Classification of peripheral nerve lesions

The peripheral nerve is made up of the internal axon and the external myelin sheath as well as the surrounding stroma. The major classification system for nerve injuries describe the injury based on the architecture of the injury to these structures. The Seddon classification divides nerve lesions into the following groupings: neuropraxia, axonotmesis, and neurotmesis.

Neuropraxia represents damage to the myelin. There is no damage to the axon, and therefore there is no Wallerian degeneration. This is the mildest form of lesion, and symptoms may resolve within seconds to up to 3 to 6 months. Axonotmesis occurs as a result of damage to the axon and myelin, but the surrounding Schwann tubes, endoneurium, and perineurium are partially or fully intact. However, axonotmesis does result in Wallerian degeneration of the axon. Wallerian degeneration begins at about 3 days and is completed over 11 days in the sensory fibers and over 9 days in the motor fibers because of the earlier failure of the neuromuscular junction. Thus, EMG/NCV may not be able to distinguish between neuropraxia and axonotmesis until Wallerian degeneration has had time to occur. Recovery begins via sprouting from the tip of the peripheral motor nerve within 1 week. Recovery via direct regrowth involving the motor and sensory aspect of the nerve is variable, but occurs at an average of 1 mm/d. However the rate of regrowth is decreased in cases with more proximal or severe lesions, older patients, and cases with significant scar tissue.

In axonotmesis, the axon and myelin are injured, but the surrounding Schwann tubes, endoneurium, and perineurium are partially or fully intact. In contrast, with neurotmesis, there is damage to the axon and myelin, and the architecture of the endoneurial tube is completely disrupted, which makes regrowth less likely. EMG/NCV is not typically able to distinguish between severe axonotmesis and neurotmesis.

Unlike motor function recovery, sensory function does not recover via sprouting. There is recovery via axonal regeneration. There may also be redistribution of sensory nerve coverage after an axonal injury, which results in the remaining uninjured fibers supplying cutaneous sensation to a larger area than was supplied before the injury.

Terms of EMG/NCV

Electromyography evaluates individual muscles at rest as well as with submaximal and maximal voluntary muscle contractions. At rest, the muscle is evaluated with 5 to 30 needle passes in different quadrants at each site. Each time the needle electrode is moved, there is a release of self-limited electrical activity. This activity is called insertional activity and may be increased when there is damage to the axon. If the muscle is fibrotic, then the insertional activity is decreased. Spontaneous abnormal electrical potentials that result from axonal damage are called positive waves and fibrillations. These abnormal electrical potentials may be seen as early as 7 to 10 days after injury, but may not be seen for 3 to 4 weeks. The number of these potentials does not correlate with the severity of the injury. Fibrillations are generally seen more acutely and tend to disappear over the next year. Chronic findings are identified by small fibrillations or complex repetitive discharges. Submaximal contraction looks at the contraction of the individual motor units. If there is subacute to chronic damage to the nerve, polyphasic potentials are seen. These potentials are wave forms with 5 or more phases that form as a result of collateral nerve sprouting, remyelination, and reinnervation. Over time, the polyphasic activity resolves and maximal contraction reveals large amplitude potential as a result of electrical summation of the multiple sprouts that have remyelinated. If there is enough damage, the remaining individual neurons and the muscle fibers that they innervate will fire at an increased rate, because there are few nerve fibers innervating the muscle. This is called decreased recruitment and may be a result of repetitive firing of the individual motor units; this may well correlate with clinical weakness. In myelinopathy, the only finding on EMG may be decreased or absent firing of the motor units because of conduction block.

NCS are performed on motor and sensory nerves. The temperature in the upper extremity should be at least 32° or the distal latency and conduction velocity may be artificially slow. The time that it takes the nerve to conduct from the point of stimulation to the active electrode over the muscle or to another electrode over the sensory nerve is called the distal latency. The electrical potential that is created with stimulation of the motor nerve is the compound muscle action potential (CMAP), whereas the sensory potential is called the compound sensory nerve action potential (SNAP). Normal values are based on the results in a normal population, but may also be derived by comparing the nerve in question to another peripheral nerve or the same contralateral nerve. The distal latency may be abnormal as a result of myelinopathy more than axonopathy, unless the axonal pathology is severe. Conduction velocity represents the speed of electrical conduction in the nerve. Severe slowing of the NCV is usually the result of myelinopathy, and mild NCV slowing is more attributed to axonopathy. Prolonged distal latency and slow conduction velocity usually do not result in clinical signs seen on physical examination.

In cases of myelinopathy, the electrical impulses travel at divergent speeds in the individual axons across a lesion, resulting in temporal dispersion when the wave form that is achieved with stimulation proximal to the lesion is 20% to 30% longer than the wave form that results from stimulation of the nerve distal to the lesion. This may or may not result in clinical signs seen on physical examination. Conduction block is seen when all or a portion of the impulses are not conducted across the lesion. Proximal stimulation results in an action potential that will achieve an amplitude more than 20% smaller than the potential evoked with stimulation distal to the conduction block.

In cases of axonopathy, the amplitude of the evoked response proximal and distal to the lesion will also be diminished secondary to Wallerian degeneration. The degree of diminution of the amplitude is relative to the unaffected side or accepted “norm” comparable to the severity of the injury. It does result in changes, which will be seen on physical examination. Conduction block and temporal dispersion are findings that assist in localization of the lesion in myelinopathy. NCV is not as useful in localizing the lesion with axonopathy, because axonal lesions result in diminished amplitude proximal and distal to the lesion. In axonopathy, the EMG is used to localize the lesion based on muscles that are abnormal.

Terms of EMG/NCV

Electromyography evaluates individual muscles at rest as well as with submaximal and maximal voluntary muscle contractions. At rest, the muscle is evaluated with 5 to 30 needle passes in different quadrants at each site. Each time the needle electrode is moved, there is a release of self-limited electrical activity. This activity is called insertional activity and may be increased when there is damage to the axon. If the muscle is fibrotic, then the insertional activity is decreased. Spontaneous abnormal electrical potentials that result from axonal damage are called positive waves and fibrillations. These abnormal electrical potentials may be seen as early as 7 to 10 days after injury, but may not be seen for 3 to 4 weeks. The number of these potentials does not correlate with the severity of the injury. Fibrillations are generally seen more acutely and tend to disappear over the next year. Chronic findings are identified by small fibrillations or complex repetitive discharges. Submaximal contraction looks at the contraction of the individual motor units. If there is subacute to chronic damage to the nerve, polyphasic potentials are seen. These potentials are wave forms with 5 or more phases that form as a result of collateral nerve sprouting, remyelination, and reinnervation. Over time, the polyphasic activity resolves and maximal contraction reveals large amplitude potential as a result of electrical summation of the multiple sprouts that have remyelinated. If there is enough damage, the remaining individual neurons and the muscle fibers that they innervate will fire at an increased rate, because there are few nerve fibers innervating the muscle. This is called decreased recruitment and may be a result of repetitive firing of the individual motor units; this may well correlate with clinical weakness. In myelinopathy, the only finding on EMG may be decreased or absent firing of the motor units because of conduction block.

NCS are performed on motor and sensory nerves. The temperature in the upper extremity should be at least 32° or the distal latency and conduction velocity may be artificially slow. The time that it takes the nerve to conduct from the point of stimulation to the active electrode over the muscle or to another electrode over the sensory nerve is called the distal latency. The electrical potential that is created with stimulation of the motor nerve is the compound muscle action potential (CMAP), whereas the sensory potential is called the compound sensory nerve action potential (SNAP). Normal values are based on the results in a normal population, but may also be derived by comparing the nerve in question to another peripheral nerve or the same contralateral nerve. The distal latency may be abnormal as a result of myelinopathy more than axonopathy, unless the axonal pathology is severe. Conduction velocity represents the speed of electrical conduction in the nerve. Severe slowing of the NCV is usually the result of myelinopathy, and mild NCV slowing is more attributed to axonopathy. Prolonged distal latency and slow conduction velocity usually do not result in clinical signs seen on physical examination.

In cases of myelinopathy, the electrical impulses travel at divergent speeds in the individual axons across a lesion, resulting in temporal dispersion when the wave form that is achieved with stimulation proximal to the lesion is 20% to 30% longer than the wave form that results from stimulation of the nerve distal to the lesion. This may or may not result in clinical signs seen on physical examination. Conduction block is seen when all or a portion of the impulses are not conducted across the lesion. Proximal stimulation results in an action potential that will achieve an amplitude more than 20% smaller than the potential evoked with stimulation distal to the conduction block.

In cases of axonopathy, the amplitude of the evoked response proximal and distal to the lesion will also be diminished secondary to Wallerian degeneration. The degree of diminution of the amplitude is relative to the unaffected side or accepted “norm” comparable to the severity of the injury. It does result in changes, which will be seen on physical examination. Conduction block and temporal dispersion are findings that assist in localization of the lesion in myelinopathy. NCV is not as useful in localizing the lesion with axonopathy, because axonal lesions result in diminished amplitude proximal and distal to the lesion. In axonopathy, the EMG is used to localize the lesion based on muscles that are abnormal.

Pitfalls of EMG/NCV

EMG/NCV is not a perfect test, and interpretation must be formulated and interpreted in the light of the clinical evaluation. This test does not determine the exact cause of the neurologic lesion. There are technical and operator-dependent errors, which may lead to incorrect conclusions. Correct wave form evaluation is subjective and operator dependent. Normal variations in the composition of fascicles in nerve roots and the peripheral nerves may result in different patterns of muscle innervation may confuse the localization of the lesion on EMG as well as the physical examination.

Only a portion of the muscle is evaluated when performing the EMG, and the muscle may look normal when it is not normal. If the study is performed too early, sufficient time may not have passed to evaluate whether or not muscle abnormalities are present. Later in the course of an injury, the signs of fibrillations and positive waves may disappear, to be replaced by the more chronic findings of polyphasicity and large amplitude potentials on needle testing. Chronic nerve injury may be difficult to identify on EMG. As patients age, a percentage of muscle fibers normally develop polyphasic potentials, which can lead to false-positive conclusions. Positive waves and fibrillations may be seen in myopathy as well as with direct trauma or injections into the muscle.

In more acute lesions with mixed axonopathy and myelinopathy, prognostication on NCS findings is unreliable. In certain nerves, it may not be feasible to stimulate the nerve proximal and distal to the injury and establish whether or not there is a myelinopathy. The number of positive waves and fibrillations do not correlate with the severity of the injury. If there is no evidence of myelinopathy, the amplitude of the evoked response can be used to understand the degree of axonal lesion in the acute phase. If the amplitude of the evoked response on the affected side is greater than 30% of the intact contralateral nerve, the prognosis for recovery is good. If the amplitude is between 10% and 30% of the contralateral nerve, the prognosis is fair, and it is poor if the amplitude is less than 10% of the other side. In the subacute to chronic phase, sprouting and regrowth result in increased amplitude of the evoked motor response, and it can no longer be used for prognostication.