title: Sensory pathophysiology in chronic acquired demyelinating neuropathy.
abstract: Pathophysiological changes in sensory fibres in chronic acquired demyelinating neuropathy (CADP) are poorly understood, and it is not known to what extent sensory loss may be due to axonal loss or to conduction block. Motor and sensory nerve condition were studied in 18 patients with CADP to delineate abnormalities in the compound sensory action potential (CSAP) recorded proximally along the limb. To distinguish small CSAPs from noise, near-nerve needle electrodes and electronic averaging were used. In all, 58 motor and 78 sensory nerves in the upper and lower limbs were studied, and in 29 nerves, motor and sensory conduction was compared over the same proximal and distal segments of the upper limbs. The proximal/distal amplitude ratio (P/D ratio) of the compound muscle action potential (CMAP) was reduced in 76% of the nerves compared with only 21% of the CSAPs. The amplitudes of CMAPs evoked and of CSAPs recorded distally were reduced to the same extent. The prolongation of the distal motor latency (DML) was linearly related to the reduction in amplitude of the CMAP whereas reduction of the distal sensory conduction velocity (SCVd) mainly occurred if the amplitude of the CSAP was reduced more than 70%. The proximal motor nerve conduction velocity (MCVp) was reduced by 40-50%, twice as much as the reduction in distal MCV (MCVd) (calculated from the reciprocal DML), and related to the reduction in the P/D ratio of the CMAP. The proximal SCV (SCVp) decreased approximately 20%, similar to the reduction in SCVd and out of proportion to the marked reduction of the MCVp. The results suggest different pathophysiological changes in sensory and motor fibres in CADP. Thus, nerve fibre loss could account for most of the abnormal parameters in sensory conduction, whereas demyelination was the dominating cause of motor nerve dysfunction.
authors.affiliation: Department of Clinical Neurophysiology, National University Hospital, Copenhagen, Denmark.
authors.forename: C
authors.initials: C
authors.lastname: Krarup
authors.forename: W
authors.initials: W
authors.lastname: Trojaborg
mesh_terms: D000200:Action Potentials / Q000502:physiology; D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002908:Chronic Disease; D003711:Demyelinating Diseases / Q000503:physiopathology*; D004558:Electric Stimulation / Q000379:methods; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D009043:Motor Activity / Q000502:physiology; D009412:Nerve Fibers / Q000502:physiology; D009420:Nervous System / Q000503:physiopathology; D009431:Neural Conduction / Q000502:physiology*; D009475:Neurons, Afferent / Q000502:physiology; D011930:Reaction Time; D012016:Reference Values; D012677:Sensation / Q000502:physiology*