Neurotoxicity is indicated by the sequelae of METH exposure, which include degeneration of axon terminals in the striatum, as shown by silver cupric impregnation [16, 17], neurochemical changes, such as decreased tyrosine hydroxylase (TH) and DAT levels, depletion of dopamine and its metabolites [16, 18–20], as well as reactive astrogliosis [16] and microgliosis (next paragraph). Here, TH is linked to toxic encephalopathy.