Traumatic Peripheral Nerve Lesions Follow-up

  • Author: Neil Holland, MBBS, FAAN; Chief Editor: Nicholas Lorenzo, MD   more...
 
Updated: Aug 19, 2011
 

Further Inpatient Care

  • An attempt should be made to classify all nerve injuries according to the completeness of the injury and the predominant pathophysiologic process involved: however, recognize that individual fascicles can be affected differently.
  • The results of nerve conduction studies may be difficult to interpret during the first 10 days after nerve injury until the effects of wallerian degeneration have had a chance to fully evolve in both motor and sensory fibers (see Case study 2 in Medical/Legal Pitfalls).
  • The best measure of axonal loss is the amplitude of the evoked CMAP response (compared to the other side) in a weak muscle from nerve stimulation distal to the injury site at least 7 days after the injury.
  • The density of denervation potentials in weak muscles is a poor measure of axonal loss. Denervation potentials may be absent for as long as 14-21 days after nerve injuries with severe axonal loss (see Case study 2 in Medical/Legal Pitfalls). Denervation potentials may be "profuse" in mixed injuries, even if the predominant pathophysiologic process is neurapraxia (see Case study 1 in Medical/Legal Pitfalls).
  • The presence of voluntary motor unit potentials in a clinically paralyzed muscle indicates that the nerve injury is partial, even if the distal CMAP response is absent (see Case study 2 in Medical/Legal Pitfalls).
  • Intraoperative nerve conduction testing often is required to differentiate axonotmesis from neurotmesis in closed nerve injuries that appear continuous. However, beware of "super normal" NAPs with more proximal nerve root avulsions (see Case study 4 in Medical/Legal Pitfalls).
 
Contributor Information and Disclosures
Author

Neil Holland, MBBS, FAAN  Partner, Neurology Specialists of Monmouth County; Associate Professor of Neurology, Drexel University College of Medicine; Director, MDA Clinic, Rehabilitation Hospital of Tinton Falls; Chief of Neurology and Director of the Stroke Program, Monmouth Medical Center; Active Staff, Medicine (Neurology), Riverview Medical Center

Neil Holland, MBBS, FAAN is a member of the following medical societies: American Academy of Neurology and American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Milind J Kothari, DO  Professor and Vice-Chair, Department of Neurology, Pennsylvania State University College of Medicine; Consulting Staff, Department of Neurology, Penn State Milton S 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.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Neil A Busis, MD  Chief, Division of Neurology, Department of Medicine, Head, Clinical Neurophysiology Laboratory, University of Pittsburgh Medical Center-Shadyside

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.

Chief Editor

Nicholas Lorenzo, MD  Consulting Staff, Neurology Specialists and Consultants

Nicholas Lorenzo, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, and American College of Physician Executives

Disclosure: Nothing to disclose.

References

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

  2. Cudlip SA, Howe FA, Clifton A, Schwartz MS, Bell BA. Magnetic resonance neurography studies of the median nerve before and after carpal tunnel decompression. J Neurosurg. Jun 2002;96(6):1046-51. [Medline].

  3. Filler AG, Maravilla KR, Tsuruda JS. MR neurography and muscle MR imaging for image diagnosis of disorders affecting the peripheral nerves and musculature. Neurol Clin. Aug 2004;22(3):643-82, vi-vii. [Medline].

  4. Elkwood AI, Holland NR, Arbes SM, Rose MI, Kaufman MR, Ashinoff RL, et al. Nerve allograft transplantation for functional restoration of the upper extremity: case series. J Spinal Cord Med. 2011;34:241-247. [Medline].

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

  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. 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].

  8. Kandenwein JA, Kretschmer T, Englhardt M, Richter HP, Antoniadis G. Surgical interventions for traumatic lesions of the brachial plexus: a retrospective study of 134 cases. J Neurosurg. 2005;103:614-621. [Medline].

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

  10. 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].

  11. Terzis JK, Kokkalis ZT, Kostopoulos E. Contralateral C7 transfer in adult plexopathies. Hand Clin. 2008;24:389-400. [Medline].

  12. Holland NR, Belzberg AJ. Intraoperative electrodiagnostic testing during cross-chest C7 nerve root transfer. Muscle Nerve. 1997;20:903-905. [Medline].

  13. Byrne P, Hilinski J, Hilger P. Facial Nerve Repair. eMedicine Journal [serial online]. 2009. Available at: http://emedicine.medscape.com/article/846448-overview. [Full Text].

  14. Chaput C, Probe R. Brachial Plexus Injuries, Traumatic. eMedicine Journal [serial online]. 2008. Available at: http://emedicine.medscape.com/article/1268993-overview. [Full Text].

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

  16. 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.

 
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Large-amplitude compound muscle action potential (CMAP) response was recorded from the right biceps muscle after intraoperative direct bipolar stimulation of the proximal right musculocutaneous nerve at low stimulus intensities (3.9 mA). The time base shown is 10 milliseconds/div and the gain is 50 mcV/div.
Electrodiagnostic testing 1 day after the injury revealed the following: (Left) Right ulnar motor conduction study showed a normal distal amplitude with conduction block across the elbow segment (gain = 2 mV/div, time base = 2 milliseconds [ms]/div). (Second from left) Right ulnar sensory response was normal (gain = 20 mcV/div, time base = 2 ms/div). (Third from left) Right ulnar F-wave responses were absent. (Right) Needle electromyographic (EMG) examination of right abductor digiti minimi was quiet at rest but showed a single fast firing unit on attempted contraction (gain = 200 mcV/div, time base = 10 ms/div).
Electrodiagnostic testing 3 days after the injury revealed the following: (Left) Right distal ulnar motor response is of lower amplitude than on day 1, approximately 50% of baseline (gain = 2 mV/div, time base = 5 milliseconds [ms]/div) with persistent conduction block across the elbow. (Right) Right ulnar sensory response is still normal (gain = 20 mcV/div, time base =2 ms/div).
Electrodiagnostic testing 6 days after the injury revealed the following: (Left) Right distal ulnar motor response is less than 10% of baseline (gain = 2 mV/div, time base = 5 milliseconds [ms]/div) with persistent conduction block across the elbow. (Right) Right ulnar sensory response amplitude still is relatively preserved at 50% of baseline (gain = 20 mcV/div, time base = 1 ms/div).
Electrodiagnostic testing 10 days after the injury revealed the following: Right ulnar motor (middle) and sensory (right) responses are absent. Needle electromyography (EMG) of first dorsal interosseus shows sparse denervation potentials with 1 fast firing unit on attempted volitional activity.
Intraoperative nerve action potentials recorded from the lateral cord (point R) with successive stimulation (at points 1, 2, 3, 4, and 5) along the course of the musculocutaneous nerve (gain = 100 mcV/div, time base = 0.5 milliseconds [ms]/div). Normal responses are recorded from stimulation at points 1 and 2. A slight increase in latency and drop in amplitude are noted on stimulation at point 3 close to the nerve injury. Stimulation at points 4 and 5 (distal to the injury) fail to evoke a recordable response.
A 25-year-old man had a "flail" right arm after injury in a motorcycle accident (Case study 4). Left panel: Somatosensory evoked potentials (SEPs) recorded at the scalp from stimulation of the (healthy) middle trunk (gain = 0.2 mcV/div, time base = 10 milliseconds [ms]/div). Middle panel: SEPs recorded at the scalp from stimulation of the lower trunk—no reproducible responses present (gain = 0.2 mcV/div, time base = 10 ms/div). Right panel: "Super normal" nerve action potentials recorded at the lower trunk from stimulation of the medial cord (time base = 1.5 ms/div, gain = 20 mcV/div).
MRN of the brachial plexus. a: Abnormal signal in the brachial plexus elements on the affected (right) side. Compare to b: normal plexus on the unaffected (left) side.
MRN image through the cervical spine showing pseudomengocele (arrows) at the site of a cervical root avulsion in a patient with traumatic brachial plexopathy.
 
 
 
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