Myofascial Pain Syndrome: MPS. A New Nomenclature for Myofascial Pain and Dysfunction: MPD

Myofascial Pain Syndrome: MPS

Relief of chronic Myofascial Pain and Dysfunction at www.ThinkBetterLife.com

Myofascial Pain Syndrome is a ewer term than Myofascial Pain and Dysfunction. It specifically takes Dysfunction out of the disorder which is a major mistake. Myofascial Pain is a disuse / misuse syndrome and is always a type of repetitive strain disorder.

TMJ Disorders, TMD,, Craniofacial Pain, Tension Headaches, Migraines,Cervicalgia and almost all chronic head and neck pain is directly related to Myofascial Pain and Dysfunction, MPD, MPS, Myofascial Pain Syndrome.  

Amazing Videos of Pain Relief from Migraines, TMJ, TMD, MPD, MPS, Fibromyalgia, Myofascial Pain Syndrome and Myofacial Pain and Dydfunction.

https://www.youtube.com/channel/UCk9Bfz6pklC7_UluWFHzLrg

Visit Dr Shapira's website to learn more and schedule an appointment.
www.ThinkBetterLife.com

 This type of change is designed to allow drug therapy instead of addressing underlying issues. It is part of an unfortunate swing in medicine to avoid cause and effect, corrrective actions, physical therapy, exercise, manual therapy and instead look at treatment with pharmaceuticals

90-95% of all pain is Myofascial Pain or pain coming from muscles and fascia. Dr Janet Travell wrote the book Myofascial Pain and Dysfunction: A Trigger Point Manual.

This youtube video is of a Fibromyalgia patient condemned by medicine to a life of constant pain. This diagnosis is faulty to say the least.
https://www.youtube.com/watch?v=A5xUFtuZe_Y
This patient has "Recovered" from fibromyalgia or never had fibromyalgia or the definition and signs and symptoms of fibromyalgia are a faulty system of diagnosis leading to faulty treatment.

Myofascial pain results from injury and chronic misuse of muscles. Repetiitive strain injury is the primary cause of SPG. Dysfunction or improper function is an essential issue in understanding these problems.

Myofascial pain is often mispronounced as Myofacial pain.

Fibromyalgia is a questionable diagnosis. How chronic MPD and Fibromyalgia are related is hotly contested. MPD patients recover and Fibromyalgia patients do not. Fibromyalgia can best be treated as systemic MPD but treating with the medical model leads to the medication model. This is a model that says recovery is not possible. I suggest treating all patients with a goal of complete remission initially. Treatment designed to promote healthy physiology is always better than treatment with medication to cover up symptoms.

Myofascial pain and Dysfunction (MPD) is a common, painful disorder that is responsible for many, if not the majority of pain clinic visits. MPD can affect any skeletal muscles in the body. Skeletal muscle accounts for approximately 50% of body weight, and there are approximately 400 muscles in the body. MP is responsible for many cases of chronic musculoskeletal pain and the diagnosis is commonly missed.

Mayo Clinic says about MPD "Myofascial pain syndrome is a chronic pain disorder. In myofascial pain syndrome, pressure on sensitive points in your muscles (trigger points) causes pain in seemingly unrelated parts of your body. This is called referred pain from muscle trigger points.."

Mayo clinic's description is actually and over-simplification. It is a result of distorted function that leads to formation of taut bands within the muscles. These are mediated through muscle spindles. The trigger points are areas of low EMG located in the taut band capable of causing pain referral to distant sites.

The term "Myofascial pain syndrome" leaves out the idea of Dysfunction. It is easy to move to medical management of functional problems when the dysfunction is discounted. MPD Typically occurs after a muscle has been contracted repetitively in an awkward manner. This can be caused by repetitive motions used in jobs or hobbies or by stress-related muscle tension. Tere is an enormous difference between healthy and unhealthy repetitive motions.

While nearly everyone has experienced muscle tension pain, the discomfort associated with myofascial pain and dysfunction syndrome persists or worsens over time if underlying issues are not corrected.. Treatment options for myofascial pain syndrome include physical therapy and trigger point injections. Pain medications and relaxation techniques also can help.

When patients also have TMJ disorders function becomes paramount.

MP can cause local or referred pain, tightness, tenderness, popping and clicking, stiffness and limitation of movement, autonomic phenomena, local twitch response (LTR) in the affected muscle, and muscle weakness without atrophy. Trigger points (TrPs), which cause referred pain in characteristic areas for specific muscles, restricted range of motion (ROM), and a visible or palpable LTR to local stimulation, are classic signs of MP. Over 70% of TrPs correspond to acupuncture points used to treat pain.[1]

An active TrP is an area that refers pain to a remote area in a defined pattern when local stimulation is applied. Satellite TrPs appear in response to a primary, active TrP and usually disappear after the primary TrP has been inactivated. Latent TrPs cause stiffness and limitation of ROM but no pain. Frequently, they are found in asymptomatic individuals.

Although MP and fibromyalgia have some overlapping features, they are separate entities; fibromyalgia is a widespread pain problem, not a regional condition caused by specific TrPs.

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TMJ AND POSTURE: THE INTIMATE CONNECTION BETWEEN CHIROPRACTIC PROBLEMS AND TMJ DISORDERS (TMD) ARE CRITICAL.

PATIENTS LIVING WITH TMJ DISORDERS, CHIROPRACTIC DISORDERS, HEADACHES AND MIGRAINES are alll suffering from the same underlying disorders. It is well recognized that it is impossible to achieve long term successful treatment without addressing both the dental, TMJ and Trigeminal components in conjunction with with the Chiropractic aspects of care.

Atlas Orthoganal Chiropractic or NUCCA chiropractic focus on the first two vertebrae. Both are excellent techniques but I usually prefer working with A/O chiropracters as they take a more universal approach to care. Many NUCCA chiropracters think that they can correct everything even though research at the prestegious Las Vegas Institue has shown that NUCCA adjustments DO NOT HOLD when the Neuromuscular Dental Occlusion is not corrected. A/o Chiropracters tend to be mor inclusive in care.

Atlas Orthoganal Chiropactic focuses on the first two vertebrae, the Atlas and the Axis. According to the website http://www.atlasorthogonality.com/index.htm the website of the Roy W Sweat Foundation:

"Atlas Orthogonal (SCALE—Stereotactic Cervical ALignment methods) is a spinal healthcare program developed by Dr. Roy Sweat in the late 1960’s based on scientific and biomechanical procedures. Dr. Sweat is considered by many to be one of the world’s foremost authorities on the cervical spine. After years of extensive research he developed a non-invasive, precision instrument to restore structural integrity from cervical vertebral malposition. The percussion instrument achieves postural restoration without manipulation or surgery. This precision treatment reduces cervical spine misalignment and its related symptomatology."

I work with two excellent A/O Chiropracters Dr Mark Freund in Lindenhurst and Dr David Menner in Lake Villa. I have also worked with severl NUCCA Chiropracters.

The connection between the Trigeminovascular system, the masticatory apparatus and the TM Joints was best described by a series ofg patients called "The Quadrant Theorem of Guzay" that describes how the actual center of rotation of the mandible (lower jaw) after accounting for both rotation and translation is on the Odontoid Process of the Axis found within the confines of the Atlas. The head rests on the Atlas on two fcets and it was named for Atlas in Greek Mythology who held the world on his shoulders.

Yoy can consider A/o Chiropracters and NUCCA Chiropracters as a herois Atlas managing the balance of the head on the top of the cervical column.

The neuromuscular Dentist is the navigator who assures that the head stays balanced so Atlas Axis stability is retained. The two treatments are intimately connected.

There are many other important areas of treatment in the body but these TOP Blocks are most important for anyone with Headaches, Migraines, TMJ, TMD, Spinal Problems, Tension-Type Headaches, SUNCY, Chronic Daily Headaches and non-infectious Sinus Pain and Sinus Headaches.

Additional information on Neuromuscular Dentistry is available at: http://www.sleepandhealth.com/neuromuscular-dentistry and at Dr Shapira's Delany Dental Care Ltd website at: http://www.delanydentalcare.com/neuromuscular.html

CENTRAL SENSITIZATION AND TMD: THE CONNECTION TO MYOFASCIAL PAIN, FIBROMYALGIA, HEADACHE, MIGRAINE AND RELATED DISORDERS.

I have frequently discussed the relation between headache, TMD and central sensitization. The trigeminal nerve is a frequent culprit in development of central sensitization which is why neuromuscular dentistry can be such an effective treatment. Decreases in nociceptive input from the trigeminal nerve can allow reversal of a sensitized state.

A new article in Pain "Pain." 2010 Oct 18. "Central sensitization: Implications for the diagnosis and treatment of pain." documents much of what we understand about central sensitization. These heightened central states are caused by noxious or nociceptive input into the brain. The trigeminal nerve carries a tremendous amount of information (nociception) into the CNS.

A recent article "Chronic Orofacial pain" proposes that "we propose the concept that because COFP and headaches share underlying pathophysiological mechanisms, clinical characteristics, and neurovascular anatomy, they should be classified together." This would be obvious to anyone who evaluates the anatomy and physiology of the brain and especially the stomatognathic system including the jaw muscles, teeth and periodontal ligaments. jaw joints and most importantly the trigeminal nerve. The trigeminal nerve is almost always indicated as a culprit or co-conspirator in chronic and episodic facial pain and headache .

The use of botox on jaw muscles to treat chronic headaches and migraines actually reduces nociceptive input to the trigeminal nerve from and brain from peripheral input. Neuromuscular dentistry also reduces nociceptive input withput the use of toxic nerve agents but utilizing antidromic TENS to relax muscles and establisha healthy physiologic rest position with minimal nociceptive input. Neuromuscular occlusion is simply a physiologic land spot that allows the muscle to return to a health rest position after function.

The computer adage "Garbage in- Garbage out" is what happens when nociceptive input to the brain exceeds our ability to comfortably adapt causing pain and central sensitization. Reduce the "garbage in" with neuromuscula dental techniques and the "garbage out" painful sequellae subside.

Curr Pain Headache Rep. 2010 Feb;14(1):33-40.
Chronic orofacial pain.
Benoliel R, Sharav Y.

Faculty of Dentistry, Department of Oral Medicine, Hebrew University-Hadassah, Jerusalem, Israel. benoliel@cc.huji.ac.il
Abstract
Chronic orofacial pain (COFP) is an umbrella term used to describe painful regional syndromes with a chronic, unremitting pattern. This is a convenience term, similar to chronic daily headaches, but is of clinically questionable significance: syndromes that make up COFP require individually tailored diagnostic approaches and treatment. Herein we describe the three main categories of COFP: musculoskeletal, neurovascular, and neuropathic. For many years, COFP and headache have been looked upon as discrete entities. However, we propose the concept that because COFP and headaches share underlying pathophysiological mechanisms, clinical characteristics, and neurovascular anatomy, they should be classified together.

PMID: 20425212 [PubMed - indexed for MEDLINE]

HEADACHES, MIGRAINES, FIBROMYALGIA, SLEEP APNEA, SWALLOWING PROBLEMS AND TMJ DISORDERS ARE ALL CLOSELY RELATED IN BOTH CAUSES AND TREATMENTS

PLEASE READ THIS ENTIRE BLOG ENTRY TO UNDERSTAND THE RELATIONSHIPS OF THESE DISORDERS. ALMOST ALL TREATMENT OF HEADACHES MUST CONSIDER THE MASTICATORY SYSTEM.

A new study "Effect of CPAP treatment on residual depressive symptoms in patients with major depression and coexisting sleep apnea: Contribution of daytime sleepiness to residual depressive symptoms." (see abstract below) suggests that treatment of sleep apnea will aid in resolution of symptoms. While this study used CPAP, Oral Appliances should have identical results.

The study concludes that "The results suggest that MDD patients with residual depressive symptoms despite pharmacotherapy who also have symptoms of suspected OSA, such as loud snoring, obesity, and daytime sleepiness, should be evaluated for sleep apnea by polysomnography and treated with an appropriate treatment such as CPAP. CPAP treatment may result in a significant improvement of residual depressive symptoms due to the improvement of daytime sleepiness in these patients.

Another study "Obstructive sleep apnea and depression." (see abstract below) reports 21-41% depression in sleep pne patients. It sites a previous study that lists sleep apnea as a risk factor for depression. It is not surprising that " Patients who have depression as well as OSA appear worse off than those with OSA only" ties together symptoms and treatments of sleep apnea, headaches and depression.

An opinion statement in Curr Treat Options Neurol. 2010 Jan;12(1):1-15 on on "SLEEP AND HEADACHES" ties together headaches, psychiatric problems and sleep apnea but stops short of what the NHLBI report that focuses on masticatory/trigeminal orgin of these problems.

The NHLBI published a report on the "CARDIOVASCULAR AND SLEEP RELATED CONSEQUENCES OF TEMPOROMANDIBULAR DISORDERS" THAT LOOKS AT MASTICATORY SYSTEM AS A COMMON CAUSE OF SLEEP APNEA, HEADACHES AND MANY OTHER PROBLEMS. Shimshak et al published two articles in Cranio that showed a 200-300% increase in medical costs in every field of medicine in patients diagnosed with TMJ disorders. This would include headache, migraine, depression and other diverse conditions.

The National Heart Lung and Blood Institue report states:
"The term TMD refers to a collection of medical and dental conditions affecting the temporomandibular joint (TMJ) and/or muscles of mastication, as well as contiguous tissue components. Symptoms range from occasional discomfort to debilitating pain and severely compromised jaw function. The masticatory apparatus is not only involved in chewing and swallowing but also in other critical tasks, including breathing and talking. Specific etiologies such as trauma and degenerative arthritides underlie some forms of TMD but there is no common etiology or biological explanation. TMD is hence comprised of a heterogeneous group of health problems whose signs and symptoms are overlapping but not identical.
Although broad longitudinal and cross-sectional epidemiological studies have not been carried out, TMD is estimated to affect about 12% of the general population, representing more than 34 million Americans. The majority of those seeking treatment are women in their reproductive years. As for many other pain conditions, the clinical scenario of TMD also tends to be more severe in women than men. TM disorders are considered a serious health problem because many individuals lose their ability to hold regular jobs and to function productively even within the context of a household environment.

The report talks about symptoms including "TMD has been used to characterize a wide range of conditions diversely presented as pain in the face or jaw joint area, masticatory muscle pain, headaches, earaches, dizziness, limited mouth opening due to soft or hard tissue obstruction, TMJ clicking or popping sounds, excessive tooth wear and other complaints."

The report also discusses effects on swallowing and breating ease: "There appears to an associated increase in coughing in subjects with sleep apnea. Occlusion of the pharynx can force residual secretions into the glottis and trigger coughing reflexes, swallowing reflexes, and other reflexes that could contribute to the disorganization of breathing during sleep. In addition to the muscles of mastication, the tongue plays an important role in the coordinated events of swallowing and breathing. The integration of breathing and swallowing is tightly linked, and these events in turn are in some manner linked to blood pressure regulation. Each of these pathways has been studied by scientists in individual disciplines, but there is a need for interdisciplinary studies to determine the interactions of the peripheral and central neural pathways controlling breathing, chewing, swallowing, and cardiovascular events. The presence of pain in patients with TMD would be expected to seriously impact upon these reflex and motor pathways. Little is known about the role of tongue position and how this may be altered in subjects with altered jaw location and structure. Sleep state has been shown to alter the central modulation of the coordination of breathing, airway dynamics, swallowing, and associated cardiovascular events. Differences in central modulation of these events in subjects with sleep apnea and TMD need to be evaluated using sleep as a dynamic change in the state of the individual. Cardiovascular, neuroendocrine, respiratory and swallowing alterations in awake and sleeping subjects need to be studied in a systematic manner in both in animal models and human subjects."

There are common developmental aspects that have been well documented between sleep apnea and TMJ disorders. There is an enormous cross over of signs and symptoms as well. While all sleep apnea may not be entirely related to masticatory structures there is unquestionably a large amount of crossover. There is a solid base of evidence based studies showing how airway issues change growth and development. There is also solid evidence based studies on treatment of sleep apnea with appliances that anteriorly position the mandible. there are numerous clinical reports and studies showing treatment of headaches and TMJ disorders with anterior positiong.

Is it time to look at a large proportion of sleep apnea as being related to jaw development. This would make it a treatment that could be treated and corrected by early interventions such as tonsilectomy and maxillary expansion. Maxillary expansion allows the mandible to automatically anteriorly position and frequently grow a healthier airway. A recent study showed that most pediatric patients having tonsils removed should also have expansion. Expansion according to many experts should precede tonsilectomy to reduce post operative risks.

The early correction of airway and jaw disorders could possibly save massive dollars in lifetime medical expenses if we extrapolate from the work of Shimshak. Shimshak did not show a correlation not cause and effect of TMJ disorders to increased medical expenses.

My opinion is that there is a definite cause and effect of TMJ disorders to massive increases in medical expenses. I believe that for the majority of patients sleep apnea are due to masticatory conditions that should be defined as a TMJ disorder. If we define sleep apnea as a TMJ disorder that other problems like ADD and ADHD are secondary TMJ disorders. This would also apply to morning headaches, cardiovascular, neurological, and psychiatric disorders


Sleep Med. 2010 Jun;11(6):552-7. Epub 2010 May 21.
Effect of CPAP treatment on residual depressive symptoms in patients with major depression and coexisting sleep apnea: Contribution of daytime sleepiness to residual depressive symptoms.
Habukawa M, Uchimura N, Kakuma T, Yamamoto K, Ogi K, Hiejima H, Tomimatsu K, Matsuyama S.

Department of Neuropsychiatry, Kurume University School of Medicine, Kurume, Fukuoka, Japan. hmitsu@med.kurume-u.ac.jp
Abstract
BACKGROUND: Although extensive studies have indicated a relationship between obstructive sleep apnea (OSA) and depressive symptoms, the effect of continuous positive airway pressure (CPAP) treatment on residual depressive symptoms in patients with both major depressive disorder (MDD) and coexisting OSA has not been examined.

METHODS: Seventeen patients with continued MDD despite pharmacotherapy such as antidepressants and/or benzodiazepines, who also had comorbid OSA, were required to complete the Beck Depression Inventory (BDI), Hamilton Rating Scale for Depression (HRSD), and Epworth sleepiness scale (ESS) at the commencement of the study and then again after 2 months of CPAP treatment.

RESULTS: BDI and HRSD scores decreased from 19.7 to 10.8 and 16.7 to 8.0 after 2 months of CPAP treatment (both p<0.01). We also found significant correlations among the improvement rates in BDI, HRSD and ESS scores (R=0.86 and 0.75, both p<0.01). The mixed effect model demonstrated a significant ESS effect on BDI and HRSD.

CONCLUSIONS: The results suggest that MDD patients with residual depressive symptoms despite pharmacotherapy who also have symptoms of suspected OSA, such as loud snoring, obesity, and daytime sleepiness, should be evaluated for sleep apnea by polysomnography and treated with an appropriate treatment such as CPAP. CPAP treatment may result in a significant improvement of residual depressive symptoms due to the improvement of daytime sleepiness in these patients.

PMID: 20488748 [PubMed - indexed for MEDLINE]

Sleep Med Rev. 2009 Dec;13(6):437-44. Epub 2009 Jul 10.
Obstructive sleep apnea and depression.
Harris M, Glozier N, Ratnavadivel R, Grunstein RR.

Australasian Sleep Trials Network, Adelaide Institute for Sleep Health, Flinders University, Adelaide, Australia. melanie.harris@flinders.edu.au
Abstract
There are high rates of depression in people with obstructive sleep apnea (OSA) in both community and clinical populations. A large community study reported a rate of 17% and reports for sleep clinic samples range between 21% and 41%. A large cohort study found OSA to be a risk factor for depression, but we are unaware of any longitudinal study of the reverse association. However correlations have not generally been found in smaller studies. Well-designed longitudinal studies are needed to examine temporal relationships between the two conditions and further research is needed to establish the role of confounders, and effect modifiers such as gender, in any apparent relationship. Symptoms common to OSA and depression, such as sleepiness and fatigue, are obstacles to determining the presence and severity of one condition in the presence of the other, in research and clinically. Sleep clinicians are advised to consider depression as a likely cause of sleepiness and fatigue. Several possible causal mechanisms linking OSA and depression have been proposed but not established. Patients who have depression as well as OSA appear worse off than those with OSA only, and depressive symptoms persist in at least some patients in short term studies of treatment for OSA. Direct treatment of depression in OSA might improve acceptance of therapy, reduce sleepiness and fatigue and improve quality of life, but intervention trials are required to answer this question.

PMID: 19596599 [PubMed - indexed for MEDLINE]

Curr Treat Options Neurol. 2010 Jan;12(1):1-15.
Sleep and headache.
Rains JC, Poceta JS.

Center for Sleep Evaluation, Elliot Hospital, One Elliot Way, Manchester, NH, 03103, USA, jrains@elliot-hs.org.
Abstract
OPINION STATEMENT: Headache has been linked to a wide range of sleep disorders that may impact headache management. There are no evidence-based guidelines, but the authors believe that literature supports the following clinical recommendations: 1. Diagnose headache according to standardized criteria. Specific diagnoses are associated with increased risk for specific sleep and psychiatric disorders. 2. Collect sleep history in relation to headache patterns. Screening questionnaires and prediction equations are cost-effective. 3. Rule out sleep apnea headache in patients with awakening headache or higher-risk headache diagnoses (cluster, hypnic, chronic migraine, and chronic tension-type headache); patients with signs and symptoms of obstructive sleep apnea warrant polysomnography and treatment according to sleep medicine practice guidelines. There is no evidence for suspending conventional headache treatment in suspected or confirmed cases of sleep apnea. Treatment of sleep apnea with CPAP may improve or resolve headache in a subset of patients. The impact on sleep apnea headache of other treatments for sleep apnea (eg, oral appliances, surgery, weight loss) is largely untested. At a minimum, sedative-hypnotic drugs should be avoided in suspected apneics until the sleep apnea is treated. 4. Among patients with migraine and tension-type headache, insomnia is the most common sleep complaint, reported by one half to two thirds of clinic patients. Patients who suffer from chronic migraine or tension-type headache may benefit from behavioral sleep modification. Pharmacologic treatment may be considered on a case-by-case basis, with hypnotics, anxiolytics, or sedating antidepressants used to manage insomnia, tailoring treatment to the symptom pattern. 5. Individuals with chronic headache are at increased risk for psychiatric disorders. Assessment for depression and anxiety may be warranted when either insomnia or hypersomnia is present. Psychiatric symptoms affect the choice of sedating versus alerting versus neutral pharmacologic agents for headache. 6. All headache patients, particularly those with episodic migraine and tension-type headaches, may benefit from inclusion of sleep variables in trigger management.

Increased Cortical Activity that causes headaches is increased with sleep apnea.

A recent study in Sleep Med on altered Cortical Excitability in sleep apnea concluded that " This TMS-based study suggests that untreated severe OSAS patients have imbalanced cortical excitabilities that enhanced inhibition or decreased brain excitability when awake during the day."

This may be a major cause of chronic headaches or migraines or other biochemical imbalances leading to stress disorders ofr depression. Many patients do not reach the clinical definition of sleep apnea but have UARS (upper respiratory resistance syndrome). This has been implicated in fibromyalgia and central sensitization as well.

I have included a few relevant pubmed articles below.

Sleep apne is the result of a TMJ disorder (http://www.nhlbi.nih.gov/meetings/workshops/tmj_wksp.pdf)

Neuromuscular Dentistry can help reduce incresed corticl activity, Treatment of sleep apnea can do the same.

Patients with sleep apnea have a smaller airway 24/7 that collapses at night. Correction of apnea and daytime jaw position may be ideal for all patients with chronic pain and sleep apnea.



Sleep Med. 2010 Oct;11(9):857-61.

Altered cortical excitability in patients with untreated obstructive sleep apnea syndrome.
Joo EY, Kim HJ, Lim YH, Koo DL, Hong SB.

Sleep Center, Department of Neurology, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.

Comment in:

Sleep Med. 2010 Oct;11(9):820-1.

Abstract
OBJECTIVE: To investigate cortical excitability in patients with obstructive sleep apnea syndrome (OSAS) during wakefulness.

METHODS: The authors recruited 45 untreated severe OSAS (all males, mean age 47.2 years, mean apnea-hypopnea index=44.6h(-1)) patients and 44 age-matched healthy male volunteers (mean apnea-hypopnea index=3.4h(-1)). The TMS parameters measured were resting motor threshold (RMT), motor evoked potential (MEP) amplitude, cortical silent period (CSP), and short-interval intracortical inhibition (SICI) and intracortical facilitation (ICF). These parameters were measured in the morning (9-10 am) more than 2h after arising and the parameters of patients and controls were compared. The Epworth Sleepiness Scale (ESS) and the Stanford Sleepiness Scale (SSS) were also measured before the TMS study.

RESULTS: OSAS patients had a significantly higher RMT and a longer CSP duration (t-test, p<0.001) compared to healthy volunteers. No significant difference was observed between MEP amplitudes at any stimulus intensity or between the SICI (2, 3, 5ms) and ICF (10, 15, 20ms) values of OSAS patients and healthy volunteers (p>0.05).

CONCLUSIONS: This TMS-based study suggests that untreated severe OSAS patients have imbalanced cortical excitabilities that enhanced inhibition or decreased brain excitability when awake during the day.

PMID: 20817550 [PubMed - in process]

Handb Clin Neurol. 2010;97:73-83.

Biological science of headache channels.
Pietrobon D.

Abstract
Several episodic neurological diseases, including familial hemiplegic migraine (FHM) and different types of epilepsy, are caused by mutations in ion channels, and hence classified as channelopathies. The classification of FHM as a channelopathy has introduced a new perspective in headache research and has strengthened the idea of migraine as a disorder of neural excitability. Here we review recent studies of the functional consequences of mutations in the CACNA1A and SCNA1A genes (encoding the pore-forming subunit of Ca(V)2.1 and Na(V)1.1 channels) and the ATPA1A2 gene (encoding the alpha(2) subunit of the Na(+)/K(+) pump), responsible for FHM1, FHM3, and FHM2, respectively. These studies show that: (1) FHM1 mutations produce gain-of-function of the Ca(V)2.1 channel and, as a consequence, increased glutamate release at cortical synapses and facilitation of induction and propagation of cortical spreading depression (CSD); (2) FHM2 mutations produce loss-of-function of the alpha(2) Na(+)/K(+)-ATPase; and (3) the FHM3 mutation accelerates recovery from fast inactivation of Na(V)1.5 channels. These findings are consistent with the hypothesis that FHM mutations share the ability to render the brain more susceptible to CSD, by causing excessive synaptic glutamate release (FHM1) or decreased removal of K(+) and glutamate from the synaptic cleft (FHM2) or excessive extracellular K(+) (FHM3).

PMID: 20816411 [PubMed - in pr

Handb Clin Neurol. 2010;97:47-71.

Pharmacology.
Bolay H, Durham P.

Department of Neurology, Gazi Hospital and Neuropsychiatry Centre, Gazi University, Besevler, Ankara, Turkey.

Abstract
Headache treatment has been based primarily on experiences with non-specific drugs such as analgesics, non-steroidal anti-inflammatory drugs, or drugs that were originally developed to treat other diseases, such as beta-blockers and anticonvulsant medications. A better understanding of the basic pathophysiological mechanisms of migraine and other types of headache has led to the development over the past two decades of more target-specific drugs. Since activation of the trigeminovascular system and neurogenic inflammation are thought to play important roles in migraine pathophysiology, experimental studies modeling those events successfully predicted targets for selective development of pharmacological agents to treat migraine. Basically, there are two fundamental strategies for the treatment of migraine, abortive or preventive, based to a large degree on the frequency of attacks. The triptans, which exhibit potency towards selective serotonin (5-hydroxytryptamine, 5-HT) receptors expressed on trigeminal nerves, remain the most effective drugs for the abortive treatment of migraine. However, numerous preventive medications are currently available that modulate the excitability of the nervous system, particularly the cerebral cortex. In this chapter, the pharmacology of commercially available medications as well as drugs in development that prevent or abort headache attacks will be discussed.

PMID: 20816410 [PubMed - in process]

Cephalalgia. 2010 Sep;30(9):1101-9. Epub 2010 Mar 19.

Cortical hyperexcitability and mechanism of medication-overuse headache.
Supornsilpchai W, le Grand SM, Srikiatkhachorn A.

Department of Physiology, Faculty of Medicine, Chulalongkorn University, Patumwan, Bangkok, Thailand.

Abstract
The present study was conducted to determine the effect of acute (1 h) and chronic (daily dose for 30 days) paracetamol administration on the development of cortical spreading depression (CSD), CSD-evoked cortical hyperaemia and CSD-induced Fos expression in cerebral cortex and trigeminal nucleus caudalis (TNC). Paracetamol (200 mg/kg body weight, intraperitonealy) was administered to Wistar rats. CSD was elicited by topical application of solid KCl. Electrocorticogram and cortical blood flow were recorded. Results revealed that acute paracetamol administration substantially decreased the number of Fos-immunoreactive cells in the parietal cortex and TNC without causing change in CSD frequency. On the other hand, chronic paracetamol administration led to an increase in CSD frequency as well as CSD-evoked Fos expression in parietal cortex and TNC, indicating an increase in cortical excitability and facilitation of trigeminal nociception. Alteration of cortical excitability which leads to an increased susceptibility of CSD development can be a possible mechanism underlying medication-overuse headache.

PMID: 20713560 [PubMed - in process]

HEADACHES, MIGRAINES, FIBROMYALGIA AND TMJ DISORDERS

There is an intimate cooection between TMD and Fibromyalgia and Tension-type and Muscle contraction headaches. These can also serve as triggers for many types of migraines and chronic daily headaches.

The connection is the Trigeminal Nerve that controls blood flow to the brain and contributes over half of all input to the brain an central nervous system from the body.

It is generally recognized by neuroscientists and neurologists that almost all headaches and migraines are primarily trigeminal in nature or influenced by the trigeminal nerve.

Neuromuscular dentistry may be the best prevention for these problems that frequently relate to sleep disorders as well.

Neuromuscular dentistry my be the ideal method to improve the your quality of lyour life without excessive medication. Both chiropractic and osteopathic medicine depend on the jaw for stability of the spine and holistic and or alternative health care methods like massage have longer lasting results when postural correction and neurofeedback from the trigemnal nerve are use as a stabilizing force rather than a continuing irritation that prevents healing and interferes with quality of life.

MYOFASCIAL TRIGGER POINTS ARE EXPLAINED: TMJ disorders discussed at 2010 American Equilibration Society Meeting: New Hope for Headache Sufferers

I just attended the 2010 American EquilibrationSociety meetng in Chicago titled "TREATING THE TMD PATIENT: Putting the Puzzle pieces together". Great news for patients with migraines, tension headaches and Temporomandibular disorders.

The meeting opened with an excellent letter by Henry Gremillion, who was recently named Dean of the Louisiana School of Dentistry. He spoke on "MYOGENOUS OROFACIAL PAIN" or pain coming from the muscles. It is well known that the majority of pain has orgins in the muscles, including tension-type headaches and chronic daily headaches as well as most pain associated with TMD disorders.

Dr Gremillion quoted a scary study where a single injection of nerver growth factor, a compound found in sore muscles and around trigger points could activate nociception (pain) for up to 7 weeks not just in the area of injection but in distant muscular and joint areas. Because nerve growth factor is also released in painful areas it explains why treatment can take weeks to show effectiveness. These biochemical changes are associated with neuralplasticity and central sensitization.

There is also a cmlative effect where up to 50 first order neurons can feed into a single second order neuron leading to referred pain and explaining some of the complexity of dealing with headaches coming from muscles but mediated thru the trigeminal nerve and trigeminovascular system resulting in biochemical changes in the brain. While many physicians and some dentists seek to treat this pain with enormous amounts of medications it is possible to change the neural input and and positively effect the CNS (central nervous system) Chemical inbalnces in the brain can be triggered by peripheral nervous system input. A point that was emphasized by the second speaker Dr Jay Shah of the NIHwhose lecture "NEW FRONTIERS IN THE PATHOSPHYSIOLGY OF MUSCULOSKELETAL PAIN : ENTER THE MATRIX" was truly extraordinary in explaining the biochemical changes that occurs in and around trigger points.

Even more exciting is the use of ultrasound imaging and especially vibrational sonoelastography to measure the stiffness around myofascial trigger points and to show the effects on blood flow in the immediate vicinity of trigger points. He also showed that the same biological and chemical changes occur around both latent and active trigger points. These peripheral changes create central nrvous sytem biochemical changes via afferent nerves. He discussed how pain can be due to noxious stimulus or loss of "DESCENDING INHIBITION OF PAIN" AND HOW INHIBITORY NERVE APOPTOSIS CAN CREATE PERMANENT PAIN STATES. TIME IS OF THE ESSENCE IN ADDRESSING NEUROMUSCULAR PAIN! Dr Shaw is a senior staff physiatrist in the rehabilitation medicine dept. After hearing him speak about the treatment of pain and basic research into underlying causes I believe at least some of our tax dollars are truly being used wisely.

His croup does micrassay of the chemicals around myofascial trigger points and they are now using miniscule accupunture needles which have two chanels prepared with lasers to collect chemical assays painlessly with minimal disruption to the tissues. The work he describes should make all patients with myofascial pain and /or fibromyalgia hopeful for better lives with pain controlled. These studies put the rest the idea that TMJ disorders are psychosocial or physical. There is no longer any doubt about the medical nature of these muscle disorders.

Patients with chronic headaches and migraines will surely benefit as this type of research flourishes. This research is also proving the validity of many basic precepts of neuromuscular dentistry. Correction of periheral problems that sey off muscle nociceptors and endogenous biochemicals cause amplification and perpetuation of peripheral and central sensitization that lead to persistent pain.

DR GREMILLION ALSO DISCUSSED VARIOUS ETIOLOGICAL HYPOTHESIS OF CHRONIC MUSCLE PAIN THAT ALL CORRELATED WITH NEUROMUSCULAR DENTISTRY TREATMENT. The central hypothesis dealth with first order to second order neuron ratios, the repetitve strain hypothesis is exactly what neuromuscular dentistry treats with microtrauma leading to macro problems. The peripheral sensitization hypothesis explains how microtrauma can cause central sensitization and the central biasing Mechanism hypothesis explains the equilibrium shifts as facilitation and inhibition ratios shift. He also discussed Sympathetic Dysregulation that can lead to Reflex Sympathetic Dystrophy (RSD) or Complex Regional Pain Syndromes (CRPS)