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Depression in Parkinson’s disease: aetiology, assessment and treatment

Published online by Cambridge University Press:  05 March 2026

Aydah Sarah Ashraf ,
Amit Nautiyal  and
Verghese Joseph Open the ORCID record for Verghese Joseph [Opens in a new window]
Aydah Sarah Ashraf
Affiliation:
A 5th-year medical student at Imperial College School of Medicine (ICSM), Faculty of Medicine, Imperial College London, UK. She has a BSc (Hons) in Business Management and is driven by a passion for advancing medicine through research and education, with a commitment to exploring innovative ‘what ifs’ that affect society, alongside an interest in teaching – delivering lectures to peers and running interview courses to inspire aspiring medical students.
Amit Nautiyal
Affiliation:
A physician in emergency medicine and pulmonary medicine, working as an attending physician in the Department of Medicine at Albany Medical College, and a critical care physician at Albany Medical Centre, Albany, New York, USA.
Verghese Joseph*
Affiliation:
A consultant adult psychiatrist with Lincolnshire Partnership NHS Foundation Trust, Stamford, UK. Trained in adult and old age psychiatry, he has used functional magnetic resonance imaging and evoked response potentials to study pathophysiology in schizophrenia. His special interests are in teaching, training and medical education.
*
Correspondence Verghese Joseph. Email: verghese.joseph@nhs.net
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Summary

Parkinson’s disease is a chronic neurodegenerative disorder with a range of movement-related and non-movement symptoms. Depression is a frequent complication and linked to faster cognitive decline, reduced daily functioning and poorer quality of life. This review looks at how often depression occurs in Parkinson’s disease, possible reasons behind it and the diverse ways it can be treated. A thorough evaluation using a biopsychosocial approach, supported by tools like the Patient Health Questionnaire, is essential. Treatment options include medications (e.g. selective serotonin reuptake inhibitors, tricyclic antidepressants and serotonin–noradrenaline reuptake inhibitors), talking therapies (e.g. cognitive–behavioural therapy and problem-solving therapy) and electroconvulsive therapy. Techniques such as transcranial magnetic stimulation and vagus nerve stimulation are being explored for individuals who do not respond to standard treatments. The findings highlight the importance of personalised, evidence-based care to improve the mental health and independence of people with Parkinson’s disease.

Keywords

Depressionneuropsychiatrymedicationcognitive–behavioural therapyParkinson’s disease

Information

Type
Article
Information
BJPsych Advances , First View , pp. 1 - 7
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Copyright
© The Author(s), 2026. Published by Cambridge University Press on behalf of Royal College of Psychiatrists

LEARNING OBJECTIVES

After reading this article you will be able to:

  • describe the aetiology of depression in Parkinson’s disease

  • recognise the clinical presentation and how to differentiate from other conditions

  • outline the range of pharmacological, psychological and novel interventions and their current evidence base.

Parkinson’s disease is degenerative neuropsychiatric disorder associated with significant physical and psychological morbidity. Although the condition is primarily classified as a motor disorder, characterised by symptoms such as resting tremor, rigidity, bradykinesia and postural instability, its effects extend beyond motor impairment. Neuropsychiatric problems such as anxiety and mood disorders, cognitive decline and psychosis are common and affect patient morbidity and quality of life. Managing Parkinson’s disease therefore requires a multidisciplinary strategy. This review concentrates on addressing depression in the Parkinson’s disease population. The case vignettes in the article are fictitious.

Depression in Parkinson’s disease

Over a year-long follow-up of individuals with Parkinson’s disease, depressive disorders were identified as the most diagnosed psychiatric complication (Lee Reference Lee, Chiou and Chang2022). Clinical signs typically include apathy, psychomotor slowing, memory difficulties, negative thinking, irrational beliefs and the presence of suicidal ideation without clear suicidal intent. Compared with major depressive disorder in the general population, depression in Parkinson’s disease is often associated with less guilt and self-reproach, but increased irritability and health-related worries (Gotham Reference Gotham, Brown and Marsden1986) (Box 1).

The presence of both depression and agitation tends to worsen functional outcomes, especially among individuals with early-onset Parkinson’s (Box 2). Emotional fluctuations commonly mirror motor fluctuations, with depressive symptoms worsening during ‘off’ motor periods (periods when symptoms return or worsen) and improving during ‘on’ phases (periods when symptoms are well-controlled) (Menza Reference Menza, Sage and Cody1990). Factors such as a psychiatric history, chronic pain, lack of social support and greater disease severity are associated with an increased risk of depression in Parkinson’s disease (Reijnders Reference Reijnders, Ehrt and Weber2008). Depression, together with disability, instability in posture and cognitive decline, significantly reduces overall quality of life (Schrag Reference Schrag, Jahanshahi and Quinn2000).

BOX 1

Case vignette: irritability and health-related worries in Parkinson’s depression

Mr A is a 72-year-old male with an 8-year history of Parkinson’s disease. He presents with moderate motor symptoms, including bradykinesia, muscle rigidity and impaired postural stability. Mild cognitive impairment has been observed over the past 2 years. He presents with increasing apathy, persistent low mood and psychomotor retardation. His wife reports that he frequently expresses concern about his health and has stopped attending social gatherings. His mood worsens significantly during ‘off’ motor states and slightly improves during ‘on’ states. He denies feelings of guilt or self-reproach, but displays marked irritability and sadness. Cognitive assessment reveals mild memory impairment.

BOX 2

Case vignette: depression in early-onset Parkinson’s disease

Ms B, a 54-year-old female, has early-onset Parkinson’s disease, diagnosed 5 years ago. She presents with severe motor symptoms affecting the right side, including tremors and rigidity. There is a history of chronic pain due to musculoskeletal problems and of anxiety disorder. She lives alone, has limited social support and works part-time. She reports persistent low mood, hopelessness and morning depression. She experiences frequent mood fluctuations that correspond to her motor states (‘on–off’ periods). She has expressed suicidal ideation, but denies any intent or plan. She exhibits significant agitation and pessimism and struggles with sleep disturbances. Previous trials of selective serotonin reuptake inhibitors (citalopram and sertraline) were ineffective.

Aetiology

The causes of depression in Parkinson’s disease are believed to be multifactorial, involving both biological and psychological elements. Brain imaging studies have improved our understanding of how Parkinson’s disease-related depression is linked to problems in corticostriatal circuits (Thobois Reference Thobois, Prange and Sgambato-Faure2017). The high prevalence of depression in Parkinson’s disease, together with its link to greater motor impairment and bradykinesia, indicates that dopaminergic denervation may be a key factor contributing to the clinical burden of depression in people with the disease (Prange Reference Prange, Klinger and Laurencin2022).

Using ¹¹C-DASB, a highly selective PET tracer for the serotonin transporter (SERT) showed depression in Parkinson’s disease was associated with increased binding in the caudal raphe nuclei, amygdala, hypothalamus and posterior cingulate cortex (Politis et al 2010, cited in Maillet Reference Maillet, Météreau and Tremblay2021). Recent evidence has shown more pronounced serotonergic pathology associated with depression across various stages of Parkinson’s disease, highlighting the critical role of serotonergic dysfunction within limbic corticostriatal circuits (Maillet Reference Maillet, Météreau and Tremblay2021).

Cortical cholinergic loss has also been linked to higher depression scores in males with Parkinson’s disease with and without Parkinson’s disease (Bohnen Reference Bohnen, Kaufer and Hendrickson2007). Furthermore, evidence suggests that non-dopaminergic pathways may be particularly involved, given the link between depression and more severe axial motor symptoms, such as rigidity and balance problems (Anguenot Reference Anguenot, Loll and Neau2002).

Assessment and management

The fundamental concepts of biopsychosocial assessment and intervention apply broadly to individuals with psychiatric disorders, although specific modifications may be necessary to meet the unique needs of each patient. In Parkinson’s disease, effective management of depression requires a multidisciplinary team, typically involving neurologists, psychiatrists, geriatricians, specialist Parkinson’s nurses and liaison psychiatrists, alongside the patient and their carer(s). Clearly communicating that depression is a frequent and intrinsic aspect of Parkinson’s disease can assist in fostering acceptance of appropriate treatment and support among both patients and caregivers.

When conducting assessments, particular emphasis should be placed on identifying cognitive symptoms of depression, as evidence suggests a strong association between the severity of depressive symptoms and the degree of cognitive dysfunction in Parkinson’s disease (Starkstein Reference Starkstein, Bolduc and Mayberg1990). Although somatic symptoms can aid in diagnosing major depression, their diagnostic significance is greatest when they are severe, out of proportion with the primary neurological illness and temporally linked with mood and cognitive disturbances. Three core affective features – depressed mood, early-morning mood deterioration, and hopelessness – are especially valuable in differentiating depressive states from non-depressive presentations in Parkinson’s disease. Symptoms such as inappropriate guilt, feelings of punishment, diminished self-esteem and suicidal ideation tend to occur less frequently in medically ill populations compared with psychiatric cohorts (Cavanaugh Reference Cavanaugh1995). In Parkinson’s disease, depressive symptoms may also manifest covertly, for example through poor adherence to treatment regimens or refusal to take necessary anti-Parkinsonian medications.

Differential diagnosis

Certain features of Parkinson’s disease can mimic depression (Chaudhuri Reference Chaudhuri, Healy and Schapira2006). Apathy can present with loss of motivation, reduced initiative and flat affect. However, sadness or guilt may not be present, and the patient is more often indifferent than distressed. Fatigue can present with overwhelming tiredness and lack of energy and it worsens with activity. However, Parkinson’s disease may not be associated with low mood. Motor slowing and bradykinesia present as reduced facial expression, monotonous speech and slow responses and may mimic psychomotor retardation, although mood may be appear to be normal if directly asked.

When evaluating low mood in Parkinson’s disease, it is crucial to consider alternative underlying causes. Emotional reactions, including sadness and frustration, are often normal responses to physical illness. Adjustment disorders, arising from the psychological stress associated with managing a chronic medical condition, are among the most frequent psychiatric diagnoses in general medical practice. Furthermore, depressive features are commonly observed in cases of delirium, particularly in its hypoactive form, which may sometimes be misinterpreted as depression during psychiatric assessments. Careful differentiation between delirium and depression is essential, as prompt and accurate treatment can prevent further cognitive deterioration and avoid exacerbating confusion, particularly given the anticholinergic side-effects of certain antidepressants. In Parkinson’s dementia, apathy, withdrawal, poor concentration and forgetfulness are seen (Otero Reference Otero2008). However, cognitive effects are prominent, and sadness and guilt are absent. Sleep disorders (insomnia, sleep apnoea, rapid eye movement (REM) sleep behaviour disorder) may present as daytime sleepiness, irritability and poor energy, and mood improves with sleep restoration (Barraud Reference Barraud, Lambrecq and Forni2009).

Potential screening tools in primary and secondary care

Williams et al (Reference Williams, Hirsch and Anderson2012) evaluated the psychometric properties of nine depression screening scales for people with Parkinson’s disease and found that the self-reported 30-item Geriatric Depression Scale (GDS-30) offered the most efficient profile owing to its brevity and strong psychometric performance. Tools like the Patient Health Questionnaire-9 (PHQ-9) (Kroenke Reference Kroenke, Spitzer and Williams2001) and the GDS-30 (Yesavage Reference Yesavage, Brink and Rose1982) can provide structured support in evaluating symptom severity and tracking treatment response over time.

Although these instruments can offer helpful additional information, they are no replacement for a full clinical assessment. Accurate diagnosis remains a cornerstone of effective treatment planning. The National Institute for Health and Care Excellence (2009) recommends thorough evaluation of depression, incorporating symptom severity, duration and the degree of functional limitation.

Pharmacotherapy

Efficacy

Selective serotonin reuptake inhibitors (SSRIs) are typically considered the first-line therapy for major depressive disorder in adults, owing to their favourable side-effect profiles. It is recommended to continue antidepressant therapy for a minimum of 6 weeks before evaluating the need to switch medications. There is some evidence supporting venlafaxine’s effectiveness in individuals who have not responded to SSRIs, although specific studies in older adults are limited (Kim Reference Kim, Blumberger and Karp2022). However, a systematic review of randomised controlled trials (RCTs) evaluating efficacy of SSRIs and tricyclic antidepressants (TCAs) for depression in Parkinson’s disease concluded that the results remained inconsistent and did not allow for firm treatment recommendations (Starkstein Reference Starkstein and Brockman2017).

The potential antidepressant effects of dopaminergic agonists have been evaluated in recent RCTs. A meta-analysis by Leentjens et al (Reference Leentjens, Koester and Fruh2009) suggested that pramipexole, a potent D2 receptor agonist, has antidepressant efficacy, a finding later confirmed by an RCT conducted by Barone et al (Reference Barone, Poewe and Albrecht2010). These results are clinically relevant, as pramipexole may offer a dual benefit in Parkinson’s disease by improving both depressive symptoms and motor symptoms, thereby reducing the need for additional pharmacological agents and minimising polypharmacy risks. Piribedil, a potent D2/D3 dopamine agonist that is highly effective in treating apathy following subthalamic nucleus deep brain stimulation, has also been shown to improve depressive symptoms (Thobois Reference Thobois, Lhommée and Klinger2013). There is increasing evidence that continuous infusion therapies, such as levodopa–carbidopa intestinal gel (Valldeoriola Reference Valldeoriola, Catalán and Escamilla-Sevilla2021) or subcutaneous apomorphine (Katzenschlager Reference Katzenschlager, Poewe and Rascol2018), may also alleviate depressive symptoms in Parkinson’s disease, in addition to their well-established benefits on motor function and quality of life.

Tolerability and side-effects of medications

Older adults often have reduced physiological reserve, making them more susceptible to rapid decompensation and loss of homeostasis. Severe depression in this population can lead to complications such as weight loss, dehydration and an increased vulnerability to medication side-effects. Tricyclic antidepressants are associated with troublesome anticholinergic side-effects, including dry mouth, sedation, constipation, blurred vision, postural hypotension and cardiac arrhythmias (Kamp Reference Kamp, Petersen and Faltermeier2024). Their high lethality index further necessitates extreme caution in individuals with suicidal ideation.

Although serotonin syndrome – a potential risk when combining selegiline with an SSRI – has been reported (Richard Reference Richard, Kurlan and Tanner1997), it remains rare. Among antidepressants, venlafaxine, a serotonin–noradrenaline reuptake inhibitor (SNRI), is noted for its anxiolytic properties and favourable side-effect profile. Gastrointestinal side-effects are a recognised problem with SSRIs, with growing concern about the risk of gastrointestinal haemorrhage in elderly people (Baldwin Reference Baldwin and Wild2004). When prescribing SSRIs alongside non-steroidal anti-inflammatory drugs (NSAIDs), caution is warranted; sertraline and citalopram are considered to carry the lowest risk for drug interactions. We found no RCTs that directly assessed mood stabilisers such as carbamazepine or lithium for depression in people with Parkinson’s disease. Lofepramine, a second-generation tricyclic antidepressant, is as effective as other tricyclics and offers an improved side-effect profile (Kerihuel Reference Kerihuel, Dreyfus and Whitford1991). Moclobemide is well tolerated in older adults and does not require dietary restrictions (Roth Reference Roth, Mountjoy and Amrein1996). Importantly, SSRIs have minimal negative effects on cognitive function in older people with depression (Schulkens Reference Schulkens, Deckers and Jenniskens2022).

Epilepsy must also be considered when selecting antidepressants, as certain agents can lower the seizure threshold (Tallarico Reference Tallarico, Pisano and Leo2023). Discontinuation symptoms, particularly with antidepressants that have a short half-life, often arise after 8 or more weeks of treatment (Henssler Reference Henssler, Schmidt and Schmidt2024). Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is commonly associated with SSRIs, but can occur with any antidepressant class (Gheysens Reference Gheysens, Van Den Eede and De Picker2024). Risk factors for SIADH include older age, female gender and concurrent use of sodium-lowering medications. Symptoms emerge when serum sodium falls below 130 mmol/L and may include lethargy, sleep disturbances, muscle cramps and headaches – clinical features that can overlap with depressive symptoms, necessitating a high index of suspicion for accurate diagnosis.

Neuromodulation strategies

Electroconvulsive therapy

Electroconvulsive therapy (ECT) remains a highly effective treatment for severe depression. ECT is typically considered when there is an urgent risk to life, such as profound malnutrition or acute suicidality, or when traditional antidepressant therapies have failed. Research indicates that ECT is particularly effective for depressive episodes with psychotic features (Petrides Reference Petrides, Fink and Husain2001).

Borisovskaya et al (Reference Borisovskaya, Bryson and Buchholz2016) conducted a systematic review of ECT in people with Parkinson’s disease, analysing 43 publications that primarily consisted of small case series or case reports, as no RCTs were available. Their review encompassed 116 patients, most of whom were diagnosed with major depression. The authors found that 93% of patients experienced improvement in depressive symptoms, and 83% also demonstrated improvements in motor function.

Comparative studies consistently show ECT’s superiority over other neuromodulatory interventions, including transcranial magnetic stimulation (TMS), in the treatment of depression (Micallef-Trigona Reference Micallef-Trigona2014). Although no absolute contraindications to ECT exist, it is advisable to carry out a thorough anaesthetic assessment to evaluate medical risks. Managing comorbid conditions such as hypertension and heart failure is critical before beginning therapy, and ECT is postponed for 3 months following recent myocardial infarction or stroke. Although older adults often respond positively to ECT, they are more susceptible to transient cognitive side-effects, such as confusion, requiring vigilant monitoring during treatment.

Transcranial magnetic stimulation

Repetitive transcranial magnetic stimulation (rTMS) exerts its therapeutic effects by modulating cortical excitability, either enhancing or inhibiting activity in targeted brain regions (Kamble Reference Kamble, Netravathi and Pal2014). It has shown established efficacy in the treatment of primary depression. The most employed rTMS protocol involves applying high-frequency stimulation to the left dorsolateral prefrontal cortex (DLPFC) and low-frequency stimulation to the right DLPFC. One key advantage of rTMS over ECT is its avoidance of general anaesthesia.

Meta-analyses suggest that, in addition to its antidepressant properties in Parkinson’s disease, rTMS improves both general and specific cognitive abilities (Xie Reference Xie, Chen and Wang2015; Wang Reference Wang, Zhang and Zang2024) and has minor motor function benefits, usually with fewer adverse effects (Xie Reference Xie, Chen and Wang2015).

Emerging therapies: vagus nerve stimulation and deep brain stimulation

Vagus nerve stimulation (VNS) and deep brain stimulation (DBS) are neuromodulatory treatments under investigation for addressing treatment-resistant depression. VNS delivers targeted electrical impulses to the vagus nerve, influencing mood-regulating circuits within the brain. Recent findings highlight the expanding clinical potential of VNS, particularly with the development of less-invasive techniques (Austelle Reference Austelle, Cox and Wills2024). DBS, in contrast, requires surgical implantation of electrodes into specific brain regions to adjust neural activity. Clinical trials report that DBS achieves response rates of about 60% in people with chronic, treatment-refractory depression. Nevertheless, further studies are needed to refine both the effectiveness and safety profiles of these interventions.

Psychological interventions

The effective management of depression requires a holistic, patient-centred approach that integrates supportive care, psychoeducation and family involvement. Facilitating opportunities for patients to address social challenges is equally essential. In hospital environments, interventions such as regular physiotherapy and occupational therapy can mitigate the impacts of isolation, discomfort and inactivity. Managing any underlying medical contributors to depressive symptoms remains crucial. If discontinuing a causative medication is not possible, pharmacological treatment with antidepressants should be considered.

Research suggests that psychological therapies may be just as effective as medications for managing mild to moderate depression in older adults (Baldwin Reference Baldwin and Wild2004). Two RCTs of cognitive–behavioural therapy (CBT) showed significant advantages of psychotherapy over placebo, with large effect sizes and high response rates (Calleo Reference Calleo, Amspoker and Sarwar2015). Cognitive-based mindfulness therapy – incorporating meditation practices, breathing exercises and yoga postures – has emerged as a promising intervention, particularly for people with mild to moderate depression and anxiety (Hofmann Reference Hofmann, Sawyer and Witt2010).

CBT continues to be the most extensively studied and evidence-supported psychological therapy for depression, particularly among older adults (Hofmann Reference Hofmann, Asnaani and Vonk2012). However, many of these studies focus on patients who are cognitively intact and physically stable, which may limit applicability in people with Parkinson’s disease. Adaptations of CBT have shown promise for frail individuals or those experiencing mild cognitive impairment, although more research is needed to establish efficacy across diverse populations.

Problem-solving therapy (PST), a structured approach aimed at enhancing patients’ coping strategies, also shows compelling evidence for efficacy in depression. A network meta-analysis by Barth et al (Reference Barth2013) indicated that PST offers moderate to large benefits compared with waiting-list control conditions. A recent multiverse meta-analysis by Plessen et al (Reference Plessen, Karyotaki and Miguel2023) further supports PST’s role in treating depression, but emphasises the need for broader validation.

Conclusion

Depression in Parkinson’s disease is multifactorial, influenced by a combination of psychological, social and biological factors. Individual characteristics such as personality, resilience and stress tolerance, as well as the presence of anxiety and fears, play a significant role. Contextual factors, including financial status and social support, also contribute, alongside biological mechanisms that are not yet fully understood. These factors affect not only the development of depression but also the likelihood of treatment success. There are no clearly defined guidelines for the treatment of depression in Parkinson’s disease, owing to the paucity of high-quality evidence from RCTs.

Managing depression in Parkinson’s disease is inherently complex and demands integrated care across neurology, geriatrics, psychiatry and primary healthcare providers. Effective treatment goes beyond optimising motor symptoms, requiring detailed biopsychosocial assessments and individualised, evidence-based interventions. Substantial evidence supports pharmacological approaches: SSRIs are the first-line treatment, with a switch to tricyclic antidepressants or SNRIs indicated in non-responders. Psychological therapies can be first choice of intervention if preferred by patients. ECT is indicated in severe depression, and emerging research points to the additional benefits of therapies such rTMS and VNS.

MCQs

Select the single best option for each question stem

  1. 1 The most common psychiatric comorbidity in Parkinson’s disease is:

    1. a generalised anxiety disorder

    2. b dementia

    3. c organic personality change

    4. d depression

    5. e self-harm.

  2. 2 Aetiology of depression in Parkinson’s disease is linked to:

    1. a serotonin (5-HT)

    2. b dopamine

    3. c psychosocial factors

    4. d choline

    5. e all of above.

  3. 3 Tricyclic antidepressants must be used with caution owing to the increased risk of:

    1. a tardive dyskinesia

    2. b hypertension

    3. c arrythmias

    4. d suicidal ideation

    5. e all of above.

  4. 4 ECT should be considered for depression in Parkinson’s disease in the following circumstances:

    1. a severe or psychotic depression

    2. b patient choice

    3. c poor tolerance/non-response to antidepressants

    4. d suicidal feelings

    5. e all of above.

  5. 5 The psychological therapy with the strongest research backing for depression in Parkinson’s disease is:

    1. a psychoanalysis

    2. b problem-solving therapy

    3. c hypnotherapy

    4. d cognitive–behavioural therapy (CBT)

    5. e eye movement desensitisation and reprocessing (EMDR).

MCQ answers

  1. 1 d

  2. 2 e

  3. 3 c

  4. 4 e

  5. 5 d

Data availability

Data availability is not applicable to this article as no new data were created or analysed in this study.

Acknowledgement

We thank Dr Vijay Waykar, consultant in old age psychiatry, for reviewing this article and offering helpful comments.

Author contributions

V.J. and A.N. were responsible for review of the literature and first draft. A.S.A. was responsible for updating the draft with current evidence and references.

Funding

This research received no specific grant from any funding agency, commercial or not-for-profit sectors.

Declaration of interest

None.

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