While many of us wait for a "cure", SCS could be a life saver for PD'ers who don't qualify for DBS, like my wife. My wife's PD psychosis is caused mainly by the large amount of sinemet she needs to move. With SCS it appears that she would not need nearly as much sinemet that she takes now. I believe SCS is used now for other health issues. Why do we need more years of clinical trials?



Restoration of locomotive function in Parkinson’s disease by spinal cord stimulation: mechanistic approach
3.6 Combination of dopamine replacement therapy and SCS

In the PD-SCS study it was reported that combined treatment with SCS and L-DOPA was superior to L-DOPA alone. On the other hand, SCS in severely dopamine depleted animals (where dopamine levels were decreased to < 1% of normal levels) could not restore locomotive capability without a small L-DOPA dose (20% of the amount required with L-DOPA alone). These data indicate that a minimum amount of dopamine is indeed required for alleviation of akinesia by SCS. This is perhaps not surprising given that dopaminergic projections are known to exist to practically all motor structures thought to regulate locomotor behavior; i.e. spinal cord, brain stem nuclei, thalamus, cortex and basal ganglia (Qu et al., 2006; Bjorklund & Dunnett, 2007; Smith & Villalba, 2008). When evaluating the mechanisms of therapeutic electrical stimulation, the focus is usually on the electrophysiological changes; however considering the crucial role of dopamine in the basal ganglia circuits it is clearly of interest to further investigate the relationship between dopamine release and changes in neuronal activity patterns. For example, it is feasible that electrical stimulation of the targets used to treat PD acts partially by boosting release of intracellular pools of dopamine in relevant brain circuits. Support for a mechanistic connection to dopamine release of this kind was presented in a recent study showing striatal release of dopamine in response to high frequency stimulation of the STN in pigs (Shon et al., 2010) and related findings have been reported for electrical stimulation of peripheral nerves in cats (Inoue et al., 2004). A better understanding of how to optimally combine dopamine replacement therapy and electrical stimulation will be a very important future goal in order to develop better strategies to alleviate motor symptoms in PD. Another interesting possibility is that a neuroprotective effect may be achieved by electrical stimulation alone or in combination with pharmacological treatments that potentially could significantly delay the progression of the disease (Gubellini et al., 2009).