# Diagnosis and Management of Parkinson Disease in Individuals with Pre-Existing Mood Disorders

**Authors:** Laura Buyan Dent

PMC · DOI: 10.3390/ijerph23020269 · International Journal of Environmental Research and Public Health · 2026-02-21

## TL;DR

This paper discusses how Parkinson disease is often missed in people with mood disorders due to overlapping symptoms and offers strategies for better diagnosis and treatment.

## Contribution

The paper provides a comprehensive review of diagnostic and management approaches for Parkinson disease in individuals with pre-existing mood disorders.

## Key findings

- Delayed diagnosis of Parkinson disease in patients with mood disorders leads to treatment complexity and worse outcomes.
- Integrated neurologic and psychiatric care models can improve detection and management of co-occurring disorders.
- Non-pharmacologic interventions like cognitive behavioral therapy and exercise enhance quality of life in these patients.

## Abstract

Public health relevance—How does this work relate to a public health issue?
Parkinson disease and mood disorders are both highly prevalent and increasing globally, and their frequent co-occurrence contributes to delayed diagnosis, treatment complexity, disability, and healthcare utilization.Symptom overlap and treatment interactions create systematic risks of misdiagnosis and fragmented care, particularly in settings with limited access to neurology or mental health specialists.

Parkinson disease and mood disorders are both highly prevalent and increasing globally, and their frequent co-occurrence contributes to delayed diagnosis, treatment complexity, disability, and healthcare utilization.

Symptom overlap and treatment interactions create systematic risks of misdiagnosis and fragmented care, particularly in settings with limited access to neurology or mental health specialists.

Public health significance—Why is this work of significance to public health?
Earlier recognition of Parkinson disease in people with pre-existing mood disorders can reduce morbidity, prevent inappropriate treatment escalation, and improve functional and quality-of-life outcomes.Integrating neurologic and psychiatric care models addresses a major gap in current service delivery for chronic brain disorders and supports more efficient, patient-centered care.

Earlier recognition of Parkinson disease in people with pre-existing mood disorders can reduce morbidity, prevent inappropriate treatment escalation, and improve functional and quality-of-life outcomes.

Integrating neurologic and psychiatric care models addresses a major gap in current service delivery for chronic brain disorders and supports more efficient, patient-centered care.

Public health implications—What are the key implications or messages for practitioners, policy makers and/or researchers in public health?
Practitioners and health systems should implement cross-disciplinary screening, referral pathways, and collaborative care models to improve detection and management of combined neurodegenerative and mood disordersPolicy makers and researchers should prioritize workforce training, access expansion, and research on early biomarkers and integrated interventions to reduce long-term disability and healthcare burden.

Practitioners and health systems should implement cross-disciplinary screening, referral pathways, and collaborative care models to improve detection and management of combined neurodegenerative and mood disorders

Policy makers and researchers should prioritize workforce training, access expansion, and research on early biomarkers and integrated interventions to reduce long-term disability and healthcare burden.

Parkinson disease (PD) and mood disorders represent two substantial global health burdens that increasingly co-occur as both conditions rise in prevalence worldwide. Diagnosing Parkinson disease in patients with pre-existing mood disorders is clinically challenging due to overlapping symptoms, medication effects, and shared neurobiological mechanisms. Apathy, psychomotor slowing, and fatigue may mimic depressive symptoms, leading to delayed recognition of early parkinsonism. Development of an underlying neurodegenerative disorder could account for some treatment-resistant symptoms or treatment failures if not recognized. Therefore, the identification of PD will change the treatment and management plan significantly. Accurate diagnosis of PD requires a detailed neurologic examination focusing on bradykinesia, rigidity, and resting tremor, supported when appropriate by dopamine transporter imaging (DaT scan) or other emerging biomarkers. Understanding the temporal relationship between psychiatric and motor features helps differentiate prodromal PD from primary mood disorders. Management of patients with both mood disorders and PD integrates dopaminergic replacement therapy for motor symptoms with individualized treatment of psychiatric comorbidities. Levodopa remains the cornerstone for motor control, while dopamine agonists, MAO-B inhibitors, and COMT inhibitors can be added as needed. For depression and anxiety, SSRIs and SNRIs are first-line choices; quetiapine or clozapine are preferred when treatment for psychosis is necessary. Intentional, thoughtful polypharmacy is frequently required. Non-pharmacologic interventions—including cognitive behavioral therapy, structured exercise, and patient–caregiver education—enhance mood, function, and quality of life. Multidisciplinary collaboration between neurology, psychiatry, and allied health professionals is essential for optimal outcomes. This review offers guidance to healthcare providers as well as other interested parties involved in patients with mood disorders who may also be developing or have PD, especially to those who may have limited access to neurologic resources.

## Linked entities

- **Chemicals:** Levodopa (PubChem CID 6047), quetiapine (PubChem CID 5002), clozapine (PubChem CID 135398737)
- **Diseases:** Parkinson disease (MONDO:0005180)

## Full-text entities

- **Genes:** MAOB (monoamine oxidase B) [NCBI Gene 4129], SLC6A3 (solute carrier family 6 member 3) [NCBI Gene 6531] {aka DAT, DAT1, PKDYS, PKDYS1}, SNCA (synuclein alpha) [NCBI Gene 6622] {aka NACP, PARK1, PARK4, PD1}, COMT (catechol-O-methyltransferase) [NCBI Gene 1312] {aka HEL-S-98n}, HTR1A (5-hydroxytryptamine receptor 1A) [NCBI Gene 3350] {aka 5-HT-1A, 5-HT1A, 5HT1a, ADRB2RL1, ADRBRL1, G-21}
- **Diseases:** motor (MESH:D000068079), REM sleep behavior disorder (MESH:D020187), Parkinson and Movement Disorder (MESH:D009069), cognitive impairment (MESH:D003072), dopaminergic (MESH:D009422), QT prolongation (MESH:D008133), akinetic rigid (MESH:D009127), serotonergic dysfunction (MESH:D006331), Parkinsonism (MESH:D010302), constipation (MESH:D003248), bipolar (MESH:D001714), Depression (MESH:D003866), dyskinesias (MESH:D004409), impulse-control disorders (MESH:D007174), musculoskeletal (MESH:D009140), loss of dopaminergic neurons (MESH:D009410), essential tremor (MESH:D020329), hyposmia (MESH:D000086582), ischemic cerebrovascular lesions (MESH:D002561), psychosis (MESH:D011618), orthostatic hypotension (MESH:D007024), neuropsychiatric (MESH:C000631768), psychomotor agitation or retardation (MESH:D011595), Psychomotor slowing (MESH:D011596), bradykinesia (MESH:D018476), resting tremor (MESH:D014202), delusions (MESH:D063726), brain disorders (MESH:D001927), Symptoms (MESH:D012816), visual hallucinations (MESH:D006212), dystonic spasms (MESH:D013035), hip arthritis (MESH:D001168), BPAD (MESH:C564108), anxiety disorders (MESH:D001008), neuroimmune dysregulation (MESH:D021081), Dopaminergic deficits (MESH:D009461), pneumonia (MESH:D011014), neuropsychiatric effects (MESH:D065606), cardiac conduction abnormalities (MESH:D006327), fatigue (MESH:D005221), Palsy (MESH:D010243), falls (MESH:C537863), cardiac arrhythmias (MESH:D001145), nausea (MESH:D009325), Mood (MESH:D019964), gait dysfunction (MESH:D020233), neuroinflammation (MESH:D000090862), anxiety (MESH:D001007), insomnia (MESH:D007319), Alzheimer disease (MESH:D000544), Psychiatric symptoms (MESH:D001523), PD (MESH:D010300), choreiform movements (MESH:D002819), sleep disturbance (MESH:D012893), anhedonia (MESH:D059445), serotonin syndrome (MESH:D020230), loss (MESH:D016388), agranulocytosis (MESH:D000380), parkinsonian syndromes (MESH:D020734), Neurodegenerative disorders (MESH:D019636)
- **Chemicals:** quetiapine (MESH:D000069348), DaT (MESH:C028145), Dopamine (MESH:D004298), desipramine (MESH:D003891), benserazide (MESH:D001545), selegiline (MESH:D012642), rasagiline (MESH:C031967), fluoxetine (MESH:D005473), sertraline (MESH:D020280), valproate (MESH:D014635), pramipexole (MESH:D000077487), ropinirole (MESH:C046649), lamotrigine (MESH:D000077213), olanzapine (MESH:D000077152), Benzodiazepines (MESH:D001569), Levodopa (MESH:D007980), D2 antagonism (-), risperidone (MESH:D018967), nortriptyline (MESH:D009661), norepinephrine (MESH:D009638), Pimavanserin (MESH:C510793), lithium (MESH:D008094), Buspirone (MESH:D002065), venlafaxine (MESH:D000069470), paroxetine (MESH:D017374), citalopram (MESH:D015283), Bupropion (MESH:D016642), escitalopram (MESH:D000089983), Carbidopa (MESH:D002230), clonazepam (MESH:D002998), amantadine (MESH:D000547), clozapine (MESH:D003024), haloperidol (MESH:D006220)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## References

74 references — full list in the complete paper: https://tomesphere.com/paper/PMC12941259/full.md

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Source: https://tomesphere.com/paper/PMC12941259