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Traumatic Peripheral Nerve Lesions Treatment & Management

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

Medical Care

Decisions regarding surgical intervention must take into account both the mechanism of injury and completeness of the nerve injury.

Incomplete injuries

Incompletely injured nerves remain in (at least partial) continuity; therefore, they are likely to recover spontaneously. In general, patients with incomplete nerve injuries should be treated conservatively. Lesions are judged to be partial when some residual motor or sensory function is noted in the distribution of the injured nerve segment.

Needle EMG examination can be used to confirm that a nerve injury is partial by demonstrating the presence of some recruited voluntary motor unit potentials or signs of reinnervation even in clinically paralyzed muscles. However, note that in some cases of mixed or multiple nerve injuries in which some branches or fascicles are injured incompletely, some are likely to recover while others are not (see Case study 3 in Medical/Legal Pitfalls). These cases are best managed as complete lesions.

Complete injuries

Complete nerve lesions caused by lacerations or penetrating injuries should be referred for early surgical exploration and direct end-to-end repair.

Management of other complete nerve injuries depends on whether the pathophysiology of injury is thought to be neurapraxic, axonotmetic, or neurotmetic. This underscores the importance of an appropriately and carefully timed electrodiagnostic study in the evaluation of all these cases.

Complete nerve injuries that are predominantly neurapraxic can be expected to recover favorably over the course of weeks to months. When such cases do not recover as expected, patients should undergo follow-up electrodiagnostic testing, which may show the presence of significant secondary axonal loss suggesting that the initial testing was done too early, before the electrophysiologic abnormalities had fully evolved (see Case study 2 in Medical/Legal Pitfalls). However, if the follow-up study shows persistent conduction block across the injury site, then the patient should be evaluated carefully for an ongoing compressive lesion (eg, hematoma) by appropriate imaging studies.

Complete lesions with electrophysiologic evidence of axonal loss may be axonotmetic or neurotmetic. Axonotmetic injuries are more likely to recover spontaneously. Neurotmetic injuries often require surgical repair for adequate recovery. The only way to differentiate these injury types noninvasively is to monitor the patient for signs of recovery. However, the chances of successful surgical repair begin to decline by 6 months after the injury. By 18-24 months, the denervated muscles usually are replaced by fatty connective tissue, making functional recovery impossible. In most cases, close clinical observation is warranted for 3-6 months after this type of nerve injury. If no clinical or electrophysiologic evidence of recovery is noted during this period, these patients should be referred for surgical exploration.

Symptomatic management of patients with nerve injury

Many patients develop neuropathic pain in addition to motor and sensory deficits from nerve injury. The author uses an escalating drug regimen for symptomatic control of neuropathic pain.

Some patients with very mild pain can be treated effectively with long-acting nonsteroidal anti-inflammatory drugs (NSAIDs).

Topical lidocaine patches are very useful or patients with small areas of cutaneous pain, eg, pain in the lateral foot after a sural nerve biopsy or other injury.

Patients with moderately severe pain usually respond to low-dose tricyclic agents such as nortriptyline or antiepileptic drugs such as gabapentin (Neurontin) and lamotrigine (Lamictal).

Patients with severe neuropathic pain, unresponsive to these agents, may require narcotic analgesia. The author usually begins with tramadol (Ultram). If and when this becomes ineffective, oxycodone (OxyContin) is used with increasing doses. The author uses fentanyl patches for patients who are allergic to codeine, morphine sulfate (MS Contin) and methadone for patients with severe pain.

Spinal cord stimulators may be useful for patients with segmental neuropathic pain.

Patients with weakness and deformity after nerve injury should be considered for physical and occupational therapy evaluation. Function may be improved significantly by the use of the appropriate assistive devices such as cock-up wrist splints (for radial nerve injuries) and AFO splints (for foot drop with peroneal or sciatic nerve injuries). Additionally, consider tendon transfer to improve residual function, depending on the precise pattern of residual injury and functional limitation.[5]

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Surgical Care

Indication for surgical exploration and (nerve graft) repair

Complete nerve lesions caused by lacerations or penetrating injuries should be referred for early surgical exploration and direct end-to-end repair.[6]

Other significant nerve injuries with no clinical or electrophysiologic evidence of recovery after 3-6 months of clinical observation are also indications for surgical exploration.

Intraoperative nerve conduction testing and surgical repair

At the time of surgical exploration, the injured nerve may be obviously severed, in which case the injured segment should be resected and an end-to-end anastomosis (usually with an intervening nerve graft) performed. If the injured nerve segment appears to remain in continuity, intraoperative nerve conduction studies can differentiate axonotmetic from neurotmetic injury.

Sterile bipolar hook electrodes are used to stimulate and record nerve action potentials (NAPs) from surgically exposed nerve segments. Low stimulus intensities and durations should be used to avoid further iatrogenic nerve injury. Responses are recorded directly from nerves, so the patients can be paralyzed pharmacologically. Lifting the electrodes and nerve out of the operative field during testing is important to avoid current spread through blood and other fluids.

The presence of an evoked NAP across the injured segment indicates that the lesion is axonotmetic and recovering spontaneously. Surgical intervention should be limited to external neurolysis in these cases;[7, 8, 9] however, note that normal (or "super normal") NAPs can also be recorded from the brachial plexus sensory fibers in cases of root avulsion.

A 25-year-old man had a "flail" right arm after in 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).

The absence of a recordable NAP across the injured nerve segment more than 2-3 months after injury suggests that the injury is neurotmetic, necessitating nerve graft repair. In this instance, a normal nerve segment should always be tested as a positive control to confirm the integrity of the stimulating and recording apparatus. Furthermore, if a tourniquet was used during surgery, it should be released for at least 30 minutes prior to testing, as ischemia may attenuate normal NAP responses.

Selective use of intraoperative NAPs with either neurolysis or graft repair, depending on results, has been shown to improve postoperative outcome in these cases.[10, 11]

Intraoperative somatosensory-evoked potential testing and surgical repair

Brachial plexus injuries may be intraspinal (eg, root avulsions). In these cases, a NAP cannot be conducted across the injured segment to test continuity without performing very extensive surgery (eg, multilevel laminectomies). Intraoperative SEP testing may be very helpful in this regard.[7, 12]

A handheld bipolar stimulator is used to electrically activate the most proximally exposed region of the plexus with recordings made from surface electrodes placed over the contralateral scalp. The absence of cortical SEP responses suggests more proximal nerve root avulsion. However, cortical SEP responses can also be absent in the presence of high doses of volatile anesthetic agents, so testing a normal plexus element as a positive control is always important (see Case study 4 in Medical/Legal Pitfalls).

Nerve root avulsions can only be repaired by neurotization from adjacent nerves, such as the spinal accessory nerve, cervical plexus, or intercostal nerves. However, in cases of complete brachial plexus avulsion, these nerves cannot provide adequate donor neurones for adequate repair, and cross-chest nerve root transfer has been used with encouraging results.[13] There is only minimal postoperative deficit in the contralateral limb, provided certain precautions are taken.[13, 14]

For further information, please see Brachial Plexus Injuries, Traumatic and Facial Nerve Repair.

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Consultations

Physicians typically involved in the care of patients with nerve injuries may include the following:

  • Peripheral nerve surgeon with experience in nerve exploration and graft repair
  • Neurologist with experience in nerve injuries and electrodiagnostic testing
  • Pain management physician
  • Physical and occupational therapists
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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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