PROPERTIES OF CUTANEOUS AFFERENTS DURING RECOVERY FROM GUILLAIN-BARRE-SYNDROME

The technique of percutaneous microneurography was used to record from 60 mechanosensitive cutaneous afferents in patients (n = 5) who were recovering from acute Guillain-Barre syndrome (GBS) and who displayed residual sensory deficits in the hands. Recordings were obtained from median and ulnar nerves, between 1 and 31 months following plasma exch ange therapy. The behaviour of all four types of cutaneous afferents k nown to innervate the glabrous skin of the normal hand (rapidly adapti ng types RA and PC and slowly adapting types SAI and SAII) was studied in response to mechanical skin stimulation. Some of the units could n ot be fully classified. Additionally, intradermal electrical stimulati on war used to study conduction velocity and absolute refractory perio d Abnormal response behaviour was encountered in RA, PC and slowly ada pting afferents. The abnormalities consisted of a generation of only a single action potential to above threshold stimuli (RA), inability to follow high frequency vibration (PC) and, in slowly adapting afferent s, reduced discharge rates during sustained skin indentations or cessa tion of discharge during indentation. Abnormally responding units were more frequently found in patients with marked, than in those with mil d, clinical sensory symptoms. In the former, half of all units in each patient responded abnormally (12 out of 23 in total). In patients wit h mild symptoms, most units (33 out of 37) were normal in response beh aviour as well as in other measures made: threshold to mechanical stim uli, static discharge rate, receptive field size, conduction velocity, absolute refractory period Spontaneous activity of unknown origin was also encountered in some patients. The activity consisted of highly r egular discharge bursts or relatively regular unitary discharges. The data indicate that the encoding capabilities of all types of cutaneous afferents (RA, PC, SAI and SAII) may be affected in GBS, contributing to the sensory deficits of the disease. The abnormal encoding most li kely reflects a limited ability of the axons to conduct trains of acti on potentials.