Does Blind Medicine see?

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14991339

J Neurol. 2004 Feb;251 Suppl 1:I19-I30.

Botulinum toxin in the treatment of rare head and neck pain syndromes: a systematic review of the literature.

Sycha T, Kranz G, Auff E, Schnider P.

Department of Neurology, Division of Neurological Rehabilitation, University of Vienna, Austria.

BACKGROUND: Botulinum neurotoxin (BoNT) is used to treat various neurological disorders associated with pathologically increased muscle tone. Botulinum toxin inhibits the release of the neurotransmitter acetylcholine at the neuromuscular junction thereby inhibiting striatal muscle contractions. Besides the reduction in muscle tone BoNT tends to reduce pain in pain syndromes associated with muscle spasm. In addition, BoNT has been proposed as an analgesic, suggesting alternative non-cholinergic mechanisms of action.Surprisingly, BoNT was reported as a potential treatment for tensiontype headache and migraine-both primary headache syndromes without an apparent muscular component-however, varying responses to BoNT have been found, overall without sufficient evidence for a general treatment.In this systematic review we set out to clarify the efficacy and safety of BoNT in the treatment of rare head and neck pain syndromes (e. g. cervicogenic headache, chronic paroxysmal hemicrania, cluster headache, trigeminal neuralgia, temporomandibular disorders, cervical dystonia and whiplash injuries).

OBJECTIVES: To assess the analgesic efficacy and safety of botulinum toxins versus other medicines, placebo or no treatment in rare head and neck pain syndromes.

SEARCH STRATEGY: We searched the bibliographic databases MEDLINE, EMBASE and PASCAL Biomed to May 2003. We also reviewed the reference lists from identified articles including reviews and meta-analyses of treatment studies. Furthermore we searched booklets of scientific congresses in the field of neurology for potentially relevant studies. Additional reports were identified from the reference list of the retrieved papers, and by contacting experts in the field.

SELECTION CRITERIA: Randomized controlled trials (RCTs) with any dose of BoNT for rare head and neck pain syndromes, describing subjective pain assessment as either the primary or a secondary outcome, were included in this review.

DATA COLLECTION AND ANALYSIS: All trials were quality scored and two independent reviewers extracted data. Results were compared for differences, and discrepancies were resolved by discussion.

MAIN RESULTS: Fourteen RCTs of BoNT in cervical dystonia were included in this review. All except one showed significant pain relief following BoNT treatment compared to placebo. Studies providing dichotomous outcome data were pooled using the Peto method. The overall effect was found to be highly significant (OR 4.795 [95% CI 5.551-6.473]). For cervicogenic headache, two RCTs-one positive study and one negative study-were included. Two studies addressing chronic neck pain were included in this review. Both studies did not reveal significant effects. Furthermore, one small trial (N = 15 patients) focussing BoNT in temporomandibular disorders was included,without demonstrating significant effectiveness but a high proportion of patients lost to follow-up and a high rate of adverse effects. For the use of BoNT in cluster headache, chronic paroxysmal hemicrania and trigeminal neuralgia no RCTs were identified.Adverse effects (AEs) were found to be mild to moderate and dose-dependent. They were summarized where possible, irrespective of the formulation used and condition treated (OR = 5.066 [95% CI 2.770-9.265], number-needed-to-harm (NNH) = 5.5 [range 4.4-17]).

REVIEWERS' CONCLUSIONS: There is convincing evidence for the effectiveness of BoNT in the treatment of pain associated with cervical dystonia. Due to the frequent adverse effects predominantly observed with higher doses, the trade off in risk and benefit should be carefully considered in each case. For all other rare head and neck pain syndromes we found no RCTs (cluster headache, chronic paroxysmal hemicrania, trigeminal neuralgia) and only a few small sized trials (cervicogenic headache, chronic neck pain, temporomandibular disorders). We were therefore unable to draw any definite conclusions.

PMID: 14991339 [PubMed - in process]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=14723558

Drugs. 2004;64(1):45-62.

Myofascial pain disorders: theory to therapy.

Wheeler AH.

Pain and Orthopedic Neurology, Charlotte Spine Center, Charlotte, North Carolina 28207, USA. pon@caro.net

Voluntary muscle is the largest human organ system. The musculotendinous contractual unit sustains posture against gravity and actuates movement against inertia. Muscular injury can occur when soft tissues are exposed to single or recurrent episodes of biomechanical overloading. Muscular pain is often attributed to a myofascial pain disorder, a condition originally described by Drs Janet Travell and David Simons. Among patients seeking treatment from a variety of medical specialists, myofascial pain has been reported to vary from 30% to 93% depending on the subspecialty practice and setting. Forty-four million Americans are estimated to have myofascial pain; however, controversy exists between medical specialists regarding the diagnostic criteria for myofascial pain disorders and their existence as a pathological entity. Muscles with activity or injury-related pain are usually abnormally shortened with increased tone and tension. In addition, myofascial pain disorders are characterised by the presence of tender, firm nodules called trigger points. Within each trigger point is a hyperirritable spot, the 'taut-band', which is composed of hypercontracted extrafusal muscle fibres. Palpation of this spot within the trigger point provokes radiating, aching-type pain into localised reference zones. Research suggests that myofascial pain and dysfunction with characteristic trigger points and taut-bands are a spinal reflex disorder caused by a reverberating circuit of sustained neural activity in a specific spinal cord segment. The treatment of myofascial pain disorders requires that symptomatic trigger points and muscles are identified as primary or ancillary pain generators. Mechanical, thermal and chemical treatments, which neurophysiologically or physically denervate the neural loop of the trigger point, can result in reduced pain and temporary resolution of muscular overcontraction. Most experts believe that appropriate treatment should be directed at the trigger point to restore normal muscle length and proper biomechanical orientation of myofascial elements, followed by treatment that includes strengthening and stretching of the affected muscle. Chronic myofascial pain is usually a product of both physical and psychosocial influences that complicate convalescence.

PMID: 14723558 [PubMed - in process]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12913709

J Urol. 2003 Sep;170(3):828-31.

Musculoskeletal dysfunction in men with chronic pelvic pain syndrome type III: a case-control study.

Hetrick DC, Ciol MA, Rothman I, Turner JA, Frest M, Berger RE.

Department of Urology, University of Washington, 1959 N.E. Pacific Street, Seattle, WA 98195, USA.

PURPOSE: Men with chronic pelvic pain syndrome (CPPS) type III experience pelvic pain of uncertain etiology. Pain has been attributed to prostatic, bladder and muscular origins. Few studies have documented pelvic and abdominal muscle function in men with CPPS or compared their muscular examination to that of men without pain. We hypothesized that the musculoskeletal examinations of men with CPPS types IIIA and IIIB would show more spasm, tenderness and dysfunction than in men without CPPS.

MATERIALS AND METHODS: A total of 62 men with CPPS and 89 healthy men without pelvic pain underwent a standardized musculoskeletal examination by a licensed physical therapist.

RESULTS: Controls and patients with pain showed a significant difference in muscle spasm, increased muscle tone, pain with internal transrectal palpation of the pelvic muscles, and increased tension and pain with palpation of the levator ani and coccygeus muscles (p <0.001). Patients with pain also had significantly greater pain and tension with palpation of the psoas muscles and groin. Patients and controls did not differ significantly in strength testing of the lower abdominal and oblique muscles.

CONCLUSIONS: Men with CPPS have more abnormal pelvic floor muscular findings compared with a group of men without pain. Abnormalities of the pelvic muscles may contribute to this pain syndrome.

PMID: 12913709 [PubMed - indexed for MEDLINE]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11320861

Nervenarzt. 2001 Apr;72(4):261-74.

Botulinum toxin A for the treatment of headache disorders and pericranial pain syndromes

[Article in German]

Gobel H, Heinze A, Heinze-Kuhn K, Austermann K.

Neurologisch-verhaltensmedizinische Schmerzklinik Kiel in Kooperation mit der Universitat Kiel, Heikendorfer Weg 9-27, 24149 Kiel. kiel@Schmerzklinik.de

For 20 years botulinum toxin A has been used for the treatment of a variety of disorders characterised by pathologically increased muscle contraction. Recently, treatment of tension headache, migraine, cluster headache, and myofascial pain syndromes of neck, shoulder girdle, and back with botulinum toxin A has become a rapidly expanding new field of research. Several modes of action are discussed for these indications. The blockade of cholinergic innervation reduces muscular hyperactivity for 3 to 6 months. Degenerative changes in the musculoskeletal system of the head and neck are prevented. Nociceptive afferences and blood vessels of the pericranial muscles are decompressed and muscular trigger points and tender points are resolved. The normalisation of muscle spindle activity leads to a normalisation of muscle tone and central control mechanisms of muscle activity. Oromandibular dysfunction is eliminated and muscular stress removed. However, the effect of botulinum toxin A cannot be explained by muscular actions only. Its retrograde uptake into the central nervous system modulates the expression of substance P and enkephalins in the spinal cord and nucleus raphe. Recent findings suggest an inhibition of sterile inflammation which may lead to a blockade of the neurogenic inflammation believed to be the pathophysiological substrate of primary headache disorders. The efficacy of botulinum toxin A in the treatment of pain disorders is being investigated in several studies at the moment. The results and experiences obtained so far present new alternatives in the treatment of chronic pain disorders. The practical use of botulinum toxin A is demonstrated.

Publication Types:
·Review
·Review, Tutorial

PMID: 11320861 [PubMed - indexed for MEDLINE]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8215965

Arch Neurol. 1993 Oct;50(10):1061-4. Related Articles, Links

Decreased nociceptive flexion reflex threshold in chronic tension-type headache.

Langemark M, Bach FW, Jensen TS, Olesen J.

Department of Neurology, Gentofte Hospital, University of Copenhagen, Denmark.

OBJECTIVE--To study nociceptive processing in chronic tension-type headache.

DESIGN--Survey of the threshold for the nociceptive flexion reflex obtained by sural nerve stimulation in a convenience sample of 40 patients with chronic tension-type headache and in 29 sex- and age-matched healthy subjects. Muscular response was recorded from the biceps femoris muscle. For each stimulation, subjects recorded pain on a visual analogue scale.

RESULTS--In seven subjects (four headache sufferers and three healthy subjects), no nociceptive flexion reflex response could be elicited. The median nociceptive flexion reflex threshold in the headache group was significantly lower (median, 10 mA) than in the control group (median, 20 mA). Pain tolerance thresholds were significantly lower in the headache group than in the control group. A high degree of correlation was found between nociceptive flexion reflex threshold and tolerated stimulus strength. The slopes of the stimulus intensity/visual analogue scale pain rating response curves were steeper in patients with headache than in control subjects.

CONCLUSIONS--Chronic tension-type headache may represent a disorder of an endogenous antinociceptive system with a lowering of tone and recruitment of descending inhibitory systems.

PMID: 8215965 [PubMed - indexed for MEDLINE]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=8219515

Clin J Pain. 1993 Sep;9(3):159-67.

Serotonin and its role in headache pathogenesis and treatment.

Marcus DA.

Department of Anesthesiology, University of Pittsburgh, PA 15213.

OBJECTIVE: This review tries to consolidate the literature on changes in serotonin and the importance of these changes for understanding headache pathogenesis and determining treatment. A model is presented that integrates previous serotonin studies and offers an explanation for apparent contradictions in the literature.

DATA SOURCES: Fifty-four journal articles that described a relationship between serotonin and headache in animal and human models were identified through Medline search and bibliography and reviewed. Alterations in serotonin, headache, and clinical situations influencing headache activity were examined.

DATA SYNTHESIS: Abnormalities in blood vessels have traditionally been implicated in the pathogenesis of migraine headaches, and excessive muscle contraction in tension-type headaches. Interestingly, both vascular and muscular changes occur in both migraine and tension-type headache. Recently, biochemical changes have been demonstrated in both types of headaches. These biochemical changes are postulated to precede and possibly cause the subsequent changes in blood vessels and muscle tone, known to occur in chronic headaches. Serotonin has been the most widely studied neurochemical in relation to headaches. Apparently contradictory results have been shown, such as increasing serotonin levels both increasing and decreasing headaches.

CONCLUSIONS: Serotonin plays an important role in the pathogenesis of headaches. Changes in serotonin may precede the vascular and muscular changes of migraine and tension-type headaches. The influence of serotonin on headaches explains a number of clinical situations that affect headache activity and the variety of classes of effective headache medications.

Publication Types:
·Review
·Review, Tutorial

PMID: 8219515 [PubMed - indexed for MEDLINE]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6115801

Fortschr Med. 1981 Aug 27;99(31-32):1226-30.

Depression in rheumatic diseases or somatic symptoms in depression

[Article in German]

Carriere B.

Depression can be produced in many different ways. Via cerebral nuclear-specific imbalance a depression can be associated with disturbances in nuclear regions regulating muscular tone. Such syndromes appear chiefly as syndromes of the cervical vertebral column or lumbal vertebral column or as a general "non-specific-pain-syndrome". Depression may also cause manifestations of "latent" rheumatic complaints by lowering the pain threshold. Chronic physical diseases may be assumed to produce depression via the "common pathway" (nuclear-specific imbalance of biogenic amines). Masked depression can assume the pattern of rheumatic pain syndrome and might be treated as such for a long time purely somatically (i.e. non-effectively because non-specifically).

PMID: 6115801 [PubMed - indexed for MEDLINE]

[bernard]

:idea: :?: What are the conlusions?

[nari]

Bon soir Bernard

Interesting references/studies. Good to see confirmation of what we suspect anyway.
My daughter receives BoTox injections every three or four months for her intermittent but severe headaches. It seems to work well, and quite quickly; probably far better than the Panadeine Forte and other strong stuff she was forced to take orally. Fortunately she works for a neurologist so it costs nothing.
What are the conclusions?
The sooner we appreciate the importance of central sensitisation the better.
I read somewhere (did not take a copy of it, and cannot remember the source) that the latest thoughts on arthritis (eg rheumatoid, psoriatic) is that the pain is centrally maintained and not just a local phenomenon.

Makes sense - when an XR of, say, a neck shows degeneration and altered IVD spaces yet the patient is painfree.....

We have a long way to go!

nari

[bernard]

Nari,

You look in a wrong side. Forget Botox, retain only the consequences of its use.

Look at the bold words, only these ones and you'll learn a simplicity?

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11252464

Scand J Med Sci Sports. 2001 Apr;11(2):64-80.

Sensorimotor control of knee stability. A review.

Solomonow M, Krogsgaard M.

Department of Orthopedic Surgery, Louisiana State University Medical Center, New Orleans, USA.

Traditionally, the concept of joint stability considered the displacement (or subluxation) of two bones relative to each other as the measurement index, and attributed the preservation of such stability in its physiologic range to the various ligaments associated with the joint. Although the ligaments are indeed the major restraints of any joint, the significant contribution of the musculature toward joint stability had been grossly overlooked or neglected until the last 15 years. The value and importance of muscular activity in that role becomes immediately apparent if one performs even a superficial functional comparison of muscles and ligaments. Ligaments are passive viscoelastic structures, whereas muscles are dynamic viscoelastic organs. The viscoelastic effects of the ligaments are activated and applied strictly upon the geometric and kinematic configuration of the joint traversing through its range of motion according to fixed force-displacement relationships. The musculature, however, can apply passive viscoelastic effects to the joint when not active (passive tone) and variable dynamic viscoelastic effects when contracting under voluntary or reflexive control, and at any desirable point in the range of motion and in response to joint speed, external load, gravity, pain, and so forth, while executing the functional objective of the movement set by the individual. Preservation of joint stability cannot be ascribed to the ligaments alone, but should be considered as a synergistic function in which bones, joint capsules, ligaments, muscles, tendons, and sensory receptors and their spinal and cortical neural projects and connections function in harmony. The objective of this report is to first review the anatomy and physiology of the various mechanoreceptors and their neural pathways about the joint, and describe some of the current concepts of the reflex arcs elicited by such receptors, with special emphasis on biomechanical outcomes relative to stability. The role of the musculature in maintaining stability while controlling joint motion is then reviewed, with data obtained from experiments performed on humans and animals. Finally, some clinical findings from patients with anterior cruciate ligament deficiency using a brace that simulates the ligament-muscle functions is described.

Publication Types:
·Review
·Review, Academic

PMID: 11252464 [PubMed - indexed for MEDLINE]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=10218243

Vet Clin North Am Equine Pract. 1999 Apr;15(1):87-96, vi-vii.

Spinal muscle pathology

Valberg SJ.

Department of Clinical and Population Sciences, Large Animal Medicine, University of Minnesota College of Veterinary Medicine, St Paul, USA.

Clinical signs that are easily referred to spinal muscle pathology include atrophy of epaxial muscles, focal swelling and palpable tenderness, as well as enlarged muscles with increased tone. Less easily recognized signs include rigidity of the spine, shortened stride, hindlimb lameness, and indicators of poor performance. Muscle biopsy is one option in evaluating sore backs and is best used when physical examination and imaging procedures do not reveal a likely diagnosis or when conventional treatments are unsuccessful. Rhabdomyolysis of spinal muscles may be due to nutritional myodegeneration (foals), recurrent exertional rhabdomyolysis, and polysaccharide storage myopathy. Atrophy of spinal muscles can be due to severe rhabdomyolysis, immune-related myopathy, or neurogenic atrophy from nerve trauma, EPM, or EMND.

Publication Types:
·Review
·Review, Tutorial

PMID: 10218243 [PubMed - indexed for MEDLINE]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9828696

Ther Umsch. 1998 Oct;55(10):618-23.

Leg pain--the contribution of the neurologist

[Article in German]

Beer S, Kesselring J.

Rheuma- und Rehabilitationszentrum, Valens.

Pain syndromes in the lower limbs are a particular challenge for the clinical neurologist. Pain may be due to various disorders of the central and peripheral nervous system or muscles of different etiologies. There is a continuum from slightly unpleasant sensory disturbances to nociception. Differential diagnosis must be sought according to topological and pathophysiological interpretation of the clinical findings. This will determine the necessary diagnostic requirements and therapeutic procedures. Within the central nervous system lesions of the nociceptive projections of the spinal cord or brain may lead to pain in the lower limbs. Furthermore, different pathologies of the peripheral nervous system (root, plexus, peripheral nerve) or muscles can cause pain. Finally, pain syndromes are known in clinical syndromes with disturbances of the muscle tone (extrapyramidal syndromes, spasticity) and secondary to postural problems in patients with muscular dysbalance due to paralysis.

Publication Types:
·Review
·Review, Tutorial

PMID: 9828696 [PubMed - indexed for MEDLINE]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9818473
Cas Lek Cesk. 1998 Oct 5;137(19):601-5.

Therapeutic effect of Myolastan on increased muscle tone of various etiologies

[Article in Czech]

Seidl Z, Obenberger J, Adam P.

Neurologicka klinika 1., Praha.

The authors tested in 101 patients the clinical effect of Myolastan (tetrazepam), generic name 1,4, benzodiazepine (BZD), in indications with increased muscular tonus of varying etiology. The drug has a balanced affinity to central and peripheral benzodiazepine receptors, it enhances the presynaptic inhibition of GABAergig neurones at the peripheral and supraspinal level. Clinical experience has shown that a decline of the increased muscular tonus in the affected segment mitigates subjective complaints, in particular pain, if the dosage and time of administration are adjusted for every individual patient. A favourable effect was proved during clinical administration to a heterogeneous group of patients which reflects the spectrum of our ambulatory patients with a locally increase muscle tonus. In addition to vertebrogenic complaints, non-discogenic and discogenic (proved by MR or CT), the group of patients comprised also some with multiple sclerosis. In the latter a favourable effect was recorded in 50%. The effect on spasticity in these patients was comparable with other drugs used by the patients before administration of Myolastan. The heterogeneous group of the remaining patients to whom Myolastan was administered suggests its possible further indications, without the possibility of significant conclusions. Possible side-effects could be eliminated by the administration of low doses in the evening or at night. Myolastan extends the range of drugs which have an impact on an increased muscular tonus.

PMID: 9818473 [PubMed - indexed for MEDLINE]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=9539669

Pain. 1998 Mar;75(1):1-17.
Understanding and measurement of muscle tone as related to clinical muscle pain.

Simons DG, Mense S.

Measurable sources of muscle tension include viscoelastic tone, physiological contracture (neither of which involve motor unit action potentials), voluntary contraction, and muscle spasm (which we define as involuntary muscle contraction). The latter two depend on motor unit action potentials to generate the tension. Total muscle tension is most accurately measured as stiffness. Thixotropy of muscle is an ubiquitous and functionally important phenomenon that is not commonly recognized. A clinical pain condition associated with increased muscle tension is tension-type headache, which is largely muscular in origin; it is often caused by myofascial trigger points, but not by a pain-spasm-pain cycle, which is a physiologically and clinically untenable concept. Clinical conditions associated with painful muscle spasm include spasmodic torticollis, trismus, unnecessary muscle tension, nocturnal leg cramps, and stiff-man syndrome.

Publication Types:
·Review
·Review, Tutorial

PMID: 9539669 [PubMed - indexed for MEDLINE]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6867124

Phlebologie. 1983 Apr-Jun;36(2):121-36. Related Articles, Links

Limping and muscle hypertonia concentrated in the calves. Relation to spasmophilia. Clinical and electromyographic study and treatment plan

[Article in French]

Boquet J, Guillerot E, Monnier JC.

The authors report several cases of patients who presented with pain in one or both calves and a limping gait. Clinical examination and the EMG confirmed that these disorders were of musculo-tendinous origin, maximal at the level of the gemellus tendon, frequently forming a tendinitis. The syndrome consists of a hypertonia of the calves which is maximal on waking and which improves on stretching the muscles. Most of the subjects examined suffered from a syndrome of restless legs and presented alterations of the autonomic nervous system and spasmophilia (simultaneous EMG recording of the left and right soleus muscles). Examination of the pathogenesis reveals the possibility of a phenomenon of tonic muscular training synchronous with variations in an elevated and unstable autonomic tone. The authors discuss a possible relationship with spasmophilia and algodystrophy. Finally, they propose a plan of treatment.

Publication Types:
·Case Reports

PMID: 6867124 [PubMed - indexed for MEDLINE]

[bernard]

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=213851

Spine. 1978 Sep;3(3):267-81.

Early and subtle signs in low-back sprain.

Gunn CC, Milbrandt WE.

The authors have previously reported myalgic hyperalgesia as a useful localizing sign in "low-back sprain" patients with no physical findings. This paper describes some other subtle signs related to the phenomenon of denervation supersensitivity which is well known to physiologists and clinicians involved in peripheral nerve disease, yet its related signs have not been applied to low-back pain. Following denervation of some neurons, muscle and peripheral receptors become supersensitive to transmitter substances and to different forms of stimuli. Since the peripheral nerve is a mixed nerve, findings are multiphasic and include autonomic dysfunction, trophic changes, cutaneous and myalgic hyperalgesia, and increased muscle tone. One or more of these signs occurred in 30 patients with secondary low-back pain but less often in 30 patients with primary or mechanical low-back pain; their presence, though slight, in asymptomatic controls may identify those individuals with a vulnerable back.

PMID: 213851 [PubMed - indexed for MEDLINE]

[rolf]

Hi Bernard!
I might be very slow but what is your intension by introducing these
articles? :?: :wink:

[bernard]

Hello Rin,

These articles have a common point. All tell us that pain, and more chronic pain brings changes in muscular tone. If in every case, we find pain with increased or perturbed tone, can we conclude that tone is an enhancer/producer of pain?

Many chances to do it, in this place. :wink: :wink:

Many chances to say that is many proves now that decreasing muscular tone decreases pain. All the Future of physiotherapy is in that way and we are pioneers, as Servaas. 8) 8) 8)

Now, theory is simple to elaborate and so is simple to find treatment for chronic pain patients?

[rolf]

hi Bernard!
In clinical pracsis i think its more corect to define what we feel when palpating the muscles asincreased or decreased stiffnes rather than tone.
As i have mentioned in noigroup earlier.Pain espesially chronick increase muscular tone (stiffness) more in the left side than the right.Increased stiffnes reduse muscular force. Thatswhy the left side also is weaker than the right side ,tested isomerticly.The right side of the brain is acording to Damasio and others your emotional spart of the brain,when the left side is the more logical part of the brain,very simply explained.
RIN

[emad]

Hi Rin:

In yuor last post, you have written about two issue :

muscle tone increase :arrow: increase pain
yes this right ,it is closed cycle ,pain leads to tension(tone increase) and the vice versa is right .


Right & left side :
Are you speaking general ,that tone is less in the left side of the body ?

Cheers
emad :lol:

[rolf]

Hi emad!
Nice to see the face of the person iam writing to!
The left and right side difference due to both increased muscular stiffness and decreased isometric strenght on the left side compared to the right side, in chronick pain patients has been discussed earlier on the noigroup.
NOBODY there answeared me if they had done the same experience if they did an isometric test on their patients.
The only person who seemed interested in these findings was Antonio Damasio,who i was interested in how these strenght and" tone" differences could be measured. :wink:
RIN

[bernard]

Hello RIN,

I had read with many interests your topic on NOI about the imbalance between the two sides of human beings. I think there is a normal one between the right and left side.
We are all right or left sided and thus we have all a normal imbalance?

But your thought is sensed because brain connection between the two brains are not equivalent and the two brains do not the same works.

But how do you feel that imbalance when as I said we are genetically oriented to have a dominant side?

[rolf]

Hi Bernard!
I quite agree that we have a dominant side and for most of us its the right side.(logical, mathematical,etc left side brain hemisphere)just cross your legs and se what feels natural to cross,this is your dominant side.
fMRI has shown scientist that our emotional part of the brain is the left side.When testing painpatient you will discover that as long as they have constant pain there will be a sidediffference in strenght,but when the pain dissapear they are in balance,strenght is no equal on the two sides.
The body dont lie.This side difference is a normal respons to stress(pain) and we all have it when we are in some cind of stress(pain)which continue for ours or days.
RIN :wink: :wink:

[emad]

HI Rin :
Looking forward to see your face

I agree that with pain ,muscle strengh decrease .ok

then you have spoken about the emotions considering pain as feel/emotion ,

Ok Rolf could you provide us by a scientific reference /evidence .
By the way
i have tried to cross legs ,i found myself cross Right over Left ,
i think the dominant/right usually easy to move /has skill/more applicable/more used .

cheers
emad :lol:

[rolf]

Hi Bernard!
I have always been the teachers "nightmare"by asking lots of questions.
Damasio foud my clinical empirical experience interesting,but he hadnt any answears him self.He was mostly interested in how to measure the muscular tone and strenght differences.
Sorry Bernard,but my clinical experience tells me that,pain is NOT proportional to muscular tone.If it was like that ,all my chronick patients should have more pain on their left side than the right but that is not my experience.Pain can be felt in the right lumbar area but the muscular tension/stiffness can be greater on the left side.

How to change tone?Decrease the reason for the painexperience!(physicaly,mentaly or" both")

By telling the patient about how tone/stiffness can change due to just your way of thinking can make the tone increase(they dont belive in me.dislike me as at herapeut)or decrease(they listen with interest,and like me as a therapeut)just in the first session.
I will be back with some hard scientific facts(i hope)not just my empirical experience.
RIN

[emad]

Hi Bernard & Rolf:

Bernard ,i find it is our priority to discuss the issue of left & right side
dominant and non
as that idea Nari , provide and reason using it

cheers
emad