Thursday, September 4, 2008
Restless legs
I saw two patients today who were grateful that their restless legs were better and they were able to sleep. RLS (restless leg syndrome) or periodic limb movement disorder is commonly seen in my Lyme practice. Sleep apnea and RLS are the two most common disorders diagnosed in sleep labs. Sleep clinics say RLS is frequently related to iron deficiency and low ferritin levels. In my practice it is related to Lyme disease. The afflicted persons limbs, especially legs move around in a jerking fashion interfering with sleep. It is a type of movement disorder. It is related to Parkinson's disease and responds to the same medicines. Drugs like Mirapex which increases dopamine activity in the brain are effective. Neuroborreliosis seems to cause a mix of conditions related to abnormal neurotransmitter activity. Rocephin's efficacy, is in part, thought to be due to its mitigating effect on glutamine, another neurotransmitter. Many patients develop a host of psychiatric symptoms which improve when neurotransmitters are "tweeked" including: serotonin, norepinephrine, GABA, glutamine, dopamine and possibly others. The cause is unclear. Is it infection of glial cells, supporting brain cells, neurotoxins, inflammation or other issues? Another day: another piece of the puzzle.
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That's really interesting- have come across a lot on Minocycline but not on Rocephin. Do you think it is direct effect, or an effect of removing cytokines or other influences of the Borrelia? How much of what you see as treatment responses do you think may be related to nonbactericidal action? I have seen a fair amount of info on the various neurotransmitter imbalances in all sorts of chronic neuro diseases. Those systems are so interrelated- you up regulate this and that down regulates. That it one heck of a puzzle. So many things bind multiple receptor sites. I could see a case for direct effect of neurotoxins and inflammatory mediators from the current work in neuroinflammation. But anything that directly effects any of structural or functional cellular components should be able to effect neurotransmitter levels. How much of what you see clinically in "tweaking" do you think might be exhaustion of that neurotransmitter type from chronic stimulation? Or I guess for that matter, from chronic suppression of the opposing neurotansmitter system? I wondered about that from some of my reading and also from watching this disease in action- there is just a lot of neural activity going on all the time in the Lymes patient I've observed and those I've read about. Sensory and motor- tingling, stabbing, twitching, tightening, ect , ect. That versus neuro disease that turn things off- Lymes seems to turn everything neurologically on all the time. In causing this irritant or whatever it is reaction that keeps these areas over reacting all the time, are we just exhausting all the up regulators like the dopamine you gave as the example? And then down regulating the down regulators to try to reachieve balance? Does that match the picture of clinical rebalancing that you find works? Or is it all over the map and no pattern? Just curious what you have seen.
Hi Lyme MD,
I have just read all the posts back to this one on your blog and want to say thank you for putting the information out there. I was bitten by a tick approx. 6 weeks ago after a trip to Texas and have had mild but strange symptoms, and beginning last night, very restless legs - actually muscles all over twitching. I currently live in New Zealand, where nothing is known about Lyme and it's co-infections. I am trying to educate myself and my doctor here, so that I get the best possible treatment at this early stage, hopefully avoiding worse symptoms. I will try to get tests done at the recommended labs, but I'm not sure if they handle international blood samples. Any advice on how to handle this situation is appreciated!
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