AUTHOR AND EDITOR INFORMATION

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INTRODUCTION

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Background

Evaluation and management of peripheral nerve injuries requires a thorough knowledge of neuroanatomy, neurophysiology, and electrodiagnostic medicine. The purpose of this article is not to describe the clinical features of every conceivable nerve injury. This type of information is well presented in other publications (eg, Stewart, 1993). Instead, this article emphasizes the use of various electrodiagnostic techniques in the evaluation and management of nerve injuries in general.

Pathophysiology

See History.

CLINICAL

Section 3 of 11  

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• Follow-up
• Miscellaneous
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History

Nerve injuries can be classified on the basis of completeness and predominant pathophysiology.

• Nerve injuries first should be classified as complete or incomplete.
• • Complete injuries disrupt all the neurons traversing the injured segment, causing total loss of distal motor or sensory function.
  • Incomplete lesions disrupt some neurons but leave others unaffected, with some sparing of distal motor or sensory function. An incomplete nerve injury implies that at least part of the nerve remains in continuity; this has important therapeutic implications.
• Although peripheral nerves may be injured in various ways, pathophysiologic responses to trauma at the neuronal level comprise only 2—demyelination and axonal loss.
• • Segmental demyelination (ie, neurapraxia): A mild stretch or compression injury may disrupt or distort the myelin sheath at the injury site, resulting in focal demyelination and leaving the axons intact. This causes a transient state of disrupted conduction along the injured segment—conduction slowing or block. Because the axons remain intact, function can be restored by focal remyelination, usually within a matter of days to weeks. This type of nerve injury is known as neurapraxia and is best considered the peripheral nervous system equivalent of "concussion."
  • Axonal injury and wallerian degeneration: Injured axons undergo a highly stereotyped process known as wallerian degeneration. Axonal function is disrupted immediately after the injury, although the disconnected distal segment initially survives and conducts externally applied stimuli; over the course of the next 5-7 days, however, the distal axonal segment slowly degenerates in a centrifugal fashion and eventually becomes inexcitable. The neuron may recover subsequently by axonal regeneration from the intact cell body, which is a slow process occurring at a rate of about 1 mm/day.
  • Axonal injuries that spare the supporting perineural connective tissue sheath are known as axonotmetic. The intact perineural connective tissue sheaths provide a conduit for axonal regeneration from the cell body to the target muscle, facilitating recovery. Injuries that disrupt the whole nerve, affecting both the axon and supporting connective tissue, are known as neurotmetic. These injuries are less likely to recover by axonal regeneration; they more often require surgical repair.
  • Mixed injuries: Individual axons can exhibit only one of these types of pathophysiologic change; however, one injured nerve is composed of thousands of axons, and a mixed pattern of segmental demyelination and axonal loss is manifested frequently. Moreover, some axons may be affected by different pathophysiologic processes at various points along their courses. This can make assessing the type of injury very difficult, even with electrodiagnostic methods, thus confounding management (see Case study 1 in Medical/Legal Pitfalls). Recovery from mixed lesions is usually biphasic. The neurapraxic component of the injury recovers quickly by remyelination and the axonal component of the injury recovers slowly by axonal regeneration.

DIFFERENTIALS

Section 4 of 11  

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• Follow-up
• Miscellaneous
• Multimedia
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WORKUP

Section 5 of 11  

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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 (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.

TREATMENT

Section 6 of 11  

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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 receive physical and occupational therapy. 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).

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.
  • 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; however, note that normal (or "super normal") NAPs can also be recorded from the brachial plexus sensory fibers in cases of root avulsion (see Image 7).
  • 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.
• 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.
  • 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, or by cross-chest nerve root transfer.
• For further information, please see Brachial Plexus Injuries, Traumatic and Facial Nerve Repair.

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

MEDICATION

Section 7 of 11  

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As outlined in the text, a wide variety of analgesic medications may be effective in the treatment of neuralgic pain. These include both narcotic and nonnarcotic medications.

Drug Category: Narcotic analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.

Drug Category: Oral analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or injuries.

Drug Category: Tricyclic antidepressants

These agents are a complex group of drugs that have central and peripheral anticholinergic effects as well as sedative effects. They have central effects on pain transmission and block the active re-uptake of norepinephrine and serotonin.

Drug Category: Anticonvulsants

These agents are used to manage severe muscle spasms and provide sedation in neuralgia. They have central effects on pain modulation.

Drug Category: Anesthetics

These agents stabilize the neuronal membrane so the neuron is less permeable to ions. This prevents the initiation and transmission of nerve impulses, thereby producing the local anesthetic action.

FOLLOW-UP

Section 8 of 11  

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Further Inpatient Care

• Summary and key points
• • 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).

MISCELLANEOUS

Section 9 of 11  

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Medical/Legal Pitfalls

• Four case studies are provided here to illustrate the use of and problems with the electrodiagnostic evaluation of nerve injuries.
• Case study 1 (see also Image 1) - This 58-year-old woman presented with a tender right neck mass associated with paresthesias radiating down the lateral border of her right forearm into digits 1 and 2. She had normal right arm strength. MRI showed a brachial plexus tumor and she underwent surgical exploration; a schwannoma was resected from the right C6 nerve root just proximal to the formation of the upper trunk of the plexus. Unfortunately, she awoke from anesthesia with pain and numbness in the lateral right arm and paralysis of the right biceps, deltoid, supraspinatus, and infraspinatus muscles.
• • One month later, when she had had no recovery of right arm function, an electrodiagnostic study was performed at another facility. Standard median and ulnar motor and sensory nerve conduction study findings were bilaterally normal without significant side-to-side asymmetries. Needle EMG showed profuse denervation potentials and no voluntarily recruited motor units in affected muscles. The cervical paraspinal and right rhomboideus muscles were reportedly normal. This study was interpreted as showing severe upper trunk brachial plexus injury without evidence of axonal continuity.
  • Based on the results of this study, the patient was taken to the operating room for surgical exploration and sural nerve graft repair. However, after surgical exposure, low-intensity, direct, bipolar electrical stimulation of the proximal right musculocutaneous nerve evoked vigorous arm movements and a large-amplitude CMAP response from the paralyzed right biceps muscle (see Image 1).
  • This indicated that the predominant pathophysiology was neurapraxic injury with proximal conduction block. The degree of axonal loss had been overestimated dramatically at the preoperative electrodiagnostic study by the profuse denervation potentials recorded from paralyzed muscles. When the surgeons were given this information, they decided to perform only a simple neurolysis and then close the wound. The patient subsequently recovered normal arm strength and sensation over the course of the following 6 weeks.
  • Comment - In this case a preoperative electrodiagnostic study misdiagnosed neurapraxia as axonal loss injury, because of the following:
    • The "density" of acute denervation potentials does not necessarily correlate with the degree of axonal loss. Distal motor-evoked response amplitude is correlated more reliably with axonal continuity.
    • "Routine" nerve conduction studies do not adequately study the upper trunk of the brachial plexus. Musculocutaneous motor and sensory nerve conduction studies would have been necessary for this case.
    • Differentiating neurapraxic from axonal injury in lower trunk and medial cord brachial plexus injuries is easy, where "routine" nerve conduction studies include recording CMAP responses from clinically affected muscles. The presence of relatively preserved evoked median and ulnar motor amplitudes recorded from distal stimulation more than 2 weeks after the injury suggests neurapraxic injury with proximal conduction block.
    • Nerve conduction studies should include stimulation at the Erb point, as demonstrating partial motor conduction block across the plexus may be possible in these cases; however, "routine" nerve conduction studies do not assess the upper trunk and lateral cord of the brachial plexus. Moreover, many plexus injuries involve a combination of neurapraxia and axonotmesis, and the degree of axonal loss frequently is overestimated by the density of denervation potentials recorded by needle EMG.
    • In this case, a musculocutaneous motor nerve conduction study would have been required to identify proximal conduction block at the time of the preoperative electrodiagnostic study, and it may have prevented unnecessary surgery. This case emphasizes the importance of recording electrically evoked CMAP responses from clinically affected muscles whenever possible in cases of peripheral nerve injury, even if this involves use of "nonroutine" nerve conduction studies, as this is the best measure of the degree of axonal loss.
• Case study 2 (see also Images 2-5) - A 55-year-old man awoke from a prolonged laparotomy with a numb and painful right hand. On examination, he had numbness and dysesthesias in the distribution of the right ulnar nerve. The ulnar-innervated intrinsic hand muscles were paralyzed completely, with relative sparing of abductor pollicis brevis. Serial electrodiagnostic testing was performed on days 1 (Image 2), 3 (Image 3), 6 (Image 4), and 10 (Image 5) after injury.
• • Comments - The serial electrodiagnostic testing in this case of acute right ulnar nerve injury illustrates the time course of axonal loss. The initial nerve conduction study showed normal distal ulnar motor and sensory response amplitudes. Even though significant axonal injury was detected at the elbow, the distal nerve segment appeared normal; however, it could not conduct across the injured segment, resulting in conduction block. Needle EMG showed a single fast firing unit, indicating that although the muscle was paralyzed, the nerve injury was partial. At this point in time (day 1), electrodiagnostic testing cannot differentiate neurapraxia from axonal loss.
  • Three days after the injury, the distal motor-evoked response was of low amplitude but the sensory response amplitude was still normal. This dissociation between the rates of motor and sensory axonal degeneration is a typical feature of wallerian degeneration. This pattern of abnormalities can be interpreted mistakenly by the unwary as showing electrophysiologic evidence of radiculopathy.
  • By the sixth day of injury, both motor and sensory fibers were degenerating.
  • By the tenth day, both motor and sensory axons had degenerated. The lesion was still partial because at least one voluntary motor unit potential still could be recruited. The injury was still too acute for denervation potentials, which typically do not appear for 14-21 days.
• Case study 3 (see Image 6): A 64-year-old man sustained multiple neurovascular injuries affecting the left arm in a motor vehicle accident. He underwent surgical repair of the left axillary artery. His initial neurological deficits were consistent with an upper trunk plexus injury. Over the course of the subsequent 18 months, he regained strength in the majority of his left arm muscles; however, the left biceps muscle remained disproportionately paralyzed. An electrodiagnostic study confirmed upper trunk brachial plexopathy, which appeared partial.
• • Voluntary motor unit potentials were recorded from all affected muscles, except for biceps, where none was detected. He was brought back to the operating room for surgical exploration. The whole upper trunk of the brachial plexus was obviously scarred and thickened; however, intraoperative NAPs were recorded from the proximal upper trunk to the median and proximal regions of the musculocutaneous nerve, across this abnormal segment, indicating that this segment of the plexus remained in continuity.
  • Then the musculocutaneous nerve was stimulated along its length, in a proximal to distal fashion, and recordings were made from the lateral cord of the left brachial plexus (see Image 6). This testing identified a focal area of musculocutaneous nerve injury that was clearly separate from the more obvious proximal plexus injury. The musculocutaneous nerve injury was postulated to have occurred at the time of the axillary artery repair after the accident. The nerve was repaired with a graft and the patient made a significant recovery.
  • Comment: This patient presented with an acute upper trunk brachial plexus injury after an accident. Despite the fact that most of his deficits improved, he was left with severe residual biceps weakness. At surgery, the upper trunk of the plexus was scarred and thickened but conducted nerve action potentials consistent with the clinical functional recovery of most affected muscles. However, intraoperative nerve conduction studies identified a second (unsuspected) injury affecting the distal musculocutaneous nerve, which accounted for the disproportionate weakness in biceps and required nerve graft repair.
• Case study 4 (see Image 7): A 25-year-old man injured in a motorcycle accident had a "flail" right arm. Three months after his injury he had experienced significant neurological recovery; however, he complained of severe residual pain and numbness affecting the medial right forearm with weakness and atrophy of the intrinsic hand muscles.
• • Electrodiagnostic testing 1 month after the accident showed a normal right ulnar sensory response, borderline low right ulnar motor response amplitude, and low median motor response amplitude. Needle EMG examination showed denervation potentials and no voluntary motor unit potentials in muscles from the right C8-T1 myotomes. He subsequently underwent surgical exploration with intraoperative electrodiagnostic testing (see Image 7).
  • Cortical SEP responses from stimulation of the right upper and middle trunk were normal. No reproducible cortical SEP responses were elicited from stimulation of the right lower trunk. NAPs recorded from the lower trunk were "super normal" from stimulation of the medial cord. These abnormalities were consistent with C8-T1 root avulsion. He underwent neurotization from the cervical plexus and accessory nerve to the lower trunk using a sural nerve graft; however, clinical recovery was disappointing.
  • Comment: This case illustrates the electrophysiologic features of root avulsions. Two weeks after the injury, nerve conduction studies usually show low-amplitude motor response amplitudes with normal sensory responses because the nerve injury is proximal to the dorsal root ganglion. Cortical SEP responses are absent from intraoperative stimulation of the brachial plexus. Intraoperative brachial plexus NAPs are "super normal" from conduction across sensory fibers.

MULTIMEDIA

Section 10 of 11  

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• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

Media file 1:  A 58-year-old woman with a tender right neck mass had paraesthesias radiating to her distal right arm, with preoperative electrodiagnostic test results interpreted as consistent with severe axonal loss (Case study 1). Postoperative right arm pain and weakness did not improve with time, and the patient was taken back to the operating room. 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.
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Media file 2:  A 55-year-old man experienced pain and numbness in his right hand after prolonged laparotomy (Case study 2). 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).
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Media type:  Graph

Media file 3:  A 55-year-old man experienced pain and numbness in his right hand after prolonged laparotomy (Case study 2). 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).
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Media type:  Photo

Media file 4:  A 55-year-old man experienced pain and numbness in his right hand after prolonged laparotomy (Case study 2). 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).
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Media type:  Graph

Media file 5:  A 55-year-old man experienced pain and numbness in his right hand after prolonged laparotomy (Case study 2). 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.
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Media type:  Photo

Media file 6:  A 64-year-old man sustained multiple neurovascular injuries affecting the left arm in a motor vehicle accident (Case study 3). Although he had considerable improvement in muscle strength in the 18 months after surgery, he had residual left biceps weakness and underwent reoperation. 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.
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Media type:  Graph

Media file 7:  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).
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Media type:  Graph

REFERENCES

Section 11 of 11

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Miscellaneous
• Multimedia
• References

• Brown WF, Veitch J. AAEM minimonograph #42: intraoperative monitoring of peripheral and cranial nerves. Muscle Nerve. Apr 1994;17(4):371-7. [Medline].
• 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].
• Chaput C, Probe R. Brachial Plexus Injuries, Traumatic. eMedicine Journal [serial online]. 2003. Available at: http://www.emedicine.com/orthoped/topic26.htm. [Full Text].
• Chaudhry V, Cornblath DR. Wallerian degeneration in human nerves: serial electrophysiological studies. Muscle Nerve. Jun 1992;15(6):687-93. [Medline].
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Article Last Updated: Oct 11, 2006