Somatosensory input and oromandibular dystonia

Abstract

Oromandibular dystonia (OMD) involving the lateral pterygoid uscles (LPs) may cause incapacitating protrusive and lateral jaw ovements, but can be alleviated with botulinum toxin (BTX) [1]. ystonia is thought to be derived from dysfunction of the basal anglia, and the excess movement to be due to loss of inhibitory otor control. Neurophysiologic and neuroimaging studies have hown abnormalities at cortical and subcortical levels, probably eflecting a dysfunction in the basal ganglia-thalamo-cortical ciruits. Although dystonia is mainly a motor problem, observations uggest a sensory component with impaired inhibitory integration f somatosensory inputs at spinal, subcortical and cortical levels o ongoing motor programs [2]. Sensory tricks involving tactile timulation alleviate symptoms in dystonia, also indicate a sensory nfluence. Further, an abnormal sensorimotor integration has been roposed. In its control of orofacial motor functions the face priary motor area (face MI) of the cerebral cortex utilises input from ace and mouth relayed in part via the face primary somatosenory area (face SI). Thus, afferent information and neuronal activity n the face SI assists in modulating orofacial motor functions, and europlastic changes in the face sensorimotor cortex may lead to ysfunctions [3].