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

Neuromuscular Dentist in Chicago, IL Accepting Patients Nationwide & Worldwide

Posted: February 23, 2018
Authored by:

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.

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.

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]