Corticospinal inhibition appears normal in patients with chronic fatigue syndrome

The pathogenesis of chronic fatigue syndrome (CFS) remains unknown. Thresho lds and latencies of motor evoked potentials (MEPs) in response to transcra nial magnetic stimulation (TMS) are normal but intracortical inhibition has not been investigated. Eleven patients with CFS were compared with 11 cont rol subjects. Each patient completed a questionnaire using visual analogue indices of pain, fatigue, anxiety and depression. Subjects released a butto n to initiate simple (SRTs) and choice reaction time (CRTs) tasks; for each task, movement times were measured between release of the initiation butto n and depression of a second button 15 cm away. Subjects held a 10 % maximu m voluntary contraction in the thenar muscles of their dominant hand while TMS was applied to the motor cortex; the duration and extent of inhibition of surface electromyographic (EMG) activity were assessed at stimulus stren gths above and below the threshold for MEPs. Patients had significantly (P < 0.05) higher mean indices of fatigue than of pain, anxiety or depression. Mean (+/- S.E.M.) SRTs (but not CRTs) were longer in patients (309 +/- 45 ms) than in controls (218 +/- 9 ms). Movement times were longer in patients for both SRTs and CRTs. TMS thresholds, expressed as a percentage of the m aximum stimulator output, were not significantly (P > 0.05) different in bo th groups for both MEPs (patients, 34 +/- 3 %; controls, 36 +/- 3 %) and in hibition of voluntary contraction (patients, 29 +/- 2 %; controls, 34 +/- 4 %). The duration and extent of inhibition did not differ significantly bet ween groups at any stimulus strength. The pattern of change in duration and extent of inhibition with increasing stimulus intensity was no different i n the two groups. The duration and extent of corticospinal inhibition in pa tients with CTS did not differ from controls, adding further evidence to th e notion that the feeling of fatigue and the slowness of movement seen in C TS is not manifest in corticospinal output pathways.