Parkinson's Disease
Read Time: 4 mins

Depression and Parkinson’s Disease

Copy Link
Published Online: Jun 4th 2011 US Neurology, 2008;4(1):67-68 DOI:
Authors: Brian D Bell
Quick Links:
Article Information

Parkinson’s disease (PD) is generally considered to be a neurological disorder. However, because of the frequency of mood and other psychiatric complications, PD could be considered a neuropsychiatric disease. In fact, James Parkinson himself observed in 1817 that depression is commonly associated with PD.1

Parkinson’s disease (PD) is generally considered to be a neurological disorder. However, because of the frequency of mood and other psychiatric complications, PD could be considered a neuropsychiatric disease. In fact, James Parkinson himself observed in 1817 that depression is commonly associated with PD.1
The estimated prevalence of depression in PD varies according to the type of mood assessment applied (interview versus self-report questionnaire), diagnostic criteria or definition of depression (the number and type of symptoms required), and research setting (community-based versus neurology clinic).1,2 However, overall the data suggest that at any given time 20–40% of individuals with PD are experiencing depression of some type. This is a higher rate than that found in the general population.3–5 Depression can be difficult to diagnose in PD because of the overlap between symptoms of depression and PD. For example, the biological symptoms typical of depression—such as low energy, insomnia or excessive sleep, weight loss, diminished sexual function, and an emotionless face—can be directly related to the neuroanatomical disruption characteristic of PD. These symptoms are not necessarily evidence of depression and, conversely, the psychomotor slowing of depression might be accidentally overlooked in a patient with PD.2,6
Depression in PD could be considered an understandable reaction to a disabling chronic illness. However, some researchers believe that depression may be a part of the disease and caused by neurological changes.2,7 This notion is supported by the fact that depression sometimes precedes the diagnosis of PD. Of course, the cause of depression in patients with PD could be a combination of a subjective reaction to the illness and the brain changes brought about by the disease.5 The consensus is that depressive symptoms should be addressed and treated by physicians regardless of whether these symptoms are part of PD itself or due to a separate cause.1,8,9
The psychiatric complications of PD require attention because they can exacerbate the already considerable physical challenges brought on by the disease. In fact, an international survey of patients with PD discovered that depressive symptoms were the most important factor in patient quality-of-life ratings.10,11 Another reason to treat depression in PD is that reports of care-giver burden correlate significantly with patients’ depression and quality of life.12
It has been recommended that optimal anti-Parkinson symptom treatment should be the first step in the treatment of PD. It is notable that some PD medications may have an antidepressant effect of their own. The antidepressant effect of dopamine agonists such as pramipexole is probably due to stimulation of D3 dopamine receptors, whereas the drug’s effect on PD symptoms is related to the D2 dopamine receptor.3 Dopamine agonists may be helpful, in particular for patients who experience on–off motor fluctuations, with their depressive symptoms being related to the ‘off’ periods. When the use of an antidepressant is considered in a patient with PD, its potential adverse effects and interactions with PD drugs must be weighed against the effects of the depression itself.3 Although it should be noted that the majority of the studies did not include a placebo control, there is evidence that antidepressant medications can have a significantly positive effect on depression in PD.1,2,6 There are different classes of antidepressant medication. The selective serotonin re-uptake inhibitors (SSRIs) (e.g. Zoloft®, Prozac®, Paxil®, and Celexa®) are prescribed most often in PD patients with depression. In general, the SSRIs are safer and better tolerated by patients than the tricyclic antidepressants (TCAs) (e.g. Elavil®, Tofranil®, and Pamelor®). For example, the SSRIs have fewer cardiac and cognitive adverse effects and, in addition, they can effectively treat anxiety and pain, which are also common in patients with PD.2,3,8
Research studies have shown that PD symptoms can worsen as a result of SSRI use, but this adverse effect occurred in only a small minority of patients and was reversed after discontinuation of the medication.8 The combination of Selegilene and SSRIs could potentially result in a deadly serotonin syndrome. One author states that when Selegilene is being taken at a dosage ≥20mg per day, it should not be used together with SSRIs.2,3 Finally, more research is necessary to determine the best therapeutic ranges for antidepressant medications in individuals with PD.1
Some patients with depression either experience medication interaction effects and do not respond to pharmacotherapy for depression or are simply reluctant to take another medication. For these patients in particular, effective psychotherapeutic options would, of course, be valuable. To date, there have been very few studies of the effectiveness of psychotherapeutic techniques such as cognitive behavioral therapy (CBT) for the treatment of depression in PD.8 The research that has been carried out suggests that non-pharmaceutical approaches can help to improve mood, quality of life, and health outcomes. In one study, those individuals with the most severe depression seemed to benefit the most from CBT.13 The use of coping strategies and other techniques for managing grief and other emotional distress can still be effective in this context.
The growing trend toward use of online support groups may serve patients with PD well. Communicating with a group via a computer allows patients to access support without leaving the home. For individuals who have difficulty typing, a friend or spouse could possibly help. A recent study in California found that participation in an online support group that included professional facilitators positively affected mood and quality of life in a group of patients with PD.14
In PD patients without dementia, electroconvulsive therapy can be an effective choice for the treatment of depression when other treatments have failed. This treatment requires close management by a psychiatrist. Regular exercise can sometimes help to improve both physical and mental health in individuals with PD.1,15 In non-demented PD patients, electroconvulsive therapy (ECT), which requires close management by a psychiatrist, can be an effective choice for depression when other treatments have failed.3,6 The usual cause of the onset of delusions, hallucinations, and paranoia in PD is either the addition of a new PD drug such as amantadine, a dopamine agonist, or Selegilene or an increase in levodopa. A head injury or metabolic imbalance can also be responsible for these types of behavioral change. If the dramatic change in behavior is actually due to a primary psychotic depression rather than an adverse medication or injury, both an antidepressant and an atypical antipsychotic medication are called for. At the same time, a reduction in or elimination of one or more of the patient’s antiparkinsonian drugs might be necessary.3
Deep-brain stimulation surgery, including bilateral subthalamic nucleus surgery, can result in the appearance or exacerbation of personality, anxiety, or mood disorders in some PD patients. In particular, a history of major depression is a risk factor for a significant post-operative mood disorder, even when surgery results in marked improvement in motor functioning.16,17 In general, it should be emphasized that current antidepressant medications and psychotherapy have shown effectiveness for patients with PD. Therefore, both the depressive symptoms and motor symptoms of the illness should be addressed.8,18


  1. Weintraub D, Depression in Parkinson’s disease, Prim Psychiatry, 2005;12:45–9.
  2. McDonald W, et al., Prevalence, etiology, and treatment of depression in Parkinson’s disease, Biol Psychiatry, 2003;54:363–75.
  3. Lieberman A, Depression in Parkinson’s disease – a review, Acta Neurol Scand, 2006;113:1–8.
  4. Rojo A, et al., Depression in Parkinson’s disease: clinical correlates and outcome, Parkinsonism Relat Disord, 2003;10:23–8.
  5. Schrag A, et al., What contributes to depression in Parkinson's disease?, Psychol Med, 2001;31:65–73.
  6. Sawabini KA, et al., Treatment of depression in Parkinson’s disease, Parkinsonism Relat Disord, 2004;10:S37–41.
  7. Ehrt U, et al., Depressive symptom profile in Parkinson’s disease: a comparison with depression in elderly patients without Parkinson’s disease, Int J Geriatr Psychiatry, 2006;21:252–8.
  8. Veazey C, et al., Prevalence and treatment of depression in Parkinson’s disease, J Neuropsychiatry Clin Neurosci, 2005;17: 310–23.
  9. Kanner AM, et al., The impact of mood disorders in neurologic disease: should neurologists be concerned?, Epilepsy Behav, 2003;4:S3–13.
  10. Behari M, et al., Quality of life in patients with Parkinson’s disease, Parkinsonism Relat Disord, 2005;11(4):221–6.
  11. Slawek J, et al., Factors affecting the quality of life of patients with idiopathic Parkinson’s disease – a cross-sectional study in outpatient clinic attendees, Parkinsonism Relat Disord, 2005;11(7):465–8.
  12. Schrag, A, et al., Caregiver-burden in Parkinson’s disease is closely associated with psychiatric symptoms, falls, and disability, Parkinsonism Relat Disord, 2006;12(1):35–41.
  13. Cole, K, et al., The feasibility of using cognitive behaviour therapy for Depression associated with Parkinson’s disease: A literature review, Parkinsonism Relat Disord, 2005;11:269–76.
  14. Lieberman MA, et al., Online support groups for Parkinson’s patients: A pilot study of effectiveness, Soc Work Health Care, 2005;42(2):23–37.
  15. Rodrigues de Paula F, et al., Impact of an exercise program on physical, emotional, and social aspects of quality of life of individuals with Parkinson’s disease, Mov Disord, 2006;21(8): 1073–7.
  16. Burn D, et al., Neuropsychiatric complications of medical and surgical therapies for Parkinson’s disease, J Geriatr Psychiatry Neurol, 2004;17:172–80.
  17. Houeto J, et al., Behavioral disorders, Parkinson’s disease and subthalamic Stimulation, J Neurology Neurosurg Psychiatry, 2002;72:701–7.
  18. Weintraub D, et al., Parkinson’s Disease – Part 3: Neuropsychiatric Symptoms, Am J Manag Care, 2008;14(2):S59–69.

Further Resources

Share this Article
Related Content In Parkinson's Disease
  • Copied to clipboard!
    accredited arrow-down-editablearrow-downarrow_leftarrow-right-bluearrow-right-dark-bluearrow-right-greenarrow-right-greyarrow-right-orangearrow-right-whitearrow-right-bluearrow-up-orangeavatarcalendarchevron-down consultant-pathologist-nurseconsultant-pathologistcrosscrossdownloademailexclaimationfeedbackfiltergraph-arrowinterviewslinkmdt_iconmenumore_dots nurse-consultantpadlock patient-advocate-pathologistpatient-consultantpatientperson pharmacist-nurseplay_buttonplay-colour-tmcplay-colourAsset 1podcastprinter scenerysearch share single-doctor social_facebooksocial_googleplussocial_instagramsocial_linkedin_altsocial_linkedin_altsocial_pinterestlogo-twitter-glyph-32social_youtubeshape-star (1)tick-bluetick-orangetick-red tick-whiteticktimetranscriptup-arrowwebinar Sponsored Department Location NEW TMM Corporate Services Icons-07NEW TMM Corporate Services Icons-08NEW TMM Corporate Services Icons-09NEW TMM Corporate Services Icons-10NEW TMM Corporate Services Icons-11NEW TMM Corporate Services Icons-12Salary £ TMM-Corp-Site-Icons-01TMM-Corp-Site-Icons-02TMM-Corp-Site-Icons-03TMM-Corp-Site-Icons-04TMM-Corp-Site-Icons-05TMM-Corp-Site-Icons-06TMM-Corp-Site-Icons-07TMM-Corp-Site-Icons-08TMM-Corp-Site-Icons-09TMM-Corp-Site-Icons-10TMM-Corp-Site-Icons-11TMM-Corp-Site-Icons-12TMM-Corp-Site-Icons-13TMM-Corp-Site-Icons-14TMM-Corp-Site-Icons-15TMM-Corp-Site-Icons-16TMM-Corp-Site-Icons-17TMM-Corp-Site-Icons-18TMM-Corp-Site-Icons-19TMM-Corp-Site-Icons-20TMM-Corp-Site-Icons-21TMM-Corp-Site-Icons-22TMM-Corp-Site-Icons-23TMM-Corp-Site-Icons-24TMM-Corp-Site-Icons-25TMM-Corp-Site-Icons-26TMM-Corp-Site-Icons-27TMM-Corp-Site-Icons-28TMM-Corp-Site-Icons-29TMM-Corp-Site-Icons-30TMM-Corp-Site-Icons-31TMM-Corp-Site-Icons-32TMM-Corp-Site-Icons-33TMM-Corp-Site-Icons-34TMM-Corp-Site-Icons-35TMM-Corp-Site-Icons-36TMM-Corp-Site-Icons-37TMM-Corp-Site-Icons-38TMM-Corp-Site-Icons-39TMM-Corp-Site-Icons-40TMM-Corp-Site-Icons-41TMM-Corp-Site-Icons-42TMM-Corp-Site-Icons-43TMM-Corp-Site-Icons-44TMM-Corp-Site-Icons-45TMM-Corp-Site-Icons-46TMM-Corp-Site-Icons-47TMM-Corp-Site-Icons-48TMM-Corp-Site-Icons-49TMM-Corp-Site-Icons-50TMM-Corp-Site-Icons-51TMM-Corp-Site-Icons-52TMM-Corp-Site-Icons-53TMM-Corp-Site-Icons-54TMM-Corp-Site-Icons-55TMM-Corp-Site-Icons-56TMM-Corp-Site-Icons-57TMM-Corp-Site-Icons-58TMM-Corp-Site-Icons-59TMM-Corp-Site-Icons-60TMM-Corp-Site-Icons-61TMM-Corp-Site-Icons-62TMM-Corp-Site-Icons-63TMM-Corp-Site-Icons-64TMM-Corp-Site-Icons-65TMM-Corp-Site-Icons-66TMM-Corp-Site-Icons-67TMM-Corp-Site-Icons-68TMM-Corp-Site-Icons-69TMM-Corp-Site-Icons-70TMM-Corp-Site-Icons-71TMM-Corp-Site-Icons-72