How can nerve conduction studies differentiate demyelinating versus axonal neuropathies?

How can nerve conduction studies differentiate demyelinating versus axonal neuropathies?

• A. Demyelinating neuropathies show reduced amplitude with preserved velocity; axonal neuropathies show slowed velocity.
• B. Demyelinating neuropathies show slowed conduction velocity, prolonged F-wave latency, and conduction block; axonal neuropathies show reduced amplitude with relatively preserved velocity.
• C. EMG shows denervation in demyelinating neuropathies only.
• D. Nerve conduction studies cannot differentiate these conditions.

Answer: (B)

Nerve conduction studies differentiate these conditions by how the nerve’s signal is affected: demyelination slows conduction and disrupts timing, while axonal loss reduces signal strength but largely preserves speed. In demyelinating neuropathies, the myelin sheath is damaged, so conduction velocity drops markedly. Distal and proximal (F-wave) latencies become prolonged, and conduction block or marked temporal dispersion can occur because impulses struggle to traverse the demyelinated segments. Amplitude of the response may stay relatively preserved early on, since many nerves still conduct, but timing and speed are the giveaway. In axonal neuropathies, there is loss of axons, so the overall signal amplitude (CMAP/SNAP) decreases. The remaining fibers conduct at near-normal speed, so conduction velocity is relatively preserved compared to the marked slowing seen with demyelination. F-waves and distal latencies may be affected, but the hallmark is reduced amplitude with retained conduction speed. Thus, the statement that demyelinating neuropathies show slowed conduction velocity, prolonged F-wave latency, and conduction block, while axonal neuropathies show reduced amplitude with relatively preserved velocity, best captures how nerve conduction studies differentiate these conditions.

Nerve conduction studies differentiate these conditions by how the nerve’s signal is affected: demyelination slows conduction and disrupts timing, while axonal loss reduces signal strength but largely preserves speed.

In demyelinating neuropathies, the myelin sheath is damaged, so conduction velocity drops markedly. Distal and proximal (F-wave) latencies become prolonged, and conduction block or marked temporal dispersion can occur because impulses struggle to traverse the demyelinated segments. Amplitude of the response may stay relatively preserved early on, since many nerves still conduct, but timing and speed are the giveaway.

In axonal neuropathies, there is loss of axons, so the overall signal amplitude (CMAP/SNAP) decreases. The remaining fibers conduct at near-normal speed, so conduction velocity is relatively preserved compared to the marked slowing seen with demyelination. F-waves and distal latencies may be affected, but the hallmark is reduced amplitude with retained conduction speed.

Thus, the statement that demyelinating neuropathies show slowed conduction velocity, prolonged F-wave latency, and conduction block, while axonal neuropathies show reduced amplitude with relatively preserved velocity, best captures how nerve conduction studies differentiate these conditions.