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Chapter Summary
• Context: Diagnostic clinical neurophysiology serves as an indispensable functional extension of history taking, physical examination, and neuroimaging in spine practice. While magnetic resonance imaging (MRI) and computed tomography (CT) document structural anatomy and canal narrowing, electromyography and nerve conduction studies (EMG/NCS) evaluate the physiological integrity and viability of motor axons, sensory fibers, neuromuscular junctions, and myotomal motor units. Diagnostic electrophysiology is crucial for confirming or refuting suspected radiculopathy, establishing disease acuity (acute vs. subacute vs. chronic reinervating), determining severity of axonal loss, distinguishing true compressive radiculopathy from peripheral entrapment neuropathies (carpal tunnel syndrome, cubital tunnel syndrome, peroneal nerve compression at the fibular head) or generalized polyneuropathies ("double crush syndrome"), and identifying motor neuron disease (amyotrophic lateral sclerosis) or plexopathies. Electromyographic changes (fibrillation potentials, positive sharp waves) require 18 to 21 days following acute axonal injury to appear in distal limb muscles, though paraspinal muscle denervation appears within 7 to 10 days. Sensory nerve action potentials (SNAPs) remain normal in preganglionic compressive radiculopathy (because dorsal root ganglion [DRG] cells lie distal to the intraspinal compression), providing a pivotal diagnostic distinction from postganglionic plexopathies or peripheral neuropathies. Understanding neurophysiological principles, optimal timing, and limitations prevents diagnostic delays and inappropriate spinal surgery.
• Chapter Objective: To present the neurophysiological methods used in evaluating spinal pathologies and demonstrate their application in differentiating radiculopathy, plexopathy, entrapment neuropathy, polyneuropathy, and motor neuron disease. The reader should be able to interpret nerve conduction studies (CMAP, SNAP, F-waves, H-reflex), understand needle electromyography findings (spontaneous activity, motor unit potential morphology, recruitment patterns), recognize the physiological timing of denervation, understand the diagnostic significance of preserved SNAPs in preganglionic root lesions, and formulate targeted electrodiagnostic requests.
• Clinical Neurophysiology and Diagnostic IntegrationDiagnostic electrophysiology comprises nerve conduction studies (NCS), late responses (F-waves, H-reflex), and needle electromyography (EMG). These modalities transform clinical symptoms into objective neurophysiological data. NCS measures compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) amplitudes and conduction velocities. Late responses evaluate proximal nerve segments: F-waves assess motor conduction to the anterior horn cells, while the H-reflex (primarily S1 reflex arc via tibial nerve stimulation) evaluates sensory afferent and motor efferent monosynaptic pathway integrity. Needle EMG evaluates insertional activity, spontaneous abnormal activity at rest (fibrillations, positive sharp waves, fasciculations), and motor unit action potential (MUAP) morphology during voluntary contraction.
• Preganglionic vs. Postganglionic Lesions (SNAP Preservation)The sensory dorsal root ganglion (DRG) is situated within or just lateral to the intervertebral foramen. In standard spinal compressive radiculopathies (e.g., disc herniation, canal stenosis), the site of nerve root compression is preganglionic (proximal to the DRG). Consequently, wallerian degeneration affects only the central axon ascending the dorsal columns of the spinal cord; the peripheral sensory axon and DRG cell body remain intact. Therefore, sensory nerve action potential (SNAP) amplitude remains completely normal in preganglionic radiculopathy, despite profound clinical sensory loss. In contrast, in postganglionic lesions (brachial/lumbosacral plexopathies, peripheral nerve lacerations, entrapment neuropathies), the peripheral axon undergoes wallerian degeneration, causing reduced or absent SNAP amplitudes. This rule is the cornerstone of electrodiagnostic localization in spine surgery.
• Timing, Denervation, and Reinnervation CascadeFollowing acute axonal compression or transection, physiological changes progress chronologically. Immediate motor block occurs, but needle EMG does not display denervation potentials immediately. Spontaneous denervation activity (fibrillation potentials and positive sharp waves) appears first in the paraspinal muscles (dorsal rami innervation) within 7 to 10 days, proximal limb muscles (14–18 days), and distal limb muscles (21–28 days). Performing EMG prior to 3 weeks following acute nerve injury yields a high rate of false-negative studies for denervation. With chronicity (>2–3 months), collateral sprouting produces polyphasic, high-amplitude, long-duration reinnervation motor unit action potentials (MUAPs) with reduced recruitment density.
• Differential Diagnosis: Entrapment, Double Crush, and ALSElectrodiagnosis effectively resolves clinical dilemmas: 1) Differentiating C8–T1 radiculopathy from carpal tunnel syndrome (CTS) or ulnar neuropathy at the elbow; 2) Differentiating L5 radiculopathy (tibialis anterior, extensor hallucis longus, and tensor fasciae latae involvement with normal superficial peroneal SNAP) from common peroneal neuropathy at the fibular head (peroneal muscles affected, tensor fasciae latae spared, abnormal superficial peroneal SNAP); 3) Identifying "Double Crush Syndrome," where proximal subclinical cervical/lumbar root compression increases susceptibility of the distal axon to entrapment neuropathy; 4) Identifying generalized sensorimotor polyneuropathy (diabetic, toxic, CIDP); and 5) Detecting Amyotrophic Lateral Sclerosis (ALS), characterized by widespread active denervation and chronic reinnervation across three or four anatomical regions (bulbar, cervical, thoracic, lumbosacral) without sensory conduction abnormalities.
• Clinical Application: Electrodiagnostic testing should be requested when clinical history and MRI are discordant, when multiple anatomical levels of stenosis exist and the clinically symptomatic culprit root must be confirmed before targeted decompression, or when peripheral neuropathy/plexopathy is suspected. Testing should be scheduled at least 3 weeks after symptom onset to allow wallerian degeneration and distal fibrillations to manifest. In suspected cervical radiculopathy with shoulder pain, EMG distinguishes C5 radiculopathy from rotator cuff tears or suprascapular/axillary neuropathy. In foot drop, EMG confirms L5 radiculopathy versus common peroneal nerve palsy. In patients with multi-level lumbar stenosis and peripheral diabetic neuropathy, EMG objectively quantifies whether active motor radiculopathy is present, guiding surgical decision-making. Testing paraspinal muscles confirms preganglionic root involvement, though prior spinal surgery causes non-specific paraspinal denervation artifact that must be interpreted cautiously.
