Depression Is Risk Factor for Impulse Control Disorders in Parkinson’s Patients, Study Finds

Depression Is Risk Factor for Impulse Control Disorders in Parkinson’s Patients, Study Finds

Patients with Parkinson’s are at a greater risk of developing impulse control disorders (ICDs) if they are depressed, according to results from an international study.

The findings also revealed that treatment with dopamine agonists increases this susceptibility, and caution is advised when prescribing such therapies to depressed Parkinson’s patients.

The study, “Depression as a risk factor for impulse control disorders in Parkinson’s disease,” was published recently in the journal Annals of Neurology.

Depression and ICDs are two of the most common non-motor symptoms of Parkinson’s disease. However, while depression often precedes the onset of motor problems, ICDs are related to Parkinson’s treatment, especially to dopamine agonists. “This association with [dopamine agonists] makes ICDs a potentially avoidable disorder,” the researchers wrote.

Prior studies have shown that depression and ICDs often coexist in people with Parkinson’s, but were not able to assess whether depression increases the susceptibility for ICDs.

A team of Spanish researchers used data from the Parkinson’s Progression Markers Initiative, a multi-center clinical trial to identify biomarkers of Parkinson’s progression, to address this gap. A total of 354 patients were included, mostly from specialized university hospitals in the U.S. and Europe. None had ICD at baseline, as assessed with the Questionnaire for Impulsive Compulsive Disorders in Parkinson’s Disease.

ICD and medication use were evaluated at follow-up evaluations every three months initially, and every six months after visit four. The researchers also evaluated anxiety with the State-Trait Anxiety Inventory, apathy with the Movement Disorders Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS), and sleep impairments via the REM sleep behavior disorder screening questionnaire.

At baseline, 54.8% of patients were aged between 60 and 75 years and 61.3% were men. The results showed that 68 participants (mean age 60.8 years, 13.3 months since diagnosis) had either depressive symptoms or were diagnosed with depression and taking antidepressants.

The prevalence of depression was higher in women than in men (27.78% vs 15.93%) and depressed patients did not receive dopamine agonists more frequently than non-depressed patients either at baseline or during follow-up.

Also, anxiety and apathy scores were higher in patients with depression (aged 61.6 years, 182 men, 12.7 months since diagnosis).

Over a median follow-up of approximately four years, the patients with depression at baseline showed a nearly two-fold greater risk of developing ICDs, as reflected in an incidence rate of 19.4 cases per 100 patient-years — a measure obtained by multiplying the number of persons at risk over time — compared to 10.3 cases in those without depression.

As shown previously, using dopamine agonists also increased the risk for ICDs. In fact, patients with depression had an ever greater risk of developing ICDs if taking these treatments. Controlling for multiple potential confounding factors — such as age, sex, apathy and anxiety — did not alter these findings.

“Our results show depression acts as a risk factor for the development of ICDs in [Parkinson’s] patients,” the scientists wrote.

“Notably, our results [also] show that the use of [dopamine agonists] in patients with depression is linked to a higher ICD risk,” they added. As such, dopamine should be used with caution in this patient population, the researchers commented.

Importantly, depression should be routinely monitored “to optimize medical decisions regarding the risk of developing ICDs.”

José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has studied Biochemistry also at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario, in London, Ontario. His work ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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Ana holds a PhD in Immunology from the University of Lisbon and worked as a postdoctoral researcher at Instituto de Medicina Molecular (iMM) in Lisbon, Portugal. She graduated with a BSc in Genetics from the University of Newcastle and received a Masters in Biomolecular Archaeology from the University of Manchester, England. After leaving the lab to pursue a career in Science Communication, she served as the Director of Science Communication at iMM.
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José is a science news writer with a PhD in Neuroscience from Universidade of Porto, in Portugal. He has studied Biochemistry also at Universidade do Porto and was a postdoctoral associate at Weill Cornell Medicine, in New York, and at The University of Western Ontario, in London, Ontario. His work ranged from the association of central cardiovascular and pain control to the neurobiological basis of hypertension, and the molecular pathways driving Alzheimer’s disease.
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