eMedicine Specialties > Neurology > Electroencephalography and Evoked Potentials

Somatosensory Evoked Potentials, Clinical Applications

Jasvinder Chawla, MBBS, MD, MBA, Chief of Neurology, Hines Veterans Affairs Hospital; Associate Professor and Director, Neurology Residency Training Program, Loyola University Medical Center
Jorge G Burneo, MD, MSPH, Assistant Professor of Neurology, Epidemiology, and Biostatistics, Department of Clinical Neurological Sciences, Epilepsy Program, London Health Sciences Centre, University of Western Ontario, Canada; Gregory L Barkley, MD, Director of the Comprehensive Epilepsy Program, Department of Neurology, Henry Ford Health System; Associate Professor, Case Western Reserve University

Updated: Dec 17, 2008

Introduction

Somatosensory evoked potentials (SEPs) are generated by stimulation of afferent peripheral nerve fibers by either physiological or electrical means. SEPs were first recorded more than 50 years ago. For an explanation of their physiologic and anatomic basis and description of techniques, see Somatosensory Evoked Potentials: General Principles. In this article, the focus is on the clinical applications of SEPs.

SEPs can be recorded after physiological stimuli (eg, muscle stretch). However, electrical stimulation usually is administered to elicit the potential. Typically, a square wave of 0.2- to 2-millisecond duration is delivered to a peripheral nerve by electrodes, usually surface electrodes. For intraoperative monitoring, needle electrodes are used for stimulation since they require smaller currents, which reduce the stimulus artifact. The usual sites for SEP stimulation are the median nerve at the wrist, the common peroneal nerve at the knee, and the posterior tibial nerve. A SEP also may be recorded by stimulating the skin in various dermatomal areas, but the response is much weaker.

In mixed peripheral nerves, the threshold for sensory perception is lower than the threshold to elicit movement. For stimulation of mixed peripheral nerves, the stimulating current is adjusted to produce a minimal movement of the joint involved. This stimulation intensity typically is well tolerated by patients. Recording electrodes are placed on the scalp and over the cervical spine. For recording upper extremity SEPs, electrodes are placed over the Erb point. For recording lower extremity SEPs, electrodes are placed over the lumbosacral spine.

Waveforms are described in terms of morphology, amplitude, and dispersion. Each laboratory should establish reference values for latencies and interpeak latencies that are based on a patient's age and height. Because limb cooling affects peripheral nerve conduction velocity, minimum skin temperature norms should be established for each laboratory.

Responses recorded are classified according to specific latencies. "Short-latency" SEPs refer to the portion of the SEP waveform that occurs within 25 milliseconds after stimulation of the upper extremity nerves, 40 milliseconds after stimulation of the peroneal nerve, or 50 milliseconds after stimulation of the tibial nerve. "Long-latency" refers to the waveforms recorded more than 100 milliseconds following stimulation of these nerves. "Middle-latency" SEP refers to waveforms that occur between these 2 periods.

Mixed nerve stimulation has become the standard for clinical use. Other methods include cutaneous nerve stimulation, dermatomal stimulation (which is more specific than cutaneous nerve stimulation), motor point stimulation, and paraspinal stimulation.

Clinical Interpretation

The SEP stimulus preferentially excites only the largest myelinated fibers in the peripheral nerve. These include cutaneous and subcutaneous fibers, somesthetic and proprioceptive fibers, and motor axons of equivalent diameter. The stimulus activates predominantly the large-diameter, fast-conducting group in muscles and group II cutaneous fibers. Stimulation produces an action potential that travels up the axon toward the spinal cord and past the cell bodies of the sensory axons of the large-fiber sensory system in the dorsal root ganglia to the ipsilateral posterior columns of the spinal cord. These signals then traverse a synapse in the dorsal column nuclei at the cervicomedullary junction.

The signals travel in second-order neurons to the ventroposterolateral nucleus of the thalamus (VPL) via the medial lemniscus. In the VPL, a synapse is made with a third-order neuron that travels to area 3b of the parietal sensory cortex. SEPs provide information concerning the integrity of the pathway through the brain, brain stem, spinal cord, dorsal roots, and peripheral nerves.

Although SEPs may reveal or localize a lesion involving the somatosensory pathways, they should be interpreted as extended neurologic examination. They do not indicate the underlying disease process and normal findings do not exclude an organic basis for symptoms. Despite these limitations, SEP studies may be helpful diagnostically as well as prognostically to determine the extent of pathologic involvement in different disorders.

Clinical Uses

Clinical uses of SEPs include the following:

Evaluation of the peripheral nervous system and the large-fiber sensory tracts in the CNS
Localization of the anatomic site of somatosensory pathway lesions
Identification of impaired conduction caused by axonal loss or demyelination
Confirmation of a nonorganic cause of sensory loss

Although SEP findings are not disease specific, they can confirm afferent conduction impairment associated with certain disorders.

Other disorders

SEPs have been used to confirm the presence of normal conduction pathways in patients with conversion disorder, malingering, or other psychological disturbances. Findings must be interpreted carefully, because normal SEPs can be seen in patients with organic sensory loss. For example, some patients with pure sensory strokes due to lacunar infarcts may have normal SEPs.

Peripheral Nervous System

SEPs may be used in evaluation of the peripheral nervous system when traditional nerve conduction studies (NCSs) are not possible (for any reason) or are not reliable (eg, technical problems, or artifacts).

Peripheral neuropathy

SEPs are rarely used to assess peripheral neuropathy since standard NCSs are the test of choice. The stimulation is applied at 2 or more sites and the responses are recorded over the scalp. In the presence of polyneuropathies and mononeuropathies, SEP waveforms recorded over the scalp may be absent or show delayed latencies with normal central conduction velocities. In this way, SEPs can be used to measure the afferent fiber conduction velocities of proximal segments. Higher stimulation currents are typically required in patients with peripheral neuropathies.

SSEP studies disclosed poorly formed and delayed cortical potentials with absent lumbar (N20) potentials, thereby suggesting the presence of proximal demyelination. SSEPs were normal in the patients with pure motor CIDP and multifocal motor neuropathy (MMN) and can thus help differentiate asymmetric forms of CIDP from MMN. These findings suggest that SSEPs may be an important complementary investigation to conventional NCSs in the diagnosis of chronic acquired demyelinating polyneuropathies (CADP).

Use of SEPs has been reported for the following peripheral nerve disorders:

Hereditary neuropathies (eg, Charcot-Marie-Tooth disease, Friedreich ataxia)
Diabetic neuropathy
Inflammatory polyradiculopathies, such as Guillain-Barré syndrome, particularly early in the course of the disease, when distal conduction and F-wave studies may be normal
Chronic acquired demyelinating neuropathies
Infectious causes (eg, HIV)
Toxic neuropathies

Focal neuropathy

The test of choice in focal neuropathy is standard NCSs. Entrapment neuropathies, such as carpal tunnel syndrome, may be found incidentally when SEPs are recorded. The use of SEP for detection of saphenous neuropathy, intercostal neuropathy, and trigeminal neuropathy has been reported. However, standard NCSs are the preferred diagnostic test for these conditions.

Plexopathy

SEPs are useful for evaluation of brachial plexopathy and traumatic plexopathies. In thoracic outlet syndrome, SEPs are of limited value with regard to the neurogenic variety of plexopathy and have no established value in diagnosis of the nonneurogenic (ie, vascular) variety. The value of SEPs in preventing or minimizing intraoperative damage of the peripheral nervous system is unproven.

Ventral rootlets and roots

Studies suggest that SEPs may have some use in the evaluation of rootlet and root dysfunction. However, needle electromyography (EMG) provides superior information in these disorders and remains the test of choice.

Lumbosacral root disease

SEPs may have some utility in the evaluation of acute lumbosacral root disease or in lumbosacral spinal stenosis.

Thoracic root disease

No data are available.

Cervical root disease

EMG is the best neurophysiological tool for evaluation of this condition. SEPs may or may not have a limited role in these conditions.

Spinal Cord

Trauma

Scalp-recorded potentials are absent in complete lesions of the cervical spinal cord. However, incomplete lesions yield varying abnormalities on SEPs. SEPs can help localize the sensory level in trauma and also may help in determining prognosis for functional outcome. Latencies and amplitudes of tibial SSEPs can change over time after spinal cord injury (SCI). The early recordability of a tibial SSEP is associated with a favorable functional and neurological status and outcome after SCI.

Surgical monitoring

SEP monitoring is used widely to assess integrity of the spinal cord during surgery in which the spinal cord is manipulated. SEPs are used most often during scoliosis correction. Ischemia of ascending somatosensory pathways produces a drop in amplitude or loss of waveforms, thus warning the surgeon in time to take corrective action. Ischemic changes are usually widespread; rarely, motor function is lost when somatosensory pathways have not been affected.

Other spinal procedures in which SEP monitoring is used include reduction of vertebral fractures and other vertebral injuries and spinal cord tumor surgery. Conduction abnormalities that selectively abolish the silent periods can distinguish between hydromyelia (a physiologically dilated central canal) and space-occupying syringomyelia.

Conditions for which SEPs might be useful

Subacute combined degeneration
Cervical spondylosis and myelopathy
Syringomyelia, to evaluate the effect of spinal cord compression
Hereditary spastic paraplegia
Transverse myelitis
Multiple sclerosis - Lower-limb SEPs produce a higher yield for detecting abnormalities
Vascular lesions
Tumors
Myelomeningocele
Tethered cord syndrome
Infectious disorders (eg, human T-lymphocytic virus 1 and HIV)

Brain Stem and Brain

Brain stem lesions and stroke

SEPs are normal in Wallenberg's syndrome but are generally abnormal when medial lemniscus is involved. SEPs are also unaffected and normal in some of the hemispheric (eg, pure motor lacunar infarctions, occipital lobe infarctions). In larger brainstem or hemispheric lesions, N20 and later waveforms may be delayed or absent. In lesions of the thalamocortical radiations, dissociation between the N20 and P22 waveform amplitudes may be observed. Changes in SEPs over time have been explored for their predictive value for recovery from stroke. This area remains investigational.

Multiple sclerosis

SEPs of the upper extremities are abnormal in about 60% of all patients with MS (definite, probable, and possible) and in about 40% of patients with asymptomatic MS. SEPs of the lower extremities have a higher frequency of abnormality, presumably since longer axons are more likely to have an area of demyelination. In clinical practice, SEPs of both the upper and lower extremities usually are performed. The change most frequently seen in MS is prolongation of central latencies. MRI has largely supplanted SEP testing in MS.

Other demyelinating diseases

Abnormalities in SEPs are seen in adrenoleukodystrophy, adrenomyeloneuropathy, metachromatic leukodystrophy, heterozygotes for adrenoleukodystrophy and adrenomyeloneuropathy.

Coma

SEPs are useful in the evaluation of a comatose patient, not only for diagnostic purposes but also for prognosis. Central conduction times are not affected significantly by level of consciousness, hypothermia, or sedative-hypnotic medications such as barbiturate anesthesia. Thus, SEPs are often useful in conditions in which clinical examination is of limited value. A favorable outcome is expected in about 53% of comatose patients with hypoxic-ischemic encephalopathy and in 49% of patients with traumatic brain injury coma who have preservation of bilateral cortical SEP responses.

The absence of cortical responses bilaterally is associated with an unfavorable prognosis (ie, an outcome of persistent vegetative state in the vast majority of patients). Unilateral preservation of cortical SEP responses offers hope for a favorable outcome. Determination of presence or absence of the N70 in patients with postanoxic coma gives additional information about the likelihood of poor outcome, but it is not precise enough to base treatment decisions solely on its absence.

Brain death

In brain death, peripheral SEP components are preserved. However, potentials generated by structures above the lower medulla are absent.

Surgical Monitoring Techniques

Intraoperative SEPs are recorded routinely using electrode strips or grids or electrodes applied directly to the exposed cortex during neurosurgical procedures in and around the somatosensory cortex. The N20 response is used to identify the primary somatosensory cortex in the postcentral gyrus. By inference, the motor cortex in the precentral gyrus can be localized as well, and this information is used to guide the surgical procedure. Scalp-recorded SEPs have also been used to monitor cerebral ischemia during vascular surgery, such as carotid endarterectomy; however, EEG monitoring is used more widely for this application. The value of regional cerebral oximetry adds nothing to the information already provided by EEG and SSEP in determining when to place a shunt during CEA.

Somatosensory response can be measured by magnetoencephalography. The generators of the N20m and later waveforms can be modeled as equivalent current dipoles. Usually, individual digits and the lip are stimulated, and the single dipoles of the cortical generators are overlaid on co-registered MRI images to create a map of the somatosensory cortex. SEPs usually are collected in outpatients several days prior to the surgery so that the information can be used by neurosurgeons to help in planning the approach to the anticipated surgery. The information also can be used to provide patients with an idea of the relative risk of neurological deficits that could result from the surgery.

Use of motor evoked potentials (MEP) and SSEP monitoring during thoracic and thoracoabdominal aortic surgery is controversial. Motor and somatosensory evoked potentials during thoracic and thoracoabdominal aortic aneurysm repair were analyzed. Irreversible changes were significantly associated with immediate neurologic deficit, and the findings were identical for SSEP and MEP in this variable, indicating that the more complex MEP measures do not add further information to that obtained from SSEP. Normal SSEP and MEP findings had a strong negative predictive value, indicating that patients without signal loss are unlikely to awake with neurologic deficit.

Combined neurophysiological intraoperative monitoring with EMG and SSEP recording and the selective use of MEPs is helpful for predicting and possibly preventing neurologic injury during cervical spine surgery.

Intraoperative SSEP monitoring was reliable in ruling out spinal injury in descending thoracic and thoracoabdominal aortic repair, but had a low sensitivity. It did not predict delayed neurologic deficit. Spinal SSEP change was an independent predictor of mortality and correlated with low preoperative glomerular filtration rate.

Degenerative Disorders

In Friedreich ataxia, SEPs recorded from the scalp usually show normal peripheral nerve conduction latencies but prolonged central conduction times. Degenerative disorders of the brain stem, such as spinal cerebellar degeneration, usually show a similar SEP pattern. In Huntington disease, latencies are normal but the amplitudes may be low (similar to the low-voltage pattern found in the EEG).

SEPs are normal in many degenerative disorders, including Parkinson disease, Alzheimer disease, and amyotrophic lateral sclerosis (particularly early in the course of the disease). An unusually large amplitude response is seen in the SEPs of patients with progressive myoclonic epilepsy. In cerebrovascular disease or head trauma, abnormal SEPs are recorded when infarction, hemorrhage, or direct injury disrupts the integrity of ascending somatosensory pathways.

Multimedia

Media file 1: Plot of 148-channel magnetoencephalographic recording of somatosensory evoked response to tapping on the tip of the left fifth digit. As magnetic fields enter and exit the skull at different locations, the deflections are upgoing at some magnetometer channels and downgoing at other magnetometer positions. The N20m latency is highlighted.

Media file 2: First cortical somatosensory response (N20m) to left fifth digit stimulation recorded by magnetoencephalography. Localization of the response is co-registered on the patient's MRI image. Note that the response localizes to the postcentral gyrus.

Media file 3: The P34m response to tapping on the tip of the left fifth digit as seen on magnetoencephalography.

Media file 4: Localization of the P34m response co-registered onto the patient's MRI image.

Media file 5: Normal baseline SSEPs. Left median on upper left corner, right median on upper right corner, left tibial on lower left corner and right tibial on lower right corner.

Media file 6: Effects of reduced temperatures from 36º to 34.5º, resulting in increase in latency throughout evoked potentials from N9-P20.

References

Achouh PE, Estrera AL, Miller CC 3rd, Azizzadeh A, Irani A, Wegryn TL, et al. Role of somatosensory evoked potentials in predicting outcome during thoracoabdominal aortic repair. Ann Thorac Surg. Sep 2007;84(3):782-7; discussion 787-8. [Medline].
Adhikary SD, Manickam BP. Unusual waveforms during SSEP monitoring--facts and artifacts. J Neurosurg Anesthesiol. Jul 2008;20(3):207. [Medline].
Aminoff MJ. Use of somatosensory evoked potentials to evaluate the peripheral nervous system. J Clin Neurophysiol. Apr 1987;DA - 19870925(2):135-44. [Medline].
Aminoff MJ, Eisen AA. AAEM minimonograph 19: somatosensory evoked potentials. Muscle Nerve. Mar 1998;21(3):277-90. [Medline].
Anderson NE, Frith RW, Synek VM. Somatosensory evoked potentials in syringomyelia. J Neurol Neurosurg Psychiatry. Dec 1986;49(12):1407-10. [Medline].
Aramideh M, Hoogendijk JE, Aalfs CM, et al. Somatosensory evoked potentials, sensory nerve potentials and sensory nerve conduction in hereditary motor and sensory neuropathy type I. J Neurol. May 1992;239(5):277-83. [Medline].
Bartholomi L, Leili S, Negrin P. Somatosensory evoked potentials in diabetes type I. Electroencephalo Clin Neurophysiol. 1991;31:43-6.
Chiappa K. Short-latency somatosensory evoked potentials: interpretation. In: Evoked Potentials in Clinical Medicine. New York: Raven Press; 1983:251-312.
Clinical Neurology [book on CD-ROM]. Philadelphia: Lippencott Raven; 1998. Chiappa KH, Hill RA, et al.
Chung I, Glow JA, Dimopoulos V, Walid MS, Smisson HF, Johnston KW, et al. Upper-limb somatosensory evoked potential monitoring in lumbosacral spine surgery: a prognostic marker for position-related ulnar nerve injury. Spine J. Aug 4 2008;[Medline].
D'Alpa F, Sallemi G, Triffiletti L, Grasso A. Cervical SEPs from radicular (digital) upper limb nerves stimulation. Acta Neurol (Napoli). Dec 1986;8(6):602-9. [Medline].
Dawson GD. Cerebral responses to nerve stimulation in man. Br Med Bull. 1950;6(4):326-9. [Medline].
Dreyfuss P, Dumitru D, Prewitt-Buchanan L. Intercostal somatosensory-evoked potentials. A new technique. Am J Phys Med Rehabil. Jun 1993;72(3):144-50. [Medline].
Friedell ML, Clark JM, Graham DA, Isley MR, Zhang XF. Cerebral oximetry does not correlate with electroencephalography and somatosensory evoked potentials in determining the need for shunting during carotid endarterectomy. J Vasc Surg. Sep 2008;48(3):601-6. [Medline].
Glover JL, Worth RM, Bendick PJ, et al. Evoked responses in the diagnosis of thoracic outlet syndrome. Surgery. Jan 1981;89(1):86-93. [Medline].
Goldie WD, Chiappa KH, Young RR, Brooks EB. Brainstem auditory and short-latency somatosensory evoked responses in brain death. Neurology. Mar 1981;31(3):248-56. [Medline].
Haupt WF, Horsch S. Evoked potential monitoring in carotid surgery: a review of 994 cases. Neurology. Apr 1992;42(4):835-8. [Medline].
Jerrett SA, Cuzzone LJ, Pasternak BM. Thoracic outlet syndrome. Electrophysiologic reappraisal. Arch Neurol. Sep 1984;41(9):960-3. [Medline].
Kakigi R. The effect of aging on somatosensory evoked potentials following stimulation of the posterior tibial nerve in man. Electroencephalogr Clin Neurophysiol. Jul 1987;68(4):277-86. [Medline].
Kelleher MO, Tan G, Sarjeant R, Fehlings MG. Predictive value of intraoperative neurophysiological monitoring during cervical spine surgery: a prospective analysis of 1055 consecutive patients. J Neurosurg Spine. Mar 2008;8(3):215-21. [Medline].
Keyhani K, Miller CC 3rd, Estrera AL, Wegryn T, Sheinbaum R, Safi HJ. Analysis of motor and somatosensory evoked potentials during thoracic and thoracoabdominal aortic aneurysm repair. J Vasc Surg. Sep 30 2008;[Medline].
Knowlton RC. Magnetoencephalography: clinical application in epilepsy. Curr Neurol Neurosci Rep. Jul 2003;3(4):341-8. [Medline].
Komanetsky RM, Novak CB, Mackinnon SE, et al. Somatosensory evoked potentials fail to diagnose thoracic outlet syndrome. J Hand Surg [Am]. Jul 1996;21(4):662-6. [Medline].
Kraft GH, Aminoff MJ, Baran EM. Somatosensory evoked potentials: clinical uses. AAEM Somatosensory Evoked Potentials Subcommittee. American Association of Electrodiagnostic Medicine. Muscle Nerve. Feb 1998;21(2):252-8. [Medline].
Krarup-Hansen A, Fugleholm K, Helweg-Larsen S. Examination of distal involvement in cisplatin-induced neuropathy in man: an electrophysiological and histological study with particular reference to touch receptor function. Brain. Oct 1993;116 ( Pt 5):1017-41. [Medline].
Krumholz A, Weiss HD, Goldstein PJ, Harris KC. Evoked responses in vitamin B12 deficiency. Ann Neurol. Apr 1981;9(4):407-9. [Medline].
Li C, Houlden DA, Rowed DW. Somatosensory evoked potentials and neurological grades as predictors of outcome in acute spinal cord injury. J Neurosurg. Apr 1990;72(4):600-9. [Medline].
Loncarevic N, Tiric-Campara M, Mulabegovic N. Somatosensory evoked cerebral potentials (SSEP) in multiple sclerosis. Med Arh. 2008;62(2):80-1. [Medline].
Louis AA, Gupta P, Perkash I. Localization of sensory levels in traumatic quadriplegia by segmental somatosensory evoked potentials. Electroencephalogr Clin Neurophysiol. Jul 1985;62(4):313-6. [Medline].
Nuwer MR. Fundamentals of evoked potentials and common clinical applications today. Electroencephalogr Clin Neurophysiol. Feb 1998;106(2):142-8. [Medline].
Olney RK, Aminoff MJ. Electrodiagnostic features of the Guillain-Barre syndrome: the relative sensitivity of different techniques. Neurology. Mar 1990;40(3 Pt 1):471-5. [Medline].
Robinson LR, Micklesen PJ. Somatosensory evoked potentials in coma prognosis. Phys Med Rehabil Clin N Am. Feb 2004;15(1):43-61. [Medline].
Roser F, Ebner FH, Liebsch M, Dietz K, Tatagiba M. A new concept in the electrophysiological evaluation of syringomyelia. J Neurosurg Spine. Jun 2008;8(6):517-23. [Medline].
Rowed DW, McLean JA, Tator CH. Somatosensory evoked potentials in acute spinal cord injury: prognostic value. Surg Neurol. Mar 1978;9(3):203-10. [Medline].
Roy MW, Gilmore R, Walsh JW. Evaluation of children and young adults with tethered spinal cord syndrome. Utility of spinal and scalp recorded somatosensory evoked potentials. Surg Neurol. Sep 1986;26(3):241-8. [Medline].
Slimp JC, Janczakowski J, Seed LJ, Kraft GH. Comparison of median and posterior tibial nerve somatosensory evoked potentials in ambulatory patients with definite multiple sclerosis. Am J Phys Med Rehabil. Dec 1990;69(6):293-6. [Medline].
Snowden ML, Haselkorn JK, Kraft GH, et al. Dermatomal somatosensory evoked potentials in the diagnosis of lumbosacral spinal stenosis: comparison with imaging studies. Muscle Nerve. Sep 1992;15(9):1036-44. [Medline].
Spiess M, Schubert M, Kliesch U, Halder P. Evolution of tibial SSEP after traumatic spinal cord injury: baseline for clinical trials. Clin Neurophysiol. May 2008;119(5):1051-61. [Medline].
Synek VM. Somatosensory evoked potentials after stimulation of digital nerves in upper limbs: normative data. Electroencephalogr Clin Neurophysiol. Nov 1986;65(6):460-3. [Medline].
Tirakotai W, Hellwig D, Bertalanffy H, Riegel T. Localization of precentral gyrus in image-guided surgery for motor cortex stimulation. Acta Neurochir Suppl. 2007;97:75-9. [Medline].
Yiannikas C, McLeod JG, Walsh JC. Somatosensory evoked responses in the diagnosis of thoracic outlet syndrome. J Neurol Neurosurg Psychiatry. Mar 1983;46(3):234-40. [Medline].
Yiannikas C, Vucic S. Utility of somatosensory evoked potentials in chronic acquired demyelinating neuropathy. Muscle Nerve. Nov 2008;38(5):1447-54. [Medline].
Zandbergen EG, Koelman JH, de Haan RJ, Hijdra A. SSEPs and prognosis in postanoxic coma: only short or also long latency responses?. Neurology. Aug 22 2006;67(4):583-6. [Medline].

Keywords

somatosensory evoked potentials, SEP, SEPs, SSEP, SEP waveform, MEP, CIDP, CADP, MMN

Contributor Information and Disclosures

Author

Jasvinder Chawla, MBBS, MD, MBA, Chief of Neurology, Hines Veterans Affairs Hospital; Associate Professor and Director, Neurology Residency Training Program, Loyola University Medical Center
Jasvinder Chawla, MBBS, MD, MBA is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Clinical Neurophysiology Society, and American Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Jorge G Burneo, MD, MSPH, Assistant Professor of Neurology, Epidemiology, and Biostatistics, Department of Clinical Neurological Sciences, Epilepsy Program, London Health Sciences Centre, University of Western Ontario, Canada
Jorge G Burneo, MD, MSPH is a member of the following medical societies: American Academy of Neurology and American Epilepsy Society
Disclosure: Nothing to disclose.

Gregory L Barkley, MD, Director of the Comprehensive Epilepsy Program, Department of Neurology, Henry Ford Health System; Associate Professor, Case Western Reserve University
Gregory L Barkley, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, American Medical Association, and Michigan State Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Donald B Sanders, MD, EMG Laboratory Director, Professor of Medicine (Neurology), Division of Neurology, Duke University Medical Center
Donald B Sanders, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, American Neurological Association, and New York Academy of Sciences
Disclosure: Nothing to disclose.

Pharmacy Editor

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

Managing Editor

Norberto Alvarez, MD, Assistant Professor, Department of Neurology, Harvard Medical School; Consulting Staff, Department of Neurology, Boston Children's Hospital
Norberto Alvarez, MD is a member of the following medical societies: American Academy of Neurology, American Epilepsy Society, and Child Neurology Society
Disclosure: Nothing to disclose.

Chief 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.

Further Reading