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February 26, 2013; 80 (9) Editorial

Dopaminergic treatment and nonmotor features of Parkinson disease

The horse lives

Angelo Antonini, Roger L. Albin
First published January 30, 2013, DOI: https://doi.org/10.1212/WNL.0b013e318285c16d
Angelo Antonini
From the Department for Parkinson's Disease (A.A.), IRCCS San Camillo, Venice, Italy; Department of Neurology (R.L.A.), University of Michigan, Ann Arbor; and Geriatrics Research, Education, and Clinical Center (R.L.A.), VAAAHS, Ann Arbor, MI.
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Roger L. Albin
From the Department for Parkinson's Disease (A.A.), IRCCS San Camillo, Venice, Italy; Department of Neurology (R.L.A.), University of Michigan, Ann Arbor; and Geriatrics Research, Education, and Clinical Center (R.L.A.), VAAAHS, Ann Arbor, MI.
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Dopaminergic treatment and nonmotor features of Parkinson disease
The horse lives
Angelo Antonini, Roger L. Albin
Neurology Feb 2013, 80 (9) 784-785; DOI: 10.1212/WNL.0b013e318285c16d

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Several years ago, Eric Ahlskog published a colorful and cogent review entitled “Beating a dead horse.” He argued that “we have reached the point of diminishing therapeutic returns with drugs acting on dopamine systems and more dopaminergic medications will provide only modest incremental benefit over current therapies.”1 Ahlskog argued correctly that excessive focus on dopaminergic features and pathology led to neglect of crucial nondopaminergic/nonmotor clinical features and pathologies. This argument was based, in part, on the perception that most of the nonmotor symptoms (NMS) in Parkinson disease (PD) would be related to degeneration in nondopamine responsive systems and that improvements in dopaminergic therapy would have little impact on NMS. Accumulated evidence now indicates the need to modify this concept.

As Ahlskog suggested, several subsequent studies substantiate the great functional burden related to NMS, their progression, and negative effect on quality of life in PD.2 Additional evidence indicates interesting relationships between striatal dopaminergic function and NMS. The basal ganglia are implicated in the modulation and integration of sensory information and pain; bladder function is under control of both inhibitory (D1) and facilitatory (D2) dopaminergic inputs; and reduced dopaminergic activity in the mesocortical and mesolimbic pathways is involved in the development of several NMS including mood, motivational, and cognitive alterations.3

These data are further supported by clinical pharmacologic studies. Some NMS fluctuate in response to dopaminergic treatment and are relieved by dopamine replacement therapy.4 Intraduodenal infusion of levodopa produces beneficial effects in 6 of the 9 domains of an NMS scale: cardiovascular, sleep/fatigue, attention/memory, gastrointestinal, urinary, and sexual function.5 Oral and transdermal dopamine agonist therapy produces significant improvements in depression6 and sleep disorders,7 highlighting the importance of studies designed to specifically address NMS features.

In this issue of Neurology®, Storch et al.8 report results of a large survey in 100 patients with fluctuating PD using a structured examination and visual analogue scales to quantify NMS. Their major findings are that some NMS are associated with motor fluctuations while others are not. Depression and anxiety are more prone to fluctuate while other symptoms appeared to be relatively unaffected by the motor state. These results are concordant with the modest prior literature and general clinical experience. Storch et al. thoughtfully evaluated NMS in both structured interviews and home-based ratings diaries. Results were similar for both the home ratings and the structured interview. Another interesting observation was that there was little correlation between several disease features and NMS frequency patterns.

These results point to complicated relationships between residual striatal dopaminergic function, dopaminergic replacement therapies, extra-nigrostriatal pathologies, and NMS. These results also indicate considerable heterogeneity of patients with PD with respect to NMS and motor fluctuations. Storch et al. are to be commended for undertaking this demanding study and their methods are very likely to be useful in future studies of this important topic.

This and prior work suggest that optimizing dopaminergic therapies is a viable avenue to improve control of some disabling NMS in PD and a worthwhile area for further clinical research. Improving consistency of delivery of dopaminergic therapies and targeting NMS specifically in well-designed studies may yield incremental but important improvements in quality of life for patients with PD. These kinds of experiments may also cast light on interesting biology related to striatal dopaminergic functions and other brain systems. The horse lives.

STUDY FUNDING

No targeted funding reported.

DISCLOSURE

A. Antonini has received honoraria for consulting services and symposia from Abbott, Boehringer Ingelheim, GSK, Lundbeck, UCB, Novartis, and Merck Serono. R. Albin reports no disclosures relevant to the manuscript. Go to Neurology.org for full disclosures.

Footnotes

  • See page 800

  • © 2013 American Academy of Neurology

REFERENCES

  1. 1.↵
    1. Ahlskog JE
    . Beating a dead horse: dopamine and Parkinson disease. Neurology 2007;69:1701–1711.
    OpenUrlAbstract/FREE Full Text
  2. 2.↵
    1. Antonini A,
    2. Barone P,
    3. Marconi R,
    4. et al
    . The progression of non-motor symptoms in Parkinson's disease and their contribution to motor disability and quality of life. J Neurol 2012;12:2621–2631.
    OpenUrl
  3. 3.↵
    1. Chaudhuri KR,
    2. Schapira AH
    . Non-motor symptoms of Parkinson's disease: dopaminergic pathophysiology and treatment. Lancet Neurol 2009;8:464–474.
    OpenUrlCrossRefPubMed
  4. 4.↵
    1. Bayulkem K,
    2. Lopez G
    . Nonmotor fluctuations in Parkinson's disease: clinical spectrum and classification. J Neurol Sci 2010;289:89–92.
    OpenUrlPubMed
  5. 5.↵
    1. Honig H,
    2. Antonini A,
    3. Martinez-Martin P,
    4. et al
    . Intrajejunal levodopa infusion in Parkinson's disease: a pilot multicenter study of effects on nonmotor symptoms and quality of life. Mov Disord 2009;24:1468–1474.
    OpenUrlCrossRefPubMed
  6. 6.↵
    1. Barone P,
    2. Poewe W,
    3. Albrecht S,
    4. et al
    . Pramipexole for the treatment of depressive symptoms in patients with Parkinson's disease: a randomised, double-blind, placebo-controlled trial. Lancet Neurol 2010;9:573–580.
    OpenUrlCrossRefPubMed
  7. 7.↵
    1. Trenkwalder C,
    2. Kies B,
    3. Rudzinska M,
    4. et al
    ; Recover Study Group. Rotigotine effects on early morning motor function and sleep in Parkinson's disease: a double-blind, randomized, placebo-controlled study (RECOVER). Mov Disord 2011;26:90–99.
    OpenUrlCrossRefPubMed
  8. 8.↵
    1. Storch A,
    2. Schneider CB,
    3. Wolz M,
    4. et al
    . Nonmotor fluctuations in Parkinson disease: severity and correlation with motor complications. Neurology 2013;80:800–809.
    OpenUrlAbstract/FREE Full Text

Disputes & Debates: Rapid online correspondence

  • Response to Ahlskog
    • Angelo Antonini, Director, Parkinson Departement, IRCCS San Camillo, Venice, Italyangelo3000@yahoo.com
    • Roger Albin
    Submitted April 03, 2013
  • Dopaminergic treatment of non-motor Parkinson's disease symptoms
    • J. Eric Ahlskog, Clinical neurologist, Mayo Clinic, Rochester, MNeahlskog@Mayo.edu
    • J. Eric Ahlskog
    Submitted March 20, 2013
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