Re: ANY FURTHER COMMENTS RE THE DYSTONIA POST?
Did anybody read Yvon's post and have any comments? I've interested.June in Toronto (beb/meige)
--modified by June in Toronto at Sat, Feb 09, 2002, 16:55:08
Re: ANY FURTHER COMMENTS RE THE DYSTONIA POST?
Hi June,
I haven't been keeping up with all the posts on the BB in a while.
I'm very intersted and appreciate the postings by you about the
Brain series on PBS as well as the information from you and Yvon
regarding Dr. Fieldings papers.
I just went over to the dystonia BB, but could not read the page of the link Yvon provided.
It says in order to sign on I have to be a subscriber to the printed
journal.
Something is working for me, so, I'm sticking to the mind/body/spirit connection. It's free, it's natural, and there's no bad side effects.
I am always longing to hear from others that it's working for also.
thanks again,
Mindy in NY
Re: ANY FURTHER COMMENTS RE THE DYSTONIA POST?
Hi Mindy, did you try the link (now on p. 3 of the Dystonia bb) by Yvon under "something that helps my dystonia"? Its a paper my Dr. Mark Hallett "Disorder of movement preparation in dystonia" - in the BRAIN - A Journal of Neurology, Oxford Journals on Line. I got in first try.June in Toronto (beb/meige)
Re: ANY FURTHER COMMENTS RE THE DYSTONIA POST?
Thanks June,
I tried again, and even tried a search. It won't let me read without
subscribing.
Mindy
Re: PAPER/MINDY Part 1
Disorder of movement preparation in dystonia Mark Hallett, MD Human Motor Control Section, NINDS, National Institutes of Health Bethesda, MD, USA "Dystonia is undoubtedly characterized by a disorder of movement execution. In many patients, the `involuntary movements' are
brought about entirely by attempted voluntary movement. Only in more severe cases are there truly involuntary movements, but even
they are exacerbated by volition. The EMG pattern underlying movement demonstrates too much motor activation. There is
excessive activation of antagonists, overflow into synergists, unnecessarily activated muscles and prolongation of muscle activation.
Such activation gives rise to abnormal muscle spasms and incoordination. A number of recent studies seem to indicate that excessive muscle activation is due to a deficiency of inhibition (Berardelli et al.,
1998; Hallett, 1998). Defective inhibition has been demonstrated at all levels of the neuraxis, spinal cord, brainstem and motor
cortex. The most direct demonstration of this has been done with paired-pulse transcranial magnetic stimulation studies, which
permit investigation of intracortical inhibition. The basal ganglia are in a good position, and seem anatomically able, to regulate some
aspects of inhibition. Indeed, it has seemed to many investigators that the basal ganglia help to select movement by facilitating the
appropriate movement and inhibiting the inappropriate ones. Then dystonia could be understood as a failure of the inhibition. The
direct pathway through the basal ganglia could be the facilitation loop and the indirect pathway the inhibitory one. While originally a surprising concept since sensation is generally thought to be normal in patients, it is now clear that there is a
significant disorder of sensory function in dystonia (Hallett, 1995). Such a problem can be highly relevant to a motor disorder since
a major role of the sensory system is to drive the motor system. Hence, disordered sensation can lead to disordered movement.
Evidence for sensory dysfunction is now direct with experiments showing defective kinesthesia (Grunewald et al., 1997), temporal
discrimination and spatial discrimination (Bara-Jimenez et al., 2000). Physiological assessment of the sensory pathway shows
enlarged sensory receptive fields of thalamic neurones (Lenz et al., 1999) and disorder in the cortical sensory homunculus
(Bara-Jimenez et al., 1998). There is also reduced sensory activation on functional PET scans in somatosensory cortex as well as
supplementary motor cortex (SMA). The efficacy of the geste manoeuvre in many patients is direct evidence for the ability of the
sensory system to affect the motor system." cont....
Re: PAPER/MINDY Part 2
"Abnormalities of the N30 component of the median nerve sensory evoked potential (SEP) are relevant to the issue of sensory
disturbances, and need to be commented on specifically for the discussion to follow. Virtually everything is controversial about the
N30. First of all, its generator is debated. The potential is maximal frontally and is affected by lesions of frontal cortex; the SMA is
often suggested as the source. Most evidence, however, suggests that it is most likely the frontal pole of a tangential dipole located in
the post-central gyrus. The best evidence for this comes from direct cortical recordings. Secondly, its alterations in disease are not
consistent in different reports. One of the reasons for this is that the N30 is a highly volatile potential, being very sensitive to the
exact stimulation methods, the psychological state and the motor task. Diminution in amplitude of the N30 was reported in patients
with Parkinson's disease, and while this has not been found by all authors, its increase in amplitude with levodopa does seem clear.
Increase in its amplitude has been reported by some investigators in patients with dystonia (Berardelli et al., 1998; Hallett, 1998).
While the N30 clearly represents early sensory processing and may be an indicator of sensory dysfunction in dystonia, its role is not
well understood. In addition to a movement execution disorder and a sensory disorder, it is now clear that there is also a disorder of movement
preparation. Movement preparation involves a number of factors, including the process of sensorimotor integration. Past evidence for
a disorder of preparation includes abnormalities in the EEG prior to a self-paced voluntary movement, including a loss of negativity
of the movement-related cortical potential and a deficit of event-related desynchronization in the beta band (Toro et al., 2000).
There is also an abnormality in the EEG during the waiting period for a go-signal (S2) after a warning signal (S1). The EEG during
this period is called the contingent negative variation (CNV), and it is also deficient in dystonia (Hamano et al., 1999). The paper in
the current issue of Brain by Murase and colleagues gives further evidence for a problem in movement preparation, showing that the
N30 is not properly modulated during this time (Murase et al., 2000). The N30 is ordinarily reduced in amplitude (gated) in the
premovement period as well as during the movement period. In dystonic patients there is no gating in the premovement period, while
normal gating occurs during movement. This suggests faulty sensory processing that might impair the developing motor program. This finding might give a partial explanation for why the N30 is found to be abnormally large in some studies. If the experimental
set-up was such that the subjects were thinking about moving their hands, then the dystonic patients would suppress their N30
potentials less than the normal subjects." cont'd...
Re: PAPER/MINDY Part 3
"Murase and colleagues found another abnormality in the premovement period. The P22 was gated more in the dystonic patients than
in the normal control subjects. The origin of the P22 is less debated than the N30, most authorities believing it to be a radial dipole
from the precentral gyrus. Hence, the P22 might reflect an aspect of motor cortex function and the N30 an aspect of sensory cortex
function. At the moment, it is difficult to be more specific than that since the physiology of gating and its significance are not well
understood. Disordered preparation for movement will certainly be a factor in faulty execution. Precise processing of all sensory stimuli from the
environment is relevant in designing an appropriate movement. The nervous system prefers to be anticipatory rather than reactive.
Murase et al. suggest that their information helps to explain the phenomenon of the sensory trick, since the added sensation might
rebalance the motor system. Whether this speculation is true or not remains to be determined, but it has already been demonstrated
that the sensory trick in patients with blepharospasm will normalize the R2 of the blink reflex (Gomez-Wong et al., 1998)." I left out the references...
Re: PAPER/June
Hi June,
Thanks so much for taking the time to post the 3 papers.
I immediately printed them out :-)
I watched part 4 - the Aging Brian last night - thought it was great.
I of course was very encouraged to hear them talk about how the brain
is capable of healing itself. This was talked about in regards to stroke victims. For those who didn't see it, by immobilizing the good arm, with practice, you can regain full use of the affected arm.
This is more or less what I have been doing to what I call re-train my brain.
Neurons continue to grow, even in old age.
Physical excercise improves memory.
Alzheimers is effected by the immune system, and they are working on a vacine with very good results.
Mindy in NY
Re: PAPER/June
You'r welcome Mindy - I was hoping you'd see it before (perhaps) it was thrown off the bb for being too long - I had to post the paper in 3 parts as only allowed a certain amount of characters per post!
I only saw part of the Aging Brain last night - taped it so will catch up on it another time. I saw the part about Alzheimers and found it very interesting - as I did the whole series. Of course I would have liked them to mention Dystonia or at least Parkinson's, but I don't think they did at all. WE should ALL TAKE NOTE that the brain can heal itself.The part about the stroke victim (which I didn't see), but as you pointed out, they immobilized the good arm - is what they did the young baby who was born witha cataract. They connected the neurons which, in adults would have already been connected, then placed a contact lens in and then taped up the good eye, to make the bad one work hard and do its job. Amazing isn't it? Yvon Breton (Dystonia board) is immobilizing his neck (he has cervical torticollis) to try and retrain the brain not to spasm - he's doing under a doctor's care but doesn't feelat this point that the neck is immobilized enough. Time will tell, but I wish himGod speed. June in Toronto (beb/meige)
Re: Further to Dr. Fielding's Exercises/Paper Discussed
Yes, June, please let us know what he says on this. Obviously he was interested.
Re: Further to Dr. Fielding's Exercises/Paper Discussed
I won't hold my breath, Kathy, that the neuro will say anything about Dr. F's papers. He said himself he was "sceptic" about such small research projects (each of Dr.F's papers only had 2 patients studied) and that "these concepts come and go without further research being done". We have tokeepytrying though.June in Toronto (beb/meige)
Re: Further to Dr. Fielding's Exercises/Paper Discussed
Boy, how in heck can someone get something published with only two patients in the study. You could probably get the same results from two people giving them a placebo if they knew what they were being given it for. I always wonder whether exercise plays a role in this disorder except that the vast majority of people that I have met who have it ( I am an exception)look to be in pretty good physical shape, certainly as far as weight is concerned. Who knows. I think that I will lose 60 pounds and see what happens. I will let you know. The only problem is that you will probably all die from old age before that happens....Alan
Re: Further to Dr. Fielding's Exercises/Paper Discussed
I agree with you, Alan, that the case studies were `minute'. I am married to a social scientist and he cringes at the thought of anything less than 1,000 patients and 10 years of study (nmaybe I'm exaggerating a bit!). Dr.F's papers were both published in `Behavioural Psychotherapy' - a respected and well-known publication.Just think of ALL the extra padding you will have to use as Santa Claus if you lose that weight - don't think you will look as authentic:-) Take care. June in Toronto (beb/meige)
Re: Further to Dr. Fielding's Exercises/Paper Discussed
Gee, I hadn't thought of that. And to think that I actually took out the old treadmill after I posted this morning and got it steamed up. I had to fight the dust and cobwebs but I actually went on it for a couple of miles. Actually, the Santa outfit was a little tight this year anyway. Can you believe it?
Re: Santa's Clothes!
Santa's clothes are supposed to be a bit tight - some of the old, old pictures of him are with some of his buttons undone, as he couldn't do them up! So you are right in fashion and you didn't know it:-) Glad you didn't fall off that old treadmill - be careful now!June in Toronto (beb/meige)
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