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I'm not a medical person or a researcher, but it seems to me this group is
making some unfounded assumptions:

1) They assume there IS such a thing as Levodopa-induced dyskinesias.  I
don't believe there's any proof of this, just theory.

2) They assume reduced dosage of Levodopa following STN is responsible for
fewer dyskinesias when patients are tested later with their stimulators off.

  In most DBS patients I know,  even with the absence of stimulation,
symptoms post-surgery never return to the severity of the symptoms
pre-surgery.  I've heard Dick's doctors theorize that the presence of the
electrode in the brain, even with the stimulator turned off, acts like a
mini-pallidotomy.   The surgery Dick had, pallidal stimulation, doesn't
usually result in a decrease in meds, yet the symptoms such as dystonia and
dyskinesia didn't return full-force, even years later, when the stimulator
was turned off.  In cases where meds weren't reduced after surgery, doesn't
that blow a hole in the "sensitization" theory?

Brian Collins, do you have an opinion on this?  Or Dr. Chris?

Margie Swindler

<< Levodopa-induced dyskinesias in Parkinson's disease: is sensitization
reversible?

 Levodopa-induced dyskinesias (LIDs) in patients with Parkinson's disease are
considered to result from the severity of dopaminergic denervation in the
striatum, which is an irrevocable phenomenon, and sensitization induced by
long-term intermittent administration of levodopa.

 Taking advantage of the 64% reduction of levodopa treatment allowed in 12
Parkinson's disease patients by continuous high-frequency stimulation of the
subthalamic nucleus, we evaluated the severity of parkinsonian motor
disability and LIDs during 2 levodopa challenges performed before the
surgical implantation of the stimulation electrodes and after 8.8 months of
continuous bilateral subthalamic nucleus stimulation that was interrupted 2
hours before the levodopa test.

 Motor disability during the "off" and "on" drug periods was unchanged.

 The severity of LIDs during the "on" period and dystonia during the "off"
period decreased by 54% and 62%, respectively.

 The reduced severity of LIDs in the absence of subthalamic nucleus
stimulation demonstrates that the sensitization phenomenon resulting from
long-term intermittent levodopa administration is partially reversible.

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