Now Antidepressant-Induced Chronic Depression Has a Name: Tardive Dysphoria

It isn't that we shouldn't take medications. It's that we shouldn't treat them like aspirin for a headache. We should take them with a real sense of risk.....

https://goo.gl/GpnFEk

This same basic mechanism—oppositional tolerance to a psychiatric drug—has been proposed to be a cause of tardive dyskinesia (TD), which develops with some frequency in long-term users of antipsychotic medications. TD is characterized by repetitive, purposeless movements, such as a constant licking of the lips, which is evidence that the basal ganglia has been damaged by the drugs. Although various explanations for TD have been put forth, one thought is that it is caused by drug-induced dopamine supersensitivity. Antipsychotics block dopamine receptors (and in particular, a subtype known as the D2 receptor), and in compensatory response, the brain’s neurons increase the density of their D2 receptors, and thus become “supersensitive” to this neurotransmitter. That may lead to the constant firing of neurons controlling motor movement (such as tongue movement), and even when the offending antipsychotic is withdrawn, TD symptoms often remain, which suggests that the brain is unable to renormalize its dopaminergic pathways.

With antidepressants, the problem may be that patients, because of the “oppositional tolerance” process, end up with a depleted serotonergic system. The postsynaptic neurons end up with a reduced density of receptors for serotonin; in rat studies, long-term treatment with an SSRI led to markedly reduced levels of serotonin in "nine areas of the brain."  El-Mallakh, in his paper, details several other ways that exposure to an SSRI may deplete serotonergic function, and notes that in experiments with young animals, such impairments are "associated with increased depressive and anxious behaviors."