EC Neurology

Mini Review Volume 13 Issue 6 - 2021

Parkinson’s Disease, the Rationale to Start Treatment Early, Start Low and Go Slow

Roy G Beran1,2,3 *

1Conjoint Professor, South Western Clinical School, University of New South Wales, Sydney, NSW, Australia
2Professor, Medical School, Griffith University, Broadbeach, Qld, Australia
3 Professor, Chair, Medical Law, Sechenov, Moscow First State University, Moscow, Russia

*Corresponding Author: Roy G Beran, Conjoint Professor, South Western Clinical School, University of New South Wales, Sydney, PO Box 598, Northbridge, NSW 1560, Australia.
Received: April 11, 2021; Published: May 27, 2021



Introduction: Parkinson’s disease (PD) is the second most common neurodegenerative disease. Idiopathic PD may be more preva- lent with the suggestion that PD is part of the natural progression of aging.

Background Information: The diagnosis of PD is a clinical diagnosis with no absolutely reliable, antemortem, objective test for diagnosis which remains reliant on the cardinal features of bradykinesia, rigidity and resting tremor with a basic requirement of at least two out of these three features. The neurones involved in PD are the same as those involved during aging. Progression of PD is more dependent upon advancing age, rather than duration, with the hall mark features of PD being significantly increased with age.

DiscussionThe interchange of PD with aging led to an alternative approach to the management reliant on early initiation of L dopa, once PD is clinically evident, starting very low and going very slow. This was subjected to an audit confirming efficacy when com- pared to current regimen.

ConclusionThere is justification for the hypothesis that idiopathic PD represents aging, rather than a true pathophysiological dis- ease, and very early introduction of dopamine replacement and supplementation, starting low and going slow is a viable alternative.

Keywords: Parkinson’s Disease; Treatment, Pathophysiology, Neuro Degeneration, Aging

  1. Blaszczyk JW. “Parkinson’s Disease and Neurodegeneration: GABA-Collapse Hypothesis”. Frontiers in Neuroscience (2016).
  2. Salari M., et al. “Demographic features and clinical characteristics of patients with Parkinson’s disease in Isfahan”. Iranian Journal of Neurology 17.1 (2018): 6-10.
  3. Hague SM., et al. “Neurodegenerative disorders: Parkinson’s disease and Huntington’s disease”. Journal of Neurology, Neurosurgery, and Psychiatry 76 (2005): 1058-1063.
  4. Fahn S and Sulzer D. “Neurodegeneration and Neuroprotection in Parkinson Disease”. Neuro Rx 1.1 (2004): 139-154.
  5. Mehta P., et al. “Population prevalence and incidence of Parkinson’s disease in an Australian community”. Journal of Internal Medicine 37.12 (2007): 812-814.
  6. Beran RG. “Is Parkinson’s Disease truly a disease or simply an indication of a long life” (Short Communication)”. Neuro Neurosurg 4 (2020): 1-2.
  7. Galvan A and Wickmann T. “Pathophysiology of Parkinsonism”. Clinical Neurophysiology 119.7 (2008): 1459-1474.
  8. Fahn S. “Description of Parkinson’s Disease as a Clinical Syndrome in Parkinson’s Disease the Life Cycle of the Dopamine Neuron”. Eds Howard J. Federoff HJ, Burke R E, Fahn S, and Fiskum G. The New York Academy of Sciences New York, New York (2003): 1-14.
  9. Parkinson J. “An Essay on the Shaking Palsy. Sherwood, Neely, and Jones”. London (1817).
  10. Mulhearn RJ. “The history of James Parkinson and his disease”. Australian and New Zealand Journal of Medicine 1 (1971): 1-6.
  11. Postuma RB., et al. “The new definition and diagnostic criteria of Parkinson’s Disease”. Lancet Neurology 15 (2016): 546-548.
  12. Marsili L., et al. “Diagnostic Criteria for Parkinson’s Disease: From James Parkinson to the Concept of Prodromal Disease”. Frontiers in Neurology 9 (2018): 156.
  13. Postuma RB., et al. “MDS Clinical Diagnostic Criteria for Parkinson’s Disease”. Movement Disorders 30 (2015): 1591-1601.
  14. Vreeling FW., et al. “Primitive reflexes in Parkinson’s Disease”. Journal of Neurology, Neurosurgery, and Psychiatry 56 (1993): 1323-1326.
  15. Galvan A and Wickmann T. “Pathophysiology of Parkinsonism”. Clinical Neurophysiology 119 (2008): 1459-1474.
  16. Rodriguez M., et al. “The degeneration and replacement of dopamine cells in Parkinson’s Disease: The role of aging”. Frontiers in Neuroanatomy 8 (2014): 80.
  17. Rodriguez M., et al. “Parkinson’s Disease as a result of aging”. Aging Cell 14 (2015): 293-308.
  18. Levy G. “The relationship of Parkinson’s Disease with aging”. Archives of Neurology 64 (2007): 1242-1246.
  19. Buchanan AS., et al. “Parkinsonism in older adults and its association with adverse health outcomes and neuropathology”. Journal of Gerontology, Series A: Biological Sciences and Medical 71 (2016): 549-556.
  20. Beran RG. “Parkinson’s Disease in Neurology for General Practitioners”. Ed Beran RG Churchill Livingstone/Elsevier, Sydney (2012): 81-94.
  21. Chow-Chuen J and Beran RG. “An independent clinical audit of an alternative treatment paradigm for the management of Parkinson’s Disease”. Journal Profile Neurology Research International 2 (2019): 180008.

Roy G Beran. “Parkinson’s Disease, the Rationale to Start Treatment Early, Start Low and Go Slow”. EC Neurology - 13.6 (2021): 65-68.

ECronicon Journal

Our Services

Quick Links

Information

Creative Commons LicenseOpen Access by ECronicon is licensed under a Creative Commons Attribution 4.0 International License
Based on a work at www.ecronicon.net