Entrapment Neuropathies

Carpal tunnel syndrome: focal median demyelination at the wrist

The median nerve is compressed beneath the transverse carpal ligament, and chronic compression demyelinates the fibres in that short segment. Demyelination slows saltatory conduction locally, so the hallmark is a prolonged distal latency — sensory before motor, because sensory fibres are more vulnerable — with normal forearm conduction velocity, since the lesion lies entirely under the ligament and the proximal nerve is healthy. This dissociation, slow across the wrist but normal above it, is the diagnosis, and it is exactly what the simulator below makes visible.

A borderline distal latency is the rule, not the exception, so the decisive test is a comparison study that pits the median against an adjacent nerve traversing a normal path over an identical distance — cancelling out temperature, age, and limb-length confounders. The high-yield pairs are the median-versus-ulnar palmar (mixed) latency over 8 cm and the median-versus-ulnar (or median-versus-radial) digit- recording sensory latency. An inter-nerve latency difference exceeding ~0.4–0.5 ms is abnormal. These internal comparisons reach roughly 85% sensitivity at ~95% specificity, substantially outperforming any single absolute latency, because each hand serves as its own control.

Ulnar neuropathy at the elbow

The ulnar nerve is entrapped at the elbow, either in the retrocondylar groove or under the humeroulnar aponeurosis of the cubital tunnel. The study stimulates below the elbow, across the elbow, and above it, and looks for slowing localised to the across-elbow segment. The quantitative thresholds are an absolute conduction velocity <50 m/s across the elbow, a drop of more than ~10 m/s relative to the forearm segment, or a focal amplitude drop (conduction block) across the elbow. A single misplaced limitation undermines the whole study: the elbow must be flexed to roughly 90–135°during measurement, because the ulnar nerve's true path lengthens with flexion. Measuring across an extended elbow underestimates the surface distance, spuriously inflates the calculated velocity, and masks real slowing. When routine segments are equivocal or fail to localise, inching — short 1 cm incremental stimulations across the elbow — pinpoints the lesion by detecting the abrupt latency jump or amplitude drop at the exact compression point.

Peroneal neuropathy at the fibular head

The common peroneal nerve is superficial as it wraps the fibular neck, where it is vulnerable to compression, trauma, and habitual leg- crossing — the classic cause of an acute foot drop. The motor study records from extensor digitorum brevis or tibialis anterior and stimulates below the fibular head, across it, and at the popliteal fossa; the signature is conduction block or focal slowing across the fibular head with normal conduction in the leg segment below. Two anatomical points discipline the interpretation. First, the nerve divides at the fibular head into the deep branch (tibialis anterior, toe extensors — ankle dorsiflexion) and the superficial branch (peroneus longus and brevis — foot eversion, plus sensation over the dorsum); recording from both branches characterises a partial lesion and weighs deep-versus-superficial involvement. Second, the indispensable differential is an L5 radiculopathy, which also causes foot drop: the discriminators are that a peroneal palsy spares ankle inversion (tibial-innervated tibialis posterior, an L5 muscle outside the peroneal territory) and spares the paraspinals, shows conduction block at the fibular head, and reduces the superficial peroneal SNAP (postganglionic), whereas an L5 root lesion denervates tibialis posterior and the paraspinals with a preserved SNAP.

Tarsal tunnel syndrome and its technical limits

Entrapment of the posterior tibial nerve beneath the flexor retinaculum behind the medial malleolus is the lower-limb analogue of carpal tunnel, but it is far harder to confirm electrically and is substantially over-diagnosed. The plantar mixed and sensory responses are technically demanding, small, and frequently absent even in asymptomatic older adults because of distance, oedema, callus, and the cool, thick tissue of the sole. Absent plantar responses are therefore non-specific, and the most useful needle finding is denervation restricted to the intrinsic foot muscles (abductor hallucis for the medial plantar, abductor digiti minimi for the lateral plantar) that spares the leg — itself confounded by the fibrillations commonly seen in normal foot muscles. The diagnosis remains primarily clinical and imaging-supported; electrodiagnosis functions mainly to exclude a polyneuropathy or a more proximal lesion.

Severity grading

Entrapments are staged along the demyelination-to-axon-loss continuum, which carries the prognosis. Mild: pure demyelination — prolonged sensory latency or an abnormal comparison study with normal motor studies and a normal needle exam (excellent recovery expected). Moderate: demyelination extends to the motor fibres — prolonged distal motor latency in addition to the sensory abnormality, still without axon loss. Severe: secondary axonal loss supervenes — low or absent sensory and CMAP amplitudes with active denervation (fibrillations) and reduced recruitment in the target muscle (e.g., abductor pollicis brevis in CTS), predicting slower and often incomplete recovery and shifting the balance toward surgical decompression.