Should treatment of Parkinson's disease be started with a dopamine agonist?

Which drugs to use when initiating pharmacotherapy in early Parkinson's disease (PD) is a complex treatment decision that depends on factors such as disease severity, functional disability, and psychosocial handicap, as well as individual aspects of age, employment status, cognitive impairment, and co-morbidity. Without clear proof of a drug's capacity to markedly alter or even stop progression of the disease, there is no pharmacologic strategy that can be currently viewed as universal first-line treatment. Dopamine (DA) replacement strategies offer greatest symptomatic relief and are needed whenever there is significant functional disability. All currently available oral DA agonists have been shown to be less effective and less well tolerated than levodopa. This has also been shown in recent double-blind controlled studies for the novel agonists such as ropinirole or cabergoline, although they appear equally effective in mild disease for the first 6-12 months of therapy. Taking into account the significant difference in cost between levodopa and DA agonists, there is at present no reason to universally start DA replacement therapy with a DA agonist in most patients. Dopamine agonists remain first-line treatment only for those at particular risk for developing levodopa-induced dyskinesias, i.e., young-onset PD patients.

[1]  A. Björklund,et al.  Short-Term GDNF Treatment Provides Long-Term Rescue of Lesioned Nigral Dopaminergic Neurons in a Rat Model of Parkinson’s Disease , 1996, The Journal of Neuroscience.

[2]  F. Hefti,et al.  Toxicity of 6‐hydroxydopamine and dopamine for dopaminergic neurons in culture , 1990, Journal of neuroscience research.

[3]  P. Löschmann,et al.  Protection of substantia nigra from MPP+ neurotoxicity by N-methyl-D-aspartate antagonists , 1991, Nature.

[4]  Bromocriptine in Parkinson's disease: a double-blind study comparing "low-slow" and "high-fast" introductory dosage regimens in de novo patients. UK Bromocriptine Research Group. , 1989, Journal of neurology, neurosurgery, and psychiatry.

[5]  M. Mena,et al.  Glia conditioned medium protects fetal rat midbrain neurones in culture from L‐DOPA toxicity , 1996, Neuroreport.

[6]  L. Carr,et al.  NF-Y activates mouse tryptophan hydroxylase transcription , 1995, Brain Research.

[7]  C. Clarke Does levodopa therapy delay death in Parkinson's disease? A review of the evidence , 1995, Movement disorders : official journal of the Movement Disorder Society.

[8]  S. Kaveri,et al.  Immunomodulating effects of intravenous immunoglobulin in autoimmune and inflammatory diseases. , 1994, Journal of neurology, neurosurgery, and psychiatry.

[9]  J. Guérit Movement disorders. Neurologic Principles and Practice, R.L. Watts, W.C. Koller. McGraw Hill, New York (1997), 780 , 1999 .

[10]  C. Nienaber,et al.  The diagnosis of thoracic aortic dissection by noninvasive imaging procedures. , 1993, The New England journal of medicine.

[11]  H. M. Geller,et al.  l‐DOPA Cytotoxicity to PC12 Cells in Culture Is via Its Autoxidation , 1995, Journal of neurochemistry.

[12]  W. Koller Selegiline monotherapy in the treatment of Parkinson's disease , 1996, Neurology.

[13]  Y. Agid,et al.  Absence of neurotoxicity of chronic L‐DOPA in 6‐hydroxydopaminelesioned rats , 1997, Neuroreport.

[14]  M. Kohno,et al.  Bromocriptine protects mice against 6-hydroxydopamine and scavenges hydroxyl free radicals in vitro , 1994, Brain Research.

[15]  M. Laga Interactions between STDs and HIV infection. , 1992, STD bulletin.

[16]  David L. Felten,et al.  Chronic dietary pergolide preserves nigrostriatal neuronal integrity in aged-Fischer-344 rats , 1992, Neurobiology of Aging.

[17]  C. Marsden,et al.  Preservation of the substantia nigra and locus coeruleus in a patient receiving levodopa (2 kg) plus decarboxylase inhibitor over a four-year period. , 1986, Movement disorders : official journal of the Movement Disorder Society.

[18]  M. Mena,et al.  Toxic effects of L-DOPA on mesencephalic cell cultures: protection with antioxidants , 1995, Brain Research.

[19]  S. Bloom,et al.  Searching for gastrinomas. , 1993, BMJ.

[20]  I. Ziv,et al.  Dopamine-induced, genotoxic activation of programmed cell death. A role in nigrostriatal neuronal degeneration in Parkinson's disease? , 1996, Advances in neurology.

[21]  M. Brin,et al.  Effects of tocopherol and deprenyl on the progression of disability in early Parkinson's disease. , 1993, The New England journal of medicine.

[22]  C. Marsden,et al.  Cabergoline in the treatment of early parkinson's disease , 1997, Neurology.

[23]  K. Hodges Census 2000 planning. , 1993, Applied demography.

[24]  J. Bhawan,et al.  Chronic dopa feeding of mice , 1982, Neurology.

[25]  Richard S. J. Frackowiak,et al.  Evidence for long‐term survival and function of dopaminergic grafts in progressive Parkinson's disease , 1994, Annals of neurology.

[26]  K. Steece-Collier,et al.  The detrimental effect of levodopa on behavioral efficacy of fetal dopamine neuron grafts in rats is reversible following prolonged withdrawal of chronic dosing , 1995, Brain Research.

[27]  M. Hallett,et al.  Clinical research criteria for the diagnosis of progressive supranuclear palsy (Steele-Richardson-Olszewski syndrome) , 1996, Neurology.

[28]  P. Jenner,et al.  Suppressive effect of L‐dopa on dopamine cells remaining in the ventral tegmental area of rats previously exposed to the neurotoxin 6‐hydroxydopamine , 1993, Movement disorders : official journal of the Movement Disorder Society.

[29]  P R Sanberg,et al.  Neuropathological evidence of graft survival and striatal reinnervation after the transplantation of fetal mesencephalic tissue in a patient with Parkinson's disease. , 1995, The New England journal of medicine.

[30]  S. Mukherji International migration in India: levels, trends and policy implications. , 1994, IIPS newsletter.

[31]  O. Rascol,et al.  Ropinirole in the treatment of early Parkinson's disease: A 6‐month interim report of a 5‐year levodopa‐controlled study , 1998, Movement disorders : official journal of the Movement Disorder Society.

[32]  A. Rascol,et al.  Early treatment with a combination of bromocriptine and levodopa compared with levodopa monotherapy in the treatment of Parkinson's disease , 1989 .

[33]  R. Nemni,et al.  Evidence of peripheral axonal neuropathy in primary restless legs syndrome , 1995, Movement disorders : official journal of the Movement Disorder Society.

[34]  Björn Gustavii,et al.  Short‐ and long‐term survival and function of unilateral intrastriatal dopaminergic grafts in Parkinson's disease , 1997, Annals of neurology.

[35]  S. Fahn,et al.  Antiparkinsonian therapies and brain mitochondrial complex I activity , 1995, Movement disorders : official journal of the Movement Disorder Society.