Within the limits of the Guillain-Barré syndrome, the pattern of clinical deficit is variable. Motor deficit may begin proximally or distally in the extremities and sensory deficit is sometimes, but not always present. Longitudinal studies were performed in 13 patients, starting during the progressive phase. The severity of the clinical deficit was related to the amplitude of the compound muscle action potentials (CMAPs) and sensory nerve action potentials (SNAPs). Two patterns were detected, but could only be reliably distinguished during the progressive phase of the disease. (I) A length- dependent reduction of the CMAP, i.e., a progressive decrease of the CMAP on moving the stimulating electrode to more proximal stimulation sites. This could often be attributed to conduction block. In this pattern (Group A), the sensory potentials were spared with only I exception. These patients had motor involvement without sensory deficit and the myotatic reflexes could be preserved up to MRC grade 3 paresis. (2) A simple reduction of the CMAP, i.e., the amplitude decreased during clinical deterioration, but during a single investigation remained similar for stimulation at all levels of the nerve. In this pattern (Group B), motor and sensory fibres were similarly involved. These patients showed both motor and sensory deficit and early myotatic areflexia. The second pattern might be explained by an immunological mechanism with a predilection for those regions of the peripheral nervous system where the blood-nerve barrier is naturally deficient. In the first pattern the discrepancy between the involvement of motor and sensory fibres raises new questions, the solution of which might be of importance for the understanding of the Guillain-Barré syndrome.