Dr. Shapira's Chicago Headache Blog

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)

Labels: CENTRAL SENSITIZATION, CGRP neuromuscular dentistry, chronic daily headaches, CRPS, facial pain, fibromyalgia, myofacial pain, neuromuscular dentistry tmd, RSD, TMD, TMJ

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]

Labels: CENTRAL SENSITIZATION, CGRP neuromuscular dentistry, Facial pain trigeminal neuralgia, TMD Migraine, TMJ Migraine, trigeminal neuralgia neuromuscular dentistry

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.

Labels: BRUXISM, CENTRAL SENSITIZATION, headaches, SLEEP APNEA, TMJ DISORDERS