First, following the peripheral nerve injury necessary to induce dystonia-like posturing in TOR1A mutant rodents, these are accompanied by significant increases in striatal dopamine and decreases in D2R receptor expression [28].This fundamental shift in dopaminergic neurochemistry has also been observed in recent post mortem studies comparing manifesting and non-manifesting carriers of the TOR1A mutant gene [29]. Here, TOR1A is linked to Dystonia.