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Year : 2019  |  Volume : 67  |  Issue : 6  |  Page : 1419--1422

Peripheral Nerve Injuries: Electrophysiology for the Neurosurgeon

Nitish Kamble1, Dhaval Shukla2, Dhananjay Bhat2,  
1 Department of Neurology, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India
2 Department of Neurosurgery, National Institute of Mental Health and Neurosciences, Bengaluru, Karnataka, India

Correspondence Address:
Dr. Nitish Kamble
Department of Neurology, National Institute of Mental Health and Neurosciences, Bengaluru - 560 029, Karnataka


Peripheral nerve injuries are a heterogeneous and distinct group of disorders that are secondary to various causes commonly including motor vehicle accidents, falls, industrial accidents, household accidents, and penetrating trauma. The earliest classification of nerve injuries was given by Seddon and Sunderland, which holds true till date and is commonly used. Neuropraxia, axonotmesis, and neurotmesis are the three main types of nerve injuries. The electrophysiological studies including nerve conduction studies (NCS) and electromyography (EMG) play a key role and are now considered an extension of the clinical examination in patients with peripheral nerve injuries. The electrophysiological results should be interpreted in the light of clinical examination. These studies help in localizing the site of lesion, determine the type and severity of lesion, and help in prognosticating. In neuropraxia, the compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) are elicitable on stimulating the nerve distal to the site of the lesion but demonstrate conduction block on proximal stimulation. The electrodiagnostic findings in axonotmesis and neurotmesis are similar. After few days of injury, Wallerian degeneration sets in with failure to record CMAP and SNAP. Intraoperative technique involves recording from the peripheral nerves during the intraoperative period and has proved useful in the surgical management of nerve injuries and helps in identifying the injured nerve, to determine whether the nerve is in continuity and in localizing the site of lesion. Intraoperative monitoring also helps in identifying the nerve close to an ongoing surgery so that surgical damage to the nerve can be prevented.

How to cite this article:
Kamble N, Shukla D, Bhat D. Peripheral Nerve Injuries: Electrophysiology for the Neurosurgeon.Neurol India 2019;67:1419-1422

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Kamble N, Shukla D, Bhat D. Peripheral Nerve Injuries: Electrophysiology for the Neurosurgeon. Neurol India [serial online] 2019 [cited 2020 Feb 24 ];67:1419-1422
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Full Text

Peripheral nerve injuries are a heterogeneous and distinct group of disorders that are secondary to various causes.[1] The common causes include motor vehicle accidents, falls, industrial accidents, household accidents, and penetrating trauma.[2] The estimated prevalence of peripheral nerve injuries in patients presenting to level I trauma centers is roughly about 2–3%.[3] Motor vehicle accidents are the predominant cause of peripheral nerve injuries amounting to 46% of total cases and commonly seen in men.[3] The most common nerve injured in the upper limbs is the radial nerve followed by the median and ulnar nerves. In the lower limbs, the most commonly injured nerve is the sciatic nerve followed by peroneal and tibial nerves.[3] Some studies have reported an incidence of 1–2% in patients with extremity trauma.[4],[5] These injures are commonly associated with head injury (60%), spinal injuries, fractures, and dislocation of nearby bones. About 10–34% of patients admitted in the rehabilitation unit have associated nerve injuries.[6] Most of the knowledge regarding peripheral nerve injuries was acquired during the World Wars and the American Civil War.[7],[8] In cases of head injury or polytrauma, peripheral nerve injuries are often missed that may subsequently lead to delay in recovery, morbidity, and poor functional outcome.[2] An early diagnosis with management is important to improve the functional outcome in these patients, and hence, it is important to identify the associated nerve injury.

The aim of this review is to describe concisely the classification, patterns of nerve regeneration, and the electrophysiological methods.

 Classification of Nerve Injuries

The earliest classification of nerve injuries was given by Seddon and Sunderland.[9],[10] These classifications even hold true till date and are commonly used. In the Seddon classification, the peripheral nerve injuries are divided into three types: neuropraxia, axonotmesis, and neurotmesis. Neurapraxia refers to a mild injury to a nerve with impairment of both motor and sensory functions. There is no loss of axon, whereas there is a temporary loss of myelin sheath. Due to this demyelination, there is impairment of impulse conduction across the nerve segment. This type of nerve injury is most commonly seen in entrapment neuropathies or pressure palsies. The prognosis is good with usually complete recovery within days to weeks.[11] The recovery is due to axon remyelination.

In axonotmesis, the axons are damaged; however, most of the covering connective tissues that form the endoneurium, perineurium, and epineurium are still partially or fully intact. There are endoneurial tubes on which the nerve regeneration can take place. This type of nerve injury is seen in crush and stretch injuries.[12]

Neurotmesis is the most severe form of nerve injuries with severe damage to the axons, myelin sheath, and the connective tissue elements. The axonal growth is nearly inadequate. This type of nerve injury is seen after massive trauma, sharp injuries, traction or avulsion injuries, and injection of noxious drugs.[13] Surgical repair is essential to enhance the reinnervation and recovery.

The Sunderland classification grades the nerve injuries into five groups. The first-degree injury corresponds to Seddon's classification of neuropraxia that has a good prognosis. The second, third, and fourth-degree injury refer to the transection of the axon (Seddon's axonetmesis) with impairment of endoneurium, perineurium, and epineurium, respectively. Prognosis is worse with this degree of injury. The fifth degree of injury corresponds to Seddon's neurotmesis.

Another sixth-degree injury has been described by some authors as a mixed lesion with the loss of axon along with conduction block.[14] This lesion is probably considered as the most common type of nerve injury.

 Changes in the Nerve and Muscle After Injury

Neuropraxic injury secondary to transient or intermittent ischemia improves quicker than injury secondary to focal demyelination. The myelin sheath is separated from the axon and predominantly affects the large fibers than the smaller fibers.[2] Due to the focal demyelination, there is leakage of the current at the nodes of Ranvier. As a result, the conduction is markedly slowed. Complete conduction block can occur with severe demyelination and is observed when the intermodal conduction time exceeds 5–600 μs.[15] The muscle is usually unaffected, but if the neuropraxia is prolonged, then the muscle may become atrophic.

The process of Wallerian degeneration is observed in axonotmesis. The cell body is separated from the axon segment distal to the injury. The transport of essential molecules and the electrical signal from the cell body to the axon fragment is disrupted.[16] There is swelling of the axon fragment due to rise in the calcium levels and consequent loss of electrical responsiveness.[17] Subsequently, there is fragmentation of both the axon and myelin. If the lesion is more proximal and close to the cell body, neuronal death occurs. Central chromatolysis (breakdown of the Nissl bodies) is the only change observed in the cell body in majority of the cases.[16] There are two possible modes of recovery in axonotmesis: collateral sprouting and regeneration. Collateral sprouting occurs when there is injury to less than 20–30% of the motor axons. The remaining axons help in collateral sprouting that takes about 2–6 months. Regeneration of the axon is the predominant mechanism when there is injury to more than 90% of the axons.[18] The process of regeneration requires an intact myelin/Schwann cell tube to support the growth of the axon. These tubes are viable for 18–24 months following injury.[19] It is important for the axon regeneration to take place within this time period; otherwise, myelin tubes will degenerate and interrupt the process of regeneration.[19] The denervated muscle becomes atrophic.

In neurotmesis, the axonal regeneration can be achieved only after the surgical repair that can be either direct approximation of the two segments or by cable grafting.[20]

 Electrophysiological Methods

Electrophysiological studies play a key role and are considered an extension of the clinical examination in patients with peripheral nerve injuries. The electrophysiological results should be interpreted in the light of clinical examination. Nerve conduction studies (NCS) and electromyography (EMG) are often used to evaluate such patients. The principal goals of the electrodiagnostic studies are localization of the lesion, determination of the type of injury and its severity, and prognostication.[21] It also informs about the fiber types involved. NCS include motor and sensory conduction studies. All patients of peripheral nerve injury must be evaluated with motor conduction studies (MCS), sensory conduction studies (SCS), and EMG of the involved muscle. In NCS, the nerves are electrically stimulated by the external electrodes and the response is recorded from the muscle (MCS) or from the nerve (SCS). The response obtained from the muscle is known as compound muscle action potential (CMAP). CMAP represents the summation of motor unit potentials beneath the recording electrode. The amplitude is proportional to the number of axons stimulated. At a particular stimulus intensity, there is no further change in the amplitude of the CMAP, suggesting that all the axons are stimulated.

The sensory potential recorded from the nerve after stimulating the nerve is known as sensory nerve action potential (SNAP). The amplitude of SNAPs is usually between 5 and 20 μV. As the amplitudes are very small, the responses need to be averaged to accurately measure the response. CMAP is about 100 times larger in amplitude when compared to the SNAP.[22] SNAPs are helpful in distinguishing whether the lesion is preganglionic or post-ganglionic. This is particularly helpful in localizing the lesions that are proximal and difficult to evaluate using routine conduction studies.

The parameters that are measured during MCS and SCS are the distal latency, amplitude, and velocity. In addition, the F-wave responses with minimum latency and persistence are measured during the MCS.

EMG involves the use of needle electrode to record the potentials directly from the muscle. Needles are either monopolar or concentric. Concentric needle electrodes are frequently employed in electrodiagnostic studies. EMG is particularly useful in distinguishing between neuropathic and myopathic cause of weakness.[22] EMG is recorded by inserting the needle electrode in the muscle when it is at rest and during voluntary contraction. EMG is used to look for the insertional activity, any abnormal spontaneous activity at rest, and motor unit potentials (MUP) during voluntary contraction of the muscle. The abnormal spontaneous activity helps in determining the time since lesion, possible site, nature, and severity of the lesion.[23] The abnormal spontaneous activity observed in peripheral nerve injuries includes fibrillations and positive sharp waves.

 Electrophysiological Findings in Peripheral Nerve Injuries

In neuropraxia, the CMAP and SNAP are elicitable on stimulating the distal part of the nerve. However, on stimulating the nerve proximal to the lesion with distal recording, there are varying degrees of loss of CMAP amplitude, partial or complete conduction block, and reduced conduction velocity across the lesion. SNAPs are also lost or reduced in amplitude on proximal stimulation. Conduction block is suggested when the amplitude falls to 50–70%.[24] These changes improve completely or partially when remyelination is complete.[25] On needle EMG, the muscle in neuropraxic lesions does not show any abnormal spontaneous activity. Some studies have shown the presence of fibrillation potentials but this has been a matter of debate.[26] On voluntary contraction of the muscle, there is poor recruitment. In complete lesion, MUPs are not recordable, but in incomplete lesions, the typical finding is reduced number of MUPs with normal amplitude, duration, and phases.[2]

Electrodiagnostic findings in axonotmesis and neurotmesis are similar. These findings depend to large extent on the duration since injury. Immediately after axonotmesis, the CMAP and SNAP are normal or mildly abnormal on stimulating distal to the lesion. This finding is observed till 7 days for CMAP and 11 days for SNAP as the motor and sensory axons are excitable till 7–11 days post-injury, respectively.[17] Hence during this period, it is difficult to distinguish neuropraxia from axonotmesis. It is only after 10–12 days that Wallerian degeneration sets in and leads to the failure to record motor and sensory responses (CMAP and SNAP) with distal stimulation. This is contrary to what is observed in neuropraxia. The responses will be preserved in neuropraxia. Presence of conduction block with preserved distal responses reliably suggests neuropraxia.[27] Hence in a suspected case of acute nerve injury, it is recommended to perform NCS 10–14 days after the injury.[27] EMG changes evolve over a period of weeks and months in axonotmesis and neurotmesis. As there is axonal loss, the needle EMG demonstrates fibrillation potentials and positive sharp waves approximately 2–3 weeks after denervation. Over a period of time, the fibrillation potentials decrease in number as reinnervation occurs.[28] With continued motor remodeling as a result of collateral sprouting, changes are observed in the MUPs. The earliest EMG changes are noted 3 weeks after the injury using single fiber EMG. These findings include presence of small, polyphasic (>4 turns), and unstable MUPs.[29] The initial unstable MUP is due to sprouting of new axons that are thin and unmyelinated with immature neuromuscular junctions. As the reinnervation continues, the MUPs become larger in amplitude and develop polyphasia with increase in the duration of MUPs. Subsequently, the MUPs also increase in number and percentage of polyphasia.

 Intraoperative Electrophysiological Studies

This technique involves recording from the peripheral nerves during the intraoperative period and has proved useful in the surgical management of nerve injuries.[30] The technique used is the same that is used for surface NCS recording. The nerve is stimulated electrically and the recording is from the innervated muscle. Mechanical stimulation also is done to determine whether the nerve is in continuity.[30] Intraoperative recordings help in identifying the nerve injured and to determine whether the nerve is in continuity.[31] Stimulation of the nerve along its course helps in localizing the site of lesion. Intraoperative monitoring also helps in identifying the nerve close to an ongoing surgery so that surgical damage to the nerve can be prevented.[30] This is especially useful in monitoring the facial nerve during removal of an acoustic neuroma. This greatly improves the surgical outcome.

Intraoperative monitoring is also useful when dealing with a lesion in-continuity (LIC). LIC is a condition that follows a nerve injury, wherein the supporting structures are preserved, but majority of the nerve fibers are damaged.[32] Any form of nerve injury can lead to LIC; axons sprout, and may fail to reach the distal myelin tubes and elongate, proliferate at the site of injury forming a neuroma.[33] This is known as neuroma in-continuity. Nerve action potential (NAP) is recorded by stimulating the nerve at a suprathreshold intensity.[33] NAP is helpful in confirming the lesion and identifying the nerves that can be treated with only neurolysis, thus avoiding excessive resections and repair.[33]

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