Basal Ganglia Perform Differencing Between ‘Desired’ and ‘Experienced’ Parameters

Abstract

The recently introduced first order SDS feedback control scheme1 has been suggested as a suitable model of the basal ganglia — thalamocortical (BTC) loops2. The first order SDS model of the BTC loops can be extended to plants of any order3 by slight modification of the original scheme. This SDS model identifies the direct and the indirect pathways of basal ganglia (BG) that respectively tend to enhance and suppress the reentrant thalamocortical excitation4 with the desired (planned) and experienced channels of the SDS scheme. The model predicts that a relatively high contribution from the desired channel results in Huntington’s disease whereas a relatively high contribution from the experienced channel results in Parkinson’s disease. The model can be considered as a mathematical framework of the phenomenological thalamic disinhibition (TDI) model of DeLong4. The TDI model suggests that if the BG output is increased (decreased) it shifts the motion towards hypokinetic (hyperkinetic) states. Despite explaining several features of the BTC loops, the TDI model also predicts that lesion to the BG output recipient zones of the thalamus results in akinesia, which is not the case. This pitfall is avoided in the SDS model. The features of the general new scheme utilized to model the BTC loops are described in this paper.