Preexisting Bipolar Disorder Worsens Parkinson’s Problems

Marta Figueiredo, PhD avatar

by Marta Figueiredo, PhD |

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A previous diagnosis of bipolar disorder negatively affects the course of Parkinson’s disease, and is associated with greater neuropsychiatric and cognitive problems, poorer treatment outcomes, and shorter survival, a study shows.

Also, a greater proportion of Parkinson’s patients with preexisting bipolar disorder had a history of either condition in the family, compared with those without bipolar disorder.

These findings suggest a genetic contribution to the development of both conditions, further supporting previous studies showing that people with bipolar disorder have a higher risk of developing Parkinson’s.

The study, “Preexisting Bipolar Disorder Influences the Subsequent Phenotype of Parkinson’s Disease,” was published in the journal Movement Disorders.

Bipolar disorder is a mood disorder characterized by cyclic episodes of emotional highs (mania or hypomania) and lows (depression). Although the mechanisms behind bipolar disorder are still not completely understood, several studies suggest that dopamine — a brain signaling molecule progressively lost in Parkinson’s — may be involved.

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An increasing number of studies have reported that people diagnosed with bipolar disorder have a higher risk — of about 3.4 times — of developing Parkinson’s, and some have suggested that the mood disorder may be a prodromal, or early, stage of Parkinson’s.

However, whether the preexistence of bipolar disorder affects the course of Parkinson’s disease remains unknown.

To address this, a team of researchers in Italy and the U.S. analyzed demographic, genetic, and clinical data of a total of 247 Parkinson’s patients with a previous history of bipolar spectrum disorders (BSD-PD group) and 502 Parkinson’s patients without such mood disorders prior and after disease onset (the PD group).

All patients had been followed for at least six years. In the BSD-PD group, bipolar spectrum disorders appeared six to 24 years before a Parkinson’s diagnosis.

Results showed that, compared with the PD group, a significantly greater proportion of patients in the BSD-PD group had a family history of Parkinson’s (48.4% vs. 22.1%) and BSDs (42.3% vs. 10.6%). This highlighted a potential genetic contribution for the development of both BSDs and Parkinson’s.

No significant differences were detected between groups in terms of motor problems and non-motor symptoms, such as sleep and gastrointestinal problems.

However, a significantly greater proportion of BSD-PD patients had neuropsychiatric symptoms, including impulse control disorders (ICDs), somatic symptoms and functional disorders (SFDs), delusions, depression, and catatonia — which is characterized by abnormal movements and behaviors, immobility, and withdrawal.

ICDs are common psychiatric conditions in which a person often is unable to resist an impulse, drive, or temptation to perform a risky behavior. SFDs are mental disorders that manifest in the form of one or multiple chronic physical symptoms that cannot be attributed to a known disease.

ICDs and SFDs were more frequent in the BSD-PD group both before and after the diagnosis of Parkinson’s.

In addition, Parkinson’s patients with preexisting BSD also had a higher risk of earlier worsening of cognitive, depressive, and psychiatric symptoms relative to the PD group. Significantly more patients in the BSD-PD group died before age 75, compared with the PD group (14.1% vs. 6.1%).

There were no significant group differences in response to pharmacological therapy.

However, despite similar exposure to dopamine agonists (mainstay treatments that mimic the action of dopamine), the BSD-PD group showed a higher risk of dopamine agonist withdrawal syndrome. This syndrome can cause symptoms such as anxiety, panic attacks, depression, irritability, and fatigue.

Notably, earlier and more frequent neuropsychiatric symptoms also were associated with BSD-PD when the team looked at a subset of 34 BSD-PD and 79 PD patients carrying mutations in the GBA and PRKN genes, which have been linked to familiar Parkinson’s.

Moreover, data from 13 BSD-PD patients and 27 matched PD patients who underwent subthalamic nucleus deep brain stimulation (STN-DBS) showed that the therapeutic approach lessened motor problems in all patients, but improved quality of life only in the PD group.

STN-DBS involves the surgical insertion of an electrode in the brain to deliver electric pulses to an area involved in motor function, to manage Parkinson’s motor symptoms.

These findings highlight that “BSDs as a prodrome to PD unfavorably shape their course and are associated with detrimental neuropsychiatric features and treatment outcomes,” the researchers wrote.

They also support the importance of conducting psychiatric examinations in people living with Parkinson’s.

More studies are needed to better clarify the association between bipolar disorders and Parkinson’s, the team noted.

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