In a recent paper in Neurology [1] Tiago et al. present the results of a meta-analysis of placebo results collected from drug trials.
Unfortunately, most of their report is behind a pay-wall, but the paper's tables can be read. These show, for a number of drugs, the improvement in motor UPDRS scores of both the active and placebo arms of the trials for that drug.
For instance,
Pramipexole, mean improvement: Active = 7.79, Placebo = 6.68
Ropinirole, mean improvement: Active = 7.17, Placebo = 7.16
Levodopa, mean improvement: Active = 8.89, Placebo = not given
A few points to note:
- the confidence intervals are wide, suggesting that for each category of data there is not statistical significance;
- the placebo results appear to be almost as good as the active control; this could be due to chance, but given this, I wouldn't have expected them to be given regulatory approval - perhaps the drugs did better in other measures;
- note that part of the power of a placebo is contextual, so the same sugar pill could have a different effect if used in a placebo controlled trial of an effective drug or of a weak drug.
A less promising, but still positive measure of the effectiveness of placebos at reducing the symptoms of PD, is given by Pham and Nogid [2]. Reporting on rotigotine they write:
"Changes on the UPDRS III (motor examination) at 6 months ranged from -3.58 to -8.7 with rotigotine transdermal system, compared with +0.38 to -4.3 in the placebo group and -10.3 in the pramipexole group (P < 0.001 vs placebo; P = NS vs pramipexole). The change in "off" time at 6 months ranged from -2.1 to -2.7 hours with rotigotine transdermal system, compared with -0.9 hour with placebo and -2.8 hours with pramipexole (P < 0.001 vs placebo; P = NS vs pramipexole). The proportion of patients achieving a >30% reduction in "off" time ranged from 55.1% to 59.7% of patients receiving rotigotine transdermal system, compared with 34.5% to 35.0% of patients receiving placebo and 67.0% of patients receiving pramipexole (P<0.001 vs placebo; P = NS vs pramipexole)."
So what? If a basic placebo can have these positive effects, just wonder what an optimally engineered placebo, or better still therebo, could have. But let's not use the possibility of making better placebos as an excuse to delay implementing the routine therapeutic use of placebos and therebos for Parkinson's. Let's make it happen NOW!
References
[1] "Another face of placebo: The lessebo effect in Parkinson disease. Meta-analyses"
Tiago A. Mestre, MD, MSc,
Prakesh Shah, MBBS, MRCP, MRCPCH,
Connie Marras, MD, FRCPC, PhD,
George Tomlinson, PhD and
Anthony E. Lang, MD, FRCPC, FAAN
Neurology April 22, 2014 vol. 82 no. 16 1402-1409
http://www.neurology.org/content/82/16/1402/suppl/DC1
Click on Tables e-1 to e-2
[2] Clin Ther. 2008 May;30(5):813-24. doi: 10.1016/j.clinthera.2008.05.007.
"Rotigotine transdermal system for the treatment of Parkinson's disease."
Pham DQ1, Nogid A
http://www.ncbi.nlm.nih.gov/pubmed/18555929
John