eMedicine Specialties > Neurology > Neuromuscular Diseases

Traumatic Peripheral Nerve Lesions: Differential Diagnoses & Workup

Author: Neil Holland, MBBS, Neurology, Neurology Specialists of Monmouth County
Contributor Information and Disclosures

Updated: Oct 11, 2006

Differential Diagnoses

Acute Inflammatory Demyelinating Polyradiculoneuropathy
Metastatic Disease to the Spine and Related Structures
Cervical Spondylosis: Diagnosis and Management
Peroneal Mononeuropathy
Diabetic Neuropathy
Polyarteritis Nodosa
Femoral Mononeuropathy
Radial Mononeuropathy
Guillain-Barre Syndrome in Childhood
Spinal Cord Hemorrhage
HIV-1 Associated Acute/Chronic Inflammatory Demyelinating Polyneuropathy
Spinal Cord Infarction
HIV-1 Associated Distal Painful Sensorimotor Polyneuropathy
Syringomyelia
HIV-1 Associated Multiple Mononeuropathies
Vasculitic Neuropathy
HIV-1 Associated Neuromuscular Complications (Overview)
Leptomeningeal Carcinomatosis

Workup

Other Tests

  • A carefully planned electrodiagnostic study is critical for determining the completeness and pathophysiology of all nerve injuries.
  • The completeness of a nerve injury can be determined any time after the injury. The presence of voluntary motor unit potentials on needle electromyography (EMG) examination of a clinically paralyzed muscle always indicates that the nerve injury, at least the branch or fascicle supplying that individual muscle, is partial.
  • In general, sensory responses are affected earlier and more severely than motor responses in peripheral nerve injuries. A reduction in sensory response amplitude of 50% or more, compared to the other (unaffected) side, is the most sensitive indication of peripheral nerve injury. Normal sensory responses are seen with nerve root injuries, even from clinically anesthetic regions, because the injured nerve segment is proximal to the dorsal root ganglion.
  • The physician performing the EMG must be fully cognizant of the time course of wallerian degeneration when performing nerve conduction studies to differentiate demyelination from axonal loss. The dissociation between the rates of degeneration of motor and sensory fibers can be a particular source of problem for the novice. A nerve conduction study performed 3-7 days after a peripheral nerve injury may show low-amplitude evoked compound muscle action potential (CMAP) with normal amplitude sensory nerve action potential (SNAP), a pattern usually interpreted as nerve root injury/avulsion (see Case study 2 in Medical/Legal Pitfalls).
    • Needle EMG findings correlate poorly with the degree of axonal loss. Denervation potentials do not appear for as long as 21 days after the nerve injury; the delay depends on the distance between the nerve injury and affected muscle. Moreover, the density of denervation potentials cannot be extrapolated to indicate the severity of axonal loss. Denervation potentials should be absent even 21 days after a pure demyelinating injury. However, most nerve injuries are mixed, and even predominantly demyelinating lesions suffer some secondary loss, often resulting in surprisingly profuse denervation potentials (see Case study 1 in Medical/Legal Pitfalls).
    • The amplitude of distal evoked CMAP and SNAP responses yields the maximum information regarding the degree of axonal loss that has occurred in motor and sensory fibers 10 or more days after a nerve injury. Evoked amplitudes must be compared to either a baseline study (immediately after the injury) or to the response evoked on the contralateral (normal) side. Adequate assessment of nerve injuries may necessitate the use of nonconventional nerve conduction studies.
    • The motor nerves used conventionally in conduction studies of the upper extremity, the median and ulnar, are both derived from the lower cord and medial trunk of the brachial plexus. A musculocutaneous motor nerve conduction study is required to assess the degree of axonal loss in cases of upper trunk plexus injuries (see Case study 1 in Medical/Legal Pitfalls).
    • The presence of a relatively preserved distal CMAP response amplitude in a paralyzed muscle more than 7-10 days after a nerve injury always should suggest more proximal conduction block. In most cases, the conduction block will be determined readily by comparing evoked CMAP response amplitudes from stimulation proximal and distal to the injury site.
    • In some instances, however, the conduction block may be too proximal to be demonstrated reliably by conventional motor nerve conduction studies (eg, conduction block at the nerve root level). In these instances, F-wave responses may be absent despite the presence of more normal distal evoked CMAP responses (see Image 2). Additionally, somatosensory-evoked potential (SEP) testing and/or nerve root stimulation may be used to demonstrate proximal conduction block even at the nerve root level.
  • In summary, a carefully planned and executed electrodiagnostic study is paramount in the evaluation of nerve injuries. Needle EMG can demonstrate whether the injury is complete or incomplete at any time after injury. Nerve conduction studies are required to differentiate demyelination from axon loss; they yield the maximal information in this regard approximately 10 days after the injury. Nerve conduction studies should be bilateral to allow side-to-side comparisons of amplitude. Some types of injuries may necessitate the use of unconventional studies to adequately assess the degree of axon loss to each individual nerve branch or fascicle.

More on Traumatic Peripheral Nerve Lesions

Overview: Traumatic Peripheral Nerve Lesions
Differential Diagnoses & Workup: Traumatic Peripheral Nerve Lesions
Treatment & Medication: Traumatic Peripheral Nerve Lesions
Follow-up: Traumatic Peripheral Nerve Lesions
Multimedia: Traumatic Peripheral Nerve Lesions
References

References

  1. Brown WF, Veitch J. AAEM minimonograph #42: intraoperative monitoring of peripheral and cranial nerves. Muscle Nerve. Apr 1994;17(4):371-7. [Medline].

  2. Byrne P, Hilinski J, Hilger P. Facial Nerve Repair. eMedicine Journal [serial online]. 2003. Available at: http://www.emedicine.com/ent/topic408.htm. [Full Text].

  3. Chaput C, Probe R. Brachial Plexus Injuries, Traumatic. eMedicine Journal [serial online]. 2003. Available at: http://www.emedicine.com/orthoped/topic26.htm. [Full Text].

  4. Chaudhry V, Cornblath DR. Wallerian degeneration in human nerves: serial electrophysiological studies. Muscle Nerve. Jun 1992;15(6):687-93. [Medline].

  5. Kline DG, Hudson AR. Nerve Injuries: Operative Results for Major Nerve Injuries. Philadelphia, Pa: WB;1995.

  6. Kliot M, Slimp J. Techniques for assessment of peripheral nerve function at surgery. In: Loftus CM, Traynelis VC, eds. Intraoperative Monitoring Techniques in Neurosurgery. New York: McGraw-Hill Inc;. 1994:275-85.

  7. Landi A, Copeland SA, Parry CB, Jones SJ. The role of somatosensory evoked potentials and nerve conduction studies in the surgical management of brachial plexus injuries. J Bone Joint Surg [Br]. Nov 1980;62-B(4):492-6. [Medline].

  8. Stewart JD. Focal Peripheral Neuropathies. New York: Raven Press;1993.

  9. Tiel RL, Happel LT Jr, Kline DG. Nerve action potential recording method and equipment. Neurosurgery. Jul 1996;39(1):103-8; discussion 108-9. [Medline].

  10. Wilbourn AJ. Assessment of the brachial plexus and the phrenic nerve. In: Johnson EW, Pease WS, eds. Practical Electromyography. Baltimore: Williams & Wilkins;1997:273-310.

Further Reading

Keywords

peripheral nerve injuries, complete nerve injury, incomplete nerve injury, segmental demyelination, neurapraxia, axonal injury, wallerian degeneration, axonal regeneration, focal remyelination, myelin sheath, evaluation of peripheral nerve injury, management of peripheral nerve injury, treatment of peripheral nerve injury

Contributor Information and Disclosures

Author

Neil Holland, MBBS, Neurology, Neurology Specialists of Monmouth County
Neil Holland, MBBS is a member of the following medical societies: American Academy of Neurology and American Association of Neuromuscular and Electrodiagnostic Medicine
Disclosure: Nothing to disclose.

Medical Editor

Milind J Kothari, DO, Professor and Vice-Chair for Education and Training, 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

Neil A Busis, MD, Chief, Division of Neurology, Department of Medicine, University of Pittsburgh Medical Center - Shadyside, Clinical Associate Professor, Department of Neurology, University of Pittsburgh School of Medicine
Neil A Busis, MD is a member of the following medical societies: American Academy of Neurology and American Association of Neuromuscular and Electrodiagnostic Medicine
Disclosure: Nothing to disclose.

CME Editor

Matthew J Baker, MD, Consulting Staff, Collier Neurologic Specialists, Naples Community Hospital
Matthew J Baker, MD is a member of the following medical societies: American Academy of Neurology
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.

 
 
HONcode

We subscribe to the
HONcode principles of the
Health On the Net Foundation

All material on this website is protected by copyright, Copyright© 1994- by Medscape.
This website also contains material copyrighted by 3rd parties.

DISCLAIMER: The content of this Website is not influenced by sponsors. The site is designed primarily for use by qualified physicians and other medical professionals. The information contained herein should NOT be used as a substitute for the advice of an appropriately qualified and licensed physician or other health care provider. The information provided here is for educational and informational purposes only. In no way should it be considered as offering medical advice. Please check with a physician if you suspect you are ill.