Central brain problems cause movement difficulty in FM (and CFS?)

Cort

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Intracortical inhibition refers to the 'voluntary preparation of movement" in the brain. I believe it has to do with movement planning and preparation. This article suggests to me that the brain is just not ready for movement . The authors suggest the problem is different in FM than muscular dystrophy. InMD - the reduced intra inhibition simply occurs because the muscles are so weak there is little need to rev the brain up (my interpretation). In FM the problem seems to be a 'central disinhibition'; central refers to the brain - this suggests to me that a global disinhibition - or inability to ully enter into the planning necessarly for movement.

This would play out I would think - in a kind of stuckness - a frozen state - which makes sense given the 'frozen muscles' and myofascial problems etc.....the muscles seem to be stuck in a contracted state.

I would expect this would play out in CFS as well.

Muscle Nerve. 2011 Feb 8. doi: 10.1002/mus.21920. [Epub ahead of print]
Central mechanisms during fatiguing muscle exercise in muscular dystrophy and fibromyalgia syndrome: A study with transcranial magnetic stimulation.

Schwenkreis P, Voigt M, Hasenbring M, Tegenthoff M, Vorgerd M, Kley RA.
Department of Neurology, BG-Universittsklinikum Bergmannsheil, Ruhr University, Buerkle-de-la-Camp-Platz 1, Bochum D-44789, Germany. peter.schwenkreis@ruhr-uni-bochum.de.
Abstract

Introduction: The aim of this study was to apply paired-pulse transcranial magnetic stimulation (TMS) to assess intracortical inhibition (ICI) during fatiguing muscle exercise in healthy humans and patients with muscular dystrophy (MD) and fibromyalgia syndrome (FMS) to obtain insight into differential central mechanisms.

Methods: We studied 23 patients with MD, 16 patients with FMS, and 23 healthy controls. All participants performed a fatiguing motor task. TMS recordings were taken pre-exercise, immediately post-exercise, and 40 minutes post-exercise.

Results: ICI was already reduced pre-exercise in MD and FMS, whereas ICI decreased significantly during fatiguing muscle exercise only in healthy subjects.

Discussion: Reduced baseline ICI in patients might prevent further utilization of this presumably compensatory mechanism during fatiguing muscle exercise. Although reduced baseline to be ICI in MD can be explained as compensatory due to peripheral weakness, in FMS reduced ICI must be considered an indicator of primary central disinhibition. Muscle Nerve, 2011.
 

Cort

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Then just prior to that this study came out - showing increased muscle stiffness. The muscles are locked down in this contracted state - which has been my experience for many years.

http://www.ncbi.nlm.nih.gov/pubmed/21298443

Eur J Appl Physiol. 2011 Feb 6. [Epub ahead of print]
Nature of passive musculoarticular stiffness increase of ankle in female subjects with fibromyalgia syndrome.

Dierick F, Detrembleur C, Trintignac G, Masquelier E.
Department of Physical Therapy, IESCA Sainte-Thrse, Haute Ecole Louvain en Hainaut (HELHa), Rue Trieu Kaisin, 134, 6061, Montignies sur Sambre, Belgium, frederic.dierick@gmail.com.
Abstract

The objective of this study was to assess the passive elastic and viscous stiffness components of ankle in young, middle-aged and old adult female fibromyalgia subjects and compare the results with age-matched healthy control subjects. The passive musculoarticular stiffness of the ankles of 60 fibromyalgia subjects and 52 controls was quantified by measuring the ankle resistance to imposed sinusoidal rotary displacements at nine different oscillation frequencies. For each frequency, the resulting torque response of the ankles was decomposed into elastic and viscous components of the total stiffness. The self-perceived stiffness intensity of the ankles was assessed in fibromyalgia subjects by means of a visual analogue scale.

Two-way ANOVA test indicated a significant effect of fibromyalgia (P < 0.001) and age (P < 0.001) on elastic stiffness results and a significant effect of age (P < 0.001) on viscous stiffness results. Post hoc Holm-Sidak test indicated that younger and middle-aged fibromyalgia subjects had a significant elastic stiffness increase of more than two times that of controls (P = 0.038 and P < 0.001, respectively). Middle-aged fibromyalgia subjects had a significant viscous stiffness increase of 1.2 times that of controls (P = 0.038). No significant differences in stiffness were observed between older fibromyalgia subjects and controls.

In conclusion, the self-perceived stiffness increase of ankle reported by younger and middle-aged fibromyalgia subjects is due to changes in elastic and/or viscous musculoarticular structures around the ankle. The absence of changes in older fibromyalgia subjects is probably related to the ageing process of controls.
 

Enid

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Gosh how familiar this sounds Cort - muscles definately locked down in a contracted state. You are marvellous finding these things ! And to see how our (ME) research speeds now. Like all we try to explain the afflication from "experiences" - mine a strange feeling of more ease after a body MRI scan. Eased something and I could actually walk back to bed.
 

Cort

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That is so true for me as well. Muscles feel locked and movement seems uncertain and difficult does it not? The grace of movement is largely gone - its effortful - as if things were frozen up......which could mean the brain is in a kind of state of shock...This could be the whole arousal idea as well - because some key planning aspects of it that usually ready us for movement are inhibited - its never really read to initiate movement. Its stuck on first base. ..
 

Enid

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Very central to the brain - some beast or collection crosses the bbb and creates havoc there in the very basic bodily functions only (amygdala involved and arousal system too - passed out three times). Up and at 'em says I we alone who can discuss the sheer horrors of it all can only guide. Hoping you are looking after your health - very important.
 
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Yes, the muscles feel very 'clunky' as if the signals aren't getting to them right. And so dropping things, etc. ( I don't have FM, just ME/CFS('just', haha))
 
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I take baclofen for my significant muscle stiffness and it helps me a lot. I have CCC CFS. My neuro doc thought I might have atypical MS so he told me to titrate up with baclofen and I stopped at 40mg per day (10mg every 4 hours). I would take more, but can't tolerate more. I have been taking it for 5 years now and live from pill to pill to reduce (but still not eliminate) stiffness.

I don't know whether my stiffness is linked to CFS (XMRV?) or whether it is a co-morbid condition, but I find it interesting that others with CFS are mentioning muscle stiffness as well.
 

Cort

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Muscle stiffness is big in FM and certainly present in CFS. Its been a major problem for me...I think of it as kind of a mild seizure state and it fits with the idea of sympathetic nervous system arousal and reduced PNS activity was well.

Interesting how many of us kind of slide between these different neurological diagnoses. They thought I might have MS at one time but while the MRI showed abnormalities...they weren't distinctive to MS.
 
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Cort:

Thanks for your wonderful site and for all that you do!

I haven't seen much discussion of baclofen on ME/CFS forums. Have you tried baclofen or considered it? Have others?

My wife has FMS (tender points, IBS, RLS), so we are a family grouping with related neuro-immune dysfunction. She has a bleeding disorder and received cryoprecipitate for an operation that came from over 20 donors. I may have picked up XMRV or other MLRV from her.

Her FMS stiffness is different from mine. Mine is a constant low-grade spasticity where there is resistance to movement and the resistance increases with speed of movement, especially while walking. It is so low-grade that it is not detected in a neurological exam where you like down and they manipulate your relaxed leg, but I certainly detect it every time I walk! Little old ladies in their sneakers blow by me during my daily 1/4 mile walk (I am 61 today).

It is coming back to me that my symptom that led to me getting baclofen was getting pain in my triceps when I picked up my (fat) cat using my biceps. Your brain is supposed to tell the opposing triceps muscle to relax at the same time that it instructs the biceps muscle to contract, and with spasticity, this opposing muscle relaxation signal isn't strong enough or is too late, or the opposing muscle doesn't really relax completely and has a low level of contraction which may increase when opposed by an opposite muscle. I believe that the baclofen acts to reduce (relax) the baseline contraction or degree of contraction of opposing muscles which allows freer movement.

As I follow the XMRV news (I am negative by PCR/culture and serology at VIP Dx) I am wondering whether the XMRV may be degrading the muscle agonist/antagonist motor neurons and synapses resulting in creeping spasticity stiffness (resistance to movement).