Findings in Disease Entities

Anterior Horn Cell Disease

Characteristic findings include normal sensory potentials unless extremity cooling occurs. Motor nerve changes progress from decreased amplitude (axonal loss) through latency prolongation and slowed velocities. At times the response is of very low amplitude, making it difficult to evaluate conduction velocities.

Root Lesion

Sensory root compression proximal to the dorsal root ganglion produces normal peripheral sensory conductions. In appropriate locations (C7 and S1), the presence of sensory nerve compression can be investigated by use of the H-reflex which would be either delayed or absent.

Motor radiculopathies may show low amplitudes and slowed conduction with severe axonal loss. Routine testing covers only C8/T1 (arm) and L5/S1 (leg) roots.

Plexus Lesions

Nerve conduction studies may be most helpful in evaluating plexus injuries. Sensory potentials diminish or absent with normal or slightly slowed conduction velocities. Motor responses show low voltage with preserved or slightly slowed velocities.

Brachial Plexus Testing: Stimulation at Erb’s point tests trunk/root lesions. Needle electrode stimulation at C7 transverse process evaluates thoracic outlet compression.

Causes: trauma, tumor infiltration, idiopathic plexitis

Lumbar Plexus: Needle electrode stimulation 2-3 cm lateral to L4 spinous process, recorded from quadriceps

Sacral Plexus: Needle electrode placed medially/caudally to posterior superior iliac spine, recorded from abductor hallucis

Compression/Entrapment Neuropathies

Nerve conduction studies are the definitive test in compression/entrapment neuropathies.

Myelin Lesions: Normal latencies below entrapment; slowed velocities or prolonged distal latency above. Conduction block may show no response or low amplitude proximally with normal amplitude distally.

Axonal Lesions: Diffusely decreased amplitude regardless of stimulation site. Conduction velocities normal until late disease.

Myopathy

Normal motor amplitudes are typical with normal sensory potentials and motor conduction velocities. Distal myopathies may show decreased motor amplitudes.

Neuromuscular Transmission Defect

Myasthenia Gravis (postsynaptic): Motor amplitudes normal to decreased early; later decreased resembling myopathy. Sensory potentials normal. Slow repetitive stimulation of an involved muscle will produce a decrement.

Lambert-Eaton Syndrome and Botulism (presynaptic): Diffusely decreased motor amplitudes with preserved latencies/velocities. Sensory potentials normal. Post-exercise testing shows significant amplitude improvement.

Polyneuropathies

Sensory fibers, with few exceptions, are always affected first.

Myelin Lesions: Increased action potential duration causes lower amplitude and prolonged distal latency

Axonal Lesions: Decreased amplitudes with minimal latency prolongation

Later stages affect motor fibers similarly. F-wave and H-reflex become abnormal before routine studies in proximal neuropathies. Mixed lesions show combined changes.

Trauma

Multiple stimulation levels assess injury location. A normal response from stimulation below the injury site suggests a conduction block lesion, partial or complete. A low amplitude response suggests that axonal damage has occurred.