Spatio-temporal impairments in limb and body movements during righting in an hemiparkinsonian rat analogue: relevance to axial apraxia in humans.

Humans with Parkinson's disease (PD) often have problems in righting themselves, in that they have difficulty in recruiting their axial musculature to rotate the body to prone. Since this "axial apraxia' is not ameliorated by L-DOPA therapy, it has been concluded that dopamine (DA) does not play a role in recruiting axial rotation of the body [14]. This hypothesis was tested by comparing the righting of rats with unilateral 6-hydroxydopamine (6-OHDA) lesions of the substantia nigra (SN) with that of intact rats. Body-on-body righting, where asymmetrical tactile stimulation of the body initiates hindquarter righting, was used to specifically test tactile righting independently of righting triggered or influenced by other sensory systems. In this behavioral test, rats are placed on their sides, their forequarters are held down and their hindquarters released. The DA-depleted rats took longer to begin righting, to complete righting, and used more limb action to right themselves than did control rats. These findings suggest that for this tactile based form of righting, DA-depletion produces axial apraxia. However, frame-by-frame analysis of righting sequences of DA-depleted rats showed that pelvis-led axial rotation could occur, but the spatio-temporal relationship between body and limb movements was disorganized. Therefore, following DA-depletion axial apraxia-like deficits appear to arise from sensorimotor disruption. This raises the issue of whether the axial apraxia in PD patients arises from damage to systems beyond the nigrostriatal DA system, or from interference with sensorimotor integration that is not ameliorated by replacement therapy.