TREAT HEADACHES, MIGRAINES AND FACIAL PAIN WITHOUT DANGEROUS DRUGS AND ASSOCIATED SIDE EFFECTS. NEUROMUSCULAR DENTISTRY IS A SAFE AND EFFECTIVE.

Neuromuscular Dentistry may be one of the most effective treatments for a wide variety of conditions including various types of "migraine", tension-type headaches, facial pain, trigeminal neuralgia, TMJ disorders, myofascial ain and muscular and neurogenic headaches. Drugs do not cure the underlying problems that cause the problems and frequently their mechanism of action is unknown. Many drugs are recalled due to dangerous or deadly side effects and a large number of patients experience rebound headaches. These patients frequently require higher doses of medication over time.

There are many varied and diverse advantages to neuromuscular dentistry over standard medical approaches. The single biggest problem in treating headaches utilizing neuromuscular dental technology is that it can be expensive. Insurance companies are aware that 50% reduction in symptoms almost always occurs with treatment. This is a higher positive respone than almost any drug regimens. Insurance companies frequently chose to deny coverage to increase profits to shareholders. Patients who have undergone numerous CAT Scans, MRI's ,Drug therapies and surgeries without adequate control of their pain frequently find that Neuromuscular Dentistry gives amazing relief and improves the quality of their lives and the lives of their loved ones and are then denied coverage for treatment. Many of these patients have exhausted their resources on unsuccessful therapies prior to learning about and experiencing relief thru neuromuscular dentistry.

The Alliance of TMD Organizations is working to address the unfair practices of insurance companies relative to the treatment of TMJ disorders and Headaches related to the masticatory system. They are also the primary group protecting the rights of TMJ patients. There is a large group of clinicians in dentistry who believe the problems patients experience are psychosocial and not physical and want medication to become the only treatment available to most patients. They would like to take away patients right to chose non-drug alternative treatments. Unfortunately this group has enormous political influence and exert control over most research funds often to the detriment of patients. This remains true even after scandals in FDA hearings led removal of some of their members from FDA panels. There are also numerous instances of unethical conflicts of interest that were not disclosed to the FDA. Additional information on the TMD alliance is available at: http://www.tmdalliance.org/

I would like to disclose that I am a representative of ICCMO to the Alliance and that I am a long term member of The American Equilibration Society, The American Academy of CranioFacial Pain and a member of The International Academy of Comprehensive Aesthetics. I am also a Diplomate of the American Academy of Pain Management. These are member organizations of the TMD Alliance. I am the chair of the insurance reimbursement commitee.


Neuromuscular Dental Treatment of headaches is usually divided into two phases: the initial treatment phase (pain reduction and elimination) and long term stabilization (long term maintenance of improved quality of life).

The initial treatment phase includes the diagnostic protocols established by the particular neuromuscular dentist, comprehensive exam including medical histroy review (extremely important), muslce palpation exam, range of motion evaluation radiographs. The use of EMG (electomyography) and computerized mandibular scans (CMS or MKG), sonography, ultra low frequency TENS and transcranial neurostimulation are frequently useful in understanding the variable in the course of the doctor establishing a working diagnosis. More advanced practitioners frequently wil do diagnostic trigger point injections, nerve blocks or autonomic blocks such as spenopalatine ganglion blocks.

The mainstay in neuromuscular dental treatment of TMJ disorders (TMD), migraines, tension-type headaches, atypical migraine, chronic daily headaches and facial pain is the diagnostic neuromuscular orthotic. THIS ORTHOTIC IS UTILIZED TO ESTABLISH A HEALTHY "LANDING POINT" THAT HAS MINIMAL MUSCULAR AND NEUROMUSCULAR ADAPTATION. This allows the body and all of the neuromuscular components a healthy environment to heal.

Doctors do not cure patients! The best doctors remove the impediments to healing! The body than returns to a healthy homeostatic condition. This is what is accomplished with the neuromuscular orthotic over a series of several appointment. If the patient experiences complete relief and /or total elimination of symptoms for an extended period the stabilization phase can be initiated. When patient have substantial relief but still have remaining symptoms they will determine whether they are ready for stabilization.

Long term stabilization can be a very expensive full mouth reconstruction but this is usually one of many possible treatments. Long term removable orthotics, orthodontics and semi-permanent appiances allow pain control without the expense of a reconstruction. WHAT IS IMPORTANT IS THAT THE PATIENT IS READY FOR LONG TERM STABILIZATION. The diagnostic orthotic is not a long term treatment. Frequently patients have dramatic improvements with their orthotics but do not precede to long term stabilization and see their symptoms return as the appliance wears down or breaks.

Sleep disturbances frequently accompany craniomandibular disorders and headaches. Patients with tiredness, morning headaches, nocturnal headaches, high blood pressur and memory problems usuallly need to be evaluated at a sleep lab utilizing a full polysomnograph array.

Sleep Appliance Causes Patient To Develop "TMJ". Is "TMJ" from Somnomed Sleep Appliance or is sleep apnea a symptom of a TMJ problem?

JEFF: I have an oral device (sonomed) for sleep apnea. It gave me TMJ. I haven't been able to tolerate cpap.


Dr Shapira: YOU STATE THAT YOU HAVE A SOMNOMED TO TREAT SLEEP APNEA BECAUSE YOU CANNOT TOLERATE CPAP.
It is excellent that you have chosen to treat the sleep apnea which can cause heart attacks, strokes, memory loss and excessive daytime sleepiness. Morning Headaches and headaches that wake patients from sleep are usually the result of sleep apnea or TMJ disorders ie "TMD"

YOU THEN STATE THAT YOU DEVELOPED TMJ BUT GAVE NO SPECIFICS AS TO SYMPTOMS. TMJ STANDS FOR TEMPOROMANDIBULAR JOINT, NOT A DISEASE. It is important to understand the SPECIFIC problems so they can be addressed. Patients wearing oral appliances for sleep apnea may experience bite changes or tooth movement but damage should not occur to the joints. It is essential to work with a dentist who has training in treating sleep apnea and TMJ disorders.

I frequently see patients whose bite changes but the feel better. Many of the changes that occur when wearing a sleep appliance are actually due to the body healing. The same developmental problems cause both sleep apnea and TMJ disorders, migraines and chronic daily headaches.

Neuromuscular Dentistry is one of the best approaches to treating headaches and TMJ disorders.

ACCORDING TO THE NHLBI SLEEP APNEA IS A TMJ DISORDER. SEE http://www.nhlbi.nih.gov/meetings/workshops/tmj_wksp.pdf You have actually developed a new symptom from the same disorder but because you didn't specify symptoms I can not specify what to do next.

The American Academy of Sleep Medicine recommends that dentists treating sleep apnea with oral appliances should be well trained in treating TMJ disorders. I SUGGEST THAT THE BEST QUALIFIED DENTISTS FOR TREATING TMJ DISORDERS ARE NEUROMUSCULAR DENTISTS.

IF YOU CAN GIVE ME SPECIFIC INFORMATION I MAY BE OF MORE HELP. Please review www.ihateheadaches.org to learn about Neuromuscular Treatment of TMJ Disorders, headaches and migraines.

The following is the result of a web form submission from:
comments: I have an oral device (sonomed) for sleep apnea. It gave me TMJ
I haven't been able to tolerate cpap

Cluster Headaches and Sleep Apnea. Cluster Headaches caused by sleep apnea and sleep apnea sequelae may be eliminated with treatment of apnea

All patients with cluster headaches that have onset during sleep should be evaluated for sleep apnea. Sleep apnea causes hypoxia (drop in oxygen) and a rise in CO2. Oxygen therapy is a recognized and effective treatment for sleep apnea. Prevention of many cluster headaches can be addressed by correcting sleep problems.

During apneic events the patients quit breathing oxygen drops followed by hypercapnia or a rise in carbon dioxide levels. This can cause acidosis that could trigger cluster headaches. This leads to an awakening and patients gasping and is associated with adrenaline release or fight or flight reflex. Repetition throughout the night can also be the trigger.

Patients with untreated sleep apnea have abnormal cortisol levels and this disturbs the ability to cope with normal life stresses. There is also an increase in insulin resistance and changes in blood sugar can also be a cluster headache trigger. The article
Timing patterns of cluster headaches and association with symptoms of obstructive sleep apnea." from Sleep Res Online. 2000;3(3):107-12 concludes that "in some patients, physiological consequences of OSA may trigger CH during the first few hours of sleep and thereby influence the timing of subsequent daytime headaches."

The National Heart Lung and Blood Institute (NHLBI) considers sleep apnea to be a Temporomandibular Disorder. The NHLBI report "CARDIOVASCULAR AND SLEEP-RELATED CONSEQUENCES OF TEMPOROMANDIBULAR DISORDERS" discusses effects of sleep apnea in detail. Learn more about the dangers of sleep apnea and oral appliance treatment at http://www.ihatecpap.com

A section of the report titled The Craniofacial Complex and its Impact on Control of Upper Airway Resistance and Cardiopulmonary Function- Jaw Biomechanics and Function" discusses sexual dimorphism and may explain why cluster headaches are more common in men. Part of that report follows: "These compartments are activated differently during the production of different oral behaviors, suggesting that they function as output elements used in different combinations by the nervous system. These muscles are complex and unique, containing fibers of phenotypes not found in limb muscles. They are smaller, and express myosin heavy chain isoforms found only in limb muscles during development. The cardiac alpha-myosin heavy chain isoforms of the masseter and temporalis muscles are unique to skeletal muscle and resemble heart muscle. Considerable sexual dimorphism has been identified in these muscles with regard to the slow and fast fibers types of the masseter. Males have predominately fast fiber types while females predominately slow fiber types. These sex differences arise in response to androgens in males but persist even in the absence of androgens."

It is widely accepted that the Trigeminal Nervous system that controls the jaws teeth and associate dental structures is implicated in the majority of all headaches including cluster headache.

Control of the upper airway often decrease or fails during sleep as seen in this excerpt: "Control of Upper Airway Collapsibility During Sleep
The upper pharyngeal airway in humans has relatively little bony or rigid support. Since there is variability in soft tissue and bony structures of the head and neck, there must be mechanisms in place that enable the pharyngeal dilator muscles to adjust for these anatomic differences. Animal and human studies indicate that there are at least three mechanisms to control the activity of the genioglossus muscle. First, negative pressure has substantial impact on this muscle and a clear linear relationship exists between negative pressure in the airway and genioglossal activation. Second, there is pre-motor neuron input to these muscles from respiratory pattern generating circuits as shown by the pre-activation of these muscles that occurs prior to the development of negative pressure in the airway. Third, tonic activity in the muscle is consistently evident, although the mechanisms that determine the level of this activity have not been studied. During sleep, the mechanisms that control upper airway resistance are importantly impacted. Specifically, tonic activity drops markedly and the negative pressure reflex is substantially attenuated or completely lost. These findings have important implications in the pathophysiology of SDB." They probably also have important implications in the physiology and pathology of cluster headaches.

The report also discusses physiological pain processes and central sensitization found in TMJD patients that is similar to findings in cluster and headache patients in this excerpt: "Craniofacial/Deep Tissue Persistent Pain and Relationships to Cardiovascular and Pulmonary Function and Disease.
Injury to peripheral tissues following trauma or surgery often results in hyperalgesia that is characterized by increased sensitivity to painful stimuli. This is a common problem in patients with TMD. Until recently, it was thought that the increase in pain was due to changes at the site of injury but it is now known that it involves central nervous system hyper-excitability leading to long-term changes in the nervous system. Animal models of hyperalgesia produced by inflammation or nerve injury that mimic persistent pain conditions have shown that an increased neuronal barrage into the central nervous system (CNS) leads to central sensitization involving activation of excitatory amino acid transmitters and their receptors. The activation of N-methyl- D-aspartate (NMDA) receptors leads to influx of calcium into neurons, the activation of protein kinases, and phosphorylation of receptors. The net effect of these responses is increased gene expression of NMDA receptors, an alteration in the sensitivity of receptors, increased excitability, and an amplification of pain. These responses appear to be most robust in response to deep tissue injury such as occurs in TMD patients.
Modulation by descending pathways from the CNS importantly influences these events. Under normal conditions, the net effect of the descending neural projections from the brain stem to the spinal cord is to inhibit or counterbalance the hyper-excitability produced by tissue injury. It is now understood that this balance can shift to a net excitatory effect whereby descending modulation results in more hyper-excitability and more pain after injury. This central sensitization appears to be a prominent component in patients suffering from deep pain conditions such as TMD and fibromyalgia. It is believed that the diffuse nature and amplification of pain is in part due to this imbalance and that these findings have important functional implications relevant to the survival of the organism in response to the presence of persistent tissue injury. It is therefore now believed that persistent pain can be attacked both at the site of injury and where it is elaborated in the nervous system."

The report also documents connections with autonomic system derangements that are normally found in headaches, migraines and cluster headaches. These autonomic symptoms are the ones that Sphenopalatine Ganglion Blocks can relieve or eliminate. The relevant section is excerpted below:
" Alteration in Baroreceptor Activity - Impact on Pain, Autonomic Function, Motor Output, and Sleep":

"Evidence has emerged that several regions of the CNS interact in complex ways to integrate sensory perception, autonomic function, motor output, and sleep architecture. The outcomes of a number of recent studies also suggest that several of the signs and symptoms associated with TMD may result, at least in part, from impairments in neural networks that coordinate the interplay between sensory systems, autonomic function, motor output, and sleep architecture. Many of the central pathways that are critically involved with the integration of these systems are regulated by visceral afferent input, including input from cardiopulmonary, carotid sinus, and aortic arch baroreceptors. In addition, abnormalities in the function and central integration of baroreceptor afferent information has been associated with abnormalities in pain perception, autonomic function, motor output, and sleep architecture, and thus may contribute to the development and maintenance of TMD and other related disorders (e.g., fibromyalgia). There is a need for additional studies that systematically examine whether abnormal baroreceptor function contributes to the pathogenesis of TMD."

Several relevant studies on TMD and Sleep Apnea are included below:

Cranio. 1997 Jan;15(1):89-93.
Cluster-like signs and symptoms respond to myofascial/craniomandibular treatment: a report of two cases.
Vargo CP, Hickman DM.

Raleigh Regional Center for Head, Neck and Facial Pain in Beckley, West Virginia, Morgantown, USA.
Abstract
Two cases with pain profiles characteristic of cluster-like headache, both within and outside the trigeminal system, are reported. One male patient would typically awaken from sleep with severe unilateral temporal head pain and autonomic signs of ipsilateral lacrimation and nasal congestion. A female patient exhibited severe unilateral boring temporal and suboccipital head pain with associated ipsilateral lacrimation and rhinorrhea. In addition, both patients presented with signs and symptoms of masticatory and/or cervical disorders. These two cases illustrate possible treatment alternatives, as well as possible influences from cervical and masticatory structures in the development of cluster or cluster-like headache.

PMID: 9586493 [PubMed - indexed for MEDLINE]

Cranio. 1995 Jul;13(3):177-81.
Sphenopalatine ganglion block: a safe and easy method for the management of orofacial pain.
Peterson JN, Schames J, Schames M, King E.

Headache and Pain Center, Hollywood Community Hospital, Los Angeles, CA 90028, USA.
Abstract
The sphenopalatine ganglion (SPG) block is a safe, easy method for the control of acute or chronic pain in any pain management office. It takes only a few moments to implement, and the patient can be safely taught to effectively perform this pain control procedure at home with good expectations and results. Indications for the SPG blocks include pain of musculoskeletal origin, vascular origin and neurogenic origin. It has been used effectively in the management of temporomandibular joint (TMJ) pain, cluster headaches, tic douloureux, dysmenorrhea, trigeminal neuralgia, bronchospasm and chronic hiccup.

PMID: 8949858 [PubMed - indexed for MEDLINE]



Ned Tijdschr Tandheelkd. 2006 Nov;113(11):474-7.
[Spontaneous pain attacks: neuralgic pain]
[Article in Dutch]

de Bont LG.

Universitair Medisch Centrum, Groningen. l.g.m.de.bont@kchir.umcg.nl
Abstract
Paroxysmal orofacial pains can cause diagnostic problems, especially when different clinical pictures occur simultaneously. Pain due to pulpitis, for example, may show the same characteristics as pain due to trigeminal neuralgia would. Moreover, the trigger point of trigeminal neuralgia can either be located in a healthy tooth or in the temporomandibular joint. Neuralgic pain is distinguished into trigeminal neuralgia, glossopharyngeal neuralgia, Horton's neuralgia, cluster headache and paroxysmal hemicrania. In 2 cases trigeminal neuralgia is successfully managed with a neurosurgical microvascular decompression procedure according to Jannetta. Characteristic pain attacks resembling neuralgic pain result from well understood pathophysiological mechanisms. Consequently, adequate therapy, such as a Janetta procedure and specific pharmacological therapy, is available.

PMID: 17147031 [PubMed - indexed for MEDLINE]


Sleep Res Online. 2000;3(3):107-12.
Timing patterns of cluster headaches and association with symptoms of obstructive sleep apnea.
Chervin RD, Zallek SN, Lin X, Hall JM, Sharma N, Hedger KM.

Sleep Disorders Center, Department of Neurology, University of Michigan, Ann Harbor, Michigan, USA. chervin@umich.edu
Abstract
Cluster headaches (CH) frequently recur at the same point in the circadian cycle, often during sleep. They may, in some cases, represent a susceptible individual's response to hypoxemia or other physiological changes induced by obstructive sleep apnea (OSA). If and when this mechanism exists, timing of CH close to the onset of sleep-and therefore OSA-might be expected. We questioned 36 subjects with CH about the times at which their CH usually occurred and about several symptoms known to be predictive of OSA, including habitual snoring, loud snoring, observed apneas and excessive daytime sleepiness. We then used logistic regression to determine whether occurrence of CH in each of six time periods was associated with OSA symptoms. The 23 subjects (64%) who reported CH in the first half of a typical night's sleep also tended to report headaches during the midday/afternoon period. Symptoms of OSA, and in particular habitual snoring, were predictive of both first-half-of-the-night and midday/afternoon CH (p<.05). Thirty-one subjects (86%) reported that their CH were sleep-related, usually occurring during any part of the night or on awakening, but symptoms of OSA were not predictive of this timing pattern. In short, several OSA symptoms showed an association with CH occurrence in the first half of the night but not with sleep-related CH in general. These findings suggest that in some patients, physiological consequences of OSA may trigger CH during the first few hours of sleep and thereby influence the timing of subsequent daytime headaches.

PMID: 11382908 [PubMed - indexed for MEDLINE]