Premium
Length‐dependent weakness and electrophysiological signs of secondary axonal loss in chronic inflammatory demyelinating polyradiculoneuropathy
Author(s) -
Harbo Thomas,
Andersen Henning,
Jakobsen Johannes
Publication year - 2008
Publication title -
muscle and nerve
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.025
H-Index - 145
eISSN - 1097-4598
pISSN - 0148-639X
DOI - 10.1002/mus.21000
Subject(s) - compound muscle action potential , polyradiculoneuropathy , medicine , weakness , electrophysiology , nerve conduction velocity , sensory loss , muscle weakness , pathophysiology , sural nerve , electromyography , anatomy , cardiology , guillain barre syndrome , surgery , physical medicine and rehabilitation , pediatrics
Abstract In chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) the pathophysiology underlying permanent muscle weakness and sensory loss was studied in 22 stabilized long‐term CIDP patients clinically characterized using isokinetic dynamometry, quantitative sensory testing, and neuropathy scores. Conduction velocity (CV), distal latency (DLAT), minimal F‐wave latency (FLAT), compound muscle action potential (CMAP), and amplitude decay between distal and proximal stimulation sites were determined in the median, ulnar, peroneal, and tibial motor nerves and sensory CV and nerve action potentials in the median and sural nerves. Amplitude of CMAP and the DLAT were related to quantitative muscle strength, whereas CV, FLAT, amplitude decay, and dispersion were not consistently related to strength. Furthermore, CMAP and muscle strength were significantly more reduced distally than proximally. In conclusion, the electrophysiological signs of axonal loss and the associated length‐dependent muscle weakness suggest secondary axonal loss in addition to primary demyelination in CIDP. Muscle Nerve, 2008