Misdiagnosis of Meiges Disease

Highlights Only
S

SirTrouserz

Well-known member
: J Behav Ther Exp Psychiatry. 1991 Sep;22(3):221-3. Links
Meige's disease misdiagnosed as anxiety disorder.Cairns SL, LeBow MD.
Department of Psychology, University of Manitoba, Winnipeg, Canada.

A woman in her late 40s with a 5 year history of anxiety was treated with relaxation training and cognitive restructuring. Her anxiety was manifested by facial twitching, hand fidgeting, vocal tremor, loss of self-esteem, and depression. Therapy seemed to reduce motor symptoms and improve her self-esteem, confidence, and mood. Six months after the start of therapy the client was found to have Meige's Disease. Following treatment with botulinum toxin, motor symptoms disappeared. This case highlights the need for psychotherapists to be more aware of neurological and medical problems which may mimic psychological ones.

PMID: 1804856 [PubMed - indexed for MEDLINE]
 
Well, you know my very good friend Steve dared me to start some trouble this week, so I was foolish enough to take him up on it ;)

whataprettyworld, could you please present some evidence to back up your statements, because my psychologist said that anxiety can only cause small nerve twitching like eye twitching and the like, not the entire peripheral nervous system twitching, cramping, exercise intolerance and fatigue, etc. that many of us have. I had a lot of anxiety when I originally developed peripheral nerve hyperexciteability. I was a disastrous wreck of a girl. Anxiety beyond what I thought humanly possible.

However, now I have no anxiety about my BFS symptoms and I still twitch and cramp even after being treated with correct medication finally by a neurologist. I'm not anxious about it anymore though because I know what it is. I have not found evidence that anxiety can cause all of the symptoms we have, though for many here they happen concurrently, at least at first. The studies just don't show that anxiety can cause these symptoms over a long term that I have found and some people have been twitching 20 + years. Have you found any studies that show how that occurs?

And Basso my dearest, loving, multitalented, philosophical friend, perhaps you were so busy speaking of love and life and chocolate and ladies and joy, that you missed my post on some scientific study of documented medical causes and treatments for conditions such as ours. Are they absolutely conclusive? No. Is here pretty good evidence for causes of BFS that are physiological in nature? Yes. But you knew that already I don't blame you for missing my previous post, and you're probably so busy enjoying life that you'll miss it again, but here it is in entirety again anywho just for kicks.


Ned Tijdschr Geneeskd. 1996 Aug 10;140(32):1655-8.Links
[Muscle cramps and fasciculations not always ominous: muscle cramp-fasciculation syndrome]
[Article in Dutch]
Vos PE, Wokke JH.
Academisch Ziekenhuis, Afd. Neurologie, Utrecht.
In three patients, men of 43, 44 and 55 years old with muscle cramps, fasciculations and easy fatiguability of muscles, cramp-fasciculation syndrome was diagnosed. This is a benign disorder which has to be differentiated from amyotrophic lateral sclerosis. Response to treatment (benzodiazepines or carbamazepine) is good.
PMID: 8815407 [PubMed - indexed for MEDLINE]

Serrao M, Cardinali P, Rossi P, Parisi L, Tramutoli R, Pierelli F.
A case of myokymia-cramp syndrome successfully treated with gabapentin.
Acta Neurol Scand. 1998 Dec;98(6):458-60.
PMID: 9875627 [PubMed - indexed for MEDLINE
Brain, Vol. 125, No. 8, 1887-1895, August 2002
© 2002 Guarantors of Brain

Neurology. 1998 May;50(5):1483-5.Links
Antibodies to ion-channel proteins in thymoma with myasthenia, neuromyotonia, and peripheral neuropathy.
Heidenreich F, Vincent A.
Department of Neurology, Heinrich-Heine University, Düsseldorf, Germany.
A patient presented with anti-acetylcholine receptor antibody-positive myasthenia gravis. After removal of a thymoma and use of cytotoxic therapy, there was worsening of myasthenia, onset of muscle stiffness and hyperexcitability, and electrophysiologic signs of peripheral neuropathy. Elevated serum titers of antibodies to neuronal voltage-gated K+ channels were present, consistent with neuromyotonia (Isaacs' syndrome). A beneficial response to treatment paralleled changes in antibody titers.
PMID: 9596015 [PubMed - indexed for MEDLINE]

Muscle Nerve. 1994 Sep;17(9):1065-7.Links
Myokymia-cramp syndrome: evidence of hyperexcitable peripheral nerve.
Smith KK, Claussen G, Fesenmeier JT, Oh SJ.
Department of Neurology, University of Alabama at Birmingham 35294.
PMID: 8065395 [PubMed - indexed for MEDLINE]

Neurology. 1991 Jul;41(7):1021-4.Links
Comment in:
Neurology. 1992 Feb;42(2):466.
Neurology. 1992 Sep;42(9):1846-7.
Cramp-fasciculation syndrome: a treatable hyperexcitable peripheral nerve disorder.
Tahmoush AJ, Alonso RJ, Tahmoush GP, Heiman-Patterson TD.
Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107.
We report nine patients with muscle aching, cramps, stiffness, exercise intolerance, and peripheral nerve hyperexcitability. Neurologic examination showed calf fasciculations in seven, quadriceps myokymia in two, and deltoid myokymia in one patient. Two patients had mild increase in serum creatine kinase. Muscle biopsy showed either no abnormality (three patients) or mild neurogenic changes (four patients). Fasciculations were the only abnormality on routine electrodiagnostic studies. Supramaximal stimulation of the median, ulnar, peroneal, and posterior tibial nerves at frequencies of 0.5, 1, 2, and 5 Hz produced showers of electrical potentials following the M response in at least one nerve. In three patients, the fasciculations and evoked electrical potentials were abolished by regional application of curare but not nerve block. Carbamazepine therapy caused moderate-to-marked reduction of symptoms and nerve hyperexcitability. We designate this hyperexcitable peripheral nerve disorder as the "cramp-fasciculation syndrome."
PMID: 1648679 [PubMed - indexed for MEDLINE]

Johns Hopkins Med J. 1976 Dec;139 SUPPL:49-60.Links
Autonomous peripheral nerve activity causing generalized muscle stiffness and fasciculations: report of a case with physiological, pharmacological, and morphological observations.
Harik SI, Baraka AS, Tomeh GF, Mire-Salman J, Kronful Z, Afifi AK.
A 14-year-old boy with generalized muscle weakness, stiffness and fasciculations associated with profuse and continuous electromyographic (EMG) activity is described. The spontaneous mechanical and electrical muscle activity was unaffected by sleep, general anesthesia, or spinal anesthesia but was abolished by small doses of curare, succinyl-choline, and gallamine. Proximal and distal peripheral nerve block caused moderate and marked reduction of EMG activity, respectively, thus indicating that the disorder is due to autonomous peripheral nerve activity. The delayed motor nerve conduction velocities and the structural abnormalities seen in some of the myelin sheaths by light and electron microscopic studies on sural nerve biopsy preparations constitute further evidence that the peripheral nerve is the site of abnormality in this disorder. Diphenyl hydantoin and carbamazepine maintenance therapy produced adequate clinical relief.
PMID: 189112 [PubMed - indexed for MEDLINE]

: J Neurol Neurosurg Psychiatry. 1998 Feb;64(2):256-8. Links
Continuous muscle fibre activity: a case treated with acetazolamide.
Celebisoy N, Colakoglu Z, Akbaba Y, Yüceyar N.
Ege University, Faculty of Medicine, Department of Neurology, Bornova, Izmir, Turkey.
A case is reported of the continuous muscle fibre activity syndrome, which includes a group of disorders characterised by sustained motor unit activity due to hyperactivity of peripheral nerve motor axons. In this patient the muscle stiffness and myokymic movements were successfully treated with acetazolamide, which acts as a membrane stabiliser either by blockade of chloride and bicarbonate membrane transport or by producing kaliuresis and raising the transmembrane potential by decreasing extracellular potassium.
PMID: 9489543 [PubMed - indexed for MEDLINE]

Ann Neurol. 1997 Feb;41(2):238-46.Links
Autoantibodies detected to expressed K+ channels are implicated in neuromyotonia.
Hart IK, Waters C, Vincent A, Newland C, Beeson D, Pongs O, Morris C, Newsom-Davis J.
Neurosciences Group, Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, United Kingdom.
Antibody-mediated autoimmunity underlies a diverse range of disorders, particularly in the nervous system where the extracellular domains of ion channels and receptors are especially vulnerable targets. We present here a novel means of detecting autoantibodies where the genes of the suspected target proteins are known, and use it to detect specific autoantibodies in acquired neuromyotonia (Isaacs' syndrome), a disorder characterized by hyperexcitable motor nerves and sometimes by central abnormalities. We expressed different human brain voltage-gated potassium channels in Xenopus oocytes by injecting the relevant alpha-subunit complementary RNA, and detected antibody binding by immunohistochemistry on frozen sections. Antibodies were detected to one or more human brain voltage-gated potassium channel in 12 of 12 neuromyotonia patients and none of 18 control subjects. The results establish neuromyotonia as a new antibody-mediated channelopathy and indicate the investigative potential of this molecular immunohistochemical assay.
PMID: 9029073 [PubMed - indexed for MEDLINE]

Muscle Nerve. 1997 Mar;20(3):299-305.3.0.CO;2-6" target=_blank3.0.CO;2-6" target=_blank
Antibodies to potassium channels of PC12 in serum of Isaacs' syndrome: Western blot and immunohistochemical studies.
Arimura K, Watanabe O, Kitajima I, Suehara M, Minato S, Sonoda Y, Higuchi I, Takenaga S, Maruyama I, Osame M.
Third Department of Internal Medicine, Kagoshima University School of Medicine, Sakuragaoka, Japan.
We investigated the pathophysiology of nerve hyperexcitability in a patient with Isaacs' syndrome, who had typical clinical and electromyographic features and responded to plasma exchange. Immunoblotting and immunohistochemistry studies showed that antibodies from this patient reacted with the lysate of a neuronal cell line (PC12). In Western blots, constituents of the patient's serum, particularly immunoglobulin M, reacted with proteins of approximately 50 and 18 kDa, whereas the control serum did not. A cross-linking study with alpha-dendrotoxin (7 kDa) showed a 57 kDa protein-peptide complex. Immunohistochemistry showed that the patient's serum reacted with PC12 cells and human intramuscular nerve axons. Our findings indicate that in Isaac's syndrome nerve hyperexcitability is the result of the immunological involvement of the voltage-dependent potassium channels located along the distal motor nerve or at the nerve terminal.
PMID: 9052808 [PubMed - indexed for MEDLINE]

Phenotypic variants of autoimmune peripheral nerve hyperexcitability
Ian K. Hart1, Paul Maddison2, John Newsom-Davis2, Angela Vincent2 and Kerry R. Mills3
1 Neuroimmunology Group, University Department of Neurological Science, Walton Centre, Liverpool, 2 University Department of Clinical Neurology, Institute of Molecular Medicine, Oxford, 3 Department of Neurophysiology, King’s College Hospital, London, UK
Correspondence to: P. Maddison, Neurology Department, Royal Victoria Infirmary, Newcastle upon Tyne NE1 4LP, UK E-mail:
We found raised titres (=" src="/math/ge.gif" border=0100 pmol/l) of serum VGKC antibodies in 15 out of 39 (38%) of group A patients and five out of 18 (28%) of group B patients tested (Fig. 2)
Although overall only 35% of patients had raised VGKC antibody titres detected by the 125I--dendrotoxin immunoprecipitation assay, this is likely to be an underestimate. We have previously discussed the relative insensitivity of this assay compared with a molecular-immunohistochemical assay that detects serum binding to frozen sections of Xenopus oocytes injected beforehand with cRNA for an individual VGKC subunit (Hart et al., 1997).
This finding emphasizes that acquired nerve hyperexcitability is not a single disease process, but a response to peripheral nerve dysfunction or damage arising from several different causes


Dr I.Hart. Senior lecturer in Neurology.
The study title is. "Characterization of autoantibodies associated with peripheral nerve hyperexcitability (PNH)".
This involves the study of the immune system in conditions causing muscle twitching and cramps. It is known that in many patients with PNH the cause is a problem with the immune system which, instead of protecting the body as it should do when functioning normally starts to produce antibodies that bind to parts of the nerve called potassium channels. This results in muscle overactivity causing twitching and cramps. The present tests however, only detect these antibodies in about 40% of patients. The aim of this study is to try to identify whether other, different antibodies can cause PNH and to analyse how these antibodies interfere with nerve function.


Muscle Nerve. 2007 Jul 18; [Epub ahead of print] Links
Interspike interval analysis in a patient with peripheral nerve hyperexcitability and potassium channel antibodies.
Kleine BU, Stegeman DF, Drost G, Zwarts MJ.
Department of Clinical Neurophysiology, Radboud University Nijmegen Medical Centre, P.O. Box 9101, 6500HB Nijmegen, The Netherlands.
Neuromyotonia or Isaacs' syndrome is a rare peripheral nerve hyperexcitability disorder caused by antibodies against potassium channels of myelinated axons. We present the high-density surface electromyographic (EMG) recordings of a patient with fasciculations and cramps due to neuromyotonia. To characterize the time course of hyperexcitability, we analyzed the interspike intervals (ISIs) between fasciculation potentials, doublet, and multiplet discharges. ISI duration increased within each burst. The ISI histograms found can be explained by the recovery cycle of the myelinated axon and its dependency on the slow potassium conductance. We conclude that ISI analysis is a useful tool to understand the membrane dynamics underlying abnormal motor unit activity. Muscle Nerve, 2007.
PMID: 17636480 [PubMed - as supplied by publisher]


Neurology. 2005 Oct 25;65:1330-1. Links
Sensory symptoms in acquired neuromyotonia.
Herskovitz S, Song H, Cozien D, Scelsa SN.
Department of Neurology, Montefiore Medical Center, Albert Einstein College of Medicine, Bronx, NY, USA.
PMID: 16247076 [PubMed - indexed for MEDLINE]

J Child Neurol. 1999 Jan;14:41-3.Links
Autoimmune syndromes at the neuromuscular junction.
Newsom-Davis J.
University of Oxford, United Kingdom.
PMID: 10223852 [PubMed - indexed for MEDLINE]

Newsom-Davis J.
Autoimmune neuromyotonia (Isaacs' syndrome): an antibody-mediated potassium channelopathy.
Ann N Y Acad Sci. 1997 Dec 19;835:111-9. Review. No abstract available.
PMID: 9616766 [PubMed - indexed for MEDLINE]
 
Geez Louise, look at all the fun I've been missing! :eek: I got yelled at by one of our attending doctors today, so what the heck, might as well roll up my sleeves and jump in.

All this debating and arguing and sniping has got to be so healthy for everyone's nerves. NOT.

Why can't we all just conclude that some of us had anxiety first, which ultimately led to our symptoms, while others developed a peripheral nervous condition first that can ultimately be exacerbated by anxiety? There may be more or less of one than another, but why should that really matter? Oh, yeah...because being extreme black or white in our thinking is one of the symptoms (or would that be causes?) of bfs. :mad:

We may never know who fits into either category, but it is probably fair to say, if you try anti-anxiolytics and cognitive restructuring and fail to feel significantly better...then mosey on over to the other camp.

Chicken or egg, egg or chicken, I think it is more important to know and acknowledge that it could be one, the other, or both. And I personally enjoy eating either one, as long as they are cooked thoroughly. ;)

Being correct, doing enough research, posting links to articles are all fine and good, but true peace can only be attained through acceptance...and moving on. Accept what we can not change, change what we can, and figure out the difference. And here's the crucial bit; it varies from person to person. Sir_Trouserz may need to put up her dukes and fight in order to establish peace in her life. Basso lights a Yankee candle and gets boinking. :mad: Neither is right or wrong in what works for them.

We can tie ourselves and our fellow board members into knots trying to determine what came first, or who has strictly anxiety vs who has a physical condition. Perhaps it was the baseline anxiety which left our immune system more vulnerable to the auto-immune condition of bfs, or maybe it was some other spiritual condition; such as self-loathing or poor self esteem. There is no doubt that our body responds to our mind, and vice versa. To attempt to place blame on one or the other is to drastically oversimplify this amazing vessel we dwell within.

Stress can contribute to heart attacks, high blood pressure, and strokes, but we wouldn't ever treat any of those conditions with stress reduction alone. And we know that these conditions in turn can then cause depression, anxiety, and a tormented spirit. Which came first? Dunno, but I sure as sh-t think it behooves us to address all of the above.

In my case, I had symptoms first. Then anxiety took over. But I can't honestly say that I didn't predispose myself to the medical condition known as "bfs," by having a lifetime of low-grade generalized anxiety that wreaked havoc on my physical person. Or maybe it was my abusive father, or some exposure to chemicals, or having taken some antibiotic for a sinus infection. There is just no telling. We can do studies, try treating this or that, but ultimately, I think it is up to each of us to figure out for ourselves.

Just my opinion, but I don't think it is particularly helpful to insist we have the only answer, not that anyone is necessarily doing that. It's flawed thinking, and arrogant; in that it fails to consider each person as a perfect, beautiful, whole.

My mother died of lung cancer almost 15 years ago. Before she died, her oncologist once told me that "prayer helps." It blew my mind, not because I disagree, but because I was shocked to hear her say it. Nonetheless, it is clinically tested and proven. A study concluded that patients who were prayed for (without their knowledge) had clinically improved outcomes over those who did not receive prayer, (also unknowingly.) Does it make sense from a biological perspective? Can we explain it? No, but that's how medicine works. It is something like 10% science, 40% trial and error and 50% fly by the seat of our pants expecting a miracle.

Hell, let's just enjoy the ride today, how 'bout it?

Blessings,
Sue
 
Some very good points LisaLM. Research and study have been my way of learning, improving and coping with different challenges in my life. There are some books based on research that have literally changed my life and way of thinking and I am a much happier person because of them.

My mother-in-law when I was going through a rough time was always and forever giving me books on her personal brand of philosophy which were always well-intended, but never helpful to me. I just couldn't relate to them. I had to find my own way.

What is helpful to me may not be to 43RichyThe43rd or Vanessa or others here, but it is my hope that they help someone who needs the same kind of reassurances that I do and may need help finding a neurologist or a medication and are having trouble finding either one to help.

My concern is that other people are being misdiagnosed and suffering needlessly like I did because they and their doctors did not know that BFS/BFCS/PNH as a condition has some documented medical causes and treatments. How other people choose to view this, live with this or what have you is a personal decision and everyone has to do what is right for them. If the woman in the original article I posted hadn't been treated just as just an 'anxiety case' she might have had helpful medical treatment sooner along with the psychological treatment that helped her, too.

And I hope you yelled back LisaLM, if that is what helps you deal with stress. If not, you can put up your dukes here if you like :LOL: ( Oh, wait a minute, I think you already did)
 
Wow you and me both Suz...I thought I would just read through this thread leisurely:))) Ang..don't listen to Steve anymore ;) And Basso...well, smooches.

The problem as Suzi most succintly put is that any medical condition comes with a variety of variants. Each person comes with a specific set of genetics and genetic predispositions, a lifetime of experiences and exposures and a unique set of circumstances. Yes there are some on this site who have anxiety as their primary and some who have BFS as their primary. Either way, we all seem to suffer from some of both in varying degress at different stages. When we finally reach that time when we have a definitive diagnois and plan of action for treatment then we can certainly call it as it is. I think for those of us more clinically minded - the prove it to me and make clear people....we need these types of studies and information, thanks for that Sir_Trouserz. Others of us need a place to be reassured and that is fine too. Medicine is not an exact science and I hope to God it never becomes one because then we will miss so much by taking the individual out of the equation and the treatment!
Kit
 
Sir_Trouserz
stop messing around with this topic. Almost everybody knows what this is....a physiological condition. Sure others have stress that gives them minor twitches for a minor amount of time. But our is different as you already know. Thanksgiving, Turkey, gravey, ham, dessert.....leave that stress causing theory in the dust. :unsure:
 
For those truly interested, here are a few links from a potential pool of literally thousands about anxiety and the physical symptoms research has documented to be associated with it. The last link might be of particular interest to some.

To try to make an "either/or" case out of this seems too narrow in focus given most "medical" problems have multiple causes, some of which are emotional or psychological in nature. Conisder medical conditions like cardiovascular disease and migraine head ache as examples of disorders that include biological, environmental, psychological and genetic factors in their genesis. We'll very likely miss something when we insist on making it singular in cause.

It is wrong for a psychotherapist to rule out a medical explanation for physical symptoms in the process of making a psychological diagnosis just as it is for a physician to dismiss something as "in your head". Coming up with an accurate diagnosis generally involves some time, thought and a process of ruling out through all sorts of tests and clinical examination. Even then, many times (barring very specific biological markers) it is more art than "science" in either profession.

Finally, I have indeed seen clients with big twitches and other interesting physical phenomena that have had a psychological cause, determined not just because I said so but after much testing and phsyician visits, etc. The havoc one's emotions can wreak on one's body is pretty amazing.

I don't see that the sharing of information needs to be adversarial. I thought we were here to be of help to one another. So, I guess I offer this up for anyone who thinks it could be helpful in managing their symptoms and for those who don't, well, keep looking.
 
kind of replying to this thread and kevintwisters here as they are both intertwined...

hoping that although i don't post here often anymore, i still have enough 'credentials' to do so ;) seriously - i don't think that anybody should need to build up as it were to any input on this forum - just because someone does not post regularly is not to say that they are not a very active 'lurker' and hence of value to a community...

i really don't understand why it is being pushed right now that bfs could be of only one origin - namely autoimmune - and that all other possibilties whether causes or ways to cope/cure are being blasted. i have to concur with tui here, who points out that whenever someone comes along with a success story, it seems they either get very little response; have their symptoms belittled in that it could never have been bfs in the first place; or are told that they are probably just in 'remission'.

personally - i find it rather arrogant to state that anxiety simply cannot be a cause of bfs... and i am also not sure how helpful it may be for some to persistently be told to delve deeper when given an 'anxiety' diagnosis... if you look hard enough in a negative way, then unpleasant things will often be found.... as a teenager i complained for years of heart palpitations etc and was always brushed off with anxiety - however i never felt that this was correct and so i pushed and pushed until finally i was diagnosed with 'long qt syndrome'. in my case this condition is hereditary and i was told that i had been a walking timebomb all my life. nevertheless - up until my diagnosis i still lived my life as though i was 'alive'... and i guess i still do... however now 2 of my children are also diagnosed with the same and it appears that they will not have the opportunity to live in such a carefree mode as i did... my children will always be on medication and must avoid all competitive sports and stress from the outset (even the egg and spoon race, for heavens sake)... so what are we? lucky that we know our diagnosis and hence may be able to prevent a fatal event, or instead forever restricted by fear of somethiong that may never have taken place... in many cases long qt in a family can have a devastating impact as jennhaz can vouch, however in my case, after trawling through our family tree, the experts cannot find one case of a fatality linked to long qt... some i guess could say i am in denial, however it looks to me that we seem to be a pretty low risk family, if such a thing exists in the documentation about long qt... i suppose at this point people may be thinking that i am posting on the wrong forum, but i guess my point is that sometimes delving so deep may not be beneficial albeit that you may uncover something that is 'medically' factual...

as for the studies, statistics and evidence that has so far been uncoverd on bfs... i find it bizarre that so much is discredited/ discounted if it does not relate to the mayo or hart studies, or has a benign enough cause to enable life to go on once fear of the symptoms has abated. i posted not so long ago about a study that my neurophysiologist has completed which followed 'twitching' in 150 or so women over 3 years - he concluded that the cause was hormonal. i received very few responses to this post and although i understand that the male members may feel that this study cannot include them - i fail to understand why it was not of more interest to many of the female twitchers out there. he is simply doing what so many of you demand should be done - researching twitching and coming up with possible explanations. incidentally - in my case - he concluded that the hormonal cause was probably not the cause of my twitching. anyway - like i said it seems that sometimes people want to discover more than a simple or benign cause... and likewise when people come up with a success story of what has worked in their case, they are dismissed as somehow not in the same boat of twitchers as all of those deeper delvers out there... why? :confused:
 
Thank you all for the input. I will read those articles Nancy and I think you're right that we should be here to help one another. The human body and the impact our emotions have on us are very complex and it is good to have input from so many knowledgable people. For me, for this condition that I now have, Steve's site, the new neuro and the new anticonvulsants, saved my sanity, but I will blame him for putting me up to all of this.

Zeke you are a laugh riot and I am so glad you stuck around. I am waaaay late in making my Turkey day grocery list and you are absolutely right that that is what I should be focusing on. :LOL: But I like to read research documents!!! (I know I'm such a geek and maybe no one wants to hear about them anyways)

Gobble Gobble!
 
Though I'm not sure my status as "Selfless Giver of Time" imbues me with the bona fides to weigh in such a weighty topic, I'll give it my best shot. I think that Suzi Q hit it right on the head (and those Attending docs should stop yelling at her because she is such a smart cookie :) ).

Anxiety exacerbates physiological conditions, and physiological conditions lead to greater anxiety. Which came first? Who knows? Are my twitching and myriad of other BFS symptoms entirely caused by anxiety? I doubt it, but I can't say for sure. How do I explain the fact that my symptoms seem to disappear when talking to a neurologist? Beats me. On the other hand, the onset of BFS symptoms happened during a time period where I was not particularly stressed about anything (and approximately 1.5 weeks after taking Cipro for a month). So what does that mean? No good answers.

The world is full of environmental risk factors that can (and do) cause physiological illness. And that is nothing new. For example, people used to die of cholera/dysentery all the time, but we now (in developed countries) have highly treated drinking water that prevents those illnesses generally; yet we still imbibe potentially carcinogenic trihalomethanes that are produced during the water chlorination process. We solve one environemental risk and inadvertantly create another. You simply can't eliminate environmental risk completely in modern society, and sometimes a person will develop a condition (BFS) and never know the reason why. There is apparently an association between MND and exposure to certain toxic materials, and few would assert that MNDs are caused by anxiety. Why is it then impossible to believe that there could a similar link between environmental/drug exposures and nerve hyperexcitability?

So bottom line is this, and Suzi Q is right on, for some people its more anxiety, for others its more physiological, and for many (myself included) its a combination of the two. I have TMJ and severe reflux, both of which are physiological, diagnosable conditions, and both of which may have had their root cause in anxiety. If CBT eliminates your twitching via counseling, then you are golden. If not, try some of the things that Sir_Trouserz is trying to control her symptoms through medicine. If they work, then again, you are golden. Or better yet, try both. There is no wrong answer in the context of BFS (other than "I think I have **S"). Get counseling for the anxiety that plagues most of us on this site, and also try any medical solutions that may be offered (anticonvulsants, etc.). Arguing about it only raises everyone's anxiety, and nobody on this site needs any more of that.

Okay, way more time than I wanted to spend on this . . . but hopefully this adds a little perspective. If not, can't say I didn't try.

J.
 
As much respect as I have for you opinion J, Suzi Q's, and everyone here, I have to say that I think there's a need for debate about this condition even if we disagree or never come to a clear consensus.

I am not happy about the way I was treated by my first neurologists and, though I wish I could say I were the only one for whom that is true, I know that I'm not. That makes looking into this further, wherever it leads us, a real necessity.

I don't like to compare this condition to any other, but as I told you in a pm, not so long ago docs were blaming CFS mostly on patient anxiety and now there are other medical causes suspected. The medical evidence for this condition having some defineable physiological causes is accumulating according to the research, in my own opinion. I know that others here disagree and that's fine.

I don't have all the answers, and no one here knows all the factors involved in the mind-body interaction with this or any other condition, but whatever part of this syndrome is physiological in nature I think we would eventually benefit by if we understand better, however that comes about.
 
Perhaps...just perhaps love is what matters anyway. Love of self, which sends out those amazing symmetrical ripples when it enters life's pond.

Basso
 
See, I knew you were biased towards love Basso, but I guess that is why everyone around here loves you so much. :D)
Sir_Trouserz
(PS I still love studies though, too. Sorry, hard to resist getting in the last word anyways. :rolleyes: )
 
What does this have to do with this thread? Nothing....but when I saw that Basso had written the words "perhaps love" it reminded me of a lovely song by john Denver.....

PERHAPS LOVE (John Denver)

Perhaps love is like a resting place, a shelter from the storm
It exists to give you comfort, it is there to keep you warm
And in those times of trouble when you are most alone
The memory of love will bring you home

Perhaps love is like a window, perhaps an open door
It invites you to come closer, it wants to show you more
And even if you lose yourself and don't know what to do
The memory of love will see you through

Love to some is like a cloud, to some as strong as steel
For some a way of living, for some a way to feel
And some say love is holding on and some say letting go
And some say love is everything, and some say they don't know


sorry to disrupt the thread, carry on.....

ristinaL91
 

Users who are viewing this thread

Total: 1 (members: 0, guests: 1)
Back
Top