Kinaesthetic neurons in thalamus of humans with and without tremor.

Increased afferent input may alter receptive field sizes, properties and somatotopographic representation in the cortex. Changes in the motor thalamus may also occur as a result of altered afferent input. Such plasticity has been implicated in both sensory and movement disorders. Using tremor as a model of augmented afferent input to kinaesthetic/deep neurons representing the shaking limbs, we studied the representation and properties of these neurons in human thalamus in patients with resting tremor (RestTr) from Parkinson's disease, patients with action- or posture-induced tremor (ActionTr), and patients without tremor (NoTr). Data were collected during stereotactic thalamotomy or insertion of deep brain stimulators for relief of pain or movement disorder. Using microelectrode recording, 58 kinaesthetic neurons responding to wrist and/or elbow movement were studied by mapping the receptive field, carefully isolating each joint during testing. There were no significant differences in the proportions of single and multijoint responsive neurons in the different patient groups (RestTr, ActionTr and NoTr). The borders between tactile-cutaneous, deep-kinaesthetic and voluntary cell representations in the thalamus were mapped in 74 patients and compared between the different tremor groups. A significant difference in kinaesthetic representation was found: both the RestTr and ActionTr groups had a significantly greater kinaesthetic representation than the NoTr patients. There was an expansion of kinaesthetic representation in patients with chronic increased afferent drive from tremor, without alteration in RF size. No decrease in tactile representation was found, suggesting that the increase in kinaesthetic representation does not occur at the expense of tactile representation. These data suggest that plasticity can occur at the thalamic level in humans and may contribute to the pathogenesis of tremor.