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 exchange therapy. The behaviour of all four types of cutaneous afferents known to innervate the glabrous skin of the normal hand (rapidly adapting types RA and PC and slowly adapting types SAI and SAII) was studied in response to mechanical skin stimulation. Some of the units could not be fully classified. Additionally, intradermal electrical stimulation war used to study conduction velocity and absolute refractory period Abnormal response behaviour was encountered in RA, PC and slowly adapting 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 afferents, reduced discharge rates during sustained skin indentations or cessation of discharge during indentation. Abnormally responding units were more frequently found in patients with marked, than in those with mild, clinical sensory symptoms. In the former, half of all units in each patient responded abnormally (12 out of 23 in total). In patients with mild symptoms, most units (33 out of 37) were normal in response behaviour as well as in other measures made: threshold to mechanical stimuli, 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 regular 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 likely reflects a limited ability of the axons to conduct trains of action potentials.