Myoclonus-dystonia (M-D), commonly caused by mutations in the SGCE gene, is characterized by reduced striatal dopamine D2 receptor density and excessive dopamine release. This receptor deficit likely contributes to the hyperkinetic motor symptoms observed in both patients and animal models. Given that D2 receptor density is not fixed but responsive to pharmacological, genetic, and environmental influences, restoring or augmenting D2 signalling represents a plausible therapeutic strategy. This review surveys the known approaches to increasing striatal D2 receptor density or availability, organized into three categories: pharmacological interventions, genetic and molecular approaches, and lifestyle modifications. For each approach, the mechanism of action, supporting evidence from animal and human studies, and relevance to M-D or related basal ganglia disorders are discussed. While no single intervention has been clinically validated for D2 upregulation in dystonia, the converging evidence suggests that a multimodal strategy—combining lifestyle optimization with emerging pharmacological or genetic tools—may offer a path toward normalizing basal ganglia output in D2-deficient conditions.