i notice throughout this site doctors are saying there's no connection between TD and SSRIs. some recent evidence disagrees

dyskinesias and dystonias emerging in patients being treated with SSRIs that could persist for weeks and months afterwards (Fitzgerald & Healy 1995) http://www.socialaudit.org.uk/58092-DH.htm

Motor neurons were challenged with fluoxetine and paroxetine at clinically relevant doses as well as at lesser and greater doses. Ethanol was used as a negative control and another group of cells was left untreated. As expected, in alcohol-treated cells, there was significant decrease in cell survival and neurite outgrowth. In untreated cells there was no effect in either cell survival or neurite outgrowth. In fluoxetine-treated motor neurons there was ~52% cell death while in paroxetine-treated cells there was 14% cell survival and both SSRIs caused significant loss of the percentage of neurite-bearing cells. Both SSRIs decreased cell survival in a dose-dependent manner. http://www.dovepress.com/effects-of-selective-serotonin-reuptake-inhibitors-on-motor-neuron-sur-peer-reviewed-article-IJGM-MVP

a selective serotonin reuptake inhibitor (SSRI) blocks the normal reuptake of serotonin from the synaptic cleft, which is the tiny gap between neurons. Serotonin now stays in the cleft longer than normal, and feedback mechanisms immediately kick into gear. The presynaptic neurons begin putting out less serotonin than usual, while the postsynaptic neurons—the neurons receiving the message—decrease the density of their receptors for serotonin. The drug is acting as an accelerator of serotonergic activity; the brain responds by putting down the brake. This basic mechanism—oppositional tolerance to a psychiatric drug—has been proposed to be a cause of tardive dyskinesia, which develops with some frequency in long-term users of antipsychotic medications and Tardive dysphoria [persistent depression] in long-term users of SSRIs http://www.psychologytoday.com/blog/mad-in-america/201106/now-antidepressant-induced-chronic-depression-has-name-tardive-dysphoria

Surgeries performed with aborted fetal tissue in the 1980’s in patients with Parkinson’s proved that the diseased brain could be repaired. The treatment aimed to replace decayed dopamine cells in the brain’s of Parkinson’s patients. Some transplanted patients showed remarkable improvement but eventually the majority developed dyskinesias. Marios Politis and colleagues in the United Kingdom and Sweden have discovered that the neurotransmitter serotonin is the culprit. They found that previously decayed dopamine neurons—a hallmark of Parkinson’s disease—were still restored and fully functional over a decade after transplantation. But Politis and colleagues also saw unexpectedly high amounts of serotonin neurons in the transplanted tissue. The finding is puzzling because the dyskinesias in Parkinson’s are thought to be a result of dopamine action, not serotonin. The researchers discovered that the deceptive ability of serotonin neurons to switch to a different neurotransmitter—to adopt and pump out dopamine—causes the dyskinesias. Administering a drug to block this action almost immediately eliminated the dyskinesias in both patients. http://phys.org/news197132585.html#jCp

shamimkhaliq

8/19/12 11:25pm

sorry, there's no "edit". i just wanted to add one more study, of the link between depression and parkinson's disease: http://www.sciencedaily.com/releases/2002/05/020528074951.htm