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Traumatic Peripheral Nerve Lesions Workup

  • Author: Neil R Holland, MBBS, MBA, FAAN; Chief Editor: Nicholas Lorenzo, MD, MHA, CPE  more...
 
Updated: Dec 28, 2015
 

Imaging Studies

Magnetic resonance neurography (MRN) uses a high resolution fast spin echo T2 imaging technique to demonstrate abnormal signal within nerve trunks at sites of major nerve injuries and compression. This technique can be particularly useful for identifying nerve injuries, such as piriformis syndrome and brachial plexus injuries, at sites inaccessible to conventional nerve conduction studies.

MRN of the brachial plexus. a: Abnormal signal in 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.

The same technique can be used to demonstrate pseudomeningoceles in the cervical spine from traumatic nerve root avulsions.[2, 3]

MRN image through the cervical spine showing pseud 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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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.

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.

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.

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. 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.[4] 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.

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Contributor Information and Disclosures
Author

Neil R Holland, MBBS, MBA, FAAN Interim Chair Neurology, Geisinger Health System; Clinical Professor of Neurology, The Commonwealth Medical College

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

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

Neil A Busis, MD Chief of Neurology and Director of Neurodagnostic Laboratory, UPMC Shadyside; Clinical Professor of Neurology and Director of Community Neurology, Department of Neurology, University of Pittsburgh Physicians

Neil A Busis, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Chief Editor

Nicholas Lorenzo, MD, MHA, CPE Founding Editor-in-Chief, eMedicine Neurology; Founder and CEO/CMO, PHLT Consultants; Chief Medical Officer, MeMD Inc

Nicholas Lorenzo, MD, MHA, CPE is a member of the following medical societies: Alpha Omega Alpha, American Association for Physician Leadership, American Academy of Neurology

Disclosure: Nothing to disclose.

Additional Contributors

Milind J Kothari, DO Professor, 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 Neurological Association, American Association of Neuromuscular and Electrodiagnostic Medicine

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. 2002 Jun. 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. 2004 Aug. 22(3):643-82, vi-vii. [Medline].

  4. Korus L, Ross DC, Doherty CD, Miller TA. Nerve transfers and neurotization in peripheral nerve injury, from surgery to rehabilitation. J Neurol Neurosurg Psychiatry. 2015 Jul 1. [Medline].

  5. 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].

  6. Kuffler DP. An assessment of current techniques for inducing axon regeneration and neurological recovery following peripheral nerve trauma. Prog Neurobiol. 2014 May. 116:1-12. [Medline].

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

  8. 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.

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

  10. 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].

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

  12. 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]. 1980 Nov. 62-B(4):492-6. [Medline].

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

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

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

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

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

  18. 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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