According to a recent study, newer, more narrowly focussed antidepressant drugs that have proven to more effectively treat serotonin imbalances may actually be less effective for subjects diagnosed with both depression and Parkinson's disease. 

Parkinson's disease's most prominent symptoms concern restrictions on physical mobility: muscle rigidity, tremor-like tics and severe discomfort in motion. But, like Alzheimer's, the disease is a progressively degenerative neurological condition that incapacitates individuals over time, eventually disabling their most basic cognitive functions. Those suffering from the disease's later stages often experience difficulty processing and communicating all types of information. 

Another near-universal element of the Parkinson's equation is depression. Independent studies estimate that at least 50% of affected subjects may be diagnosed with clinical depression as well. And these mood changes are not emotional responses to the disease itself. They may, in fact, precede the diagnosis. Subjects who've suffered from chronic anxiety or other mood problems prior to being diagnosed with Parkinson's are nearly guaranteed to develop concurrent depression. 

The psychiatric components of Parkinson's often take a backseat to its more obvious physical symptoms, and they may be treated as minor complications. But successful reduction of mood disorders can make the entire experience less painful for subjects and their families. And a new study indicates that the newer SSRI antidepressants commonly used to treat Parkinson's patients are considerably less effective than their predecessors. 

Parkinson's can compromise the body's ability to produce both dopamine and serotonin, so SSRIs have been the medications most commonly used to treat depressed Parkinson's patients (most of whom still, unfortunately, receive no psychiatric treatment at all. This study, published in the online magazine Neurology, dosed three groups of patients with either an SSRI, a placebo or an older tricyclic antidepressant designed to target both serotonin and neropenephrine receptors in the brain. Amazingly, they found that the tricyclic subjects were nearly five times as likely to report emotional improvement over the study's eight week course. Researchers are not yet certain exactly why this is the case, but the results imply that depression among Parkinson's patients involves variables beyond serotonin shortages.   

The most important conclusion drawn from this study is the fact that depression is a symptom of Parkinson's rather than a reaction to it and that subjects should continue to seek treatment for both. Depression among Parkinson's patients does respond successfully to treatment. Reducing the physical discomforts of the disease is not sufficient if depression plays a role, and subjects who refuse to seek psychiatric treatment should be referred by their family members or other loved ones.