent consults for follow-up and advice of the following specialists may be required:
    • Neurosurgery/spinal orthopedics: This consultation should assess the need for urgent surgical spinal decompression. Posterior decompression and stabilization offers at least equivalent neurologic outcomes as nonoperative or anterior approaches and has the additional benefits of surgeon familiarity, shorter hospital stays, earlier rehabilitation, and ease of nursing care.1
    • Plastic surgery: Plastic surgery may be needed if severe skin breakdowns occur.
    • Rehabilitation: This initial consultation may prevent possible complications, including contractures, and may offer the patient advice on bladder/bowel management, wound management, and the required physical therapy/occupational therapy and assistive devices; this would include follow-up, involvement of social workers, and vocational rehabilitation experts for home adaptation (needed on discharge).
    • Dietitian: A dietitian is needed to advise on optimizing the diet to ensure adequate caloric and protein intake. Patients with these syndromes often have an increase in metabolism associated with the healing process.

Diet

See Consultations.

Activity

The rehabilitation team, especially the spinal cord injury rehabilitation physician and occupational and physical therapists, should be involved as soon as possible.

  • This entails setting goals in the rehabilitation unit toward maintaining and improving endurance, with the ability to be independent in activities of daily living on discharge from the hospital or long-term care facility.
  • The rehabilitation goals are to maximize the medical, physical, psychological, educational, vocational, and social function of the patient. This involves the following rehabilitation modalities:
    • Medical - Ensure adequate prevention and treatment of possible medical complications already discussed, especially deep venous thrombosis, bladder and bowel problems, and decubitus ulcers
    • Physical therapy - Range of motion and strengthening exercises, sitting balance, transfer training, and tilt table as tolerated (because of tendency to orthostatic hypotension). Tilt table should start at 15 degrees, progressing by 10 degrees every 15 minutes up to about 80 degrees with the necessary precautions. Other activities include wheelchair propulsion training, standing table exercises, functional electrical stimulation for increased muscle tone, use of lower extremity orthoses to aid balance and walking, along with ambulation exercises, family training and community skills, and a home exercise program.
    • Occupational therapy - Wheelchair training, especially for advanced wheelchair activities; transfer training; activities of daily living program with assistive devices for dressing, feeding, grooming, bathing, and toileting; motor coordination skills training; shower program; upper extremities training to increase strength for the increased demands of wheelchair propulsion and walking with assistive devices; home evaluation; family training; and a home exercise program.
    • Orthotic/assistive devices - May be needed for functional household ambulation and, if possible, community ambulation.
      • This entails prescribing and training in proper use of knee-ankle-foot orthoses (KAFO) with forearm crutches for support; for lower lesions, KAFOs or AFOs with canes or crutches may be needed.
      • In addition to the above, bathtub bench, transfer boards, pressure-relieving seats, and wheelchairs are devices that may be needed. The patient should be assessed for these needs prior to discharge from the acute rehabilitation setting.

Medication

The rationale for the medications listed in this section was outlined in Medical Care.

Corticosteroids

These agents have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.


Methylprednisolone sodium succinate (Adlone, Medrol, Solu-Medrol)

Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing increased capillary permeability. This prevents further worsening of injury.
Treatment must be started within 8 h of injury; apparently has no benefit if started > 8 h after injury. Late treatment may have detrimental effects.

Adult

30 mg/kg IV over 15 min followed by a 45-min break, then restart IV infusion at 5.4 mg/kg/h for 23 h; medication must be started within 8 h after injury; starting after 8 h may have detrimental effect

Pediatric

0.5-1.7 mg/kg/d or 5-25 mg/m2/d PO/IV/IM divided q6-12h

Digoxin may increase digitalis toxicity secondary to hypokalemia; estrogens may increase levels; phenobarbital, phenytoin and rifampin may decrease levels (adjust dose); monitor patients for hypokalemia when taking concurrent diuretics

Documented hypersensitivity; viral, fungal or tubercular skin infections

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

Hyperglycemia, edema, osteonecrosis, peptic ulcer disease, hypokalemia, osteoporosis, euphoria, psychosis, growth suppression, myopathy, and infections are possible complications of glucocorticoid use

Anticoagulants

These agents are taken as prophylaxis for deep venous thrombosis and/or pulmonary embolism.


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. Administer low dose.

Adult

5000 U SC q8-12h

Pediatric

Not established

Digoxin, nicotine, tetracycline, and antihistamines may decrease effects; NSAIDs, aspirin, dextran, dipyridamole, and hydroxychloroquine may increase toxicity

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

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 (gasping syndrome) by benzyl alcohol, which is used as preservative; caution in severe hypotension and shock

Skeletal muscle relaxants

These agents are thought to work centrally by suppressing conduction at the spinal level.


Baclofen (Lioresal)

May induce hyperpolarization of afferent terminals and inhibit both monosynaptic and polysynaptic reflexes at spinal level.

Adult

5 mg PO bid, with gradual increase q3d as tolerated to 30-80 mg qd in divided doses (tid/qid)
Intrathecal: Test dose 50-100 mcg, doses >50 mcg should be given in 25-mcg increments separated by 24h; maintenance: after positive response to test dose, initial dose (via intrathecal pump) is twice test dose, given over 24-h period

Pediatric

Generally not recommended for children <12 y for safety reasons
<12 years: 2.5 to 5 mg PO bid with gradual increase q3d as tolerated
<8 years: Not to exceed 30 mg/d
8-12 years: Not to exceed 60 mg/d
>12 years: Administer as in adults

Opiate analgesics, benzodiazepines, alcohol, TCAs, guanabenz, MAOIs, clindamycin, and hypertensive agents may increase effects

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 patients with history of autonomic dysreflexia and when spasticity is utilized to obtain increased function; autonomic dysreflexia can result from withdrawal of this medication


Dantrolene (Dantrium)

Stimulates muscle relaxation by modulating skeletal muscle contractions at site beyond myoneural junction and acting directly on muscle itself. Prevents calcium release from sarcoplasmic reticulum.

Adult

Begin with 25 mg PO qd; increase to 25 mg bid/qid, then by 25-mg increments to as high as 100 mg, bid/qid prn

Pediatric

Start with 0.5 mg/kg PO bid, increase to 0.5 mg/kg bid/qid, then by increments of 0.5 mg/kg to 3 mg/kg bid/qid prn; not to exceed 100 mg qid

Toxicity may increase with coadministration of clofibrate and warfarin; coadministration with estrogen may increase hepatotoxicity in women older than 35 y

Documented hypersensitivity; active hepatic disease (hepatitis and cirrhosis)

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

May cause hepatotoxicity (use only for recommended indications); caution in impaired pulmonary function and severe cardiac insufficiency; may cause photosensitivity with exposure to sunlight

Benzodiazepines

These agents may act in the spinal cord to induce muscle relaxation.


Diazepam (Diastat, Diazemuls, Valium)

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA.
Individualize dosage and increase cautiously to avoid adverse effects.

Adult

Mild spasms: 5-10 mg PO q4-6h prn
Moderate spasms: 5-10 mg IV prn
Severe spasms: Mix 50-100 mg in 500 mL D5W and infuse at 40 mL/h

Pediatric

Mild spasms: 0.1-0.8 mg/kg/d PO divided tid/qid
Moderate or severe spasms: 0.1-0.3 mg/kg IV q4-8h

Phenothiazines, barbiturates, alcohols, and MAOIs increase CNS toxicity when administered concurrently

Documented hypersensitivity; narrow-angle glaucoma

Pregnancy

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

Precautions

Caution with other CNS depressants, low albumin levels, or hepatic disease (may increase toxicity)

Alpha 2-adrenergic agonist agents

May reduce sympathetic outflow, which may produce a reduction in muscle tone.


Clonidine (Catapres)

Stimulates alpha2-adrenoreceptors in brain stem, activating an inhibitory neuron, which in turn results in reduced sympathetic outflow.

Adult

1 mg PO bid; titrate to effect; not to exceed 2.4 mg/d

Pediatric

5-30 mcg/kg/d PO

Tricyclic antidepressants inhibit hypotensive effects of clonidine; coadministration of clonidine with beta-blockers may potentiate bradycardia; tricyclic antidepressants may enhance hypertensive response associated with abrupt clonidine withdrawal; hypotensive effects of clonidine are enhanced by narcotic analgesics

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 cerebrovascular disease, coronary insufficiency, sinus node dysfunction, and renal impairment


Tizanidine (Zanaflex)

Centrally acting muscle relaxant metabolized in the liver and excreted in urine and feces.

Adult

4-8 mg PO q8h prn; not to exceed 36 mg/d

Pediatric

Not established

May interact with alcohol (increase somnolence, stupor) and oral contraceptives (which decrease its clearance), and can cause increased hypotensive effects when administered concurrently with diuretics

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 renal impairment

Neuromuscular blocker agent, toxin

These agents inhibit transmission of impulses in neuromuscular tissue.


Botulinum Toxin Type A (BOTOX®)

Binds to receptor sites on motor nerve terminals and inhibits release of acetylcholine, which in turn inhibits transmission of impulses in neuromuscular tissue.
Most useful for treating spasticity in the gastrocnemius and soleus muscles; less effective in larger muscles such as quadriceps. Re-examine patients 7-14 d after initial dose, to assess for response. May be repeated q3-4mo.

Adult

1.25-2.5 U (0.05-0.1 mL) IM injection into most active muscles; give q3-4mo

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Aminoglycosides or drugs that interfere with neuromuscular transmission may potentiate effects of botulinum toxin

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

Do not exceed recommended dosages and frequencies of administration; presence of antibodies to botulinum toxin type A may reduce effects of therapy; when used for cervical dystonia it may cause dysphagia, upper respiratory infection, neck pain, or headache; ptosis may occur when used for blepharism or strabismus
When used cosmetically for glabellar lines may cause headache, respiratory infection, flu syndrome, blepharoptosis, or nausea

Bisphosphonate derivatives

Analogs of pyrophosphate and act by binding to hydroxyapatite in bone-matrix, thereby inhibiting the dissolution of crystals. Prevent osteoclast attachment to the bone matrix and osteoclast recruitment and viability.


Etidronate disodium (Didronel)

Inhibits normal and abnormal bone resorption. Appears to inhibit bone resorption without inhibiting bone formation and mineralization.

Adult

20 mg/kg PO qd for 2 wk, then 10 mg/kg for as long as 12 wk

Pediatric

Not established

Coadministration with calcium containing products and other multivalent cations decrease absorption

Documented hypersensitivity; hypocalcemia, renal impairment

Pregnancy

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

Precautions

Monitor hypercalcemia-related parameters (eg, serum levels of calcium, phosphate, magnesium and potassium); maintain adequate intake of calcium and vitamin D to prevent severe hypocalcemia; caution if active upper GI problems; do not administer with alendronate for osteoporosis in postmenopausal women

Phosphodiesterase (type 5) enzyme inhibitors

These agents increase vasodilatory effects of nitric oxide by inhibiting the enzyme phosphodiesterase type 5, which in tun increases sensitivity for erections.


Sildenafil (Viagra)

Phosphodiesterase type 5 (PDE5) selective inhibitor. Inhibition of PDE5 increases cGMP activity, which increases vasodilatory effects of nitric oxide. Effective in men with mild-to-moderate ED. Take on an empty stomach about 1 h before sexual activity. Sexual stimulation is necessary to activate response. The increased sensitivity for erections may last 24 h. Available as 25-, 50-, and 100-mg tabs.

Adult

25-100 mg PO 1 h before sexual activity

Pediatric

Not established

Potentiates vasodilatory effect of NO, resulting in potentially fatal drop in blood pressure; coadministration with ketoconazole, erythromycin, or cimetidine increases plasma sildenafil concentrations; coadministration with rifampin decreases plasma levels of sildenafil

Documented hypersensitivity; concurrent or intermittent using of organic nitrates in any form

Pregnancy

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

Precautions

Adverse effects include headaches (16%), flushing (10%), upset stomach (7%), nasal congestion (4%), and a blue haze at the periphery of vision (3%); adverse effects occur more often in men taking the 100-mg dose; serious adverse effects occur in patients with severe heart disease and those who are taking nitrates; rates of MI were 1.7 and 1.4 per 100 man-years for sildenafil and placebo groups


Vardenafil (Levitra)

Phosphodiesterase type 5 (PDE5) selective inhibitor. Inhibition of PDE5 increases cGMP activity, which increases vasodilatory effects of nitric oxide. Effective in men with mild-to-moderate ED. Take on empty stomach about 1 h before sexual activity. Sexual stimulation is necessary to activate response. Increased sensitivity for erections may last 24 h. Available as 2.5-mg, 5-mg, 10-mg, and 20-mg tabs.

Adult

10 mg PO 1 h before sexual activity; may increase to maximum recommended dose of 20 mg or decreased to 5 mg based on efficacy and side effects
Concurrent administration with ritonavir: Not to exceed 2.5 mg PO q72h
Concurrent administration with indinavir, ketoconazole (400 mg PO qd), or itraconazole (400 mg PO qd): Not to exceed 2.5 mg PO q24h
Concurrent administration with ketoconazole (200 mg PO qd), itraconazole (200 mg PO qd), or erythromycin: Not to exceed 5 mg PO q24h

Pediatric

Not established

CYP3A4 inhibitors (eg, erythromycin, ketoconazole, itraconazole, indinavir, ritonavir) may significantly increase levels of vardenafil; vardenafil potentiates hypotensive effect of nitrates or alpha-blockers; avoid coadministration with other drugs that prolong QT interval (eg, quinidine, procainamide, amiodarone, sotalol)

Documented hypersensitivity; concurrent or intermittent use of alpha-blockers or organic nitrates in any form

Pregnancy

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

Precautions

Common adverse effects include headache, flushing, rhinitis, dyspepsia, or indigestion; assess cardiovascular status before use; caution with left ventricular outflow obstruction or conditions aggravated by hypotension or prolonged QT interval; caution with hepatic impairment (decrease dose); may cause prolonged or painful erection (<2%)


Tadalafil (Cialis)

Phosphodiesterase type 5 (PDE5) selective inhibitor. Inhibition of PDE5 increases cGMP activity, which increases vasodilatory effects of nitric oxide. Sexual stimulation is necessary to activate response. Increased sensitivity for erections may last 36 h. Available as 5-mg, 10-mg, and 20-mg tabs.

Adult

10 mg PO before sexual activity; may increase to maximum recommended dose of 20 mg or decreased to 5 mg based on efficacy and adverse effects; not to exceed 1 dose per day; may be taken without regard to food
Concurrent administration with potent CYP3A4 inhibitors (eg, ketoconazole, ritonavir): Not to exceed 10 mg PO q72h prn
Moderate renal impairment (CrCl 30-50 mL/min): 5 mg PO qd prn initially; may increase to 10 mg PO q48h prn
Severe renal impairment (CrCl <30 mL/min): Do not exceed 5 mg PO qd prn
Mild-to-moderate hepatic impairment: Do not exceed 10 mg PO qd prn

Pediatric

<18 years: Not established

CYP3A4 inhibitors (eg, erythromycin, ketoconazole, itraconazole, indinavir, ritonavir) may significantly increase levels of vardenafil; vardenafil potentiates hypotensive effect of nitrates or alpha-blockers; concurrent alcohol consumption may increase orthostatic hypotension risk

Documented hypersensitivity; concurrent or intermittent use of alpha-blockers (eg, doxazosin, terazosin, prazosin) or organic nitrates in any form

Pregnancy

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

Precautions

Common adverse effects include headache, flushing, rhinitis, dyspepsia, or indigestion; assess cardiovascular status before use; caution with left ventricular outflow obstruction or conditions aggravated by hypotension; caution with hepatic or renal impairment (decrease dose); may cause prolonged or painful erection; may cause back pain or myalgias

More on Cauda Equina and Conus Medullaris Syndromes

Overview: Cauda Equina and Conus Medullaris Syndromes
Differential Diagnoses & Workup: Cauda Equina and Conus Medullaris Syndromes
Treatment & Medication: Cauda Equina and Conus Medullaris Syndromes
Follow-up: Cauda Equina and Conus Medullaris Syndromes
Multimedia: Cauda Equina and Conus Medullaris Syndromes
References

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Further Reading

Keywords

lower spinal cord injury, compressive lumbosacral polyradiculopathy, cauda equina syndrome, conus medullaris syndrome, spinal cord compression, back pain, spinal cord injury, upper motor neuron symptoms, UMN symptoms, lower motor neuron symptoms, LMN symptoms, spinal cord syndromes

Contributor Information and Disclosures

Author

Segun T Dawodu, MD, JD, MBA, FAAPMR, FAANEM, CIME, DipMI(RCSed), Former Clinical Instructor, Mount Sinai Medical School; Current Director, Pain and Injuries Rehabilitation Services, PMRehab Pain and Sports Medicine Associates
Segun T Dawodu, MD, JD, MBA, FAAPMR, FAANEM, CIME, DipMI(RCSed) is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American College of Sports Medicine, American Medical Association, American Medical Informatics Association, Association of Academic Physiatrists, International Society of Physical and Rehabilitation Medicine, and Royal College of Surgeons of England
Disclosure: Nothing to disclose.

Coauthor(s)

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

Medical Editor

Milind J Kothari, DO, Professor and Vice-Chair, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Hershey Medical Center
Milind J Kothari, DO is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and American Neurological Association
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

James H Halsey, MD, Professor, Department of Neurology, University of Alabama Medical Center
James H Halsey, MD is a member of the following medical societies: American Academy of Neurology, American Heart Association, American Medical Association, American Neurological Association, American Society of Neuroimaging, Medical Association of the State of Alabama, New York Academy of Sciences, Pan American Medical Association, Sigma Xi, Society for Neuroscience, and Southern Medical Association
Disclosure: Nothing to disclose.

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

Nicholas Y Lorenzo, MD, Chief Editor, eMedicine Neurology; Consulting Staff, Neurology Specialists and Consultants
Nicholas Y Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Neurology
Disclosure: Nothing to disclose.

 
 
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