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  • Comprehensive Management of Parkinson’s Disease: Current Therapeutics, Risk Factors and Future Perspectives

  • 1 Department of Physiotherapy Vivekananda Global University India.

    2Department of Pharmaceutical Science University of Kashmir India.

Abstract

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by the degeneration of dopaminergic neurons in the substantia nigra pars compacta and the presence of intracellular inclusions known as Lewy bodies. The resulting dopamine deficiency in the basal ganglia leads to the classical motor symptoms of the disease, including tremor, rigidity, akinesia, and postural instability. Although the condition was first described by James Parkinson nearly two centuries ago, the exact etiology of the disease remains incompletely understood. Parkinson’s disease is primarily diagnosed clinically, though modern imaging techniques such as functional magnetic resonance imaging and nuclear imaging may assist in differentiating it from other parkinsonian disorders. Without treatment, the disease progresses gradually over several years, eventually leading to severe motor impairment and loss of independence. The management of Parkinson’s disease aims to improve patients’ quality of life through a combination of pharmacological, surgical, and supportive therapies. Pharmacological treatment includes drugs such as levodopa, dopamine agonists, monoamine oxidase-B inhibitors, anticholinergics, and other agents that enhance dopaminergic activity. In addition, multidisciplinary care involving physiotherapy, occupational therapy, speech therapy, and social support plays an essential role in disease management. Although current therapies significantly improve functional mobility and extend life expectancy, treatment remains primarily symptomatic, highlighting the need for continued research into more effective therapeutic strategies.

Keywords

Parkinson’s Disease, . progressive neurodegenerative disorder, Therapeutics, Risk Factors

Introduction

Parkinson's disease (PD) is a neurodegenerative ailment that begins with a loss of dopaminergic neurons in the substantia nigra and progresses throughout the central nervous system. Despites  the fact that James Parkinson's original report of "shaking palsy" was published nearly 200 years ago, there is still a dearth of understanding of the aetiology of Parkinson disease (1) Parkinson's disease remains a clinical diagnosis, characterized by cardinal motor symptoms such as akinesia, stiffness, and tremor. However, developments in various imaging techniques, such as functional magnetic resonance imaging or nuclear imaging techniques, provide further information, allowing a precise distinction from differential diagnosis, such as essential tremor or other parkinsonian disorder (2) There are many therapeutic methods available for the treatment of Parkinson's disease, including medications, surgical procedures, and physical therapies. They are not all equally available, and their true clinical value, as assessed by their impact on clinically relevant outcomes, is generally not demonstrated through high-quality, randomly and controlled clinical trials. In contrast, certain therapeutic methods have been thoroughly investigated in controlled clinical trials and appear to be underutilized (3) Underuse may be attributed to a lack of awareness of clinical data reported in medical literature. Furthermore, industry frequently establishes research projects on specific treatment interventions or procedures as part of the drug development process, rather than to address gaps in the available clinical evidence (4) The Movement Disorder Society (MDS) has commissioned an evidence-based evaluation of current pharmacological and specific non-pharmacological treatments frequently used to manage patients with Parkinson's disease (PD) in order to contribute to the practice of EBM. Clinical pharmacologists and specialists in clinical movement disorders formed a task group to achieve this goal (5) The pathological hallmark of Parkinson's disease is a loss of the pigmented dopaminergic neurones of the substantia nigra pars compacta in the brain, with the formation of intracellular inclusions known as Lewy bodies(6) In the early 1960s, researchers discovered an important challenge that is a hallmark of the disease, the loss of brain cells that make dopamine, a crucial neurotransmitter that's involved in muscular control. Normal ageing has been described by progressive loss of dopamine-containing neurons, the most people do not lose the 70% to 80% of dopaminergic neurones needed to cause symptomatic Parkinson's disease (7) Without treatment, Parkinson's disease advances over 5 to 10 years to a stiff, akinetic state in which the patients cannot care for themselves. Immobility-related consequences, such as aspiration pneumonia and pulmonary embolism, can cause death (8) Attempts to restore dopaminergic activity with levodopa and dopamine agonists have been successful in reducing many of the clinical symptoms of Parkinson’s disease (9) An alternate, but complimentary, strategy has been to use anticholinergic medicines to restore the proper balance of cholinergic and dopaminergic impacts on the basal ganglia. The recent development of efficient pharmacological treatment has dramatically transformed the future prospects of Parkinson's disease; in most cases, good functional mobility can be maintained for many years, and the life expectancy of effectively treated patients has been significantly extended (10)

Management of Parkinson Disease

Parkinson's disease management aims to enhance the quality of life for patients. Drug treatment is not the only option. In order to solve the many needs of patients and their families and other allied health professionals must be appropriately involved. Nurses, social workers, and occupational, physiotherapy, and speech therapy services will frequently play a significant role (11) Patients in various stages of the disease might require different medical therapy as well as additional choices from a multidisciplinary team that manages their condition (12) The main objective of medical intervention is to allow the patient to operate as much as possible normally whereas avoiding adverse consequences from treatment. The signs of early disease are often not problematic, and treatment is rarely required (13) The management of PD is complex and involves the treatment of both the motor and nonmotor aspects of the disease in early as well as advanced stages of the disease (14) However, it is crucial to emphasize that Parkinson's disease medication must be adjusted to each patient's specific needs. If the symptoms are mild, drugs such as monoamine oxidase inhibitors (e.g., selegiline, rasagiline, safinamide), dopamine agonists, and anticholinergic medications are frequently used in addition to nonpharmacological therapy (15) Levodopa medication is often given when symptoms become severe and interfere with everyday activities or working conditions. As the disease advances and motor disorders (such as motor fluctuations and dyskinesias) arise, surgical and experimental therapies should be considered (16) Although no effective neuroprotective medications have been discovered, several studies are currently in progress to identify possible disease-modifying therapies. Treatments to prevent or eliminate toxic α-synuclein include inosine, which raises urates, and isradipine, a calcium channel blocker, among others (17) Since these and other medicines are proven to reduce or prevent disease progression, an intensive exercise program is currently recommended as the best way for potentially affecting disease progression. In this sense, exercise and physical therapy, particularly resistance and endurance training, and other rigorous training modalities, have been found most useful (18) As a result, pharmacological treatment should begin with Monoamine Oxidase B inhibitors or dopamine agonists, followed by levodopa as soon as needed, especially in younger adults, where motor problems tend to arise earlier and more severe. The intermittent, nonphysiological pulsatile stimulation of dopaminergic receptors by oral levodopa is one of the processes that causes motor fluctuations and LID (19) When symptoms cannot be optimally alleviated by standard oral drugs, it is necessary to apply the techniques of continuous dopaminergic delivery by introducing the so-called advanced therapies or "device-aided treatments (20)

 

Table 1.

Drug class

Mechanism of Action

Side effects

Specific drugs

Daily therapeutic dose range

Frequency Dose

 

Anticholinergics

 

Block acetylcholine

Dry eyes, Urinary retention, glaucoma

Trihexyphenidyl benztropine

Ethopropazine

1-6mg

1-6mg

25-100mg

TID

TID

TID

 

Levodopa

Metabolism to dopamine in cell that contain dopamine decarboxylase

Nausea, dystonic and choreiform

Levodopa and carbidopa

100-2000mg/d as condition advances

TID

 

 

Amantadine

 

 

Blocks

NMDA receptors and acetylcholine receptors and promotes release of dopamine

Cognitive dysfunction, peripheral edema and skin rash

Amantadine

50-200mg

Monoamine Oxidase (MAO) inhibitors

Block MAO -B receptor to reduce dopamine metabolism

Nausea, sleep disorder and impaired cognition

Selegiline

1-10mg

BID

Catechol 0 methyltransferase (comt) Inhibitors

Block peripheral COMT activity to improve levodopa pharmacokinetics

Levodopa related side effect exacerbation, urine discoloration

Entacapone

200mg

It depend

Dopamine agonists

Directly stimulate dopamine receptor

Hypotension, psychosis and peripheral edema

Bromocriptine

Ropinirole

15-30mg

6-24mg

TID

 

RISK FACTORS

Herbicide use, working near industrial plants, and pesticide exposure are all causes of Parkinson's disease (21) According to two neurologists, influenza infection is the principal cause of Parkinson's disease, although according to other studies, influenza infection cannot develop or raise the risks of Parkinson disease (22) These are the some of the risk factors of Parkinson’s disease.

1. Cigarette smoking several research have focused on the inverse relationship between cigarette smoking and Parkinson's disease risk. In meta-analyses, smoking was safeguarding against Parkinson's disease, with pooled probability ratios ranging from 0.23 to 0.70 (23) An inverse correlation was reported between the number of cigarettes per day, the number of years of smoking, the number of pack-years and the risk for PD, as well as a correlation between the number of years since quitting and the risk for PD (24)

2. Fat and obesity its quickly increasing in the United States (25) and it is well known that obesity increases the risk of Parkinson's disease and reduces life expectancy. A study revealed that greater skinfold thickness in middle age was connected with Parkinson's disease (26) in addition, some evidence shows that body mass index is associated with a risk of Parkinson’s disease and the effect is graded and independent of other risk factors (27)

3. Age is a crucial determinant in the onset of dyskinetic movements. Patients who get Parkinson's disease at a younger age are more likely to develop dyskinesia, and they do so considerably earlier in the course of the disease. Younger age has been documented to be a risk factor both as the present age and the age of disease onset (28) Although epidemiologic evidence is limited, many additional risk variables have been proposed. Factors such as well water use, milk consumption, excess body weight, exposure to hydrocarbon solvents, living in rural or agricultural areas, exposure to copper, manganese, and lead, high iron intake, history of anaemia, and higher levels of education can all contribute to anaemia (29)

4. Environmental factors are considered significant contributors to Parkinson’s disease, particularly when combined with genetic susceptibility. Exposure to pesticides, herbicides, heavy metals, and industrial chemicals has been associated with an increased risk of developing the disease (30) Certain pesticides, such as paraquat and rotenone, have been shown to induce oxidative stress and mitochondrial dysfunction, which can damage dopaminergic neurons (31) These chemicals interfere with cellular respiration in neurons, leading to energy depletion and cell death. Agricultural workers and individuals living in rural environments may therefore have higher exposure to these substances (32) Exposure to heavy metals such as manganese and lead has also been linked to neurotoxicity and degeneration of dopaminergic neurons. These metals can accumulate in the brain and disrupt normal neuronal signaling (33) Long-term exposure to industrial solvents and environmental pollutants may further increase the risk of Parkinson’s disease by triggering inflammatory responses and neuronal damage.

5. Head Trauma traumatic brain injury (TBI) has been identified as a potential risk factor for Parkinson’s disease. Individuals who experience repeated or severe head injuries may have a higher likelihood of developing Parkinson’s disease later in life (34) Head trauma can cause damage to brain tissues, chronic inflammation, and disruption of normal neuronal function. Injury to the brain may also trigger the abnormal accumulation of proteins such as α-synuclein, which are implicated in Parkinson’s disease pathology (35) In addition, traumatic injury can damage dopaminergic neurons in the substantia nigra, leading to reduced dopamine production (36) Repeated head injuries, such as those seen in contact sports or accidents, may cause long-term neurodegenerative changes (37) Chronic inflammation and oxidative stress following traumatic injury may gradually contribute to neuronal degeneration and increase the risk of Parkinson’s disease (38)

 

FUTURE PERSPECTIVES

The paper highlights several areas that may influence the future management of Parkinson’s disease. One important direction involves the continued search for therapies capable of modifying disease progression. Although current treatments mainly focus on improving symptoms, ongoing studies are investigating potential neuroprotective strategies aimed at slowing neuronal degeneration. Research is currently exploring treatments that may reduce or eliminate toxic α-synuclein accumulation, which is believed to contribute to neuronal damage in Parkinson’s disease. Agents such as inosine, which increases urate levels, and isradipine, a calcium-channel blocker, have been investigated as potential therapeutic options that may influence disease progression. Another important perspective is the development of improved treatment strategies that provide more continuous dopaminergic stimulation. Traditional oral levodopa therapy may lead to motor complications such as motor fluctuations and levodopa-induced dyskinesia due to intermittent stimulation of dopamine receptors. Therefore, advanced therapeutic approaches involving continuous dopaminergic delivery and device-aided treatments are being considered when symptoms cannot be adequately controlled with conventional oral medications. In addition to pharmacological approaches, non-pharmacological strategies are also expected to play a growing role in future management. Regular exercise programs, physical therapy, resistance training, and endurance training have been suggested as beneficial interventions that may help maintain mobility and potentially influence disease progression. Overall, future management of Parkinson’s disease is expected to involve improved pharmacological therapies, advanced treatment technologies, and a stronger emphasis on multidisciplinary care to enhance patient outcomes.

CONCLUSIONS

Parkinson’s disease is a chronic and progressive neurological disorder that significantly affects motor function and overall quality of life. The disease is primarily associated with the loss of dopaminergic neurons in the substantia nigra, leading to dopamine deficiency and the development of characteristic motor symptoms. Although the exact cause of Parkinson’s disease remains unclear, several environmental and lifestyle factors have been associated with increased risk. The management of Parkinson’s disease requires a comprehensive and individualized approach aimed at improving functional ability and maintaining independence for as long as possible. Pharmacological therapies such as levodopa, dopamine agonists, monoamine oxidase-B inhibitors, and other medications remain the cornerstone of treatment, while surgical and advanced therapies may be considered in later stages of the disease. In addition, multidisciplinary care involving physiotherapy, occupational therapy, speech therapy, and social support is essential in addressing the diverse needs of patients. Despite considerable progress in treatment strategies, Parkinson’s disease remains incurable, and current therapies primarily focus on symptomatic relief. Continued research is therefore essential to improve understanding of the disease mechanisms and to develop more effective therapeutic approaches that may slow disease progression and further improve patient outcomes.

REFERENCES

  1. BraakHDel TrediciKRubUde VosRAJansen SteurENBraakEStaging of brain pathology related to sporadic Parkinson’s diseaseNeurobiol Aging200324219721112498954
  2. KaufmanMJMadrasBKSevere depletion of cocaine recognition sites associated with the dopamine transporter in Parkinson’s-diseased striatumSynapse19919143491796351
  3. Manyam BV. Ayurvedic approach to neurologic illness. In: Weintraub MI, ed. Alternative Medicine in Neurologic Illness. Philadelphia, Mosby: 2000 (in press).
  4. Lang AE, Blair RDG. Anitcholinergic drugs and amantadine in the treatment of Parkinson´s disease. In: Calne DB, ed. Handbook of experimental pharmacology, Vol. 88: Drugs for the Treatment of Parkinson´s Disease. Berlin Heidelberg: Springer-Verlag, 1989
  5. Feldburg W. Present views on the mode of action of acetylcholine in the central nervous system. Physiol Rev 1945;25:596-642.
  6. Lang AE, Lozano AM. Parkinson’s disease. First of two parts. N Engl J Med. 1998;339:1044–1053. doi: 10.1056/NEJM199810083391506.
  7. Braak H, Braak E. Pathology of Alzheimer’s disease. In: Calne DB, editor. Neurodegenerative Diseases. Philadelphia, PA: WB Saunders; 1994. pp. 585–614.
  8. National Parkinson Foundation About Parkinson disease: Who gets Parkinson’s disease? April 2008. Available at: www.parkinson.org/netcommunity/page.aspx?pid=225&srcid=201
  9. Albin RL. Parkinson’s disease: Background, diagnosis, and initial management. Clin Geriatr Med. 2006;22:735–751. doi: 10.1016/j.cger.2006.06.003.
  10. Bower JH, Maraganore DM, McDonnell SK, et al. Incidence and distribution of parkinsonism in Olmsted County, Minnesota, 1976–1990. Neurology. 1999:1214–1220. doi: 10.1212/wnl.52.6.1214.
  11. Mouradian MM. Recent advances in the genetics and pathogenesis of Parkinson’s disease. Neurology 2002;58:179-85.
  12. Miyasaki JM, Martin WRW, Suchowersky O, Weiner WJ, Lang AE. Practice parameter: initiation of treatment for Parkinson’s disease: an evidence based review. Neurology 2002;58:11-7
  13. Rascol O, Brooks DJ, Korczyn A, De Deyn PP, Clarke CE, Lang AE. A five-year study of the incidence of dyskinesia in patients with early Parkinson’s disease who were treated with ropinirole or levodopa. N Engl J Med 2000;342:1484-91
  14. Löhle M., Ramberg C.-J., Reichmann H., and Schapira A. H. V., Early versus delayed initiation of pharmacotherapy in Parkinson’s disease, Drugs. (2014) 74, no. 6, 645–657, https://doi.org/10.1007/s40265-014-0209-5, 2-s2.0-84899887840.
  15. Hughes AJ, Daniel SE, Kilford L, Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico-pathological study of 100 cases. J Neurol Neurosurg Psychiatry 1992;55(3):181-4.
  16. Verhagen Metman L, Del Dotto P, van den Munchkhof P, Fang J, Mouradian MM, Chase TN. Amantadine as treatment for dyskinesias and motor fluctuations in Parkinson’s disease. Neurology 1998;50:1323-6.
  17. Warren Olanow C., Kieburtz K., Rascol O. et al., Factors predictive of the development of Levodopa-induced dyskinesia and wearing-off in Parkinson’s disease, Movement Disorders. (2013) 28, no. 8, 1064–1071, https://doi.org/10.1002/mds.25364, 2-s2.0-84881558752.
  18. Chase T. N., Striatal plasticity and extrapyramidal motor dysfunction, Parkinsonism & Related Disorders. (2004) 10, no. 5, 305–313, https://doi.org/10.1016/j.parkreldis.2004.02.012, 2-s2.0-2942541214.
  19. Nutt J. G., Continuous dopaminergic stimulation: is it the answer to the motor complications of Levodopa?, Movement Disorders. (2007) 22, no. 1, 1–9, https://doi.org/10.1002/mds.21060, 2-s2.0-33847744193.
  20. Fox S. H., Katzenschlager R., Lim S.-Y. et al., International Parkinson and movement disorder society evidence-based medicine review: update on treatments for the motor symptoms of Parkinson’s disease, Movement Disorders. (2018) 33, no. 8, 1248–1266, https://doi.org/10.1002/mds.27372, 2-s2.0-85044254104.
  21. Herbicide use, working near industrial plants, and pesticide exposure are all causes of Parkinson's disease.
  22. Estupinan, D., Nathoo, S., and Okun, M. S. (2013). The demise of Poskanzer and Schwab’s influenza theory on the pathogenesis of Parkinson’s disease. Parkinsons Dis. 2013:167843. doi:10.1155/2013/167843

(PDF) Parkinson Disease: A Review. Available from: https://www.researchgate.net/publication/376096793_Parkinson_Disease_A_Review [accessed Mar 08 2026].

  1. R.E. Strowd et al. Association between subthalamic nucleus deep brain stimulation and weight gain: results of a case-control study Clin Neurol Neurosurg (2016)
  2. P. Ibáñez et al. Causal relation between α-synuclein locus duplication as a cause of familial Parkinson's disease Lancet (2004)
  3. Mokdad A. H., Serdula M. K., Dietz W. H., Bowman B. A., Marks J. S., and Koplan J. P., The spread of the obesity epidemic in the United States, 1991–1998, Journal of the American Medical Association. (1999) 282, no. 16, 1519–1522, 2-s2.0-0032697493, https://doi.org/10.1001/jama.282.16.1519.
  4. Abbott R. D., Ross G. W., White L. R., Nelson J. S., Masaki K. H., Tanner C. M., Curb J. D., Blanchette P. L., Popper J. S., and Petrovitch H., Midlife adiposity and the future risk of Parkinson′s disease, Neurology. (2002) 59, no. 7, 1051–1057, 2-s2.0-0037044236.
  5. Hu G., Jousilahti P., Nissinen A., Antikainen R., Kivipelto M., and Tuomilehto J., Body mass index and the risk of Parkinson disease, Neurology. (2006) 67, no. 11, 1955–1959, 2-s2.0-33845700948, https://doi.org/10.1212/01.wnl.0000247052.18422.e5.
  6. J.J. Lin Genetic polymorphism of the angiotensin converting enzyme and l-dopa-induced adverse effects in Parkinson’s disease J Neurol Sci (2007)
  7. Jankovic J, H Hurtig, J Dashe: Etiology and pathogenesis of Parkinson Disease. UpToDate. Retrieved on 7/22/2013 from www.uptodate.com. (2013)
  8. Andrew J. Lees, John Hardy, Thomas Revesz. Lees AJ, Hardy J, Revesz T. Parkinson’s disease. Lancet. 2009;373(9680):2055–2066.
  9. C. Warren Olanow, Anthony H. V. Schapira. Olanow CW, Schapira AHV. Therapeutic prospects for Parkinson disease. Annals of Neurology. 2013;74(3):337–347.
  10. Joseph Jankovic. Jankovic J. Parkinson’s disease: clinical features and diagnosis. Journal of Neurology, Neurosurgery & Psychiatry. 2008;79(4):368–376.
  11. Heinz Reichmann. Reichmann H. Clinical criteria for the diagnosis of Parkinson’s disease. Neurodegenerative Diseases. 2010;7(5):284–290.
  12. Anthony E. Lang, Connie Marras. Lang AE, Lozano AM. Parkinson’s disease. New England Journal of Medicine. 1998;339(15):1044–1053.
  13. J. William Langston. Langston JW. The Parkinson’s complex: Parkinsonism is just the tip of the iceberg. Annals of Neurology. 2006;59(4):591–596.
  14. Caroline M. Tanner. Tanner CM, Goldman SM. Epidemiology of Parkinson’s disease. Neurologic Clinics. 1996;14(2):317–335.
  15. Stanley Fahn, Joseph Jankovic. Fahn S, Jankovic J, Hallett M. Principles and Practice of Movement Disorders. 2nd ed. Elsevier; 2011.

Reference

  1. BraakHDel TrediciKRubUde VosRAJansen SteurENBraakEStaging of brain pathology related to sporadic Parkinson’s diseaseNeurobiol Aging200324219721112498954
  2. KaufmanMJMadrasBKSevere depletion of cocaine recognition sites associated with the dopamine transporter in Parkinson’s-diseased striatumSynapse19919143491796351
  3. Manyam BV. Ayurvedic approach to neurologic illness. In: Weintraub MI, ed. Alternative Medicine in Neurologic Illness. Philadelphia, Mosby: 2000 (in press).
  4. Lang AE, Blair RDG. Anitcholinergic drugs and amantadine in the treatment of Parkinson´s disease. In: Calne DB, ed. Handbook of experimental pharmacology, Vol. 88: Drugs for the Treatment of Parkinson´s Disease. Berlin Heidelberg: Springer-Verlag, 1989
  5. Feldburg W. Present views on the mode of action of acetylcholine in the central nervous system. Physiol Rev 1945;25:596-642.
  6. Lang AE, Lozano AM. Parkinson’s disease. First of two parts. N Engl J Med. 1998;339:1044–1053. doi: 10.1056/NEJM199810083391506.
  7. Braak H, Braak E. Pathology of Alzheimer’s disease. In: Calne DB, editor. Neurodegenerative Diseases. Philadelphia, PA: WB Saunders; 1994. pp. 585–614.
  8. National Parkinson Foundation About Parkinson disease: Who gets Parkinson’s disease? April 2008. Available at: www.parkinson.org/netcommunity/page.aspx?pid=225&srcid=201
  9. Albin RL. Parkinson’s disease: Background, diagnosis, and initial management. Clin Geriatr Med. 2006;22:735–751. doi: 10.1016/j.cger.2006.06.003.
  10. Bower JH, Maraganore DM, McDonnell SK, et al. Incidence and distribution of parkinsonism in Olmsted County, Minnesota, 1976–1990. Neurology. 1999:1214–1220. doi: 10.1212/wnl.52.6.1214.
  11. Mouradian MM. Recent advances in the genetics and pathogenesis of Parkinson’s disease. Neurology 2002;58:179-85.
  12. Miyasaki JM, Martin WRW, Suchowersky O, Weiner WJ, Lang AE. Practice parameter: initiation of treatment for Parkinson’s disease: an evidence based review. Neurology 2002;58:11-7
  13. Rascol O, Brooks DJ, Korczyn A, De Deyn PP, Clarke CE, Lang AE. A five-year study of the incidence of dyskinesia in patients with early Parkinson’s disease who were treated with ropinirole or levodopa. N Engl J Med 2000;342:1484-91
  14. Löhle M., Ramberg C.-J., Reichmann H., and Schapira A. H. V., Early versus delayed initiation of pharmacotherapy in Parkinson’s disease, Drugs. (2014) 74, no. 6, 645–657, https://doi.org/10.1007/s40265-014-0209-5, 2-s2.0-84899887840.
  15. Hughes AJ, Daniel SE, Kilford L, Lees AJ. Accuracy of clinical diagnosis of idiopathic Parkinson's disease: a clinico-pathological study of 100 cases. J Neurol Neurosurg Psychiatry 1992;55(3):181-4.
  16. Verhagen Metman L, Del Dotto P, van den Munchkhof P, Fang J, Mouradian MM, Chase TN. Amantadine as treatment for dyskinesias and motor fluctuations in Parkinson’s disease. Neurology 1998;50:1323-6.
  17. Warren Olanow C., Kieburtz K., Rascol O. et al., Factors predictive of the development of Levodopa-induced dyskinesia and wearing-off in Parkinson’s disease, Movement Disorders. (2013) 28, no. 8, 1064–1071, https://doi.org/10.1002/mds.25364, 2-s2.0-84881558752.
  18. Chase T. N., Striatal plasticity and extrapyramidal motor dysfunction, Parkinsonism & Related Disorders. (2004) 10, no. 5, 305–313, https://doi.org/10.1016/j.parkreldis.2004.02.012, 2-s2.0-2942541214.
  19. Nutt J. G., Continuous dopaminergic stimulation: is it the answer to the motor complications of Levodopa?, Movement Disorders. (2007) 22, no. 1, 1–9, https://doi.org/10.1002/mds.21060, 2-s2.0-33847744193.
  20. Fox S. H., Katzenschlager R., Lim S.-Y. et al., International Parkinson and movement disorder society evidence-based medicine review: update on treatments for the motor symptoms of Parkinson’s disease, Movement Disorders. (2018) 33, no. 8, 1248–1266, https://doi.org/10.1002/mds.27372, 2-s2.0-85044254104.
  21. Herbicide use, working near industrial plants, and pesticide exposure are all causes of Parkinson's disease.
  22. Estupinan, D., Nathoo, S., and Okun, M. S. (2013). The demise of Poskanzer and Schwab’s influenza theory on the pathogenesis of Parkinson’s disease. Parkinsons Dis. 2013:167843. doi:10.1155/2013/167843

(PDF) Parkinson Disease: A Review. Available from: https://www.researchgate.net/publication/376096793_Parkinson_Disease_A_Review [accessed Mar 08 2026].

  1. R.E. Strowd et al. Association between subthalamic nucleus deep brain stimulation and weight gain: results of a case-control study Clin Neurol Neurosurg (2016)
  2. P. Ibáñez et al. Causal relation between α-synuclein locus duplication as a cause of familial Parkinson's disease Lancet (2004)
  3. Mokdad A. H., Serdula M. K., Dietz W. H., Bowman B. A., Marks J. S., and Koplan J. P., The spread of the obesity epidemic in the United States, 1991–1998, Journal of the American Medical Association. (1999) 282, no. 16, 1519–1522, 2-s2.0-0032697493, https://doi.org/10.1001/jama.282.16.1519.
  4. Abbott R. D., Ross G. W., White L. R., Nelson J. S., Masaki K. H., Tanner C. M., Curb J. D., Blanchette P. L., Popper J. S., and Petrovitch H., Midlife adiposity and the future risk of Parkinson′s disease, Neurology. (2002) 59, no. 7, 1051–1057, 2-s2.0-0037044236.
  5. Hu G., Jousilahti P., Nissinen A., Antikainen R., Kivipelto M., and Tuomilehto J., Body mass index and the risk of Parkinson disease, Neurology. (2006) 67, no. 11, 1955–1959, 2-s2.0-33845700948, https://doi.org/10.1212/01.wnl.0000247052.18422.e5.
  6. J.J. Lin Genetic polymorphism of the angiotensin converting enzyme and l-dopa-induced adverse effects in Parkinson’s disease J Neurol Sci (2007)
  7. Jankovic J, H Hurtig, J Dashe: Etiology and pathogenesis of Parkinson Disease. UpToDate. Retrieved on 7/22/2013 from www.uptodate.com. (2013)
  8. Andrew J. Lees, John Hardy, Thomas Revesz. Lees AJ, Hardy J, Revesz T. Parkinson’s disease. Lancet. 2009;373(9680):2055–2066.
  9. C. Warren Olanow, Anthony H. V. Schapira. Olanow CW, Schapira AHV. Therapeutic prospects for Parkinson disease. Annals of Neurology. 2013;74(3):337–347.
  10. Joseph Jankovic. Jankovic J. Parkinson’s disease: clinical features and diagnosis. Journal of Neurology, Neurosurgery & Psychiatry. 2008;79(4):368–376.
  11. Heinz Reichmann. Reichmann H. Clinical criteria for the diagnosis of Parkinson’s disease. Neurodegenerative Diseases. 2010;7(5):284–290.
  12. Anthony E. Lang, Connie Marras. Lang AE, Lozano AM. Parkinson’s disease. New England Journal of Medicine. 1998;339(15):1044–1053.
  13. J. William Langston. Langston JW. The Parkinson’s complex: Parkinsonism is just the tip of the iceberg. Annals of Neurology. 2006;59(4):591–596.
  14. Caroline M. Tanner. Tanner CM, Goldman SM. Epidemiology of Parkinson’s disease. Neurologic Clinics. 1996;14(2):317–335.
  15. Stanley Fahn, Joseph Jankovic. Fahn S, Jankovic J, Hallett M. Principles and Practice of Movement Disorders. 2nd ed. Elsevier; 2011.

Photo
Mohammed Maina Jawa
Corresponding author

Department of Physiotherapy Vivekananda Global University India

Photo
Alhaji Kolo Shettima
Co-author

Department of Pharmaceutical Science University of Kashmir India

Mohammed Maina Jawa, Alhaji Kolo Shettima, Comprehensive Management of Parkinson’s Disease: Current Therapeutics, Risk Factors and Future Perspectives, Int. J. of Pharm. Sci., 2026, Vol 4, Issue 4, 2086-2252, https://doi.org/10.5281/zenodo.19589809

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