Evidence for an Abnormal Cortical Sensory Processing in Dystonia: Selective Enhancement of Lower Limb P37-N50 Somatosensory Evoked Potential *Michele Tinazzi, MD, ²Emma Frasson, MD, ²Alberto Polo, MD, *Frediano Tezzon, MD, *Paolo Bovi, MD, *Luciano Deotto, MD, ‡Francois Mauguiere, PhD, ²Antonio Fiaschi, MD, and *Giuseppe Ferrari, MD *Divisione di Neurologia Ospedale Civile Borgo Trento, Verona, Italy; ²Dipartimento di Scienze Neurologiche e della Visione, Sez. di Neurologia Riabilitativa, Verona, Italy; and ‡Functional Neurology and Epileptology Department, Hopital Neurologique, Lyon, France Summary: We evaluated brain stem P30, contralateral frontal N37, and the vertex-ipsilateral central P37, N50 somatosensory evoked potentials (SEPs) obtained in response to stimulation of the tibial nerve in 10 patients with idiopathic dystonia. Results were compared with those obtained in 10 healthy subjects matched for age and sex. The amplitude of the brain stem P30 potential and of the contralateral frontal N37 response in dys- tonic patients was not significantly different from that recorded in normal subjects. The vertex- ipsilateral central P37-N50 complex, which is thought to originate in the pre-rolandic cor- tex, was significantly enhanced in patients compared with the control group. These results suggest the enhancement of the vertex-ipsilateral central P37-N50 complex might reflect an abnormal response to somatosensory inputs of a precentral cor- tex which is excessively activated because of a disorder of the basal ganglia. Such inefficient sensory processing in motor areas might contribute to motor impairment in dystonia. Key Words: Lower limb SEPs—Somatosensory evoked potentials—Dystonia—Somatosensory cortex. The precise nature of motor disorders in dystonia is not fully understood. As far as the motor system is con- cerned, the primary abnormality is thought to be located in the basal ganglia which controls movement through the cortico-striato-thalamocortical circuit. 1–6 However, the presence of a number of clinical phenomena docu- menting a modulatory effect of sensory input on motor patterns suggests that the somatosensory system may also play an important role in the motor disorders that characterize dystonia. 7 For example, sensory tricks can relieve dystonic spasm 4,6,8 ; further, vibration can induce dystonia in patients with hand cramps whereas afferent block can relieve it. 9 Finally, patients with focal hand dystonia may have discriminative sensory processing problems 10 and an abnormal perception of movement. 11 Despite these findings, subclinical involvement of the sensory system is still a matter of debate. Using the so- matosensory evoked potential recording (SEP) tech- nique, Reilly et al. 12 first found an enlargement of the median nerve-derived P22-N30 response in patients with writer’s cramp. Similar findings have been recently re- ported by Kanovsky et al. 13,14 in patients with spasmodic torticollis, but not by Mazzini et al. 15 who found a re- duced P22-N30 response, although it must be noted that patients in these studies had no apparent upper limb involvement. There are no reports of cortical SEPs to tibial nerve stimulation in dystonia. In normal subjects, the scalp distribution of cortical SEPs consists of a “paradoxical lateralization,” because the main P37 response which is followed by the N50 response distributes on the vertex and on the ipsilateral silent hemisphere with a sort of phase-reversal N37 response of lower amplitude, usually over the contralateral pre-rolandic regions. An increasing number of observations suggests that the generators of the N37 and P37-N50 are respectively related to the ac- tivation of the postcentral and precentral cortex. 16–22 To assess possible abnormalities of scalp SEPs from the lower limb in dystonia, we studied subcortical and Received July 17, 1998; revision received November 2, 1998. Ac- cepted January 27, 1999. Address correspondence and reprint requests to Dr. Michele Tinazzi, Divisione di Neurologia ospedale Civile Borgo Trento, Piazzale Stefani 1, 37126 Verona, Italy. Movement Disorders Vol. 14, No. 3, 1999, pp. 473–480 © 1999 Movement Disorder Society 473