|Briefing||Hot Off The Press|
|The Consortium continues to evolve and gain national recognition. We were recently joined by colleagues at the West Haven, Las Vegas, Omaha, San Juan, and Fort Harrison VAMCs, bringing our network to a total of 47 Consortium Centers. As the 2008 Conference approaches, we anticipate another successful program and encourage the exchange of ideas and suggestions in the development of the agenda. We will also be putting out a call for poster and case presentations in the near future. Please mark your calendars for September 3rd-5th to partner with fellow thought leaders at this important event!||
Cervical dystonia (CD) is effectively treated with both botulinum toxin type A (BoNT-A) and type B (BoNT-B). This international, double-blinded multi-center study was designed as a noninferiority trial between BoNT-A and BoNT-B, the first to compare effectiveness, safety and duration of response in toxin-naïve subjects with CD receiving their first BoNT treatment. Subjects were randomized, treated (BoNT-A [150 U]; BoNT-B [10,000 U]), and assessed in a double-blinded fashion at baseline, and assessed every 4 weeks following injection. The primary outcome measure was the Toronto Western Spasmodic Torticollis Rating Scale (TWSTRS) measured at 4 weeks post-injection. Secondary measures included change in the TWSTRS-subscale scores, pain, global impressions, duration of response, and safety assessments. 111 subjects were randomized to participate in the study. The results met noninferiority criteria for efficacy. Similarly, there was no statistically significant difference in duration of response, injection site pain measures or safety. These results suggest that either BoNT-A (150 U) or BoNT-B (10,000 U) can be used effectively in previously untreated CD subjects to achieve a similar degree of benefit and duration of response.
Move Disord 2008 March 15; 23: 510-517 http://www.ncbi.nlm.nih.gov/pubmed/18098274?ordinalpos=1
Previous studies have shown that men with higher serum urate levels have lower risk of developing Parkinson's Disease (PD). The Parkinson's Study Group's PRECEPT study evaluated over 800 early PD patients (who were not on dopaminergic therapy). In this study, that group was studied to see how urate levels might affect PD progression. All subjects had urate levels drawn and b-CIT SPECT imaging done at the beginning of the study and were followed for an average of 21 months. Subjects with urate levels in the highest quintile reached need for dopaminergic therapy at only half the rate of those in the lowest quintile. Furthermore, these same high-urate subjects had significantly less loss of b-CIT uptake in the striatum on repeat SPECT imaging. The researchers concluded that these two findings suggest a slower rate of PD progression and that "targeting urate... could be an effective disease-modifying therapy in PD."
Arch Neurol. 2008 April; 65 (6); e-published ahead of print http://www.ncbi.nlm.nih.gov/pubmed/18413464?ordinalpos=1
To investigate a possible neuroprotective effect of some antihypertensive drugs, a case-control study was performed using the UK-based General Practice Research Database. The use of calcium channel blockers, ACE Inhibitors, beta-blockers, and angiotensin II blockers was assessed (classified by timing (current or past) and length of exposure) in about 3600 cases of early Parkinson's Disease (PD) and 3600 age/sex-matched controls. A logistic regression analysis was performed controlling for several factors, including vascular risk factors and dementia. Subjects who had current long-term use (>30 prescriptions filled) of calcium channel blockers (CCBs) had significantly reduced risk of a PD diagnosis (OR =0.77) when compared to non-use of CCBs. ACE inhibitors, beta-blockers, and angiotensin II blockers did not show any significant effect. The effect of CCBs was stronger in patients over 80 years old, and in women. The authors referenced a recent publication in Nature (by Chan CS, Guzman JN, Ilijic E et al) which found that blocking calcium channels may be neuroprotective because it causes substantia nigral cells to revert from a theoretically harmful calcium-channel based pacemaking function to a less harmful one based on sodium channels.
Neurol. 2008 April 15; (70) 1438-1444 http://www.ncbi.nlm.nih.gov/pubmed/18256367?
|Dates To Remember||Committee Recap|
|June 22nd-26th, 2008
Congress on PD and
July 28th-31st, 2008
18th Annual Course
for the Clinical
August 7th-9th, 2008
6th Annual Young
September 3rd-5th, 2008
|Clinical Care Committee
April 08 Transmitter
May 08 Transmitter
July 08 Transmitter
September 08 Transmitter
November 08 Transmitter
January 09 Transmitter
March 09 Transmitter
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