Sequential electrodiagnostic abnormalities in acute inflammatory demyelinating polyradiculoneuropathy

TLDR

Delayed sensory abnormalities in AIDP may result from intraneural edema and compression at vulnerable sites. The study reviewed 180 EMG studies of patients with acute inflammatory demyelinating polyradiculoneuropathy. Electroneuromyography was employed to track temporal patterns of demyelination and axonal changes. EMG showed demyelination in 87 % of patients within 5 weeks, with motor deficits peaking at week 3 and sensory deficits at week 4 (often sparing the sural nerve), while fibrillation potentials appeared 2–5 weeks post‑onset and conduction abnormalities began resolving by weeks 6–10, indicating functional recovery.

Abstract

Abstract We reviewed 180 electroneuromyographic (EMG) studies from patients with acute inflammatory demyelinating polyradiculoneuropathy. EMG criteria suggestive of demyelination were met during the first 5 weeks in 87% of patients; an additional 10% had indeterminate electrodiagnostic evaluations, and 3% demonstrated axonal degeneration only. Motor nerve conduction abnormalities initially predominated, with the nadir of abnormality occurring at week 3. Sensory nerve conduction abnormalities peaked during week 4 and were atypical for polyneuropathy, with 52% of patients having normal sural but abnormal median sensory studies, perhaps reflecting distal nerve involvement. Delayed sensory abnormalities may reflect, in part, secondary involvement related to increased intraneural edema accentuated by compression at sites of anatomic vulnerability. Fibrillation potentials and increased polyphasia appeared between weeks 2 and 5 in proximal and distal muscles simultaneously, which is consistent with either random axonal degeneration at any point along the axon or distal involvement. Resolution of conduction abnormalities began between weeks 6 and 10, with increased mean motor‐evoked amplitude best reflecting functional clinical recovery.