Commentary, Jtsdt Vol: 13 Issue: 6

Parkinson's disease and Neuropsychiatric Sequelae: From Depression to Psychosis

Mei Ling Zhang^*

Psychopathology Research Centre, University of Hong Kong, Hong Kong

*Corresponding Author: Mei Ling Zhang
Psychopathology Research Centre, University of Hong Kong, Hong Kong
E-mail: mei.zhang@email.com

Received: 30-Nov-2024, Manuscript No. JTSDT-24-153726;
Editor assigned: 02-Dec-2024, PreQC No. JTSDT-24-153726 (PQ);
Reviewed: 13-Dec-2024, QC No. JTSDT-24-153726;
Revised: 16-Dec-2024, Manuscript No. JTSDT-24-153726(R);
Published: 22-Dec-2024, DOI:10.4172/2324-8947.100430

Citation: Zhang ML (2024) Parkinson’s disease and Neuropsychiatric Sequelae: From Depression to Psychosis. J Trauma Stress Disor Treat 13(6):430

Copyright: © 2024 Zhang ML. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution and reproduction in any medium, provided the original author and source are credited.

Introduction

Parkinson's disease (PD) is a progressive neurodegenerative disorder that primarily affects motor functions, such as tremors, bradykinesia, and rigidity, due to the degeneration of dopaminergic neurons in the substantia nigra. However, it is now recognized that PD affects more than just motor function. Neuropsychiatric sequelae, including depression, anxiety, cognitive impairment, and psychosis, are common in individuals with Parkinson’s disease and often cause significant distress, impair quality of life, and complicate disease management [1].

Depression is one of the most common neuropsychiatric disorders in Parkinson's disease, with an estimated 40-50% of PD patients experiencing significant depressive symptoms during the course of their illness. Depression in PD is not merely a reactive response to the physical challenges of the disease but is considered a core feature of Parkinson’s pathology. The pathophysiology of depression in PD involves complex interactions between neurochemical changes and brain circuitry affected by the disease. Dopaminergic, serotonergic, and noradrenergic deficits in brain regions such as the prefrontal cortex, limbic system, and basal ganglia are implicated in the development of depression [2].

The inflammation and oxidative stress associated with neurodegeneration in PD may also play a role in mood disorders by further disrupting neurotransmitter systems and impairing neuroplasticity. Depression in PD may present differently from typical major depressive disorder. PD patients often report a lack of motivation, energy, and pleasure (anhedonia), rather than overt sadness or low mood. Additionally, symptoms such as fatigue, sleep disturbances, and changes in appetite may overlap with the motor symptoms of PD, making diagnosis more challenging [3].

Managing depression in PD involves a combination of pharmacological and non-pharmacological interventions. Selective serotonin reuptake inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors (SNRIs) are commonly prescribed to alleviate depressive symptoms, though their efficacy may be limited by the neurochemical complexities of PD. Dopaminergic agents, such as pramipexole and ropinirole, can sometimes improve mood due to their effects on dopamine receptors. Psychotherapy, particularly cognitive-behavioral therapy (CBT), has shown promise in treating depression in PD, helping patients develop coping strategies and address negative thinking patterns [4].

Anxiety is another prevalent neuropsychiatric complication in PD, affecting approximately 25-40% of patients. Anxiety in PD may manifest as generalized anxiety disorder, panic attacks, or social phobia, and is often comorbid with depression. The neurobiological mechanisms underlying anxiety in PD involve disturbances in both dopaminergic and serotonergic systems. Dysregulation of the limbic system, particularly the amygdala, which is responsible for processing fear and emotional responses, may contribute to heightened anxiety in PD patients. Additionally, autonomic dysfunction—a common non-motor symptom of PD—can exacerbate anxiety by causing palpitations, sweating, and shortness of breath, mimicking panic attacks [5].

Anxiety can significantly impact the daily lives of PD patients, leading to avoidance of social situations, increased disability, and reduced participation in rehabilitation programs. Furthermore, anxiety can worsen motor symptoms, creating a vicious cycle where increased tremors or rigidity further heighten anxiety. Treatment options for anxiety in PD include both pharmacological and psychotherapeutic interventions. SSRIs and SNRIs are often used to manage anxiety, although their effects may vary. Benzodiazepines may be prescribed for short-term relief of acute anxiety symptoms, but they are used cautiously due to the risk of sedation and falls in PD patients [6].

Cognitive-behavioral therapy (CBT) and mindfulness-based therapies have been shown to be effective in reducing anxiety in PD by teaching patients relaxation techniques and helping them manage catastrophic thinking. Cognitive decline is a common feature of Parkinson’s disease, with many patients experiencing mild cognitive impairment (MCI) in the early stages of the disease, which may progress to Parkinson’s disease dementia (PDD) in the later stages. Cognitive impairments often involve deficits in executive function, attention, and visuospatial abilities [7].

Cognitive impairment in PD is thought to result from the widespread neurodegeneration that affects not only the dopaminergic system but also cholinergic, serotonergic, and noradrenergic pathways. The accumulation of alpha-synuclein protein aggregates (Lewy bodies) in cortical and subcortical regions further disrupts cognitive processing and contributes to the development of dementia. Additionally, vascular pathology and cerebral small vessel disease, which are common in elderly populations, may exacerbate cognitive decline in PD patients [8].

Cholinesterase inhibitors, such as rivastigmine, are commonly prescribed to manage cognitive symptoms in PD, particularly in patients with Parkinson’s disease dementia. These medications work by enhancing acetylcholine levels in the brain, improving attention and memory. However, their benefits are often modest, and more research is needed to develop effective treatments for cognitive decline in PD. Cognitive rehabilitation programs, which involve structured exercises to improve memory, attention, and problem-solving, may also help PD patients maintain cognitive function and improve daily living skills [9].

Psychosis is one of the most distressing neuropsychiatric sequelae in Parkinson’s disease, affecting up to 20-40% of patients, particularly in the later stages of the disease. Psychosis in PD often manifests as visual hallucinations, delusions, or paranoia. The exact mechanisms underlying psychosis in PD are not fully understood, but it is thought to involve an imbalance in dopaminergic and serotonergic neurotransmission. Antiparkinsonian medications, particularly dopamine agonists and levodopa, can exacerbate psychosis by increasing dopaminergic activity in areas of the brain associated with perception and reality testing [10].

Conclusion

Parkinson’s disease is a complex neurodegenerative disorder that extends far beyond its motor symptoms. Neuropsychiatric sequelae, including depression, anxiety, cognitive decline, and psychosis, are common in PD and significantly impact the quality of life of patients and their families. Early identification and treatment of these neuropsychiatric symptoms are essential to improving outcomes and supporting long-term care. By integrating pharmacological, psychological, and rehabilitative interventions, healthcare providers can offer a more holistic approach to managing these challenging symptoms and promoting better overall well-being in Parkinson’s disease patients.

References

1. Schrag A, Taddei RN (2017) Depression and anxiety in Parkinson's disease. Int Rev Neurobiol;133:623-55.

Indexed at, Google Scholar

2. Aarsland D, Marsh L, Schrag A (2009) Neuropsychiatric symptoms in Parkinson's disease;24(15):2175-86.

Indexed at, Google Scholar, Cross Ref

3. Hershey LA, Coleman-Jackson R (2019) Pharmacological management of dementia with Lewy bodies. Drug Aging;36:309-19.

Indexed at, Google Scholar, Cross Ref

4. Ravina B, Camicioli R, Como PG, Marsh L, Jankovic J (2007) The impact of depressive symptoms in early Parkinson disease. Neurology;69(4):342-7.

Indexed at, Google Scholar, Cross Ref

5. Protoc R. Consistency of neuropsychiatric syndromes across dementias: Results from the European Alzheimer Disease Consortium. Dement Geriatr Cogn Disord Cogn.11:231-9.

Indexed at, Google Scholar, Cross Ref

6. Santangelo G, Barone P, Cuoco S, Raimo S, Pezzella D (2014) Apathy in untreated, de novo patients with Parkinson’s disease: validation study of Apathy Evaluation Scale. J Neurol;261:2319-28.

Indexed at, Google Scholar, Cross Ref

7. Kalinderi K, Bostantjopoulou S, Fidani L (2016) The genetic background of Parkinson's disease: current progress and future prospects. Acta Neurologica Scandinavica;134(5):314-26.

Indexed at, Google Scholar, Cross Ref

8. Poewe W (2003) Psychosis in Parkinson's disease;18(S6):80-7.

Indexed at, Google Scholar, Cross Ref

9. Friedman JH, Factor SA (2000) Atypical antipsychotics in the treatment of drug-induced psychosis in Parkinson's disease;15(2):201-11.

Indexed at, Google Scholar, Cross Ref

10. Titova N, Chaudhuri KR (2018) Non-motor Parkinson disease: new concepts and personalised management. Med J Aust;208(9):404-9.

Indexed at, Google Scholar, Cross Ref