That goes without saying. I'm angry at this condition, which to me is more like torture. I remember my three straight nights of no sleep well. I have IBS, IC, GERD, DDD (everyone does), allergies, constant fatigue, a symptomatic Schatzki's ring and a Morton's neuroma. They are all child's play in comparison to RLS. It angers me when I read about people suffering from this ridiculous condition. Have you ever heard of any other condition in the world where the discomfort is relieved by standing up and walking?
Which reminds me, if you really want to go crazy, I reread the report about those autopsies of the brains of people who had primary RLS during their lifetime and realized that it is really only one or two regions of the brain that have low levels of iron and bad receptors and really mostly the d2 receptors in those regions. What the heck is that all about??? That's like saying the tissue in the middle finger is low on iron but not the other fingers. How does that happen? AND in another project unrelated to RLS, researchers wanted to find out the affect of iron deficiency on the brains of newborns so they fed newborn mice iron deficient diets. Guess what. Iron deficiency was only noted to affect the striatum and only the receptors therein lacked density. Does that mean when iron is in low supply only the really important parts of the brain get any. You would think that the part of the brain that calms our peripheral nervous system and allows us to sleep is important? Well my space ship is here, time to return to earth.
Med trials/insomnia/depression
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figflower
Re: Med trials/insomnia/depression
Ok, one last article, by none other than Dr. E. See what I mean about the striatum:
The dopamine transporter is decreased in the striatum of subjects with restless legs syndrome.
Earley CJ1, Kuwabara H, Wong DF, Gamaldo C, Salas R, Brasic J, Ravert HT, Dannals RF, Allen RP.
Abstract
STUDY OBJECTIVES:
Prior studies, all using SPECT techniques, failed to find any differences for dopamine transporter (DAT) in restless legs syndrome (RLS) subjects. The distinct pharmacokinetic properties associated with SPECT-determined DAT along with rapid biodynamic changes in DAT may, however, have missed membrane-bound DAT differences. The current studies assessed real-time DAT binding potentials (BP) in striatum of RLS patients using (11)C-methylphenidate and PET techniques.
DESIGN:
RLS medications were stopped at least 11 days prior to the PET study. Clinical severity of RLS was also assessed. PET scans were performed at 2 different times of day (starting at 08:30 and 19:30) in separate groups of subjects. The primary outcome measure was total striatal DAT BP.
PARTICIPANTS:
Thirty-six patients with primary RLS and 34 age- and gender-matched controls.
RESULTS:
RLS subjects had significantly lower DAT binding in the striatum compared to controls on both the Day and the Night scans. DAT was decreased in putamen and caudate but not the ventral striatum of RLS subjects. There were no diurnal differences in DAT for the total group or for control and RLS separately. DAT BP did not correlate with any clinical measures of RLS.
CONCLUSION:
The current study found a significant decrease in DAT BP in two independent studies. These results when viewed along with prior RLS SPECT and autopsy studies of DAT, and cell culture studies with iron deficiency and DAT, suggest that membrane-bound striatal DAT, but not total cellular DAT, may be decreased in RLS.
The dopamine transporter is decreased in the striatum of subjects with restless legs syndrome.
Earley CJ1, Kuwabara H, Wong DF, Gamaldo C, Salas R, Brasic J, Ravert HT, Dannals RF, Allen RP.
Abstract
STUDY OBJECTIVES:
Prior studies, all using SPECT techniques, failed to find any differences for dopamine transporter (DAT) in restless legs syndrome (RLS) subjects. The distinct pharmacokinetic properties associated with SPECT-determined DAT along with rapid biodynamic changes in DAT may, however, have missed membrane-bound DAT differences. The current studies assessed real-time DAT binding potentials (BP) in striatum of RLS patients using (11)C-methylphenidate and PET techniques.
DESIGN:
RLS medications were stopped at least 11 days prior to the PET study. Clinical severity of RLS was also assessed. PET scans were performed at 2 different times of day (starting at 08:30 and 19:30) in separate groups of subjects. The primary outcome measure was total striatal DAT BP.
PARTICIPANTS:
Thirty-six patients with primary RLS and 34 age- and gender-matched controls.
RESULTS:
RLS subjects had significantly lower DAT binding in the striatum compared to controls on both the Day and the Night scans. DAT was decreased in putamen and caudate but not the ventral striatum of RLS subjects. There were no diurnal differences in DAT for the total group or for control and RLS separately. DAT BP did not correlate with any clinical measures of RLS.
CONCLUSION:
The current study found a significant decrease in DAT BP in two independent studies. These results when viewed along with prior RLS SPECT and autopsy studies of DAT, and cell culture studies with iron deficiency and DAT, suggest that membrane-bound striatal DAT, but not total cellular DAT, may be decreased in RLS.