ARE MY HEADACHES CAUSED BY TMJ? BOTOX: Diagnosing TMD (TMJ) Disorders with BOTOX

Are my headaches caused by TMJ?  

Headache Relief from BOTOX Injections is Diagnostic of a TMJ/TMD Disorder.

Edited from article in www.ThinkBetterLife.com

Patients frequently want to know whether their migraines or chronic daily headaches are caused by TMJ disorders.   This depends on how you differentiate  TMJ and/or  TMD disorders from headaches and migraines if the pain symptoms are identical.   The TMJ (Jaw Joint) is the TemporoMandibular Joint, TMD stands for TemporoMandibular Disorder.  The term TMJ often creates confusion in medical profesions, especially dentists who believe that TemporoMandibular Joints have to be clicking or poppping for a patient to be diagnosed with a TMJ disorder.  Diagnosing TMD or TemporoMandibular Dysfuction Syndrome requires examining  the entire complex of muscles, joints, teeth, habits, nervous system and understanding the complex underlying physiology of the entire system.

I have seen patients whose headaches are very easy to treat but they never had complete evaluation becaause they were told their headaches were not TMJ or TMD because there were no joint sounds or locking.  Patients can be critically deprived of proper treatment due to lack of apprpriate diagnosis.

TMD or TemporoMadibular Dysfunction includes the TMJoint, The joint capsule,  the muscles, the teeth, the periodontal ligaments,  the sinus linings, the tongue and its connections to the hyoid bone and associated muscles and ligaments, The posterior cervical muscles, the upper cervical spine including the atlas and axis vertebrae,the airway, the ears and most importantly the Trigeminal  Nervous System.

I will explain what the connection of TMJ to Headaches initially and at the end of this article how TMD treatment with a Diagnostic Neuromuscular Orthotic is an essential component in the diagnosis and treatment of all headache patients.

All headache specialists agree that the Trigeminal Nervous System is involved in almost 100% of all headaches. Specifically, two components of the Trigeminal Nerve are of critical importance to headache patients. The first is the Tigeminalvascular System which is the critical nervous component of all Migraine and Vascular Headaches as well as all autonomic Cephalgias. It controls the blood flow to the anterior two thirds of the brain thru the meninges or dura of the brain.

Most migraine preventive and treatment medications address the TrigeminoVascular System and the Trigeminal-Cervico Complex.

The second Trigeminal component is the Trigemino- Cervico Complex which is connected to almost all types of headaches including tension headaches, cervicogenic headaches and chronic daily headaches and more importantly is responsible for CENTRAL SENSITIZATION. Central Sensitization is the key connection that connects headaches and Fibromyalgia and other chronic pain syndromes.  

“The nociceptive (painful input) inflow from the meninges to the spinal cord is relayed in brainstem neurones of the trigemino-cervical complex (TCC). Two important mechanisms of pain transmission are the convergence of nociceptive trigeminal and cervical afferents and sensitization of trigemino-cervical neurones. ” (Schmerz. 2004 Oct;18(5):404-10.)

The same article also stated “These mechanisms have clinical correlates such as hyperalgesia, allodynia, spread and referral of pain to trigeminal or cervical dermatomes."  Trigemino-cervical complex neurones act as "integrative relay neurones between peripheral and central pain mechanisms. The understanding of these mechanisms has implications for the understanding of the clinical phenomenology in primary headache syndromes and the development of therapeutical options.”

The Central Nervous System thru the Trigeminal nerves causes referred pain and hyperalgesia, an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves.

Dermatones are actually road maps of where different nerves go, understanding where nerves come from and go to is essential in diagnosing what processes are causing pain.

Peripheral treatment of Migraine, Tension Headache, Chronic Daily Headache and Chronic Migraine with Botox is currently in vogue and should be considered an important diagnostic procedure as well as a treatment procedure. When Botox is administered to Trigeminally innervated muscles and gives substantial relief it should be considered diagnostic proof of a TMD problem.  This is especially true in patients diagnosed with fibromyalgia,  MPD or Myofascial Pain and Dysfunction problems.  

While there is nothing wrong with injecting Botulinum Toxin every three months into headache and migraine patients if it relieves their symptoms and improves their quality of life it is ridiculous to ignore the underlying causes necessitating use of BOTOX.  Our bodies are not designed or evolved to require BOTOX injections but need them due to failure to achieve healthy homeostasis of physiologic systems.

Relief of Migraine and other headaches by BOTOX should be considered proof of the existence of a TMD disorder.  

The Trigeminal Nerve is often called the Dentist’s Nerve, it innervates all of the pulpal tissue of the teeth as well as the periodontal ligaments (PDL). The PDL has at least 29 known nerve receptors and is the largest input to the proprioceptive system of the human body. The Trigeminal dwarfs input from the middle ear especially after impulses are amplified inthe Reticular Activating System of the brain.  

The trigeminal nerve also innervates the Jaw Joints or TMJoints, the joint capsules and the retrodiscal lamina of the TMJoints where most primary TMJ pain originates. Referred pain to the TMJoint can come from Trigeminally innervated masticatory muscles including the masseter muscles, the temporalis muscles, the medial pterygoid muscles the lateral pterygoid muscles, the diagatric muscles and the very specialized muscles that tense the ear drum (Tensor Veli Tympani) and the muscle that opens and closes the eustacian tubes the Tensor Veli Palatini.

Referred pain to the TMJoint area can also be referred fron neck and shoulder musculature via the Trigemino-Cervical Complex.  The upper cervical musculature should always be considered as an intimate component of the masticatory system and be evaluated in TMJ and/or TMD patients.

The tongue is also partially innervated by the Trigeminal Nerve and an extremely important function of the Trigeminal Nerve is to maintain a patent airway. The National Heart Lung and Blood Institute (NHLBI) of the NIH wrote an incredibly important report “The Cardiovascular and Sleep Related Consequences of TemporoMandibular Disorders” It emphasizes the effects of airway on a wide variety of problems. Sleep Apnea is a TMD problem or Jaw Problem, the most important function of our jaws, teeth tongue and muscles is to maintain an airway, essential for life.

Forward head posture is implicated in almost all chronic head and neck problems and is actually largely a response to diminished airway. A more accurate description would be a forward neck posture with excessive rotation at Atlas-Axis-Occipital Joints. This airway head position connection is the link to all chiropractic patients and TMD patients. As long as forward head posture is uncorrected adverse mechanical forces will be affecting the spine and posture. Atlas Orthoganol Chiropractic and NUCCA Chiropractic address this connection concentrating on the Occipital -Atlas-Axis connections which they feel is the primary  key to successful treatment.

The effect of the Trigeminal nerve including TrigeminoVascular and Trigemino-Cervico Complexes is that of  variable nociceptive and proprioceptive input into our CNS or Central Nervous System. In computer language chronic pain is an I/O error or input/uotput error. In English, GARBAGE IN-GARBAGE OUT!  Too much Nociceptive input will create temporary and eventually premanent changes in brain function.  Our Brain is our computer and nociceptive and garbled input to the body creates biochemical changes in our brain, at one threshold they cause pain at a higher or more continuous level they cause chronic pain and at their worst they cause Central Sensitiztion or a meltdown of normal fuction with creation of Hyperalgesia (increased pain response) and Allodynia (inappropriate pain response). The use of Botox TOXIN is to disconnect the Trigeminal Nerve from the Trigeminal Muscles. If it improves headache it is proof of the TMD disorder.

The most Ethical approach to these problems is the use of a Neuromuscular Diagnostic Orthotic to correct physiologic function of the masticatory system, decrease trigminal nociception, to create homeostasis of the proprioceptive systems, decrease Central Sensitization, correct airway and posture and to remove adverse mechanical forces to the cervical spine and to the entire spinal structure.

When the neuromuscular diagnostic orthotic is used many patients respond extremely favorably and utilization of dangerous medications is reduced or eliminated. The frequency of physical therapy, massage therapy, chiropractic and osteopathic adjustments is reduced and the overall quality of life is improved.  This is due to the unique ability of the diagnostic orthotic to change input to the brain thru the Trigeminal Nervous System.

Patients who respond positively to treatment with a neuromuscular diagnostic orthotic can move forward with  definitive treatment or have long term removable orthotics made.  Patients can titrate the amount of time they wear removable orthotics based on their symptoms.  

The adaptability of the human body is great and the joints and muscles can adapt to less than perfect physiology and position but this results in excess nociception into the CNS and can result in Central Sensitization.   There are certain publications such as "Treating TMDs with Permanent Mandibular Repositioning: is it Medically Necessary?" by  Charles S. Greene, DDS, Ales Obrez, DMD, PhD that use adaptability as a reason not to create permanent changes in the bite for TMD.   

The conclusion is any position, no matter how awful is always correct because of adaptability.  You can change the position but not for TMD.  

The arcticle states " The continuing adaptability of the teeth, muscles and TMJs throughout life is described in terms of homeostasis, leading to the conclusion that each person current TMJ position is biologically correct. Therefore, that position does not need to be changed as part of a TMD treatment protocol. This means that irreversible treatment procedures such as equilibration, orthodontics, full mouth reconstruction and orthognathic surgery cannot be defended as being medically necessary.

Dr Greene has a long history of working with Insurance companies to deny patients legitimate coverage.  In this paper Dr Greens wants to use insurance contract medical language used to deny claims and raise it to the level of science.  

The following is a footnote in the article:  "The term “medical necessity” appears often in the medical literature in regard to treating patients with various diseases/disorders. However, it is almost never defined in an operational manner. The authors were unable to find a complete or consistent definition for this term by searching medical dictionaries, PubMed, or various internet search engines (e.g., Google, Bing, Yahoo). Instead, the main source for the above list has been certain insurance company contracts, in which they inform doctors and hospitals about what will or will not be covered. The authors have modified those statements to develop the 6-point definition presented here. 

What Doctor Greene is stating:   THE SCIENTIFIC DIAGNOSIS OF WHAT IS MEDICALLY NECESSARY SHOULD BE BASED ON WHAT INSURANCE COMPANIES COVER.

The article is correct in stating there is adaptability but nervous system adaptability (or lack) creates central sensitization.

There are many aspects to treatment of TMJ disorders and this article is meant to address just the treatment effects of diagnostic orthotics.  Diagnostic Orthotics change jaw position and joint position but long term treatment is a clinical decision made by doctors and their patients together.

Each patient is in essence a clinical study of one. This is evidenced based medicine but it is the evidence obtained by evaluating and treating a single individual. There is an enormous benefit to prospective studies involving hundreds of patients to give us evidenced based approaches to fit populations. Unfortunately, the field of TMD has so many variables that the most efficatious method to study an individual is to do a clinical study that includes all of the variable unique to this specific patient. In utilizing a Neuromuscular Diagnostic Orthotic we accomplish that goal.

The patient can discontinue the non-invasive treatment at any time but if treatment improves symptoms in a life changing way the patient can elect to make definitive changes utilizing a position that has been shown to be effective and therapeutic.

IMPROVEMENT IN QUALITY OF LIFE IS ALWAYS THE GOAL OF TREATMENT

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]

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]

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)

Neuromuscular Dentistry, Central Sensitization and Trigeminal Neuralgia: Is Neuromuscular Dentistry an ideal method to prevent central sensitization?

A new article in Medical Hypothesis (see Pub Med abstract below) on Atypical Trigeminal Neuralgia discusses the pathogenisis of Central Sensitization in patients with Trigeminal Neuralgia. A percentage of patients with Trigeminal Neuralgia will have pressure on the trigeminal nerve either from blood vessels or tumors usually in the area of the foramen ovale.

Many patients who have trigeminal neuralgia have no overt cause for the disorder. When there is a tumor or blood vessel creating undue pressure on the nerve a surgiclal approach is usually corrective but the central sensitization may remain. This article postulates that time is of the essence and the longer the pain persists the more likely that brain plasticity will lead to long term central sensitization. Decompression should be done ASAP according to that line of thought.

The majority of patients diagnosed with trigeminal neuralgia do not have tumor or blood vessels encroaching on the trigeminal nerve. It is well known that treatment of TMJ disorders is highly effective in reducing pain and that Neuromuscular Dentistry has been shown to be "overwhelmingly successful" according to Dr Barry Cooper and published in Cranio Journal.

The same rationale that says the key to preventing central sensitiztion is to address the problem as soon as possible also holds true with neuromuscular problems affecting the jaws, bite, jaw muscles and TMJ (TM Joints).

The effects of pressure on the trigeminal nerve are periferrral effects (noxius input) afecting the CNS. Neuromuscular bite problems are also noxious input from the periferal nervous system.

A second article in Medical Hypothesis "Migraine, neuropathic pain and nociceptive pain: towards a unifying concept." brought this to light and pushed the unifying concept of mifgraine and neuropathic pain. The basic concepts are identical. Correction of noxious input is the key to treating the pain and preventing central sensitization. This is exactly the concepts behind Neuromuscular Dentistry.

This is also explained in an excellent article on Myofascial pain and TMD published in J Pain. 2009 Nov;10(11):1170-8 (see PubMed Abstract below)"Bilateral widespread mechanical pain sensitivity in women with myofascial temporomandibular disorder: evidence of impairment in central nociceptive processing." that is interesting because it looks at a group of 20-28 year old patients with myofascial pain, TMD and central sensitization. This group of patients definitively show how periferral pain manifestations induce central sensitization. The time to intervene with neuromuscular dentistry is at an earlier stage before central sensitization occurs.

There is also a concern about the quality of sleep as TMD patients have a much higher incidence of sleep apnea which I believe predisposes patients to central nervous system changes. Migraines, Chronic Daily Headaches, Tension-Type headaches and TMD are all directly effected by the trigeminal nerve and the trigeminovascular connection. Neuromuscular Dentistry can effect the central nervous system by changing the quality of neuro input.

Med Hypotheses. 2010 Feb 19. [Epub ahead of print]

Atypical trigeminal neuralgia: A consequence of central sensitization?
Hu WH, Zhang K, Zhang JG.

Beijing Neurosurgical Institute, Capital Medical University, Beijing, China; Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.

Trigeminal neuralgia (TN) is characterized by sudden, recurrent, usually unilateral, severe brief stabbing pains in the distribution of trigeminal nerve. Although it is widely accepted that blood vessel or tumor compression contributes to paroxysms of TN, the pathogenesis of persistent background pain in atypical TN patient is unclear. Central sensitization is pain hypersensitivity caused by central neural plasticity. It is responsible for many temporal and symptomatic features of acute and chronic pain. We hypothesize that central sensitization might account for some symptoms of atypical TN. Based on this hypothesis, we postulate that early medical intervention predicts good outcomes in TN and medicines which are effective on central sensitization may be potential agents for the treatment of atypical TN. Copyright © 2010 Elsevier Ltd. All rights reserved.

PMID: 20172658 [PubMed - as supplied by publisher]

Med Hypotheses. 2010 Feb;74(2):225-31. Epub 2009 Sep 17.

Migraine, neuropathic pain and nociceptive pain: towards a unifying concept.
Chakravarty A, Sen A.

Department of Neurology, Vivekananda Institute of Medical Sciences, Calcutta, India. saschakra@yahoo.com

Migraine, neuropathic pain and nociceptive pain are the three commonest pain syndromes affecting human. In the present article, we first present the salient features of the pathophysiology of the three conditions particularly highlighting the core features that are similar in the three conditions. We argue on the validity of the prevailing concept that maintenance of structural integrity of the nervous system differentiates nociceptive pain from neuropathic pain and point out that the fundamental pathophysiology of lasting nociceptive pain (like cancer pain) and neuropathic pain (like nerve injury pain) is essentially same. Migraine pathophysiology is complex and complicated by two opposing views on site of migraine pain generation - peripheral versus central. We hypothesize that this dichotomy has resulted from focusing on two different sites on a single, somewhat complicated, pain mediating circuitry from the peripheral meningeal and vascular structures through several cell stations in the brain stem and thalamus up to the sensory cortical matrix. At the end, we suggest that fundamentally all the three pain syndromes referred to in the article share a common pathophysiological mechanism, namely peripheral pain perception, peripheral sensitization at dorsal root ganglion or its intracranial counterpart (like trigeminal ganglion) and central sensitization at the spinal cord (dorsal horn for somatic pain), brain stem nuclei and thalamus before final pain perception at the sensory cortical matrix.

PMID: 19765908 [PubMed - in process]
that cause central sensitization and pain.

J Pain. 2009 Nov;10(11):1170-8. Epub 2009 Jul 9.
Bilateral widespread mechanical pain sensitivity in women with myofascial temporomandibular disorder: evidence of impairment in central nociceptive processing.

.
Fernández-de-las-Peñas C, Galán-del-Río F, Fernández-Carnero J, Pesquera J, Arendt-Nielsen L, Svensson P.

Department of Physical Therapy, Occupational Therapy, Rehabilitation and Physical Medicine, Universidad Rey Juan Carlos, Alcorcón, Madrid, Spain. cesar.fernandez@urjc.es

Our aim was to investigate bilateral, widespread pressure-pain hypersensitivity in nerve, muscle, and joint tissues in women with myofascial temporomandibular disorders (TMD) without concomitant comorbid conditions. Twenty women with myofascial TMD (aged 20 to 28 years old), and 20 healthy matched women (aged 20 to 29 years), were recruited. Pressure-pain thresholds (PPT) were bilaterally assessed over supra-orbital (V1), infra-orbital (V2), mental (V3) nerves, median (C5), radial (C6) and ulnar (C7) nerve trunks, the C5-C6 zygapophyseal joint, the lateral pole of the temporo mandibular joint (TMJ), and the tibialis anterior muscle in a blinded design. The results showed that PPTs were significantly decreased bilaterally over the supra-orbital, infra-orbital, and mental nerves, median, ulnar, and radial nerve trunks, the lateral pole of the TMJ, the C5-C6 zygapophyseal joint, and the tibialis anterior muscle in patients with myofascial TMD as compared to healthy controls (all sites: P < .001). There were no significant differences in the magnitude of PPT decreases between the trigeminal and extratrigeminal test sites. PPT over the mental nerve, the TMJ, C5-C6 zygapophyseal joint and tibialis anterior muscle were negatively correlated to both duration of pain symptoms and TMD pain intensity (P < .05). Our findings revealed bilateral, widespread pressure hypersensitivity in women presenting with myofascial TMD, suggesting that widespread central sensitization is involved in myofascial TMD women. PERSPECTIVE: This article reveals the presence of bilateral and widespread pressure-pain hypersensitivity in women with myofascial TMD, suggesting that widespread central sensitization is involved in myofascial TMD. This finding has implications for development of management strategies.

PMID: 19592309 [PubMed - indexed for MEDLINE]

Sleep and TMJ Disorders

Patients with TMJ disorders should be evaluated for sleep disorders according to a new article in Sleep. Primary Insomnia was associated with hyperalgesia or an increased pain response. It may also be associated with central senssitazation that is found in migraines, fibromyalgia and TMD and may be a causitive factor in idiopathic pain (pain of unknown orgins)

The NHLBI (National Heart Lung and Blood Institute considers Sleep Apnea to be a TMJ disorder. The paper "Cardiovascular and Sleep Related consequences of TMJ Disorders can be found at http://www.nhlbi.nih.gov/meetings/workshops/tmj_wksp.pdf

PATIENTS WITH TMJ DISORDERS AND SLEEP PROBLEMS SHOULD BE EVALUATED BY A SLEEP PHYSICIAN! FOR MORE INFORMATION ON SLEEP APNEA, DANGERS AND TREATMENT SEE http://www.ihatecpap.com

MORNING HEADACHES ARE USUALLY THE RESULT OF TMD OR SLEEP APNEA
BRUXISM IS OFTEN A SECONDARY RESULT OF SLEEP APNEA


PubMed abstract is supplied for your convenience.
Sleep. 2009 Jun 1;32(6):779-90.
Sleep disorders and their association with laboratory pain sensitivity in temporomandibular joint disorder.

Smith MT, Wickwire EM, Grace EG, Edwards RR, Buenaver LF, Peterson S, Klick B, Haythornthwaite JA.
Johns Hopkins University School of Medicine, Department of Psychiatry and Behavioral Sciences, Baltimore, MD, USA. msmith62@jhmi.edu
STUDY OBJECTIVES: We characterized sleep disorder rates in temporomandibular joint disorder (TMD) and evaluated possible associations between sleep disorders and laboratory measures of pain sensitivity. DESIGN: Research diagnostic examinations were conducted, followed by two consecutive overnight polysomnographic studies with morning and evening assessments of pain threshold. SETTING: Orofacial pain clinic and inpatient sleep research facility. PARTICIPANTS: Fifty-three patients meeting research diagnostic criteria for myofascial TMD. INTERVENTIONS: N/A. MEASUREMENTS AND RESULTS: We determined sleep disorder diagnostic rates and conducted algometric measures of pressure pain threshold on the masseter and forearm. Heat pain threshold was measured on the forearm; 75% met self-report criteria for sleep bruxism, but only 17% met PSG criteria for active sleep bruxism. Two or more sleep disorders were diagnosed in 43% of patients. Insomnia disorder (36%) and sleep apnea (28.4%) demonstrated the highest frequencies. Primary insomnia (PI) (26%) comprised the largest subcategory of insomnia. Even after controlling for multiple potential confounds, PI was associated with reduced mechanical and thermal pain thresholds at all sites (P < 0.05). Conversely, the respiratory disturbance index was associated with increased mechanical pain thresholds on the forearm (P < 0.05). CONCLUSIONS: High rates of PI and sleep apnea highlight the need to refer TMD patients complaining of sleep disturbance for polysomnographic evaluation. The association of PI and hyperalgesia at a nonorofacial site suggests that PI may be linked with central sensitivity and could play an etiologic role in idiopathic pain disorders. The association between sleep disordered breathing and hypoalgesia requires further study and may provide novel insight into the complex interactions between sleep and pain-regulatory processes.