Evidence for an abnormal cortical sensory processing in dystonia: Selective enhancement of lower limb P37-N50 somatosensory evoked potential

Abstract

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 dystonic 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 cortex, 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 cortex 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.

Abnormalities of cortical excitability and cortical inhibition in cervical dystonia

“…We found both cortical functions significantly altered in patients with cervical dystonia. This fact only provides further evidence, following the recent similar findings of other authors [17,18,23,29,49,51,52,59] and of our previous studies involving SEP recordings [33,34,35]. SEP recordings in focal dystonia (and in other types of dystonic disorders) indicate that SEP changes can represent a disorder of cortical excitability in motor areas.…”

“…The lateralized cortical involvement in dystonic disorders has been reported several times, using diverse methods of assessments: in our SEP studies [33][34][35]; in the study of Tinazzi et al, using tibial SEP recordings [59]; in the study of Naumann and Reiners, using longlatency reflex examination [42]; in the studies of Grünewald et al and Yoneda et al, where the tonic vibration reflex was studied [19,64]; and recently, in the study of Frasson et al, using conditioned median SEP recordings [17]. The lateralized abnormality, respective of the body side pattern of dystonia, was also found in Deuschl et al studies of movement related cortical potentials (MRCP) [14] and Ikeda et al and Hamano et al studies of contingent negative variation (CNV) [22,26].…”

“…Despite some early conflicting reports, this disorder has been found in several studies using somatosensory evoked potential recordings [17,29,49,59]. Our own studies have shown that this cortical disorder in dystonia is lateralized [33,34,35].…”

A kinesthetic motor imagery study in patients with writer' cramp

“…Some studies demonstrated that patients with Parkinson's disease were slower than normal subjects regarding mental simulation of simple hand movements and rotational tasks 2,16 . However in WC there are many findings indicating that in addition to the basal ganglia there are abnormalities in primary motor cor- tex, prefrontal motor areas and also in the somatosensory areas [24][25][26] , and there appear to be distinct cortico-subcortical neural circuits involved in imagined movements including bilateral premotor, prefrontal, supplementary motor and left parietal areas 27 . The primary motor cortex is not the main suspected area for KMI slowing since it is not essential for imagery, and we know that damage restricted to the primary motor area does not result in impairment of KMI 3,28 .…”

Surgical therapy for dystonia

“…The hypothesis of increased excitability of premotor cortex is supported by increased precentral components of somatosensory evoked potentials (SEP) evoked by stimulation of the median and/or tibial nerves [16][17][18][19][20]. Transcranial magnetic stimulation studies have also shown abnormal corticocortical inhibition in dystonia [21].…”