Both increased and decreased
dyskinesias have been reported from open label clinical trials of
transplantation of human embryonic
dopamine rich tissue in
Parkinson's disease patients. In the first double-blind clinical
transplantation trial, 15% of the grafted patients developed severe postoperative
dyskinesias in the "off" phase. Since then, postoperative off-medication
dyskinesias have been reported from two additional series of grafted patients. However, such
dyskinesias are probably not a novel phenomenon. These
dyskinesias have shown a different temporal development postoperatively compared to the antiparkinsonian graft effects, and no significant relationship with the magnitude of graft-derived dopaminergic reinnervation or symptomatic relief. However, positron emission tomography studies have indicated that an unbalanced putaminal dopaminergic function may contribute to this postoperative complication. While there is little doubt that intrastriatal grafts can induce
dyskinesias, these appear to differ from common
drug-induced dyskinesias. The term graft-induced
dyskinesias (GID) is therefore suggested to more clearly identify this complication. While GID bear some phenomenological resemblance to biphasic
drug induced dyskinesias, the mechanism(s) behind this complication remains obscure. Available data are scarce but allow for hypotheses to be generated that could (and should) be addressed in experimental animals.