Electrodiagnosis in spinal disorders

1

List the common reasons for requesting electrodiagnostic tests for the evaluation of patients with spinal disorders.

• To establish and/or confirm a clinical diagnosis . Electrodiagnostic tests (EDX) may help determine whether extremity symptoms are due to radiculopathy, peripheral entrapment neuropathy, or polyneuropathy.

• To localize nerve lesions . EDX can assist in differentiation between root lesions (radiculopathy), brachial or lumbosacral plexus lesions (plexopathy), and peripheral nerve lesions (entrapment neuropathy). EDX can help distinguish central lesions (e.g., motor neuron disease) from peripheral neuropathy and spinal stenosis.

• To determine the severity and extent of nerve injury . EDX can differentiate myelin injury (conduction block or neurapraxia) from either axonal degeneration alone (axonotmesis) or axonal degeneration along with damage to a nerve’s supporting structures (neurotmesis). EDX can help to determine whether a lesion is acute or chronic, progressive or improving, and preganglionic or postganglionic. EDX can provide information regarding prognosis and a timeline for recovery after nerve injury. It is the only diagnostic test that assesses the function of a nerve.

• To correlate findings noted on spinal imaging studies . EDX may help determine whether an abnormality noted on spinal magnetic resonance imaging (MRI) is contributing to a patient’s neurologic complaints.

• To provide documentation in medicolegal settings .

2

When should EDX be avoided in the assessment of patients with spinal disorders?

• During the first 2–4 weeks after symptom onset . During this time many EDX findings are difficult to detect, and testing is not recommended, unless a baseline study for comparison would be useful.

• When the diagnosis of radiculopathy is unequivocal . EDX adds little to the treatment plan.

• When findings will not change medical or surgical management. For example, patients with extreme illness, patients who refuse treatment, or patients with isolated neck or back pain without radiculopathy.

• Patients with potential contraindications to EDX testing. For example, anticoagulated patients whose needle electromyography (EMG) test would require studying muscles that are not easily compressible in the case of bleeding; patients with open skin lesions; or patients with pacemakers and defibrillators whose nerve conduction studies (NCS) would require studying nerves near the pacemaker and pacing leads.

3

What are the basic components of an electrodiagnostic examination?

EDX is an extension of the history and physical examination. Its goal is to help differentiate the variety of causes for numbness, weakness, and pain. The standard EDX examination consists of two parts: EMG and NCS.

EMG (needle electrode examination) uses a needle “antenna” to detect and record electrical activity directly from a muscle. The distribution of abnormalities is used to identify the site of nerve or muscle pathology. EMG is the most useful electrodiagnostic test for the evaluation of radiculopathy . Muscles are assessed at rest and during contraction to evaluate four characteristics:

• 1.

  Insertional activity: EMG needle insertion into normal muscle generates brief electrical discharges by muscle fibers.

• 2.

  Spontaneous activity: In a normal relaxed muscle there should be no electrical activity.

• 3.

  Motor-unit action potentials: Slight contraction of the target muscle generates motor unit action potentials which are assessed for amplitude, duration, and configuration.

• 4.

  Recruitment: With more forceful muscle contraction of a normal muscle, a larger number of motor units are recruited and their firing rate increases.

NCS record and analyze biological electrical waveforms elicited in response to a nonbiological electrical stimulus over a nerve or nerves. NCS assess the ability of a specific nerve or nerves to transmit an impulse between two sites along the nerve following an electrical stimulus. When NCS are abnormal, they provide information that a specific nerve is not conducting impulses properly in the measured nerve segment. Both sensory and motor NCS can be performed, allowing for the evaluation of sensory, motor, and mixed nerves. NCS are most useful for diagnosis of peripheral entrapment neuropathy and peripheral neuropathy . NCS are generally expected to be normal in radiculopathy. Specialized NCS—H-reflex, F-wave, and somatosensory evoked potentials (SEPs)—have limited value in specific clinical settings for diagnosis of radiculopathy (see questions 8–11).

4

What is the anatomic basis for EDX as it relates to the assessment of spinal disorders?

The purpose of the EDX is to assess the function of the peripheral sensory and motor nervous system. Each spinal nerve contains both motor and sensory fibers which contribute to the formation of a peripheral nerve. The cell bodies of the motor axons that comprise the ventrally exiting motor roots are situated within the anterior horn of the spinal cord (primary motor neurons). The cell bodies of the sensory axons (primary sensory neurons) are located outside the spinal cord within the dorsal root ganglion (DRG). The DRG are bipolar cells with central projections that form the sensory roots, which enter the dorsal aspect of the spinal cord, and peripheral projections, which continue as sensory nerve fibers in peripheral nerves. After the dorsal and ventral roots join to form the mixed spinal nerve, usually in the region of the intervertebral foramina, the mixed spinal nerve divides into anterior (ventral) and posterior (dorsal) rami. The anterior rami supply the anterior trunk muscles and, after entering the brachial or lumbosacral plexus, the muscles of the extremities. The posterior rami supply the paraspinal muscles and skin over the neck and trunk ( Fig. 17.1 ).

Lesions can be classified as either preganglionic (localized to spinal cord or sensory nerve root proximal to the DRG) or postganglionic (localized anywhere along the motor nerve root, sensory nerve root distal to the DRG, brachial or lumbosacral plexuses, or peripheral nerves). Myelin lesions within the spinal canal (myelopathy, most radiculopathies) are undetectable with standard NCS studies, as it is impossible to stimulate proximally to these lesions. Axonal lesions within this same region compromise sensory fibers proximal to their cell bodies in the DRG. Such lesions do not affect the sensory NCS, because the injured sensory fibers degenerate centrally between the cell body in the DRG and the nerve root. Cells in the DRG continue to supply nutrition to the peripheral sensory fibers, thereby preserving sensory nerve conduction in this region, even though physical examination findings of sensory loss can be present. With more peripheral lesions (e.g., those affecting the plexuses or peripheral nerves), sensory fibers degenerate distally, resulting in abnormal sensory NCS. In contrast, nerve root compression distal to the motor cell bodies in the anterior horn cell results in distal degeneration of motor fibers that can be detected with EMG studies and sometimes motor NCS. Note that the muscles most commonly recorded from during NCS are innervated by at least two nerve roots, and thus only severe single- or multi-level root compression will result in abnormal motor NCS waveforms (the waveform amplitude is maintained due to numerous unaffected nerve root fibers that contribute to the amplitude), while needle EMG may be able to detect even mild axonal lesions. For these reasons, needle EMG is the single most valuable electrodiagnostic test for diagnosis of radiculopathy affecting motor fibers.

It is possible for the DRG to be situated more proximally in the neural foramina, or even in an intraspinal location. In these instances, the DRG and/or more distal fibers can be affected by direct compression or indirectly by vascular insult and edema formation. While sensory NCS are typically normal in discogenic radiculopathies, they may be affected if the DRG is located more proximally, which is relatively common in the case of the L5 DRG (12%–21% of cases of L5 radiculopathy may have reduced superficial peroneal SNAP amplitudes). The DRG can also be damaged in diseases such as diabetes mellitus, herpes zoster, and malignancy. In these conditions, the sensory NCS may be abnormal.

5

Explain how EMG is used to assess radiculopathy in patients with spinal disorders.

Specific muscles are selected for EMG assessment. Six upper limb muscles, including paraspinal muscles, consistently identify more than 98% of cervical radiculopathies that are confirmable by electrodiagnosis . For upper-limb EMG evaluation, a suggested screen includes deltoid, triceps, pronator teres, abductor pollicis brevis, extensor digitorum communis, and cervical paraspinal muscles. Six lower limb muscles, including paraspinal muscles, consistently identify more than 98% of lumbosacral radiculopathies that are confirmable by electrodiagnosis . A suggested lower-limb EMG screen for optimal identification includes the vastus medialis, anterior tibialis, posterior tibialis, short head of biceps femoris, medial gastrocnemius, and lumbar paraspinal muscles. For both lumbosacral and cervical disorders, when paraspinal muscles are unreliable to study, eight distal muscles are needed to achieve optimal identification. It is important to note, however, that a significant percentage of radiculopathies are not confirmable by electrodiagnosis, regardless of the number of muscles tested (see question 16).

Localization of a nerve injury to a specific root level is achieved by testing a variety of muscles in a multisegmental distribution that are innervated by different peripheral nerves. If the abnormalities are confined to a single myotome and cannot be localized to the distribution of a single peripheral nerve, the diagnosis is consistent with radiculopathy. The paraspinous musculature is generally affected in radiculopathies. However, on occasion, especially in cervical radiculopathies and long-standing radiculopathies, the paraspinous muscles may be normal.

EDX findings must be interpreted in view of the time interval between the onset of the lesion and the performance of the electrical study, as the development of specific EMG abnormalities occur in a somewhat predictable time course ( Table 17.1 ). Specific diseases are more likely to develop certain abnormalities than others. Table 17.2 identifies the EMG abnormalities commonly associated with various pathologies.

6

What are fibrillation potentials? Why are they important in assessing radiculopathy?

Fibrillation potentials are spontaneous, regularly firing action potentials of individual denervated muscle fibers. Fibrillation potentials are a sensitive indicator of motor axon loss. They can be observed in neuropathy, direct nerve and muscle trauma, myopathy, and some neuromuscular transmission disorders. Fibrillation potentials appear approximately 14 days after nerve fiber injury. However, they appear within 1 week in paraspinal muscles and within 3–6 weeks in the distal limb. Fibrillations can persist for 18–24 months or longer, until muscle fibers are reinnervated. Importantly, while the presence of fibrillations is indicative of motor axonal loss, it is not indicative of the degree of motor axonal loss (i.e., a muscle with countless fibrillations could have minimal axonal loss, while a muscle with few fibrillations could have significant axonal loss, and vice versa).

7

How are NCS obtained? For what diagnoses are NCS most likely to be helpful?

NCS are obtained by application of an electrical impulse at one point, resulting in an action potential (motor or sensory) that is recorded at a second point at a predetermined distance along the nerve. The NCS measures the time (latency) required to travel between the stimulating and recording site as well as the velocity (nerve conduction velocity [NCV]) and amount of potential conducted (amplitude). Sensory responses (sensory nerve action potential [SNAP]) are recorded over a sensory nerve, whereas motor responses (compound motor action potential [CMAP]) are recorded over a muscle. The SNAP amplitude represents the sum of the action potentials of the sensory fibers of individual sensory or mixed nerves. The CMAP amplitude represents the sum of the action potentials of individual muscle fibers innervated by a motor nerve. Special types of nerve conduction studies include F-wave, H-reflex, SEPs, and motor-evoked potentials (MEPs).

NCS are most likely to yield positive findings in conditions that may mimic the symptoms of radiculopathy, such as compression neuropathy or peripheral neuropathy. Sensory NCS are expected to be normal in radiculopathy because the pathologic lesion is often preganglionic. Motor NCS can be abnormal in severe radiculopathy (i.e., reduced CMAP amplitude).