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Subject: DBS Reprogramming Improves Stable Benefits; Parkin Lowers Age of Onset Date: 8/16/2006 1. Subthalamic nucleus stimulation: Improvement in outcome with reprogramming A Moro, YYW Poon, AM Lozano, JA Saint-Cyr, AE Lang Arch Neurol 2006;63:Epub ahead of print Reprogramming deep brain stimulation electrodes can improve motor outcome in Parkinson’s disease, even after a prolonged period of stable and satisfactory response, according to this study. Forty-four PD patients with long-term (mean 3.5 years) stable response to subthalamic DBS underwent reprogramming at a routine follow-up visit. Patients were off medication and underwent Total UPDRS assessment, followed by a standardized reprogramming protocol. Medications were adjusted to reduce dyskinesia as needed. Reprogramming and adjustments were performed by a movement disorders specialist familiar with DBS programming and medication adjustment. At a mean of 5 months after reprogramming: --55% of patients had sustained improvement compared to baseline, with an average motor improvement of 29%. Half these patients had a transient increase in dyskinesias, which required further adjustment of stimulation and medications over 1-2 weeks. --31% of patients required no change in stimulation settings, and had no change in motor scores. --14% of patients had worse speech and gait after reprogramming, requiring a restoration of the original settings. The authors conclude, “Further improvement of parkinsonian signs can be achieved in the majority of patients even after long-term stable stimulation. Improved patient outcomes from STN DBS are obtained when postoperative care is personally managed by a neurologist expert in movement disorders and DBS who is directly responsible for stimulation programming and simultaneous drug adjustments based on observed clinical responses to changing stimulation parameters.” 2. Influence of heterozygosity for parkin mutation on onset age in familial Parkinson disease M Sun, JC Latourelle, GF Wooten, MF Lew, C Klein, HA Shill, L Golbe, et al. Arch Neurol 2006;63:826-832 Increased dosage of parkin gene mutations correlates with younger age of onset in familial PD, according to this study. Genotyping of families in the GenePD study revealed 23 families with parkin mutations, including 10 compound heterozygotes, 3 homozygotes, and 10 heterozygotes. Age at onset was 11.7 years earlier for those with 1 mutation compared to patients in the study with no mutations. Those with 2 mutations had an age of onset 13.2 years earlier than those with no mutations. E-MOVE Editor: Richard Robinson, NASW, WE MOVE
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