Electrodiagnostic Testing
Venu Akuthota
Jason Friedrich
INTRODUCTION
Electrodiagnostic (EDX) testing can be a useful tool in the evaluation of athletes with neurologic problems (1,26).
Although clinical recognition of patterns of pain and sensory or motor abnormalities is the first step toward the identification of a nerve problem, EDX testing can augment the clinical examination to better localize and characterize neuropathology (2).
A thorough EDX consultation integrates the history, physical examination, and selected nerve conduction and electromyographic studies into a meaningful diagnostic conclusion.
Whereas imaging studies identify structural abnormalities, EDX studies evaluate the physiology and function of the peripheral nervous system.
A negative EDX examination does not rule the possibility of pathology because electrophysiologic studies are time and severity dependent (1,2).
Clinical judgment is used in EDX; therefore, EDX studies are highly dependent on the quality of the electromyographer (7,11,12).
This chapter will describe the pathophysiology of nerve injury and associated chronology of electrophysiologic findings, as well as describe the components of an EDX evaluation.
EDX testing involves both nerve conduction studies (NCS) and needle examination (NE). The NE is also referred to as electromyography (EMG).
The purpose of this chapter is to provide the clinician a basis for ordering EDX consultations and understanding proper EDX reports.
ANATOMY
Standard EDX studies typically give little information regarding central nervous system pathology (upper motor neuron pathway).
The components of the peripheral nervous system include afferent sensory nerves and efferent motor nerves.
Sensory (Afferent) Pathway
Cutaneous receptors → sensory axons → pure sensory or mixed nerves → nerve plexus (e.g., brachial plexus, lumbosacral plexus) → cell bodies in the dorsal root ganglion (usually within intervertebral foramina) → dorsal roots synapse in the dorsolateral spinal cord.
This pathway is evaluated during NCS of pure sensory or mixed nerves.
Motor (Efferent) Pathway
Anterior horn cell (spinal cord) → spinal nerves, subsequently dividing into ventral and dorsal rami. Ventral rami → nerve plexus → peripheral motor nerve → neuromuscular junction → muscle fibers. Entire pathway is referred to as a motor unit.
This pathway is evaluated during NCS of motor or mixed nerves, from the point of stimulation to the recording site.
Individual motor units can be evaluated during NE with voluntary muscle activation.
PATHOPHYSIOLOGY OF NERVE INJURY
Peripheral nerves can either be myelinated or unmyelinated.
Myelinated fibers conduct much more rapidly by way of saltatory (“jumping”) conduction, in which depolarization occurs only at interspersed nodes of Ranvier, allowing current to jump from node to node (2).
NCSs evaluate the fastest-conducting fibers within a given nerve; typically, these are the A alpha myelinated fibers.
Seddon Classification
Divides peripheral nerve injury into neurapraxia, axonotmesis, and neurotmesis (Table 20.1).
Neurapraxia
Neurapraxia is a comparatively mild injury that affects only the myelin sheath and causes focal conduction slowing or conduction block as a result of current leakage between nodes of Ranvier (32). Although the myelin is injured, the
nerve fibers remain in axonal continuity. This results in motor or sensory loss from impaired conduction across the demyelinated segment. However, impulse conduction is normal in the segments proximal and distal to the injury, where the myelin remains intact.
Table 20.1 Classification of Nerve Pathophysiology (2)
Type
Pathology
EDX Correlation
Prognosis
Neurapraxia
Myelin injury
CV slowing across segment
DL prolonged across segment to months
Loss of amplitude proximal but not distal
NE normal
Recovery in weeks
Axonotmeses
Axonal injury with variable stromal disruption
Loss of amplitude distal and proximal
NE shows spontaneous activity
NE shows abnormal voluntary motor units
Longer recovery and more variable
Neurotmeses
Severance of entire nerve
No waveform with proximal or distal stimulation
NE shows spontaneous activity
NE shows no recruited motor units
Poor recovery, surgery required
CV, conduction velocity; DL, distal latency; NE, needle examination.
Demyelination is typically seen with focal nerve entrapments (e.g., carpal tunnel syndrome). It may also occur in peripheral polyneuropathies either as a patchy process (e.g., Guillain-Barré syndrome) or a diffuse process (e.g., diabetic peripheral neuropathy).
Axonotmesis and Neurotmesis
Axonotmesis and neurotmesis refer to axonal injury with Wallerian degeneration of nerve fibers disconnected from their cell bodies. These types of injuries result in loss of nerve conduction at the site of injury and distally. Axonotmetic injuries involve damage to the axon, with some preservation of the surrounding stroma (endoneurium, perineurium, epineurium), whereas neurotmetic injuries imply complete disruption of the enveloping nerve sheath (2,32).
EDX studies typically cannot distinguish axonotmesis from neurotmesis.
Athletes can experience axonal injury with conditions such as radiculopathy.
SPECIFIC ELECTRODIAGNOSTIC STUDIES
EDX studies typically consist of NCS and NE.
Nerve Conduction Studies
NCSs may be performed on motor, sensory, or mixed nerves.
There are numerous pitfalls associated with performing NCSs (Table 20.2). Both motor and sensory NCSs test only the fastest, myelinated axons of a nerve; thus, the lightly myelinated or unmyelinated fibers (e.g., C pain fibers) are not examined (7,18,19).
Motor nerves are stimulated at accessible sites, and the compound motor action potential (CMAP) is recorded over the motor points of their target muscles. Motor points represent regions of high concentration of neuromuscular junctions, typically in the central muscle belly.
Deep motor nerves and deep proximal muscles are more difficult to study and interpret (15).
Sensory nerves can be studied along the physiologic direction of the nerve impulse (orthodromic) or opposite the physiologic direction of the afferent input (antidromic).
A stimulated sensory nerve produces the recorded sensory nerve action potential (SNAP).
Frequently, sensory nerves are tested within mixed nerves, such as the plantar nerves, and produce a mixed nerve action potential (MNAP).
CMAP, SNAP, and MNAP waveforms are analyzed and interpreted by the clinician.
▪ Temperature
▪ Inadequate or excessive stimulation
▪ Improper placement of electrodes
▪ Tape measurement error
▪ Not adjusting values for age
▪ Anomalous innervation
▪ Volume conduction of impulse to nearby nerve
▪ Improper filter settings
▪ Improper electrode montage setup
▪ Involuntary muscle contractions
Waveform parameters include amplitude, latency, and conduction velocity.
Amplitude evaluates the number of functioning axons in a given nerve and, for motor nerves, the number of muscle fibers activated.
Latency refers to the time (milliseconds) from the stimulus to the recorded action potential.
With motor NCSs, latency accounts for peripheral nerve conduction (distal to the site of stimulation), neuromuscular junction transition time, and muscle fiber activation time (12).
With sensory nerves, latency measures only the conduction time within the segment of nerve stimulated. Conduction velocity is calculated by dividing the distance travelled between a distal and proximal stimulation site by the impulse conduction time.
Late Responses
Whereas routine NCSs typically evaluate distal nerve segments, late responses, such as the H reflex and F wave, travel the full length of a nerve.
H Reflex
The H reflex is the electrophysiologic analog to the ankle stretch reflex. It measures afferent and efferent conduction along the S1 nerve root pathway (16).
A latency difference of at least 1.5 milliseconds is significant in most laboratories.
Amplitude of < 50% compared with the uninvolved side is also significant.
Because the amplitude of this reflex is sensitive to contraction of the plantar flexor muscles, amplitude changes without associated latency abnormalities should be interpreted with caution (31).
The H reflex evaluates the afferent and efferent pathway; thus, it gives information about the sensory pathway that is not tested on NE.
The S1 nerve injury can be due to S1 radiculopathy from a herniated disc or lumbar stenosis, peripheral neuropathy (usually with bilaterally abnormal H reflexes), or sciatic/tibial nerve injuries (2).
F Wave
The F wave is a late muscle potential that results from a motor nerve volley created by supramaximally stimulated anterior horn cells (16). Thus, the F wave represents conduction up and down a motor nerve, without any sensory afferent contribution.
Unlike the H reflex, the F wave can be elicited at many spinal levels and from any muscle.
Like the H reflex, F wave studies examine long nerve pathways, which consequently obscure small focal abnormalities.
Abnormalities of F wave values may be due to injury anywhere along the pathway evaluated; thus, specificity may be limited.
Magnetic Stimulation
Potential advantages over conventional electrical stimulation are less discomfort with stimulations and improved access to deeper nerve segments, including roots of the lumbosacral plexus and the proximal sciatic nerve (5).
Needle Examination
Evaluates the entire motor unit (lower motor neuron pathway), but not the sensory pathway.
Assesses muscles at rest (to detect potential axonal injury) and with volitional activity (to evaluate voluntary motor unit morphology and recruitment) (9).
Needs to be timed such that abnormalities are optimally detected.
If performed too early (i.e., < 2-3 weeks after the initial injury), spontaneous muscle fiber discharges (denervation potentials) may not have had time to develop (2).
If performed too late (i.e.Related posts:
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