Abstract
Increased striatal dopaminergic functions with heightened postsynaptic receptor sensitivity has been proposed to underlie the major clinical symptoms of Tourette's syndrome (TS). The beneficial response of the majority of TS patients to haloperidol supports the hyperdopaminergic pathophysiological concept of TS. However, in 5 recently encountered TS patients, haloperidol failed to ameliorate self-injurious behavior (SIB) while the opiate antagonist, naloxone, attenuated SIB, implicating deranged endorphinergic mechanisms in the pathophysiology of this disorder. Brain damage is commonly associated with partial neuronal denervation, denervation supersensitivity and neuronal habituation (Cannon's Law). While the motor tics of TS possibly reflect neuronal denervation of striatal dopaminergic neurons. SIB may represent opioid denervation with alterations in opioid receptor sensitivity possibly involving striato-limbic-hypothalamic circuits. The effect of naloxone on SIB in TS could thus be explained on the basis of a modulatory effect of this drug on opioid receptor sensitivity.
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