Radiculopathy

Root localisation by myotome

A nerve root distributes its motor fibres through the plexus into several different peripheral nerves. The defining electrodiagnostic move is therefore to find denervation in muscles that share a root level but are supplied by different peripheral nerves. Tibialis anterior (deep peroneal) and tibialis posterior (tibial) are both predominantly L5; if both fibrillate, the common factor cannot be either peripheral nerve — it must be the L5 root. This same-root, different-nerve dissociation is what separates a radiculopathy from a mononeuropathy or a plexopathy, and it is why at least two muscles per root are required before a level can be claimed. The spared muscles are as informative as the abnormal ones: normal levels above and below sharpen the localisation by exclusion.

A working myotome map

The DRG rule: why sensory studies stay normal

The dorsal root ganglion, the pseudounipolar sensory cell body, sits in the intervertebral foramen — distal to where a herniated disc or a foraminal lesion typically compresses the root. A radiculopathy is, in the overwhelming majority of cases, a preganglionic lesion: it severs the central (intraspinal) projection while leaving the peripheral sensory axon and its cell body intact and in continuity. Because the recorded sensory nerve action potential depends on the integrity of the peripheral axon and its soma, the SNAP remains normal even when the corresponding dermatome is densely numb. The numbness is real — central transmission is interrupted — but the peripheral generator that the machine records is untouched. This preserved-SNAP-with-numbness pattern is the single most powerful separator between a radiculopathy (SNAP preserved) and a plexopathy or peripheral lesion (SNAP reduced or absent, because the lesion is postganglionic).

Motor versus sensory root involvement

The motor and sensory roots are not equally interrogable. The motor (ventral) root carries no ganglion in its path, so motor axon loss produces Wallerian degeneration that the needle exam detects directly as fibrillations and reinnervation. The sensory (dorsal) root, by the DRG geometry above, is electrically silent to routine sensory studies. This asymmetry has two consequences. First, the needle examination of muscle is the workhorse of radiculopathy diagnosis, while sensory NCS function mainly to exclude a more distal process. Second, a purely sensory radiculopathy — pain and numbness with no motor axon loss — can be entirely electrodiagnostically normal, because there is no motor denervation to detect and the SNAP is preganglionically preserved. A normal study never excludes radiculopathy; it excludes significant motor axon loss.

Timing: fibrillations and the reinnervation sequence

Denervation unfolds on a stereotyped clock that lets the needle exam date the lesion and stage its level. After acute axonal injury, fibrillation potentials and positive sharp waves do not appear immediately — they require Wallerian degeneration and denervation hypersensitivity to develop. They emerge earliest in the most proximal muscles, with paraspinals fibrillating at roughly 1–2 weeks and distal limb muscles at 3–6 weeks, simply because the degenerating distal stump takes longer to disconnect over a longer axon. A study performed too early will be falsely negative for active denervation; the optimal window for fibrillation yield in the limb is about 3 weeks after onset. Reinnervation then proceeds over months: large-amplitude, long-duration, polyphasic motor unit potentials with reduced recruitment signal chronic reorganisation. The combination — fibrillations plusreinnervated units — marks an active-on-chronic process; reinnervated units without fibrillations indicate an old, stable, or recovering lesion. The temporal gradient from paraspinal to distal also lets you infer roughly when the insult occurred.