TRIGEMINAL AUTONOMIC CEPHALGIAS, Chronic Headaches Related To Trigeminal Nerve Respond well to Neuromuscular Dentistry & Sphenopalatine Ganglion Block

The Trigeminal Nerve is often called the Dentist's Nerve because it goes to the teeth, jaw muscles, jaw joints (TMJ),and periodontal ligament. Trigeminal innervation of the sinuses, eustacian tubes, tensor of the ear drum (tensor tympani), soft palate, tongue and meninges of the brain explain why there are so many disorders associated with jaw function, TMJ and TMD.

There are a special group of disorders called the Trigeminal Autonomic Cephalgias (See National Institute of Neurological Disorders and Stroke web information below). Sphenopalatine Ganglion Blocks are an autonomic block that can be used to treat many types of migraine, Tension-tyoe headaches and chronic daily headaches but the SPG block are especially useful for autonomic cephalgias.

Cluster Headaches are primarily found in males and frequently awake patients from sleep. Oxygen is also an excellent treatment if it is administered immediately. Triptans, neurosurgery as well as antipsychotics and calcium channel blockers are also used prophylactically. Utilization of implanted electrodes and or neurosurgery where the nerves are resected are techniques that are often used. The Sphenopalatine Ganglion block (an autonomic block can be used both diagnostically and therapeutically) is probably one of the safest and most effective treatments for cluster headaches and when done with plain lidocaine are almost free of side effects. Paroxysmal hemicrania and SUNCT (Short-lasting, Unilateral, Neuralgiform headache attacks with Conjunctival injection and Tearing) are other Autonomic trigeminal that have similarities to cluster headaches. The National Institute of Neuromuscular Disorders and Stroke can be found below)

A diagnostic neuromuscular orthotic can also be utilized prophylactically with cluster headaches. A diagnostic neuromuscular orthotic is used to treat both the sommatic and autonomic aspects of the trigeminal nerves. They are particularly effective at treating muscle spasm, myofascial pain and trigger points in masticatory muscles. The combination of both therapies, a diagnostic neuromuscular orthotic and self administered autonomic Sphenopalatine Ganglion Blocks (SPG Block) can virtually "Cure" cluster headaches in some patients. An added advantage to the diagnostic orthotic is that it can frequently eliminate tension-type headaches and chronic daily headaches (muscular orgin headaches) that are almost always trigeminally modulated.

The SPG block is a simple procedure that my patients learn to self administer in one or two appointments. The block is done transmucosally with a cotton tipped applicator with lidocaine (no epinephrine or preservatives). No needles ever penetrate the patient but rather the saturated cotton is passed intranasally (though the nose) to the area adjacent to the ganlion. The anaesthetic passes through the tissue to the ganglion.

According to Wikipedia the Sphenopalatine Ganglion is also called the "The pterygopalatine ganglion (Synonym: ganglion pterygopalatinum, meckel's ganglion, nasal ganglion, sphenopalatine ganglion) is a parasympathetic ganglion found in the pterygopalatine fossa. (This is where the cotton tip applicator contacts mucosa) It is one of four parasympathetic ganglia of the head and neck. The others are the submandibular ganglion, otic ganglion, and ciliary ganglion. The flow of blood to the nasal mucosa, in particular the venous plexus of the conchae, is regulated by the pterygopalatine ganglion and heats or cools the air in the nose.

(The structure of the Sphenopalatine Ganglion also from Wikipedia below)

The pterygopalatine ganglion (of Meckel), the largest of the parasympathetic ganglia associated with the branches of the Maxillary Nerve (branch of trigeminal nerve), is deeply placed in thepterygopalatine fossa, close to the sphenopalatine foramen. It is triangular or heart-shaped, of a reddish-gray color, and is situated just below the maxillary nerve as it crosses the fossa.

The pterygopalatine ganglion supplies the lacrimal gland (tear ducts), paranasal sinuses, glands of the mucosa of the nasal cavity and pharynx, the gingiva, and the mucous membrane and glands of the hard palate. It communicates anteriorly with the nasopalatine nerve.

According to Wikipedia (below) there are sensory, sympathetic and parasympatheic roots

Its sensory root is derived from two sphenopalatine branches of the maxillary nerve; their fibers, for the most part, pass directly into the palatine nerves; a few, however, enter the ganglion, constituting its sensory root.

Parasympathetic root

Its parasympathetic root is derived from the nervus intermedius (a part of the facial nerve) through the greater petrosal nerve.

In the pterygopalatine ganglion, the preganglionic parasympathetic fibers from the greater petrosal branch of the facial nerve synapse with neurons whose postganglionic axons, vasodilator, and secretory fibers are distributed with the deep branches of the trigeminal nerve to the mucous membrane of the nose, soft palate, tonsils, uvula, roof of the mouth, upper lip and gums, and upper part of the pharynx. It also sends postganglionic parasympathetic fibers to the lacrimal nerve (a branch of the Ophthalmic nerve, also part of the trigeminal nerve) via the zygomatic nerve, a branch of the maxillary nerve (from the trigeminal nerve), which then arrives at the lacrimal gland.

The nasal glands are innervated with secretomotor from the nasopalatine and greater palatine nerve. Likewise, the palatine glands are innervated by the nasopalatine, greater palatine nerve and lesser palatine nerves. The pharyngeal nerve innervates pharyngeal glands. These are all branches of maxillary nerve.

Sympathetic root

The ganglion also consists of sympathetic efferent (postganglionic) fibers from the superior cervical ganglion. These fibers, from the superior cervical ganglion, travel through the carotid plexus, and then through the deep petrosal nerve. The deep petrosal nerve joins with the greater petrosal nerve to form the nerve of the pterygoid canal, which enters the ganglion.

TRIGEMINAL AUTONOMIC CEPHALGIAS

Some primary headaches are characterized by severe pain in or around the eye on one side of the face and autonomic(or involuntary) features on the same side, such as red and teary eye, drooping eyelid, and runny nose. These disorders, called trigeminal autonomic cephalgias (cephalgia meaning head pain), differ in attack duration and frequency, and have episodic and chronic forms. Episodic attacks occur on a daily or near-daily basis for weeks or months with pain-free remissions. Chronic attacks occur on a daily or near-daily basis for a year or more with only brief remissions.

Cluster headache - the most severe form of primary headache-involves sudden, extremely painful headaches that occur in "clusters," usually at the same time of the day and night for several weeks. They strike one side of the head, often behind or around one eye, and may be preceded by a migraine-like aura and nausea. The pain usually peaks 5 to 10 minutes after onset and continues at that intensity for up to 3 hours. The nose and the eye on the affected side of the face may get red, swollen, and teary. Some people will experience restlessness and agitation, changes in heart rate and blood pressure, and sensitivity to light, sound, or smell. Cluster headaches often wake people from sleep.

Cluster headaches generally begin between the ages of 20 and 50 but may start at any age, occur more often in men than in women, and are more common in smokers than in nonsmokers. The attacks are usually less frequent and shorter than migraines. It's common to have 1 to 3 cluster headaches a day with 2 cluster periods a year, separated by months of freedom from symptoms. The cluster periods often appear seasonally, usually in the spring and fall, and may be mistaken for allergies. A small group of people develop a chronic form of the disorder, which is characterized by bouts of headaches that can go on for years with only brief periods (1 month or less) of remission. Cluster headaches occur more often at night than during the day, suggesting they could be caused by irregularities in the body's sleep-wake cycle. Alcohol (especially red wine) and smoking can provoke attacks. Studies show a connection between cluster headache and prior head trauma. An increased familial risk of these headaches suggests that there may be a genetic cause.

Treatment options include oxygen therapy-in which pure oxygen is breathed through a mask to reduce blood flow to the brain-and triptan drugs. Certain antipsychotic drugs, calcium-channel blockers, and anticonvulsants can reduce pain severity and frequency of attacks. In extreme cases, electrical stimulation of the occipital nerve to prevent nerve signaling or surgical procedures that destroy or cut certain facial nerves may provide relief.

Paroxysmal hemicrania is a rare form of primary headache that usually begins in adulthood. Pain and related symptoms may be similar to those felt in cluster headaches, but with shorter duration. Attacks typically occur 5 to 40 times per day, with each attack lasting 2 to 45 minutes. Severe throbbing, claw-like, or piercing pain is felt on one side of the face-in, around, or behind the eye and occasionally reaching to the back of the neck. Other symptoms may include red and watery eyes, a drooping or swollen eyelid on the affected side of the face, and nasal congestion. Individuals may also feel dull pain, soreness, or tenderness between attacks or increased sensitivity to light on the affected side of the face. Paroxysmal hemicrania has two forms: chronic, in which individuals experience attacks on a daily basis for a year or more, and episodic, in which the headaches may stop for months or years before recurring. Certain movements of the head or neck, external pressure to the neck, and alcohol use may trigger these headaches. Attacks occur more often in women than in men and have no familial pattern.

The nonsteroidal anti-inflammatory drug indomethacin can quickly halt the pain and related symptoms of paroxysmal hemicrania, but symptoms recur once the drug treatment is stopped. Non-prescription analgesics and calcium-channel blockers can ease discomfort, particularly if taken when symptoms first appear.

SUNCT (Short-lasting, Unilateral, Neuralgiform headache attacks with Conjunctival injection and Tearing) is a very rare type of headache with bursts of moderate to severe burning, piercing, or throbbing pain that is usually felt in the forehead, eye, or temple on one side of the head. The pain usually peaks within seconds of onset and may follow a pattern of increasing and decreasing intensity. Attacks typically occur during the day and last from 5 seconds to 4 minutes per episode. Individuals generally have five to six attacks per hour and are pain-free between attacks. This primary headache is slightly more common in men than in women, with onset usually after age 50. SUNCT may be episodic, occurring once or twice annually with headaches that remit and recur, or chronic, lasting more than 1year.

Symptoms include reddish or bloodshot eyes (conjunctival injection), watery eyes, stuffy or runny nose, sweaty forehead, puffy eyelids, increased pressure within the eye on the affected side of the head, and increased blood pressure.

Cephalalgia. 2009 Jul 13. [Epub ahead of print] LinksSluder's neuralgia: a trigeminal autonomic cephalalgia?

SUNCT is very difficult to treat. Anticonvulsants may relieve some of the symptoms, while anesthetics and corticosteroid drugs can treat some of the severe pain felt during these headaches. Surgery and glycerol injections to block nerve signaling along the trigeminal nerve have poor outcomes and provide only temporary relief in severe cases. Doctors are beginning to use deep brain stimulation (involving a surgically implanted battery-powered electrode that emits pulses of energy to surrounding brain tissue) to reduce the frequency of attacks in severely affected individuals.

Oomen KP, van Wijck AJ, Hordijk GJ, de Ru JA.
Department of Otolaryngology, Central Military Hospital, Utrecht, The Netherlands.
Oomen KPQ, van Wijck AJM, Hordijk GJ & de Ru JA. Sluder's neuralgia: a trigeminal autonomic cephalalgia? Cephalalgia 2009. London. ISSN 0333-1024The objective was to formulate distinctive criteria to substantiate our opinion that Sluder's neuralgia and cluster headache are two different clinical entities. A systematic review was carried out of all available, original literature on Sluder's neuralgia. Pain characteristics, periodicity and associated signs and symptoms were studied and listed according to frequency of appearance. Eleven articles on Sluder's neuralgia were evaluated. Several differences between Sluder's neuralgia and cluster headache became evident. Based on described symptoms, new criteria for Sluder's neuralgia could be formulated. Sluder's neuralgia and cluster headache could possibly be regarded as two different headache syndromes, and Sluder's neuralgia could be a trigeminal autonomic cephalalgia.
PMID: 19614698 [PubMed - as supplied by publisher]

Can Dentists Prevent Migraines? The Answer Is Yes According To New Research Out Of Germany.

The Journal of Neuroscience (J Neurosci. 2011 Feb 9;31(6):1937-43) recently published an article titled "Trigeminal nociceptive transmission in migraineurs predicts migraine attacks"

I have long advocated that the majority of Migraines and Tension-Type headaches are actually input-output errors. Nociceptive information entering the Trigeminovascular system are the pathology that triggers migraines and other headaches.

This study looked at fMRI or functional MRI studies of the brain.

They found that predicting migraine by trigeminal nociceptive activity could predict migraines.

Whers does most nociceptive trigeminal input arise?

In the Jaw Muscles, Muscle Spindles, Golgi Tendon Organs and periodontal ligaments of the teeth.

Neuromuscular Dentistry is very effective in eliminating and preventing migraines and muscular tension-type headaches. The majority of "sinus headaches" are actually referred muscle pain. The reason for the success of Neuromuscular Dentistry is the ability to eliminate nociceptive input.

Input/output errors are often described in computer lingo as Garbage In / Garbage Out.

The neurofeedback loops from periodontal ligaments , muscles, muscle spindles etc send nociceptive input (ie Garbage in) into the trigeminovascular system.

Migraines and other headaches are the "Garbage Out " part of the equation.
The article states that:
"Remarkably, the distance to the next headache attack was predictable by the height of the signal intensities in the spinal nuclei. Migraine patients scanned during the acute spontaneous migraine attack showed significantly lower signal intensities in the trigeminal nuclei compared with controls, demonstrating activity levels similar to interictal patients. Additionally we found-for the first time using fMRI-that migraineurs showed a significant increase in activation of dorsal parts of the pons, previously coined "migraine generator." Unlike the dorsal pons activation usually linked to migraine attacks, the gradient-like activity following nociceptive stimulation in the spinal trigeminal neurons likely reflects a raise in susceptibility of the brain to generate the next attack, as these areas increase their activity long before headache starts. This oscillating behavior may be a key player in the generation of migraine headache, whereas attack-specific pons activations are most likely a secondary event."

Another article in Neurology. 2011 Jan 18;76(3):206-7 states "Photophobia is an abnormal sensitivity to light experienced by migraineurs during attacks. The pathophysiology of photophobia is poorly understood. Nevertheless, 2 facts appear to have a link with photophobia: visual cortex hyperexcitability on the one hand and interactions between visual pathway and trigeminal nociception on the other."

The photophobia or sensitivity to light during a migraine attack is also due, in part to trigeminal nociception (Garbage in. The nociceptive input from the teeth,jaws, periodontal ligaments are the "garbage in" and the migraines and photophobia are the Garbage out".

Experimental studies on rats "J Neurosci. 2010 Oct 27;30(43):14420-9.
Changes of meningeal excitability mediated by corticotrigeminal networks: a link for the endogenous modulation of migraine pain." confirm the effect of trigeminanl nociception on meningeal migraines. The Trigeminovascular system is always paramount in migraine. The Trigeminal nerve controls the blood flow to the anterior 2/3 of the meninges of the brain.

Primary Stabbing Headaches are also trigeminally innervated as reported in"
J Headache Pain. 2011 Jan 6. [Epub ahead of print]
Incidence and influence on referral of primary stabbing headache in an outpatient headache clinic." The article states that "Primary stabbing headache (PSH) is a pain, as brief, sharp, jabbing stabs, predominantly felt in the first division of trigeminal nerve." The trigeminal nerve you will remember is the Dentist's nerve.


PubMed Abstract below:

J Neurosci. 2011 Feb 9;31(6):1937-43.
Trigeminal nociceptive transmission in migraineurs predicts migraine attacks.

Stankewitz A, Aderjan D, Eippert F, May A.

Department of Systems Neuroscience, University Medical Center Hamburg-Eppendorf, D-20246 Hamburg, Germany.
Abstract

Several lines of evidence suggest a major role of the trigeminovascular system in the pathogenesis of migraine. Using functional magnetic resonance imaging (fMRI), we compared brain responses during trigeminal pain processing in migraine patients with those of healthy control subjects. The main finding is that the activity of the spinal trigeminal nuclei in response to nociceptive stimulation showed a cycling behavior over the migraine interval. Although interictal (i.e., outside of attack) migraine patients revealed lower activations in the spinal trigeminal nuclei compared with controls, preictal (i.e., shortly before attack) patients showed activity similar to controls, which demonstrates that the trigeminal activation level increases over the pain-free migraine interval. Remarkably, the distance to the next headache attack was predictable by the height of the signal intensities in the spinal nuclei. Migraine patients scanned during the acute spontaneous migraine attack showed significantly lower signal intensities in the trigeminal nuclei compared with controls, demonstrating activity levels similar to interictal patients. Additionally we found-for the first time using fMRI-that migraineurs showed a significant increase in activation of dorsal parts of the pons, previously coined "migraine generator." Unlike the dorsal pons activation usually linked to migraine attacks, the gradient-like activity following nociceptive stimulation in the spinal trigeminal neurons likely reflects a raise in susceptibility of the brain to generate the next attack, as these areas increase their activity long before headache starts. This oscillating behavior may be a key player in the generation of migraine headache, whereas attack-specific pons activations are most likely a secondary event.

PMID: 21307231 [PubMed - indexed for MEDLINE]


Neurology. 2011 Jan 18;76(3):213-8. Epub 2010 Dec 9.
A PET study of photophobia during spontaneous migraine attacks.

Denuelle M, Boulloche N, Payoux P, Fabre N, Trotter Y, Géraud G.

Service de Neurologie et Explorations Fonctionnelles du Système Nerveux, CHU Rangueil, Toulouse, France. denuelle.m@chu-toulouse.fr

Comment in:

* Neurology. 2011 Jan 18;76(3):206-7.

Abstract

BACKGROUND: Photophobia is an abnormal sensitivity to light experienced by migraineurs during attacks. The pathophysiology of photophobia is poorly understood. Nevertheless, 2 facts appear to have a link with photophobia: visual cortex hyperexcitability on the one hand and interactions between visual pathway and trigeminal nociception on the other.

METHODS: We used H(2)(15)O PET to study photophobia induced by continuous luminous stimulation covering the whole visual field in 8 migraineurs during spontaneous migraine attacks, after headache relief by sumatriptan and during attack-free interval. The intensity of the luminous stimulation provoking photophobia with subsequent headache enhancement was specifically determined for each patient.

RESULTS: We found that low luminous stimulation (median of 240 Cd/m(2)) activated the visual cortex during migraine attacks and after headache relief but not during the attack-free interval. The visual cortex activation was statistically stronger during migraine headache than after pain relief.

CONCLUSION: These findings suggest that ictal photophobia is linked with a visual cortex hyperexcitability. The mechanism of this cortical hyperexcitability could not be explained only by trigeminal nociception because it persisted after headache relief. We hypothesize that modulation of cortical excitability during migraine attack could be under brainstem nuclei control.

PMID: 21148120 [PubMed - indexed for MEDLINE]

J Neurosci. 2010 Oct 27;30(43):14420-9.
Changes of meningeal excitability mediated by corticotrigeminal networks: a link for the endogenous modulation of migraine pain.

Noseda R, Constandil L, Bourgeais L, Chalus M, Villanueva L.

Department of Anesthesia, Critical Care, and Pain Medicine, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215, USA.
Abstract

Alterations in cortical excitability are implicated in the pathophysiology of migraine. However, the relationship between cortical spreading depression (CSD) and headache has not been fully elucidated. We aimed to identify the corticofugal networks that directly influence meningeal nociception in the brainstem trigeminocervical complex (Sp5C) of the rat. Cortical areas projecting to the brainstem were first identified by retrograde tracing from Sp5C areas that receive direct meningeal inputs. Anterograde tracers were then injected into these cortical areas to determine the precise pattern of descending axonal terminal fields in the Sp5C. Descending cortical projections to brainstem areas innervated by the ophthalmic branch of the trigeminal nerve originate contralaterally from insular (Ins) and primary somatosensory (S1) cortices and terminate in laminae I-II and III-V of the Sp5C, respectively. In another set of experiments, electrophysiological recordings were simultaneously performed in Ins, S1 or primary visual cortex (V1), and Sp5C neurons. KCl was microinjected into such cortical areas to test the effects of CSD on meningeal nociception. CSD initiated in Ins and S1 induced facilitation and inhibition of meningeal-evoked responses, respectively. CSD triggered in V1 affects differently Ins and S1 cortices, enhancing or inhibiting meningeal-evoked responses of Sp5C, without affecting cutaneous-evoked nociceptive responses. Our data suggest that "top-down" influences from lateralized areas within Ins and S1 selectively affect interoceptive (meningeal) over exteroceptive (cutaneous) nociceptive inputs onto Sp5C. Such corticofugal influences could contribute to the development of migraine pain in terms of both topographic localization and pain tuning during an attack.

J Headache Pain. 2011 Jan 6. [Epub ahead of print]
Incidence and influence on referral of primary stabbing headache in an outpatient headache clinic.

Guerrero AL, Herrero S, Peñas ML, Cortijo E, Rojo E, Mulero P, Fernández R.

Neurology Department, Hospital Clínico Universitario, Avda Ramón y Cajal 3, 47005, Valladolid, Spain, gueneurol@gmail.com.
Abstract

Primary stabbing headache (PSH) is a pain, as brief, sharp, jabbing stabs, predominantly felt in the first division of trigeminal nerve. Population studies have shown that PSH is a common headache. However, most people suffer attacks of low frequency or intensity and seldom seek for medical assistance. There are few clinic-based studies of PSH, and its real influence as a primary cause for referral to neurology outpatient offices is to be determined. We aim to investigate the burden of PSH as main complaint in an outpatient headache clinic. We reviewed all patients with PSH (ICHD-II criteria), attended in an outpatient headache clinic in a tertiary hospital during a 2.5-year period (January 2008-June 2010). We considered demographic and nosological characteristics and if PSH was main cause of submission. 36 patients (26 females, 10 males) out of 725 (5%) were diagnosed of PSH. Mean age at onset 34.1 ± 2.9 years (range 10-72). Mean time from onset to diagnosis 68.8 ± 18.3 months. Twenty-four patients fulfilled ICHD-II criteria for other headaches (14 migraine, 6 tension-type headache, 2 hemicrania continua, 1 primary cough headache and 1 primary exertional headache). 77.7% of patients were submitted from primary care. In 14 patients (39%), PSH was main reason for submission, its intensity or frequency in 5 (35.7%) and fear of malignancy in 9 (74.3%). Only two patients of those who associated other headaches were submitted due to PSH. In conclusion, PSH is not an uncommon diagnosis in an outpatient headache office. However, and according to our data, it is not usually the main cause of submission to a headache clinic.

PMID: 21210176 [PubMed - as supplied by publisher]

intense jaw pain on left side, swollen jaw and cheek, no dental issues per dentist and endodontist...tmj or trigeminal neuralgia?

I recently received a e-mail from a patient with the following complaint:

intense jaw pain on left side, swollen jaw and cheek, no dental issues per dentist and endodontist...tmj or trigeminal neuralgia?

The question TMJ or Trigeminal Neuralgia is very limited. 95% of all pain that patients experience is muscle pain. Many patients have severe or even excruciating pain but their TM Joints are normal. These are neuromuscular problems and may have many contributing factors. Trigeminal Neuralgia is rarely the cause of pain and when it is there is usually very specific triggers. The pain usually comes and goes going from normal to intense pain after stimulating trigger.

KI have seen patients with similar symptoms that are later tracked back to cracked toooth syndrome that was not evident early on. Vacumn sinusits can also give similar symptoms.

That said, the most common cause of pain is myofascial pain acute muscle spasm, myositis or other pain of muscular orgin.

A simple test that all general dentists and/or endodontists should know is how to do trigger point deactivation with a vapocoolant and stretch that can often give instanyt pain relief. Use of a diagnostic block to the muscle can also correct these problems when used to make a differential diagnosis.

The patient did not describe whether the pain was affected by jaw movement, if there was limited opening, or many other vital facts to know if there was joint involvement.

The correct approach is to make an accurate diagnosis. This involves a thorough evaluation of the jaw musclesand (TMJ) joints but also the head and neck musculature.

The best route is to seek out a neuromuscular dentist who is trained to evaluate and correct these problems.

I frequently see patients in Chicago who have not found help locally.

Diagnosis is the key to successful treatment. Treatment should be reversible until significant pain relief is accomplished and both the patient and the doctor are comfortable with primary and secondary diagnosis.

WHAT IS THE BEST TMJ TREATMENT?

THERE IS NO SINGLE "BEST TREATMENT" FOR TMJ BECAUSE TMJ IS NO A SINGLE DISEASE OR PROBLEM. TMJ actually stands for TemporoMandibular Joint and it is a joint not a disease. Everyone has two TM Joints. TMD stands for TemporoMandibular Dysfunction but it is also a general term.

The following should help guide patients in finding the "right " doctor.

To receive the "Best TMJ Treatment" it is first necessary to have the "Best TMJ Diagnosis".

The diagnosis is actually the most complex part of treating this group of disorders.

The medical SOAP model is an essential part of arriving at the right diagnosis and treatment and is frequently not followed.

The "S" in SOAP is the subjective findings. These come from the patients history. Many dentists and physicians short change patients by not getting a thorough and complete history. Often, relevant facts about a patient's history are missed or revealed later by patients. I usually set aside a minimum of one hour for a first visit with a patient with chronic pain. My team will often schedule much longer appointments when a case appears complicated. The tentative diagnosis or diagnostic tree (differential diagnosis) is made from the patient's history and interview. It is the confirmed or reevaluated based on Objective findings.

The "O" in SOAP is the objective findings. Before objective testing is done the subjective history helps determine the proper testing that is appropriate for each patient. Objective testing includes Radiographs or x-rays. These may be plain film, cone beam, CT scans, MRI's. These are used to diagnose bony changes and soft tissue changes to the joints.

There are specific objective testing that helps determine the "Best TMJ Treatment" and confirms details of the working diagnosis. Neuromuscular Dentists use the following diagnostic tools to elucidate the complete nature of this disorder.

THE FOLLOWING OBJECTIVE DEVICES ARE USED BY NEUROMUSCULAR DENTISTS TO AID IN DIAGNOSIS AND TREATMENT OF CRANIOMANDIBULAR DISORDERS (TMJ, MPD, MPD,ETC)

EMG or Electromyography that is used to determine starting levels of muscle activity, symmetry of muscle activity, funCtional activity as it relates to posture and function. Spectral Analysis of EMG help to determine underlying physiologic sTatus of the muscles. EMG can also be used to fine tune bite corrections and to measure efficacy of treatment.

Sonography and/or JVA (joint vibration analysis) Can be used to measure the health of the joint and determine thru spectral analysis the amount of joint damage or changes.

MKG (mandibular kinesiograph) , CMS (computerized Mandibular Scans) are used to evaluate function and movement and in conjunction with ULF TENS to measure rest position.

ULF TENS is used diagnostically and as a treatment tool. The the dimensional position of the jaw is evaluated before and after muscle relaxation (as confirmed by EMG)

Blood Tests, urine chemistry, thyroid function are all objective tests that are used when appropriate. Sleep studies are an often under utilized diagnostic tool in finding the "BEST TMJ TREATMENT". Patients with morning headaches, snoring, high blood pressure and excessive daytime sleepiness should always be evaluated with polysomnography. The NHLBI (National Heart Lung and Blood Institute) of the NIH (National Institute of Health) considers Sleep Apnea to be a TMJ disorder.

Psychometric tests are also objective tests that are used in diagnosis. Unfortunately, many doctors believe that there are no real physical ailments and the TMJ is a "psychco-social" disease to be treated with drugs and psychotherapy. There are frequently psycho-social overlays to TMJ problems. Being in chronic pain changes patients in many ways. Psychometric testing often reveals the results of chronic pain rather than the cause.

The "A" in SOAP is the assessment, where all of the subjective and objective information allows the doctor to have a "working diagnosis" and to lay out an initial treatment plan.

The "P" in Soap is the PLAN or methods determined by the Physician or Dentist to be used to treat the patient. This may include use of medications, therapy or diagnostic orthopedic appliances. Many patients need numerous methods of treatment to address the disorders and problems diagnosed and revealed in Subjective and Objective examination. Frequently more than one practitioner will be involved in treatment.


DIAGNOSIS DOES NOT END WHEN A NEUROMUSCULAR DIAGNOSTIC ORTHOTIC IS PLACED IN A PATIENTS MOUTH!

It is essential to understand that diagnosis and treatment is an ongoing procedure and that a SOAP approach is used at subsequent appointments. The "BEST TMJ TREATMENT" is ongoing and as the patients improve it is frequently appropriate for the focus of treatment to change. It is important for the patient and doctor to be open and honest to achieve the best results.

I strongly believe that the Neuromuscular Dentistry approach is the best "TMJ" treatment but it is only a part of the total diagnosis.

Facial Pain, Normal Sinus CT scans, Headache, Migraine and TMD

An older study in the Laryngescope is on 104 patients with facial pain who had normal CT scans. Twenty nine of the patients had previous unsuccessful sinus surgery. The patients were approximately 80% women, TMJ disorders are usually (80%) found in female patients.

The study showed " Four percent of patients seen by a neurologist had an unsuspected serious intracranial diagnosis." It is essential that organic neurologic causes are ruled out but the 100 remaining patients had headaches of undetermined causes. Facial pain and sinus pain are a alert for MPD (myofascial pain) and TMD (temporomandibular pain). Treatment of patients with chronic headaches, migraines sinus and/or facial pain is frequently done without a neuromuscular dental evaluation even though NMD has extremely high success rates.

The Trigeminal nerve innervates the sinus cavities. It is often called the Dentist's nerve because the trigeminal nerve primarily goes to the teeth, jaw muscles, jaw joints, periodontal ligaments and is responsible in full or part for most headaches. It also controls blood flow to the anterior 2/3 of the brain thru the meninges.

Correction of underlying neuromuscular problems often allows drug free effective treatment. When CT scans are normal patients with sinus pain and facial pain should always be evaluated by a neuromuscular dentist. Neurologists should evaluate all patients with organic brain disorders but functional treatment is preferred to heavy drug therapy for the majority of patients.

Frequently Chiropracters and dentists can get miraculous results by working together especially NUCCA and A/O (Atlas Orthogonal) chiropracters. The Dentists can correct nociceptive trigeminal nerve input while the chiropracters correct cervical and head posture. Long term correction of those problems usually requires correction of descending conditions associated with improper jaw function.



Laryngoscope. 2004 Nov;114(11):1992-6.
Neurologic diagnosis and treatment in patients with computed tomography and nasal endoscopy negative facial pain.
Paulson EP, Graham SM.

Department of Otolaryngology--Head and Neck Surgery, University of Iowa, Iowa City, Iowa 52242-1093, USA.
Abstract
OBJECTIVE: To determine the helpfulness of specialist neurology referral for patients with facial pain, a normal sinus computed tomography (CT) scan, and normal nasal endoscopy findings.

STUDY DESIGN: Prospective identification of patients and analysis of data approved by the Institutional Review Board.

METHODS: The data of 104 consecutive patients presenting with facial pain, a normal sinus CT scan, and normal nasal endoscopy findings were reviewed. The patients presented to a single rhinologist in a tertiary care institution. All patients were referred for specialist neurologic evaluation and potential treatment. Further information was obtained from a patient survey.

RESULTS: Of the 104 patients, 81 were women and 23 were men. The average age was 46 years (range, 22-85). Fifty-six had clear CT scans, 48 had minimal change, and all had negative endoscopies. Twenty-nine had previous unsuccessful sinus surgery. The average follow-up period was 10.5 months. Forty of 75 patients seeing a neurologist were seen on multiple occasions. Four percent of patients seen by a neurologist had an unsuspected serious intracranial diagnosis. The most common diagnoses were migraine (37%), rebound headache (17%), chronic daily headache (17%), and obstructive sleep apnea (16%). Overall, 58% improved on medical therapy; 60% of those with a clear CT scan improved, and 53% of those with minimal change on CT scan improved (P = .749).

CONCLUSIONS: Facial pain remains a difficult symptom to diagnose and treat in rhinologic practice. Patients often undergo surgery without help. Most patients with facial pain, a normal sinus CT scan, and normal endoscopy findings benefit from neurologic consultation. Serious intracranial pathologic conditions can be excluded and diagnosis-specific pharmacogenetic therapy instituted with improvement in more than 50%.

PMID: 15510029 [PubMed - indexed for MEDLINE]

Chronic daily headaches and meds don't work. What should I do? Neuromuscular Dentistry may be the answer.

Chronic headaches without a cause are frequently related to the Trigeminal nervous system and have no specific diagnosis. When headaches are not helped by routine medical care a neuromuscular dentist may be the best answer.

Question from Tiffany: I have been having headaches everyday now for about a year and 9 months now. Had no accidents or head trama btu i have headaches everyday ..No meds work for me only excedrin for about an hours and the head aches is right back. I really dont know the cause but i would like to find out more or what could be causing this.

Dr Shapira Response.

Tiffany, chronic headaches are usually coming from head and neck musculature, especially those muscle innervated by the Trigeminal Nerve. There may or may not be any joint noise or discomfort. A thorough medical evaluation with your physician to rule out organic disease is alway in order.

I start patients with a consultation appointment and usually can relieve a significant amount of pain during the appointment. Most muscle pains can be allieviated or eliminated temporarily with vapocoolant spray and stretch techniques to confirm muscle problems.
I start treatment with a thorough head and neck exam and a neuromuscular dental work up and than a neuromuscular diagnostic orthotic. Most patients see drastic improvement in just a couple of visits. There are no magic cures and it takes time for a chronic problem to unwind completely.

IF NEUROMUSCULAR DENTISTRY IS SO EFFECTIVE IN TREATING TENSION TYPE HEADACHES AND MIGRAINES WHY DON'T MORE PHYSICIANS REFER PATIENTS TO DENTISTS.

THE ANSWER TO THIS HAS TO DO WITH HOW PHYSICIANS ARE GENERALLY TRAINED AND THE FACT THEY ARE COMFORTABLE REFERRING TO OTHER PHYSICIANS. DENTISTS ARE USUALLY OUTSIDE THE TYPICAL REFERRAL PATTERNS FOR PHYSICIANS.

A SECOND REASON IS MANAGED CARE. PHYSICIANS ARE FREQUENTLY FINANCIALLY RESPONSIBLE FOR COSTS OF REFERRALS THEY MAKE AND DO NOT WANT TO BE STUCK WITH A LARGE BILL (OR DECREASE IN PAYMENTS).

MANY YEARS AGO I WORKED WITH CHICAGO HMO AND SHOWED THEM I COULD SAVE THEM SUBSTANTIAL AMOUNTS OF MONEY IN TREATING CHRONIC PAIN PATIENTS. AS A RESULT THEY GAVE ME A PREFERRED STATUS WHERE THERE WAS LITTLE OUT OF POCKET COST FOR THE PHYSICIANS WHEN REFERRING PATIENTS FOR TMJ THERAPY. DR TRUBITT WHO WAS THE MEDICAL DIRECTOR OF CHICAGO HMO SAID THAT THE COMPANY SAVED APPROXIMATELY $250.000 IN THE FIRST 6 PATIENTS WE TREATED (TOTAL COST ABOUT $25,000). CHICAGO HMO PAID 100% OF ALL MY TMD TREATMENT COSTS (PHASE 1) FOR SEVERAL YEARS BECAUSE THEY SAVED MONEY ON EVERY PATIENT TREATED. THE PATIENTS GAVE THE INSURANCE COMPANY VERY POSITIVE FEEDBACK. CHICAGO HMO DID NOT COVER PHASE 2 TREATEMNT SO PATIENTS WERE MADE AN APPLIANCE WITH A CAST BASE. PATIENTS DESIRING ORTHODONTICS OR RECONSTRUCTION DID SO AS AN OUT OF POCKET EXPENSE.

I WAS REFERRED PATIENTS FOR MANY YEARS WITH GREAT SUCCESS UNTIL CHICAGO HMO WAS BOUGHT BY ANOTHER COMPANY. THE NEW COMPANY WAS NOT INTERESTED IN LEARNING HOW THEY COULD SAVE MONEY. THEY DID WRITE CONTRACT LANGUAGE SAYING THAT TMJ DISORDERS WERE NOT COVERED.

THE EXPRESSION IS PENNY WISE AND POUND FOOLISH. TWO STUDIES PUBLISHED IN CRANIO BY SHIMSHAK ET AL SHOWED THAT PATIENTS WITH TMJ DISORDERS USE MEDICAL CARE IN ALL FIELDS OF MEDICINE AT 200-300% INCREASES ABOVE NON-TMJD PATIENTS. THE TOTAL MEDICAL SAVINGS DWARF THE COST OF TREATMENT BUT INSURANCE COMPANIES ONLY LOOKED AT THE COSTS NOT THE FUTURE SAVINGS.

QUALITY OF LIFE IS NEVER LOOKED AT BY INSURANCE COMPANIES IN THEIR CALCULATIONS.

THE SAME PROBLEM EXISTS IN TREATMENT OF SLEEP APNEA WHERE PATIENTS ARE ROUTINELY REFERRED FOR CPAP EVEN THOUGH 60% OF PATIENTS ABANDON IT COMPLETELY. ALMOST ALL STUDIES SHOW PATIENTS PREFER ORAL APPLIANCES TO CPAP.

THIS IS ALSO TRUE IN TREATMENT OF GUM DISEASE THAT CREATES CARDIAC PROBLEMS, DIABETES PROBLEMS, INCREASES IN PULMONARY INFECTIONS, PREMATURE BIRTH AND OTHER CONDITIONS BUT MOST PHYSICIANS KNOW LITTLE TO NOTHING ABOUT ORAL HEALTH AND ITS EFFECT ON OVERALL HEALTH. MOST MEDICAL INSURANCE COMPANIES DO NOT COVER THE COST OF TREATING PERIODONTAL DISEASE.

PATIENTS IN CHICAGOLAND AREA CAN CONTACT ME ABOUT TMJ DISORDERS AT 1-800-TM-JOINT AND ABOUT ORAL APPLIANCES FOR TREATING SLEEP APNEA AT 1-8-NO-PAP-MASK.

HEADACHES,TMJ AND ORTHOMOLECULAR MEDICINE

Question rrom Phil Bohnert, MD How about ortho-molecular treatments?

Reply: Orthomolecular Medicine is a term originally coined by Linus Pauling one of the greatest minds of the last century. It is medicine that idealizes the health of the total individual by correcting or optimizing the nutritional and biochemical stautus of the body.

Neuromuscular Dentistry is a form of orthomolecular medicine optimizing and correcting not nutritional but neurological input into the trigeminal nerve. The trigeminal nerve accounts for almost half of total input to the brain.

There are corrections in biochemical homeostasis at neurojunctions when it is optimized. There are also major changes to brain chemistry from control of blood flow to the brain br the trigeminal nerve.

Thank You Dr Bonnert

TMJ Treatment: Is Neuromuscular Dentistry the TMJ Treatment?

Neuromuscular Dentistry treats TMJ disorders by correcting the underlying problems rather than just treating the symptoms. The old fashioned mechanical approach to TMD treatment only addresses the current symptoms. Long term correction of chronic headaches, joint pain and muscle pain is actually the result of healing when underlying pathology is eliminated. Neuromuscular Dentistry is the best way to correct function and permit long term healing.