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Sinus Headache, Sinusitis, Sinus Pain and TMJ Disorders

Dr. Shapira Blog, Chicago, Highland Park, Lake Bluff, Lake Forest, Libertyville, TMJ, Uncategorized 0 Comments

Chronic Sinus Headache and other Sinus Pains are closely related to TMJ Disorders. The connections between these problems is multifacted.

The Trigeminal Nerve also called the Dentist’s Nerve is the underlying common source of all of these problems.

Dentists are the experts on the Trigeminal Nerrve Disorders and in particular neuromuscular dentists who optimize eliminating noxious input to the trigeminal system. The term “TMJ: The Great Imposter” was coinded because patients with TMJ disorders frequently report symptoms not specifically related to the joints.

Dentists who practice TMD and Neuromuscular Dentistry are well versed in Myofascial Pain and Dysfunction or MPD as it relates to upper body, head neck and facial pain referred from active myofascial trigger points.

The Sphenopalatine Ganglion (SPG), the largest parasympathetic ganglion in the head is on the maxillary division of the trigeminal nerve. I have taught hundreds of neuromuscular dentists both from the USA and from across the world how to utilize SPG Blocks as part of Neuromuscular Treatment.

The Sphenopalatine Ganglion also contains Sympathetic fibers of superior cervical change responsible for “Fight or Flight” reflex and when not controlled create a wide variety of stress, pain and emotional issues.

The Myomonitor utilized by Neuromuscular Dentistry effectively neuromodulates the sympathetic and parasympathetic autonnomic input from the Trigeminal Nervous System.

The majority of sinus pain and sinus headache are NOT primary issues or infections within the sinuses. Antibiotics may actually create new sinus issues related to fungal infections.

Sinus pain and Headaches can be relieved with SPG Blocks very quickly.

Long term sinus improvements are related to function and structure.  The following is a video of a patient who has experienced a cure of her lifetime sinus issues with DNA Appliance.  Neuromuscular Dentistry treated her TMJ disorders and the DNA is used for long term stabilization and to increase the size of her airway.

There are over 150 additional videos on treatment of TMJ Disorders, Headaches, Migraines, MPD, Fibromyalgia, Sinus pain, Sleep Apnea and snoring mat this link:  https://www.youtube.com/channel/UCk9Bfz6pklC7_UluWFHzLrg/videos


TMJ Chicago


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The number of abbreviations in medicine and dentistry is amazing.  In this short post I am going to give only a small number of definitions routinely utilized in literature and culture concerning TMJ disorders, often called “the Geat Imposter”  This will be an open Blog and will be added to over time.  Please come back and visit and if you have abbreviations you think need explanation please send the to me.

The most obvious is TMJ.  It is not a disease or a disorder but an abbreviation for the TemporoMandibular Joint.  The TM Joint is made up of the Temporal Bone of the skeuu “T” and the Mandible “M” where the come together is the Joint “J”  TMJ is not a diagnosis but a body part, like saying knee or Elbow.  The Fossa of the TMJ is located in the Temporal Bone which also forms the articular eminence.  The condyle is the part of the mandible in the TM Joint.  There is also an articular Disc the divides the Joint into upper and lower compartments, the lower is where rotation takes place and the upper is where translation or sliding takes place.  Both of these movements happen simultaneously in a heathy joint as the condyle dick assembly slides forward and back, side to side or obliquely while retaining ability to rotate.  The right and left joints always work in tandem but do not mirror the actions of each other in most movements.

TMD stands for TemporoMandibular Dysfunction or TMJ Disorders and is a disorder.  It can include internal derangemets which are problems inside the joint capsule.  These can include different types of arthritis and inflammatory conditions, the can include disc displacement disorders which are often referred to as clicking.  The clicking noises often represent the sounds of the condyle going on or off the disc.  Disc displacement can occur in different dimensions and to different extents.  There are reducible and not reducible clicks which refers to the ability to recapture the disc during function.  There are also closed lock dislocations of the disc where it is displaced without reduction. A displaced disc can be extremely painful. There can also be an open lock of the TMJ which is a subluxation where the condyle hyperextends over the articular evidence.  There are disorders like joint mice that are often diagnosed incorrectly as disc disorders.  You can also have inflamation , tearing and destruction of the retrodiscal lamina that connects the disc to the posterior parts of the joint including the joint capsule.  It is also possible to hacve a capsulitis of inflammation of Joint Capsule.

TMJ DISORDERS OR TMD DO NOT ALWAYS HAVE CLICKING, POPPING OR JOINT PAIN!  The disorder can be related to joint function without having internal derangements.

TMD also includes extracapsular Disorders and this is where the fun begins.

MPD is the most common extracapsular disorder.  It stands for Myofascial Pain and Dysfunction as defined by Travell and Simmons.  It is a muscular disorder that is distinct from Muscle Spasm or Myositis.  It is a disorder of muscle dysfunction secondary to improper muscle usage.  The muscle disorder is the result of a repetitive strain injury.  Myo is for  muscle and Fascia is connective tissue.  This is NOT Myo Facial Pain referring to the face though it is frequently seen written that way.

Myofascial Pain has muscles that contain taut bands and trigger points that can cause referred pain often far from the trigger points.  There are common patterns of referred pain that are often shown in textbooks but these patterns are not for a single patient but rather a frequency diagram based on thousands of patients.  The website www.triggerpoints.net is interactive and is an excellent reference for anyone with chronic pain anywhere in the body.

NUCCA and AO or A/O  are all terms for treatment directed at the complex articulation of the head to the first and second vertebrae of the Neck.  The occiput sits on top of the first vertebrae which is the Atlas.  It is named after Atlas of Greek Mythology who held and carried the world on his shoulders.  The head sits on two shoulders of the Atlas.  The TM Joints and The Atlas Occiput joints will tend to match three dimensionally.  The Axis is the second Vertebrae and has an upward protruding part called the Dens.  The Quadrant Theorem of Guzay is a mathematical explanation of the movements of the mandible after looking at both rotation and translation and shows that the middle of these combined movements is on the Dens of the Axis.  The DENS is the centrer of rotation for mandibular movements.  NUCCA is the National Upper Cervical Chiropractic Association which is a group of Chiropractors with special traing and focus on the upper cervical spine.  A?O or Atlas Orthoganol Chiropractors utilize a specific adjustment technique for the upper cervical spine.  

This is an important area of concern for TMJ Patients because of postural connections of the jaw, jaw joints, head and upper cervical areas in creating homeostasis.  Even small changes in jaw position can affect the upper cervical spine.  Changes in head position due to upper cervical spine can crearte TMJ symptoms.

CO stands for Centric Occlusion.  It describes where the upper and lower teeth fit together with mouth closure.  MIP .is the Maximal Intercuspal Position where occlusion is totally seated even if it means a pathological slide.

CR   or Centric Relation is a more complicated issue, it is an artificial location that has at least 26 different definitions and is utilized to transfer information to an articulator be CR dentists.  CR Dentists believe that joint position of the condyle in the Fossa are key to Occlusion.  CR may be very different depending on who is determining the position.  A CR Occlusion or Centric Relation occlusal scheme will usually have a CR-CO slide because most patients cannot tolerate the CR border position and create a new centric occlusion to function.    I Do Not Utilize CR or Centric Relation position.  Long Centric is another definition of this discrepancy between CR and CO.  CO is sometimes called MIP maximum intercuspal position or a fully seated CP which may actually require some adaptive movement of the tooth in the socket which is allowed by the periodontal ligament.  This freedom disappears with implants that are immovable.

Myocentric is the neuromuscular occlusion utilized by Neuromuscular Dentists.  NMD is short for Neuromuscular Dentistry.  There are many amazing videos about NMD at https://www.reddit.com/r/NeuroMuscularDent/.   It is where the teeth meet when the muscles move the jaw from rest position to closure.  There should be minimal muscle adaptation and following closure the jaw should return to rest position and the muscles should maintain health and normal function.  Myocentric is a reset position for the mandible that allows function without inducing muscle pathology.  It is specifically designed not to induce MPD or myofascial Pain.

TENS and ULF-TENs are abbreviations for Transcutaneous Neural Stimulation and Ultra Low Frequency TENS.  Neuromuscular Dentistry utilizes ULF TENS to relax the muscles to create a healthy physiological condition in the muscles which is necessary to find neuromuscular rest and to determine neuromuscular occlusion.  Creating a healthy musculature is an important first step in neuromuscular dentistry.  EMG is Electromyography which is used to measure the electrical activity of the muscles.  MKG is a Mandibular Kinesiograph often called a CMS or computerized Mandibular Scan.  It measures in real time three dimensional movement of a magnet attached to the mandible that allows precise measurement of the magnet and infer what is happening during mandibular function.

The ULF-TENS sends current thru the coronoid notch bilaterally and causes a single synapse contraction of all of the mandibular elevator muscles as well as all other Trigeminal Nerve and Facial Nerve innervated  muscles.  The underlying basis of NMD is healthy muscles.  The condyle assumes a position within the joint based on health muscle tone.  The condyle is never forcer into an unstable orthopedic border position like CR but it can go there.

Changing the position of the head can change jaw relations and changing jaw position can change head position.  It is important to establish a very stable jaw position in neuromuscular dentistry, this is done with a diagnostic neuromuscular orthotic.

The AES is the American Equilibration Society and is the oldest TMJ organization.  I have been to their meeting for 30 years but in general the majority of members believe in CR Based occlusion.

ICCMO is the International College of CranioMandibular Orthopedics and it is primarily Neuromuscular Trained dentists  It was founded by Barney Jankelson the “Father of Neuromuscular Dentistry” as a non-commercial scientific organization.  Typically, the best neuromuscular dentists are ICCMO members.

NMD stands for either NeuroMuscular Dentistry or Dentists.  This is the philosophy of treatment where muscle health is center to all treatment.

OFP is short for OroFacial Pain or Oral Facial Pain.  This is pain centered in the head and facial regions.  Some orofacial pain doctors do not look at TMJ disorders as primarily physical medicine issues but believe they are best managed by medications.  There is a wide spectrum of doctors who treat orofacial pain but there is a group that is seeking specialty even after being denied specialty by the ADA or American Dental Association multiple times.  They are now creating a specialty outside of the ADA, a dangerous precedent.  The AAOP is the American Academy of OroFacial Pain.  This group does not believe occlusion or how teeth meet have anything to do with TMJ disorders.  They tend to utilize prescription medications and CBT or cognitive behavioral therapy a lot.  Cognitive Behavioral Therapy is valuable for many disorders.

CMD stands for CranioMandibular Dysfunction or dysfunction it the articulation which would include TMD and MPD and maybe cervical issues.  CMCD is CranioMandibular Cervical Dysfunction.

AACP is the American Academy of CranioFacial Pain and was previously the AAHNFP or the Academy of Head Neck and Facial Pain.

SPG Blocks were made famous in the best selling book “MIRACLES ON PARK AVENUE!   Celebrities and patients flocked to see Dr Mlton Reder in NYC for these blocks.  

SPG stands for Sphenopalatine Ganglion also called the Pterygomandibular Ganglion, Sluders Ganglion, Nasal Ganglion or Meckel’s Ganglion.  It is located on the maxillary branch of the Trigeminal Nerve and is associated with many of the autonomic and stress related aspects of TMJ and MPD disorders.  Many believe the TMJ disorders were first described in 1908 by Sluder as Sluder’s Neuralgia others believe this is the first description of cluster headaches.  SPG Blocks can be self-administered and are one of the most amazing treatments for a wide variety of issues.

SPG Blocks  are often used in treatment of TMJ Disorders, Migraine and Cluster headaches.

Learn more about SPG Blocks at https://www.SphenoPalatineGanglionBlocks.com

ADD and ADHD are often associated with TMJ disorders because of common developmental patterns of sleep apnea and TMJ.  Sleep disordered breathing is primary cause of both Attention Deficit Disorder and Attention Deficit Hyperactivity Disorder.

RSD stands for Reflex Sympathetic Dystrophy more commonly called CRPS today or Complex Regional Pain Syndrome.

In Sleep issues we have AADSM or American Academy of Dental Sleep Medicine, the AASM or American Academy of Sleep Medicine, DOSA the Dental Organization for Sleep Apnea.  SA or Sleep Apnea, AHI= Apnea-Hypopnea Index, AI= Apnea Index, RDI = Respiratory distress index, RERE is Respiratory Related Arousal , UARS is Upper Airway Resistance Syndrome which is related to Fibromyalgia via the Alpha Intrusion into Delta Sleep.  REM is short for Rapid Eye Movement seen during dream sleep.

NIH is National Institute of Health.  The NIDCR is the National Institute of Dental and Facial Research who believes TMJ (TMD) is not related to occlusion but the NHLBI or National Heart Lung and Blood Institute  of the NIH wrote the report “Cardiovascular and Sleep Related Consequences of TemporoMandibular Disorders”  The HPA Axis is the Hypothalamus-Pituitary- Adrenal System that includes the reticular Activating System and is part of the Limbic system where we feel emotions.  Pain is an emotional response to noxious input.  Neuromuscular Dentistry addresses the HPA by stimulation of the SPG with ULF-TENS.  The is control of the autonomic nervous system with science .  This has been shown to increase permeability of the Blood Brain Barrier.…

Chicago: Orofacial Pain, TMD, TMJ, Headaches, Migraines and More

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Orofacial Pain Referral:   https://thinkbetterlife.com/referrals/

View patient video testimonials: https://www.youtube.com/channel/UCk9Bfz6pklC7_UluWFHzLrg/videos

What is Orofacial Pain and how does it relate to TMJ Disorders and Headaches.

Please visit this entire site to learn about help available for treating your Orofacial Pain and visit the patient testimonials about how they received help with their Orofacial Pain.
The term Craniofacial pain, is also commonly used by dental groups as well as universities such as Tufts.


According to the Academy of Orofacial Pain the term covers the following subjects that I have expanded on:
1. TMJoint Disorders or TemporoMandibular disorders. These can be internal derangements or intracapsular disorders, capsular problems and extracapsular problems.

2. Pain in the Masticatory Muscles including but not limited to Myofascial Pain and Dysfunction

3. Cervical musculoskeletal pain also including but not limited to Myofascial Pain and Dysfunction

4. Neurovascular pain: I have gone into great lengths discussing the Trigeminovascular system and the trigeminal cervical complex in previous posts describing the role of the trigeminal nerve in all headaches.

5. Neuropathic pain:  Pain is perceived in the Limbic system of the brain where we feelemotions.  Pain is actually an emotional response to nociceptive input.

Dr Shapira has a website dedicated to the Sphenopalatine Ganglion System, Blocks and Neuromodulation.


5A.  Under Neuropathic pain there is a category of autonomic pain and the function of the autonomic nervous system on all chronic pain problems.  Dr Shapira routinely teaches courses on the use of Sphenopalatine Ganglion Blocks to treat the autonomic nervous system.  Cranio Journal is publishing his paper on Neuromuscular Dentistry and the Autonomic Nervous System in the May 2019 issue.  He is already scheduled to give a course on the subject in May in Moscow and in  September in Kansas city.  He has recently given courses in Buenos Aires, Argentina, Seattle, Washington and Phoenix Arizona.

6. Sleep disorders related to orofacial pain which would include sleep apnea, snoring bruxism, nocturnal clenching and other movement disorders or parasomnias

7. Orofacial Dystonias The Dystonia Society website describes these a:
“In oromandibular dystonia the muscles that move the mouth and jaw are affected by involuntary spasm. This unwanted muscle contraction can pull the mouth and/or tongue into different positions. This often happens when people are using their mouths e.g. talking or eating, but can happen at rest as well.Like most types of dystonia it can be made worse when people are anxious or tired. It does not affect the mind or senses.
Although oromandibular dystonia most commonly develops following spread of dystonia from the neck or eyes, it can also appear in isolation. Where the condition comes on in mid-life without obvious cause, it will not usually spread further.
In some people, previous treatment with medicines that work by blocking the chemical dopamine in the brain (which can be used to treat a variety of conditions including nausea, vertigo or anxiety as well as psychiatric conditions such as schizophrenia and depression) can be the cause of oromandibular dystonia.”
Dr Brendan Stack has done very interesting work with changing maxillo -mandibular relations in many patients with movement disorders utilizing non-drug treatment regimens. I strongly Rx patients with these disorders at least become aware of the work Dr Stack is doing.

8. Headaches, Migraines ,autonomic cephalgias and various types of referred pain to the head. There is obvious overlap to neurovascular pain and referred cervicall pain.

Intraoral, intracranial, extracranial, and systemic

According to the AOP website “The field of Orofacial Pain is concerned with the prevention, evaluation, diagnosis, treatment, and rehabilitation of orofacial pain disorders. Such disorders may have pain and associated symptoms arising from a discrete cause, such as postoperative pain or pain associated with a malignancy, or may be syndromes in which pain constitutes the primary problem, such as TMJ disorder pain, neuropathic pains or headaches.”



J Pain Res. 2014; 7: 99–115.
Published online 2014 Feb 21. doi:  10.2147/JPR.S37593
PMCID: PMC3937250

Orofacial pain management: current perspectives



Orofacial pain (OFP) can arise from different regions and etiologies. Temporomandibular disorders (TMD) are the most prevalent orofacial pain conditions for which patients seek treatment.   THIS IS VERY IMPORTANT…PATIENTS ARE AWARE  THAT TMD IS THEIR PROBLEM.  Temporomandibular disorders include a number of clinical problems that involve the masticatory musculature THE PRIMARY MUSCULAR DISORDER IS MYOFASCIAL PAIN AND DYSFUNCTION AS DESCRIBED BY DR JANET TRAVELL AND IS ESSENTIALLY A REPETITIVE STRAIN DISORDER FROM CHRONIC MISUSE OF MUSCLES., the temporomandibular joint (TMJ) or both. Trigeminal neuropathic pain conditions can arise from injury secondary to dental procedures SUCH AS DENTAL EXTRACTIONS, ORTHOGNATHIC SURGERY AND LONG DENTAL APPOINTMENTS, infection, neoplasias, or disease or dysfunction of the peripheral and/or central nervous system. Neurovascular disorders, NEUROVASCULAR DISORDERS RESULT WHEN NOCICEPTION INTO TO TRIGEMINAL NERVE RESULTS IN RELEASE OF VASOACTIVE PEPTIDES IN THE ANTERIOR TWO THIRDS ON THE MENINGES OF THE BRAIN CONTROLLED BY THE TRIGEMINAL NERVES AND IS RESPONSIBLE FOR ALMOST 1005 OF HEADACHES, MIGRAINES, AUTONOMIC CEPHALGIAS AND OTHER REFERRED HEADACHES SUCH AS TENSION HEADACHES INCLUDING CERVICAL AND OCCIPITAL HEADACHES.  such as primary headaches, can present as chronic orofacial pain, such as in the case of facial migraine, where the pain is localized in the second and third division of the trigeminal nerve  THE LOCATION OF WHERE PATIENTS PERCEIVE PAIN IS NOT NEARLY WELL UNDERSTOOD BUT THE COMMON INITIATING FACTOR IS NOCICEPTION. Together, these disorders of the trigeminal system impact the quality of life of the sufferer dramatically. A multidisciplinary pain management approach should be considered for the optimal treatment of orofacial pain disorders including both non-pharmacological and pharmacological modalities.

Orofacial pain disorders

Orofacial pain disorders are highly prevalent and debilitating conditions involving the head, face, and neck. These conditions represent a challenge to the clinician since the orofacial region is complex and therefore, pain can arise from many sources  THE LARGEST INPUT INTO THE TRIGEMINAL SYSTEM IS UNQUESTIONABLY TEETH, PERIODONTAL LIGAMENTS, TONGUE, GINGIVAE, MUCOSAL TISSUES JAW MUSCLES AND JAW JOINTS.  THESE ARE PRIMARILY THE TERRITORY OF GENERAL DENTISTS AND IS WHY THE TRIGEMINAL NERVE IS CONSIDERED THE DENTISTS NERVE.  IN ADDITION THE TRIGEMINAL NERVE GOES TO THE TENSOR OF THE EAR DRUM, AND THE MUSCLE THAT OPENS AND CLOSES THE EUSTACIAN TUBES.. The clinician needs to have solid knowledge of the pain conditions that arise from these structures for proper diagnosis and a multidisciplinary approach of management is strongly recommended.

The orofacial pain classification as outlined by Okeson is divided into physical (Axis 1) THIS INCLUDES THE STRUCTURES GENERALLY CONSIDERED TO BE PRIMARILY THE REALM OF GENERAL DENTISTRY, AND IT IS FOR THIS REASON MOST OF THE CLINICIANS TREATING TMD ARE GENERAL DENTISTS. and psychological (Axis 2) conditions. Physical conditions comprise temporomandibular disorders (TMD), which include disorders of the temporomandibular joint (TMJ) and disorders of the musculoskeletal structures (eg, masticatory muscles and cervical spine) THERE IS A VERY CLOSE CONNECTION BETWEEN JAW POSTURE AND HEAD AND NECK POSTURE.  THIS HAS BEEN WELL DESCRIBED IN MATHEMATICAL TERMS IN THE QUADRANT THEOREM OF GUZAY AND EXPLAINS WHY DENTISTS FREQUENTLY WORK WITH CHIROPRACTORS ESPECIALLY A/O AND NUCCA CHIROPRACTORS. ; neuropathic pains, which include episodic (eg, trigeminal neuralgia [TN]) and continuous (eg, peripheral/centralized mediated) pains and neurovascular disorders NEUROOVASCULAR DISORDERS ARE A RESULT OF RELEASE OF VASOACTIVE PROTEINS RELEASED IN ANTERIOR 2/3 OF THE MENINGES OF THE BRAIN BY THE TRIGEMINAL NERVE TYPICALLY IN RESPONSE TO NOCICEPTIVE INPUT.(eg, migraine).

AXIS 2  IS REPRESENTED BY …Psychological conditions include mood and anxiety disorders.  IT IS ESSENTIAL THAT PATIENTS SHULD CLEARLY UNDERSTAND WHETHER DOCTORS ARE ADDRESSING AXIS 1 OR AXIS 2.   This review focuses on the current perspectives in orofacial pain management, and only TMD, neuropathic pains, and headaches will be discussed. For a more comprehensive discussion about pathophysiology and diagnosis of the disorders depicted in this classification and other painful disorders arising from the head, face, and neck, other texts should be reviewed.


“TMD” defines a number of clinical problems that involve the masticatory musculature, the TMJ, and associated structures.   TMD is considered to be a subclassification of musculoskeletal disorders  and is the most prevalent condition for which patients seek treatment.  IT SHOULD BE VERY CLEAR THAT PATIENTS ARE SEEKING TREATMENT FOR A PHYSICAL MUSCULOSKELETAL COMPLAINT.  The careful evaluation of these facial structures in conjunction with clinical symptoms is crucial in forming a proper differential diagnosis. The patient may present with jaw ache, earache, toothache, facial pain, and/or headache; however, the complaint may be as benign as general facial fullness or pressure.  PAIN THAT HAS LASTED MORE THAN A FEW WEEKS IS NEVER BENIGN AS THE RISK OF DEVELOPING CHRONIC PAIN SYNDROMES INCREASE WITH THE DURATION OF THE PAIN.  Treatment planning depend on various factors, including the chief complaint, medical history, presenting symptoms, examination, and diagnosis. In the past, TMD cases have sometimes been considered to be difficult to diagnose and problematic to treat; however, thanks to ongoing research in orofacial pain and pain management, clinicians are able to use a more standardized classification and better diagnostic and therapeutic methods to offer patients a wide range of treatment modalities with higher success rates.  THERE ARE MANY PATIENTS WHO RESPOND EXTREMELY WELL TO DEFINED ORTHOPEDIC APPROACHES TO MUSCULOSKELETAL ISSUES.  IT IS IMPERATIVE THAT THE PHYSICAL SYMPTOMS ARE TREATED AS SOON AS POSSIBLE.

Natural history and epidemiology of TMD

Most epidemiological studies clearly demonstrate that TMD symptoms are more commonly seen in women than in men, and that many symptoms seem to arise in adolescence or the early twenties  THE JANUARY AND FEBRUARY 2016 ISSUES OF THE JOURNAL OF THE AMERICAN DENTAL ASSOCIATION PRESENTS CLEAR IRREFUTABLE EVIDENCE ON A MUCH EARLIER ONSET OF SYMPTOMS IN ADOLESCENTS AND YOUNG CHILDREN IN A SIGNIFICANT PERCENTAGE OF THE POPULATION.and may continue intermittently, well into middle age; however, TMD symptomatology does get better with time, supporting a conservative management approach.  TYPICALLY, POST MENOPAUSAL WOMEN WILL EXPERIENCE DECREASES IN SYMPTOMS BUT LIVING IN PAIN CAN HAVE LIFE ALTERING DESTRUCTIVE EFFECTS ON PATIENTS LIVE. In a study by Solberg et al,  76% of subjects aged 18–25 years had one or more signs associated with TMD and 26% had at least one symptom associated with TMD. Of this group, only 10% had symptoms that were considered by the subjects to be severe enough to seek treatment. THAT LEAVES LARGE NUMBERS OF PATIENTS SEEKING TREATMENTS AND VERY LARGE NUMBERS OF PATIENTS WHO MIGHT EXPERIENCE A BETTER QUALITY OF LIFE WITH TREATMENT.  Rasmussen found that most cases of a clicking TMJ did not evolve into an open or closed locking state.  SHOULD PATIENTS BE TOLD THAT THEY HAVE CLICKING AND WHAT FUTURE IMPLICATIONS IT MIGHT HOLD?  SHOULD THEY BE OFFERED MINIMALLY INVASIVE TREATMENT EARLY?   Rasmussen noted that, in the natural progression of internal derangement, acute TMD symptoms lasted a mean of 5.5 years and that, although joint noises generally did not disappear, most painful and disabling symptoms subsided in time.  RASMUSSEN MAY NOT CONSIDER 5.5 YEARS OF PAIN SIGNIFICANT BUT PAIN MANAGEMENT USUALLY DIRECTS RAPID ELIMINATION OF SYMPTOMS IS IDEAL.  AT WHAT POINT DURING THOSE 5.5 YEARS DO AXIS 2 SYMPTOMS BEGIN?   Similar results were shown by Könönen et al, who followed 128 Finnish adults over 9 years, in whom the incidence of clicking increased with age.  None of the patients, however, developed locking.   In a more recent study, the presence of degenerative joint disorders was found to be the discriminating factor in two different age subgroups: patients with a mean age range of 52 years presented a prevalence of crepitus, while patients with a mean age range of 38 years did not.  THIS BEGS THE QUESTION IS WHEN DID DISK DISPLACEMENT AND DESTRUCTION OF ARTICULAR SURFACES OCCUR SINCE THESE TYPICALLY PRECEDE CREPITUS?


Disorders of the TMJ **TMJoint** are a result of a disc–condyle incoordination that influences the TMJ biomechanics. These disorders comprise the disc interference disorders or internal derangements, such as disc displacements with and without reduction, that can be asymptomatic or symptomatic due to inflammation THEY ARE ALWAYS SYMPTOMATIC BUT NOT ALWAYS PAINFUL BUT BECOME PAINFUL WHEN THE LEVEL OF INFLAMATION INCREASES.  INFLAMATION CREATES AN ENVIRONMENT FOR ADDITIONAL JOINT INJURY.  (eg, capsulitis/synovitis). Disc displacements with reduction may present as a painful or non-painful click.  REDUCTION REFERS TO REDUCING OF THE DISLOCATION OR RETURN TO HEALTHIER CONDITION. Disc displacements without reduction may present with a painful limitation at opening.   IDEALLY, PATIENTS CAN BE PREVENTED FROM DEVELOPING DISPLACEMENTS THAT ARE INCREASING IN DAMAGE, PAIN AND INFLAMATION. Retrodiscitis and TMJ subluxation  (CONDYLE DISLOCATION OVER EMINENCE)  may present symptomatology when the pain is a result of inflammation arising from the retrodiscal tissues or capsulitis or synovitis processes. RETRODISCAL TISSUES BECOME INFLAMED AND PAINFUL DUE TO IMPROPER PHYSIOLOGICL FUCTION WITHIN THE TMJoint. Osteoarthritic changes can originate in the TMJ articular surfaces and, when they are influenced by a systemic disease, can become aggressive and progressive, such as in the case of polyarthritis.  THIS IS TRUE OF ALL JOINTS IN THE BODY BUT THE TMJoint IS UNIQUE IN THAT IT  CAN OFTEN BE STABILIZED TO PREVENT FUNCTIONAL CHANGES AND RESULTANT INFLAMMATORY ARTHRITIS. 

Muscular disorders

Myalgia  THE TERM MYALGIA SPECIFICALLY REFERS TO MUSLCE PAIN NOT WHY THERE IS MUSCLE PAIN  usually presents as a dull aching pain due to muscle injury  MICRO INJURY AND REPETITIVE STRAIN ARE VERY COMMON or strain. It is commonly seen in acute forms THE MOST COMMON PRESENTATION IS MYOFASCIAL PAIN AND DYSFUNCTION AS DESCRIBED BY DR JANET TRAVELL, though, with continued muscle tension,CHRONIC MUSCLE SHORTENING LEADS TO PHYSIOLOGIC CHANGES IN THE MUSCLE FIBERS INCLUDING TAUT BANDS AND TRIGGER POINTS can present for longer periods of time. Treatment may include, rest, hot or cold compresses, stretching exercises, and muscle relaxants.   MYOFASCIAL PAIN IS MYALGIA OR MUSCLE PAIN  Myofascial pain (MFP) also presents as a dull, continuous aching pain that varies in intensity. MFP produces pain upon palpation that is local and may refer to other sites, as mapped out by TRAVELL & Simons et al.  MFP tends to be seen in muscle pain conditions of a more chronic nature,  DOES THIS MEAN THAT LACK OF TREATMENT EARLY RESULTS IN MYOFASCIAL PAIN FORMATION?   in which the tension is unremitting.  TRIGGER POINTS IN MYOFASCIAL PAIN ARE NOT NON-REMMITING BUT ACTUALLY GO THROUGH TWO PHASES LATENT AND ACTIVE WHERE ACTIVE CREATES MUCH MORE PAIN AND PASSIVE IS PAINFUL ON PALATION BUT IS STILL A PHYSIOLOGICAL PROBLEM.   Trigger points can often be  USUALLY seen in MFP and may be localized to a taut band of muscle. In addition, trigger points are associated with decreased muscle length and, when stimulated, can result in a local twitch response.  THIS IS DUE TO AN AUTONOMIC DYSFUCTION WITHIN THE MUSCLE RELATING TO THE MUSCLE SPINDLES Palpation of the trigger points should duplicate the patient’s pain complaint, THIS IS ONLY TRUE WHEN THE TRIGGER POINT IS IN AN ACTIVE PHASE BUT THEY DO NOT CAUSE REFERRED PAIN IN LATENT PHASE. thus confirming diagnosis. Blocking the source of the pain (ie, masseter muscle) by using a vapocoolant spray or local anesthetic injection can also provide a definitive diagnosis.  THE USE OF VAPOCOOLANT SPRAY AS DESCRIBED BY TRAVELL IS ACTUALLY A TREATMENT OF THE TAUT BAND AND TRIGGER POINT.  DEACTIVVATION AND ELIMINATION OF TRIGGER POINT IS ACCOMPLISHED BY UTILIZING TECHNIQUES DESCRIBED IN THE PAIN GATE THEORY, THE COLD SPRAY FLOODS THE AFFERENT NERVE INPUT BLOCKING THE PAIN OF THE STRETCH ALLOWING BREAKING UP OF TAUT BANDS BY BLOCKING ACTION OF MUSCLE SPINDLES TO PROTECT AREA OF PAIN.


Patient evaluation

TMD assessment should include a general examination of the head and neck, a detailed examination of the masticatory muscles,AS WELL AS CERVICAL AND POSTURAL MUSCULATURE, EVALUATION OF SUPRA NA INFRAHYOID MUSCLES AND SPECIAL ATTENTION TO THE SCALENE GROUP OF MUSCLES DUE TO THEIR IMPORTANCE IN BOTH POSTURE AND BREATHING an evaluation of the TMJs, an evaluation of mandibular range of motion (ROM), and a detailed intraoral examination.13

Evaluation of the TMJs and mandibular ROM

The evaluation of the TMJs includes examination for any signs of dysfunction or pain symptomatology. Fingertips are placed over the lateral and posterior aspects of the TMJs applying light but steady force and performed when the mandible is at rest/closed position and opening. Symptomatology reported in response to force applied to the lateral aspect of TMJs may be a sign of capsulitis/synovitis. Symptomatology reported in response of force applied to the posterior aspect of the condyle may be a sign of retrodiscitis or posterior capsulitis.  AN EXCELLENT METHOD OF EVALUATING THE TMJoints IS THE INTRA-MEATAL EXAMINATION WHERE POSTERIORIZATION OF THE CONDYLE INTO THE EAR CANAL CAN BE EASILY PALPATED.  I FREQUENTLY HAVE PATIENTS DO THIS WHITH THEIR PINKIES SO THEY CAN FEEL THE TISSUE DISPLACEMENT INTO THE EARS.  DO THE CONDYLES BELONG IN THE EARS?  COSTEN, THE ENT WHO ORIGINALLY DESCRIBED TMJoint DISORDERS WAS WELL AWARE OF THE POSTERIOR DISPLACEMENT ESPECIALLY IN EDENTULOUS AND DENTURE PATIENTS.  WHEN COSTEM DID HIS EXAMS PARTIAL AND COMPLETE EDENTULISM OCCURED AT A MUCH YOUNGER AGE THEN TODAY.

The clinician should be aware of joint sounds, which could present as clicks, pops, or crepitus.  CREPITUS IS THE SOUND SIMILAR TO SAND OR BROKEN GLASS IN A JOINT FROM BONE ON BONE CONTACT  These sounds are evaluated with the help of a stethoscope placed in the TMJ area or sometimes perceived during palpation. SONOGRAPHY AND  JOINT VIBRATIONAL ANALYSIS CNA QUANTIFY THESE SOUNDS.  SPECTRAL ANALYSIS OF THESE SOUNDS CORRESPONDS WITH FINDINGS ON MRI AND CAT SCANS.  Clicks and pops are commonly related to disc displacements with reduction and crepitation is commonly associated with osteoarthritic changes in the articular surfaces of the TMJ.  THIS SIMPLE STATEMENT IS THE RATIONALE FOR EARLY NON-INVASIVE TREATMENT TO PREVENT FURTHER DEGRADATION OF THE TMJoint. Imaging of the TMJ may also be useful during examination. Moreover, it is very important to identify any TMJ restrictions. The clinician should view the patient’s opening and closing patterns to note any mandibular deviations.  THIS CAN BE MEASURED MORE ACCURATELY AND QUANTIFIED WITH VARIOUS COMPUTERIZED SCANS SUCH AS THOSE AVAILABLE BY MYOTRONICS AND BIORESEARCH. The evaluation of mandibular ROM consists of measuring comfort opening, active opening, passive opening, protrusion, and left and right lateral excursions with a millimeter ruler  COMPUTERIZED TESTING IS MORE REVEALING AND ACCURATE while noting the severity and location of pain with jaw movement. This can be particularly helpful in differentiating between joint and muscle pain. FREQUENTLY THERE IS BOTH MUSCLE AND JOINT PAIN OCCURING SIMULTANEOUSLY   Comfort opening is determined by the patient opening as wide as possible without any pain, active opening is determined by the patient opening as wide as possible with pain, and passive opening is determined by the clinician gently stretching the patient presumably past active opening while noting a soft or hard end feel.   PAIN ASSOCIATED WITH JOINT NOISES SHOULD BE CONSIDERED VERY IMPORTANT  A reasonably normal interincisal distance is approximately 40 mm,THIS VARIES BY SEX OF PATIENT AND OVERALL SIZE OF PATIENT or the width of three of the patient’s fingers as a crude measure. Usually, with proper questioning, the patient will reliably reveal any recent limitations in ROM. The occurrence of TMJ clicking, crepitus, or jaw opening interferences with or without pain should also be noted at the initial examination. These baseline findings ARE FAR MORE ACCURATE WHEN TAKEN WITH BIOMEDICAL INSTRUMENTATION will aid in establishing the differential diagnosis and treatment options, as well as providing a comparison for future change in TMD symptoms.

Evaluation of the muscles of mastication

The muscles of mastication should be palpated bilaterally for firmness and tenderness, utilizing approximately 2–3 lbs of pressure, or the amount of pressure needed to cause blanching of the fingernail. Upon muscular palpation, the patient should be asked to report the severity of the tenderness, pain referral to multiple sites or single-site pain localization, and replication of the chief complaint upon palpation. It may be pertinent to ask the patient about their use of analgesics prior to palpation in order to account for reduced symptoms upon examination.  IT IS ESSENTIAL TO MAP OUT REFERRAL PATTERNS AND TO PALPATE BOTH ORGIN, INSERTIONS AND BODIES OF EACH MUSCLE.  THE POSTURE OF THE PATIENT WILL AFFECT THE RESPONSE TO PALPATION.  THIS PART OF THE EXAM IS INCREDIBLE IMPORTANT IN UNDERSTANDING THE UNDERLYING CAUSES OF PAIN.  SURFACE AND NEEDLE EMG BBOTH HAVE A PLACE IN DIAGNOSIS AND TREATMENT IN SOME PATIENTS.  SURFACE EMG IS ESPECIALLY REVEALING NON-SYMETRICAL RESTING  VALUES AND FUNCTIONING MUSCLE ACTIVITY.

Management of TMD

Most of the time, patients will visit the clinician when pain and dysfunction, such as limitation of opening, episodes of joint locking (open lock/TMJ subluxation), pain with mandibular function (chewing), facial pain, or headache are present.

The treatment goals for TMD are decreasing pain, restoring normal ROM, and restoring normal masticatory and jaw function. Many TMDs can be cyclical and self-limiting, with periods of complete remission of symptoms.  A MAJOR GOAL OF THE CLINICIAN SHOULD BE TO CLEARLY EXPLAIN THE FUNCTIONAL ETIOLOGIES OF THESE PROBLEMS AND THE BEST AVAILABLE CARE NOT JUST TREAT THE SYMPTOMS

In the case of disc-condyle LACK OF coordinations, studies suggest that for some patients even though they may be progressive (for example, a disc displacement with reduction may progress to a disc displacement without reduction), they are self limiting, suggesting an adaptation of the condition and with no significant disability.  DISABILITY IS IN THE EYES OF THE PATIENTS.  THE IDEA THAT LIVING IN PAIN FOR AN EXTENDED TIME IS SELF LIMITING IS A LIE.  LIVING IN PAIN CAN BECOME A CHRONIC PAIN PROBLEM AND HAVING MANY EMOTIONAL AND SOCIAL EFFECTS FAR BEYOND THE CLICKING OR JOINT PAIN.  It is very important to emphasize that patients have no recurrence of symptoms with the use of conservative, reversible treatments, IS CONSERVATIVE TREATMENT ONE THAT ALLOWS CONTINUAL DESTRUCTION OF THE JOINTS EVEN IF PAIN IS NOT CONSTANT?  thus conservative treatment is the modality that needs to be used at all times. CONSERVATIVE TREATMENT SHOULD BE USED AT ALL TIME IS A STATEMENT THAT CAN BE VERY DAMAGING TO THE HEALTH OF PATIENTS.  Initial treatment should therefore stress a conservative ABSOLUTELY  and reversible approach. Primary treatment options include home care (self-care program), medical care (non-surgical care), and surgical care.  SURGERY IS ALMOST ALWAYS BEST AVOIDED.  IF CONSERVATIVE NON-REVERSIBLE TREATMENT CAN PREVENT THE NEED FOR FUTURE INVASIVS AND POSSIBLY DISABLING SURGERY SHOULD THE PATIENT ALWAYS BE PRESENTED WITH LONG TERM TREATMENTS THAT MAY PREVENT FURTHER JOINT DEGRADATION.

Patient education: home care program

Home care I WOULD PREFER TO SAY EDUCATION OF THE PATIENT  should generally be INCLUDED the initial approach, at least as part of a more extensive treatment plan. The use of a home care program has proved to be effective in the management of TMD.   It has been shown that patients have reported feeling less pain immediately after their initial patient education/counseling visit, perhaps as a consequence of an immediate reduction in stress/tension-related parafunctional activity.   THERE IS A NATURAL PROGRESSION OF THE DISEASE AND RANDOM FLUCTUATIONS OF INCREASED AND DECREASED PAIN FREQUENTLY OCCUR WITH OR WITHOUT INTERVENTION.  Patient education is a crucial aspect of home care and is one of the most subtle and underappreciated, yet effective, treatments for TMD. Therefore, informing and reassuring the patient regarding their condition and presenting symptoms may alleviate a great deal of anxiety and improve treatment outcomes.  THIS DOES NOT RELIEVE THE DOCTOR OF EXPLAINING POSSIBLE ADVERSE OUTCOMES FROM LACK OF MORE DEFINITIVE TREATMENTS.

A successful home care program consists of resting the masticatory muscles by limiting jaw movements, parafunctional habit modification, emphasizing a soft diet, and moist heat and/or ice therapy.  IT IS INTERESTING THAT ELSEWHERE IN THE BODY ORTHOPEDIC PHYSICIANS AND PHYSICAL THERAPISTS FREQUENTLY UTILIZE LONG TERM ORTHOTICS AND PROSTHETICS TO TREAT MUSCLES AND JOINT BUT IN THE FAR MORE COMPLEX AND HIGHLY INNERVATED CRANIAL FACIAL REGIONS WE ARE MORE APT TO FOLLOW DEGENERATION RATHER THAN ATTEMPT TO PREVENT IT.  Muscle rest may involve limited jaw activity (eg, reduced talking, chewing, yawning) for the treatment duration, and perhaps as a preventive measure, even after symptoms have resolved.  DON’T USE YOUR JAWS IS NOT A CURE IT IS A DISABILITY, IDEALLY FULL FUNCTION SHOULD BE THE DESIRED OUTCOME. Patients with disc displacement without reduction should be instructed to avoid any forceful attempt to open the mouth wider when the condition is acute and have explained to them that, with the care provided, the ROM will improve and return to normal.


Restricting the mandibular movements as much as possible would facilitate healing and prevent further injury.  THIS IS NOT THE CASE IF THERE IS A CLOSE-LOCK DISLOCATION OR BLEEDING IN THE JOINT WHERE LIMITED MOVEMENT COULD LEAD TO ANKYLOSIS. This could be attained with a soft food diet, avoiding chewing gum and hard foods, and limitation of opening during yawning, as well as habit awareness, such as avoiding biting objects, clenching, or bruxing.   Patients may have a diurnal (daytime) parafunctional habit (clenching, grinding, posturing) that is often not conscious, and this should be addressed to decrease sustained masticatory muscle contractions.  MANY PATIENTS HAVE FUNCTIONAL PROBLEMS AND DEVIATE SWALLOWS THAT ACTUALLY PROTECT THE JOINT DURING SWALLOWING BUT LEAD TO OTHER PROBLEMS.  WHEN ONE LOOKS AT THE ENTIRE SYSTEM IT FAILS AT THE WEAKEST POINT.  THE WEAKEST POINT IS NOT ALWAYS EASILY ISOLATED.  Patient education and understanding of the physiological rest position (lips together, teeth apart) is imperative in reducing and eventually halting the daytime activity that contributes to the progression of TMD. THE UTILIZATION OF AN ORAL MYOFUNCTINAL THERAPIST MAY BE THE MOST VALUABLE INTERVENTION FROM A BEHAVIORAL POINT OF VIEW.  If asked to pay attention to their jaw position over time, many patients will return for follow-up with the recognition that they are in fact engaging in some jaw activity that contributes to their symptoms. OTHER PATIENTS MAY ACTUALLY FRE WORSE BECAUSE OF INCREASED OCCLUSAL AWARENESS THAT IS OFTEN A SIGNIFICANT FACTOR  EFFECTING WELL BEING. Additionally, suggesting habit-controlling cues may be helpful in reminding the patient throughout the day to check the position of their bite. As an example, saying the letter “N” throughout the day can remind the patient to unclench or discontinue grinding their teeth. A soft diet is also crucial for muscle and TMJ pain management so that the condition is not exacerbated while treatment is provided. Finally, a trial of moist heat and/or ice therapy overlying the painful areas of the face, head, and neck can be recommended. Moist heat tends to work better for muscle pain or tension by increasing circulation and relaxing involved muscles, and ice for TMJ capsulitis by reducing inflammatory symptoms.  UNFORTUNATELY NOT ALL PATIENTS RESPOND TO THESE TECHNIQUES AND MANY OFTEN CAN SUFFER ADDITIONAL INJURY FROM DELAYING APPLIANCE THERAPY.

Medical care (non-surgical)

Physical therapy

Instructing the patient to apply moist heat or cold compresses, or alternating both modalities, has been proven to be beneficial, since it stimulates analgesia and relaxation and may improve movement.

Physical therapy is beneficial in restoring the normal function of the TMJ, muscles of mastication, and cervical muscles, as well as in reducing inflammation, promoting repair, and strength.    Physical therapy can be performed by an experienced physical therapist or can be provided by a qualified clinician who is treating the TMJ disorder. Primary goals of the physical therapy component of treatment are to stretch chronically contracted and fatigued muscles, increase ROM, and reduce muscular trigger point activity. A number of exercises are commonly used to treat TMJ-associated muscle disorders, including N-stretch (placing the tip of the tongue on the roof of the mouth and stretching the jaw)  chin to chest (gently pulling the head forward, bringing the chin toward the chest); and head tilt (turning the head to one side and then tilting it posteriorly). These exercises must be done four to six times per day to be effective. In addition, the patient should use moist heat for 10–15 minutes followed by ethyl chloride spray prior to stretching the muscles. Vapocoolant spray provides a temporary anesthesia effect to the muscles so that a more intense stretch can be achieved without pain.  THS IS ESSENTIAL IF THE TAUT BANDS AND TRIGGER POINTS ASSOCIATED WITH MYOFASCIAL PAIN ARE GOING TO BE SUCCESSFULLY TREATED.  TRIGGER POINT INJECTIONS COMBINED WITH IMMEDIATE STRETCH PER TRAVELL AND PHYSICAL THERAPY IS EXTREMELY POWERFUL THERPY.  YOUNGER PHYSICAL THERAPISTS ARE OFTEN TRAINED IN UTILIZING DRY NEEDLING AS PART OF PHYSICAL THERAPY PROTOCOLS .  The heat and cooling spray should be used for at least three of the six exercising sessions throughout the day.  THE BEST RESULTS ARE WHEN A HEATING PAD IS USED TO HEAT THE CORE (STOMACH) FOR 20 MINUTES PRIOR TO UTILIZING VAPOCOOLANT SPRAY.  THE HEATING OF THE CORE CAUSES THE BODY TO SHUNT BLOOD TO THE FIVE LIMBS, HEAD, ARMS AND LEGS SO THE VAPOCOOLANT COOLS THE SKIN BUT NOT THE UNDERLYING MUSCLE. Patients can expect an even higher likelihood of treatment success if transcutaneous electrical nerve stimulation is added to a strict stretching regimen, and if biofeedback training is used as a cognitive behavioral procedure to teach the patient to maintain reduced muscular tension and pain.  ULTRA LOW FREQUENCY TENS USED BY NEUROMUSCULAR DENTISTRY IS THE MOST EFFECTIVE AT ELIMINATING MUSCLE SPASM AND IS PRIMARILY A PERIFERAL EFFECT ON THE MUSCLES RATHER THAN PRIMARILY A CNS EFFECT WITH OTHER TENS.


Medications are an effective addition in managing the symptomatology of intracapsular disorders.  Commonly used pharmacological agents for the treatment of TMJ disorders include analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), local anesthetics, oral and injectable corticosteroids, sodium hyaluronate injections, muscle relaxants, botulinum toxin injections, and antidepressants.   The analgesics and corticosteroids are indicated for acute TMD pain; the NSAIDs, local anesthetics, and muscle relaxants are used for both acute and chronic conditions; and tricyclic antidepressants are usually used more for chronic TMD pain in association with tension-type headaches.  THEY ARE ALSO VERY EFFECTIVE AT CONSOLIDATING DELTA SLEEP AND DELAYING REM SLEEP THAT IS HELPFUL IN TREATING MUSCLE PAIN FROM FIBROMYALGIA AND MYOFACIAL PAIN.  THEY MAY BE HELPFUL IN DECREASING NOCTURNAL BRUXISM IN SOME PATIENTS.  Research demonstrating the efficacy of botulinum toxin for muscular disorders related to TMD is limited, although there is some data to support the benefit of using low concentrations and large injection volumes of botulinum toxin at multiple muscular sites.  THE MECHANISM OF BOTOX IS TO DECREASE THE NOCICEPTIVE INPUT TO THE TRIGEMINAL NERVOUS SYSTEM BY USING THE TOXIN TO PARALYZE THE NEUROMUSCULAR JUNCTION AND THEREFORE DECREASE PARAFUNCTION AND PAIN.  CORRECTION OF NEUROMUSCULAR INPUT WITH A NEUROMUSCULAR ORTHOTIC IS SAFER AND MORE EFFECTIVE FOR MOST PATIENTS BUT BOTOX CAN BE USED ON AN INTERIM BASIS TO BREAK A PAIN CYCLE.


NSAIDs are indicated for mild-to-moderate acute inflammatory conditions. Commonly used NSAIDs include ibuprofen and naproxen. NSAIDs should be used by the patient for a minimum of 2 weeks, with time-contingent usage as opposed to dosing based on the presence of pain.  Long-term NSAID use is not recommended as long as the activity resulting in the inflammatory process can be reduced. In some chronic arthritic cases, the long-term use of NSAIDs, such as the COX-2 inhibitors, including celecoxib, may be considered; however, possible side effects, such as gastrointestinal upset, should be taken into account.  IT IS ESTIMATED THAT AS MANY AS 40,000 DEATHS OCCUR ANNUALLY FROM SIDE EFFECTS OF NSAIDS.

Local anesthetics

Local anesthetics are primarily used when a myofascial trigger point is present. Myofascial trigger points are usually detected in the mastication muscles, but can also be found in numerous other muscles, such as the splenius capitis and upper trapezius. Due to its low toxicity to muscles, 1% procaine (1 cc) is recommended, but 1% or 2% lidocaine is also commonly used. THIS AUTHOR PRFERS THE USE OF 2% LIDOCAINE WITH NO PRESERVATIVES OR VASOCONSTICTORS.   The trigger point injection technique involves locating the trigger point, which is usually found in a taut band of muscle, and needling the area.  THE USE OF DRY NEEDLING VS LIDOCAINE INJECTION CAN VARY IN EFFECTIVENESS BY THE PATIENT.  THE USE OF VAPOCOOLANT SPRAY CAN ELIMINATE THE PAIN FROM PENETRATION THROUGH THE SKIN. DR JANET TRAVELL IN HER LANDMARK TEXT MYOFASCIAL PAIN AND DYSFUNCTION : A TRIGGER POINT MANUAL CLEARLY STATES THAT INJECTION AND STRETCH IS VERY IMPORTANT, NOT JUST INJECTION.  THE COMBINING OF ALL THREE MODALITIES WILL GIVE THE BEST RESULTS. The patient should be instructed that the muscles may be sore for the first 48 hours after the injection, but should begin to improve thereafter. I FIND THAT MOST PATIENTS HAVE IMMEDIATE RELIEF THAT IMPROVES OVER 24-72 HOURS AND SORENESS IS USUALLY FELT ONLY IF PRESSURE IS APPLIED OVER INJECTION SITES.  The efficacy of trigger point injections is highly variable and dependent, for the most part, on the patient’s compliance with a strict physical therapy regimen in conjunction with the injections.  MANY PATIENT ARE FAR MORE COMPLIANT WITH EXERCISE WHEN TRIGGER POINT THERAPY ELIMINATES MOST OF THE FUNCTIONL PAIN. In addition, local anesthetics can be used to block the likely source of pain to confirm a diagnosis.

TMJ injections


Intracapsular injection of corticosteroids significantly reduces TMJ pain.  THERE IS EXCELLENT EVIDENCE THAT INTRA-ARTICULAR INJECTIONS CAN INCREASE ARTHRITIC CHANGES WHEN USED REPEATEDLY SO THEY SHOULD BE USED SPARINGLY FOR ACUTE CONDITIONS.   It is indicated for acute and painful arthritic TMJ that has not responded to other modalities of treatment and when the joint is still acutely inflamed, such as in the case of polyarthritic disorders and in acute disc displacements without reduction.  ACUTE DISK DISPLACEMENTS WITHOUT REDUCTION ARE BEST TREATED IMMEDIATELY.  THE STIMULATION OF A SEVERE GAG REFLEX CAN OFTEN IMMEDIATELY REDUCE A CLOSE LOCK DISLOCATION.  THE GAG REFLEX IS A PROTECTIVE REFLEX THAT PREVENTS VOMIT FROM ENTERING THE LUNGS AND CAUSES IMMEDIATE AND COMPLETE RELAXATION OF THE MANDIBULAR ELEVATOR MUSCLES AND CONTRACTION OF ALL THE SUPRA AND INFRA HYOID MUSCLES AS WELL AS POSTERIOR CERVICAL MUSCLES AND THE JAW OPENS STRAIGHT DOWN RATHER THAN ROTATING AND TRANSLATING TEARING ON THE RETRODISCAL TISSUES. The use of triamcinolone or dexamethasone, in addition to 2% lidocaine without epinephrine, is generally used for TMJ injections. SOMETIMES THE JAW CAN BE MANIPULATED UNDER IV SEDATION TO MANUALLY MANIPULATE THE MANDIBLE TO REDUCE A CLOSE-LOCK.  Tomograms of the TMJ or other radiographic studies are required prior to injecting into the joint space. It has been suggested in animal studies that steroid injections may increase osteoclastic activity.  There is no evidence that a single steroid injection causes damage; however, multiple injections may do, therefore the quantity of steroid injections should be carefully considered due to the possibility of bone resorption in the site of injection.  THERE IS A PROCEDURE CALLED HYDRAULIC DISTENSION THAT CAN BE USED TO REDUCE A CLOSE LOCK.  THE JOINT IS EXPANDED WITH ANAESTHETIC AND THEN MANIPULATED TO REDUCE THE DISLOCATION FLOATING THE DISK TO PLACE.

Injections of sodium hyaluronate in osteoarthritis of the knee has shown improvement of symptoms; however, results for the management of TMD have been inconclusive and more studies are warranted.  THERE IS LITTLE DOWNSIDE TO UTILIZING SODIUM HYLALURONATE .

Muscle relaxants

Muscle relaxants may be prescribed for acute muscle tension associated with TMJ disorders.  These are commonly taken at night before bed, due to possible associated drowsiness. Thus, for patients with poor sleep patterns, these drugs are particularly helpful in alleviating insomnia in addition to their muscle-pain preventive properties. A commonly used and effective muscle relaxant is cyclobenzaprine, started at lower dosages (5–10 mg) and taken 1–2 hours before bedtime.  CYCLOBENZAPRINE O FLEXERIL IS A UNIQUE MUSCLE RELAXER IN THE TRICYCLIC FMILY SIMILAR TO ANTIDEPRESSNTS AND IT IS ALSO EFFECTIVE IN CONSOLIDATING DELTA SLEEP AND DELAYING REM ONSET.  SEE ANTIDEPRESSANT BELOW.


Tricyclic antidepressants like amitriptyline and nortriptyline may be used for more chronic MFP.   In addition, they can be prescribed for the TMD patient who has tension-type headache (TTH), depression, poor sleep, and/or poor appetite. It is important to inform the patient that these medications are used in dosages that will not usually have anti-depressive effects when prescribed to treat muscle pain and/or headaches. Nortriptyline at usual doses of 10–30 mg and amitriptyline at doses of 10–25 mg should be gradually tapered up until the desired therapeutic effect is achieved or side effects develop, such as drowsiness, dry mouth, or weight gain. The tricyclic antidepressants have anti-nociceptive effects as well as maintaining the patient in deeper stages of DELTA  SLEEP AND DELAYING REM SLEEP . Caution should be used in patients who have comorbid heart conditions, concurrent psychotropic use, and/or psychiatric illness, eg, bipolar disorder.  DRY MOUTH AND WEIGHT GAIN ARE POSSIBLE SIDE EFFECTS OF THESE DRUGS.

Occlusal appliance therapy

Oral appliances (OAs) are processed acrylic devices that have been used for the management of TMD for years, with different designs. Studies have reported a reduction in TMD symptoms or at least sufficient evidence to justify their use for myalgia and arthralgia of the masticatory system.   In an extensive review about the use of OAs and the management of TMD, it was concluded that OAs are still regarded as a useful adjunct therapy for some TMD cases.  ALL ORAL APPLIANCES ARE NOT THE SAME.  THERE ARE MNY PHILOSOPHIES ABOUT THE BEST APPLIANCES.  THE TMD ALLIANCE IS A GROUP THAT INCLUDES THE ORGANIZATIONS WHOSE MEMBERS ARE INVOLVED IN TMD TREATMENT.  I AM CURRENTLY THE CHAIR OF THE ALLIANCE.

Stabilization appliances (flat plane splints)  are used for the purpose of equally distributing jaw parafunctional forces, reducing the forces placed on the masticatory muscles, and protecting the occlusal surfaces of the teeth from chronic nocturnal bruxing.  THERE IS EVIDENCE THAT THEY CAN MAKE SLEEP APNEA WORSE IN SOME PATIENTS. For the case of nocturnal bruxism, OAs will protect the teeth from excessive tooth wear but may not stop parafunctional habits; they may, however, decrease the frequency, duration, and intensity of these habits.  IF PATIENTS FEEL THEY HAVE MORE PAIN WITH THE APPLIANCES THEY SHOULD DISCUSS OTHER APPLIANCE DESIGNS WITH THEIR DENTIST. Usually, the patient is instructed to wear the splint only at night as long as parafunctional activity is controlled during the day with education and bite relation awareness, teaching the patient to be aware of when they are clenching their teeth during the day. The splint should cover all of the maxillary or mandibular teeth and have bilateral posterior contacts with little to no anterior contacts. The stabilization appliance should feel comfortable to the patient when fitted for the first time and be re-evaluated after 1 week. Adjustments should continue every 3–6 months due to changes that may result in the form and function of the splint due to chronic bruxing.

Anterior repositioning splint prescription varies among clinicians, but it is usually used for the chronic intermittent closed-locking patient.   With the possibility of permanent occlusal and bite changes with long-term use of repositioning appliances, short-term (6 weeks) use of this appliance is strongly recommended in addition to close monitoring.  THE QUESTION IS SOMETIMES WHETHER TO DEAL WITH OCCLUSAL CHANGES OR PERMANENT DAMAGE TO THE JOINTS OR INCREASING PAIN.  QUALITY OF LIFE SHOULD ALWAYS WEIGH IN THIS DISCUSSION.  WHEN APPLIANCE THERAPY IS DISCONTINUED IT IS CALLED A WALK BACK BUT OFTEN THE PATIENT IS WALKING BACK INTO THEIR PREVIOUS PATHOLOGY.  If bite changes start to develop, then the patient should be instructed to discontinue the use of the splint and the splint may need to be converted to a stabilization non-repositioning appliance. A few patients may experience increased pain with the use of a splint. In this case, the splint and the initial diagnosis should be re-evaluated and, if the pain persists, discontinuation of the splint is recommended.


In a systematic review and meta-analysis of randomized controlled trials, it was found that well-adjusted hard stabilization appliances are more effective in treating joint and muscle pain when compared with the use of no appliance, soft stabilization appliances, anterior bite appliances, and non-occluding appliances.  THESE STUDIES OFTEN DO NOT CLEARLY SPECIFY WHAT APPLIANCE ARE UTILIZED AND THOUSANDS OF PATIENTS HAVE HAD EXCELLENT RESULTS WITH LONG TERM APPLIANCE AND/OR RECONSTRUCTION.  THE TWO JOINTS AND TEETH FORM A TRIPOD THAT IS UNSTABLE IS ANY OF THE THREE LEGS ARE UNSTABLE, IE BITE OR EITHER JOINT.  Even though these OAs presented some evidence of reducing joint and muscle pains, the potential adverse events (eg, occlusal changes) were higher.  WELL THIS ARTICLE CONSIDERS OCCLUSAL CHANGES TO BE AN ADVERSE EVENT WHAT ACTUALLY IS OCCURING IS THE NATURAL PROCESS OF HEALING.  AS THE TISSUES HEAL AND REHYDRATE THEY CHANGE THE CONDYLAR POSITION.

Occlusal adjustment

There is not enough evidence to show that occlusal adjustments are useful in treating or preventing TMD.  As a general rule, TMD should be treated in a conservative manner and occlusal adjustments are an irreversible modality.  THERE ARE INCREDIBLE AMOUNTS OF IRREVERSIBLE CHANGES DONE DURING ROUTINE DENTISTRY.  WHILE THIS ARTICLE FROWNS ON OCCLUSAL CHANGES ANYONE WHO HAS EVER HAD A HIGH FILLING OR CROWN KNOW EVEN A FRACTION OF A MILLIMETER OFF ON THE BITE CAN CREATE TREMENDOUS PROBLEMS.


Surgical care


TMJ surgery is only indicated when non-surgical therapy has been ineffective, and it is not indicated in patients who are asymptomatic or mildly symptomatic or as a preventive measure.  MANY TIME SURGERY CAN BE AVOIDED IF NON-REVERSIBLE BITE CHANGES ARE MADE.  CHANGING THE TEETH IS FAR MORE CONSERVATIVE THAN JOINT SURGERY.  Surgical recommendations, such as arthrocentesis and arthroscopy, depend on the degree of internal derangement as well as previous TMJ treatment history in addition to moderate-to-severe pain and disabling dysfunction.  It is important to discourage patients from undergoing surgical procedures if physical medicine, pharmacological management, and splint therapy have not been attempted. PERMANENT BITE CHANGE IS PREFERRED OVER SURGERY .Working closely with an oral and maxillofacial surgeon who has expertise in TMJ surgery is highly advisable in dealing with this particular group of patients.

Arthrocentesis is a conservative treatment that involves an intra-articular lavage with or without deposit of corticosteroids that is useful when there are intra-articular restrictions to movement, as in disc displacement without reduction.   This procedure is often used with HYDRAULIC DYSTENSION AND mandibular manipulation and is recommended for patients who have joint restrictions and for those individuals who have developed an acute or chronic closed lock.

Arthroscopy is a closed surgical procedure that allows direct observation and sampling of joint tissue, useful in hypomobility due to joint derangement as well as fibrosis.  It is performed mainly in the upper joint space and is utilized primarily for lysis and lavage but also for ablation of adhesions and biopsy.

Arthrotomy is an open surgical procedure that modifies joint anatomy, such as total or partial joint reconstruction or replacement, which is required for the patient who has advanced TMD that meets the surgical criteria and has been refractory to other modalities.  It is used in cases of neoplasia, bony or fibrous ankylosis, severe chronic arthritis, and severe chronic dislocations.   It is important to work closely with an experienced TMJ surgeon to assess the necessity of this procedure if other conservative treatments have not produced positive results.

Acupuncture and TMD

Acupuncture has been studied as a complementary and alternative medicine treatment modality for various orofacial pain disorders, mostly those of musculoskeletal origin. Acupuncture is a form of Traditional Chinese Medicine (TCM) that involves the stimulation of acupuncture points that are thought to stimulate the flow of energy believed to be blocked. It has been proposed that the reason why acupuncture research has not been as definitive about its benefits in pain treatment is because these studies often fail to include other treatments, such as herbal remedies and Qigong.  A study that focused on TMD showed reductions in pain and, more importantly, a reduction in NSAID use in subjects who had been treated with traditional acupuncture.   Further research compared TCM including acupuncture to specialty care that included self-care, patient education, occlusal splint therapy, physical therapy, and psychosocial counseling and found that the TCM arm had a significantly greater reduction in pain and psychosocially contributing factors.  In addition, MFP, when teased apart from TMD, has been shown to benefit from acupuncture when compared to a sham acupuncture procedure.  THIS MAY BE DUE TO THE FACT THAT THERE IS AN 80% CORRELATION BETWEEN ACCUPUNCTURE POINTS AND TRIGGER POINTS.  THE ACCUPUNCTURE MAY BE ACCOMPLISHING WHAT DRY NEEDLES AND /OR TRIGGER POINT INJECTIONS ACCOMPLISH.  THIS AUTHOR TRIED UTILIZING ACCUPUNCTURE NEEDLES TO DRY NEEDLE TRIGGER POINTS BUT FOUND THAT 30 GUAGE HOLLOW NEEDLES GAVE A BETTER RESULT THAN THE VERY SLENDER ACCUPUNCTURE NEEDLES.  VAPOCOOLANT SPRAY ELIMINATES PAIN FROM SKIN PUNCTURE.  It is crucial to educate MFP patients about the difference between acupuncture and traditional trigger point injection therapy, as patients may confuse the two because of the similarity of the procedures.  Acupuncture appears to be a beneficial treatment in conjunction with traditional therapies for TMD and perhaps as an alternative if pharmacological treatment is contraindicated.

 Neuropathic pain

Basic and clinical research support that neuroplastic changes involving the peripheral and central nervous system as well as immune mechanisms are involved in the development and maintenance of chronic neuropathic pain.  It has been estimated that the incidence of chronic orofacial neuropathic pain is five to ten per 100,000 people.   Commonly, neuropathic pain conditions in the orofacial region are divided into episodic pain disorders, including trigeminal neuralgia (TN) and glossopharyngeal neuralgia, and continuous pain disorders that frequently result from deafferentation after injury in the peripheral and central nervous system, which is the case in neuromas and idiopathic trigeminal neuropathic pains ( THE TERM IDIOPATHIC MEANS THAT THE DOCTORS ARE IDIOTS AS TO THE CAUSE OF THE PAIN, WE DO NOT KNOW THE CAUSE!) such as atypical odontalgia (AO).  NEUROPATHIC PAINS ASSOCIATED WITH TMD ARE OFTEN RESOLVED WITH LONG TERM NEUROMUSCULAR ORTHOTICS. There is considerable variability in prevalence, cause, and treatment of these disorders. More detailed reviews on neuropathic pains classification, etiology, and pathophysiology can be found elsewhere.  THE USE OF SPG BLOCKS OR SPHENOPALATINE GANGLION BLOCKS ARE OFTEN EXTREMELY EFFECTIVE IN TREATING NEUROPATHIC PAIN.  THE GANGLIA IS THE LARGEST PARASYMPATHETIC GANGLION OF THE HEAD AND  I UTILIZED FOR  WIDE VARIETY OF DISORDERS THAT INVOLVE THE AUTONOMIC NERVOUS SYSTEM.  There are still limited data in regard to the treatment of trigeminal neuropathic pain. Its management is based on the evidence associated with pain management in other parts of the body. Good reference guides are those by Dworkin et aL  and Zakrzewska.  I have never been a fan of Dworkins work not because of the psychological aspects but because of the neglect of the Axis 1 treatment.

The use of anticonvulsant medications has shown to be effective in the management of trigeminal neuropathic pain, and they are the first-line treatment choice for the management of neuralgic type of pains.  THE USE OF DRUG CORNUCOPIA IS FREQUENTLY USED IN TREATING NEUROLOGICAL PAIN, WHILE THIS MAY FALL UNDER THE UMBRELLA OF OROFACIAL PAIN IT SHOULD ACTUALLY BE CONTROLLED AND MANAGED BY PHYSICIAN NEUROLOGISTS RATHER THAN DENTISTS.  THE SPECIALTY OF NEUROLOGY HAS THE BEST TRAINED PRACTITIONERS FOR PRESCRIBING THESE MEDICATIONS Tricyclic antidepressants and serotonin noradrenaline reuptake inhibitors, as well as topical medications such as capsaicin and lidocaine,are used for the more continuous type of pain, such as in the case of idiopathic trigeminal neuropathic pain, for example, in AO.  THESE DRUGS ARE WITHIN THE SCOPE OF PRACTICE OF OROFACIAL PAIN DOCTORS AND GENERAL DENTISTS IN LOW DOSES BUT HIGH DOSES SHOULD BE PRESCRIBED BY PHYSICIANS, NEUROLOGISTS AND PSYCHIATRISTS.


Trigeminal neuralgia

TN is a chronic paroxysmal neuropathic pain condition that is described as a severe, lancinating, and electric-like unilateral pain. It is localized most often to the second and third distributions of the trigeminal nerve (V2 and V3) intraorally and extraorally and can present in both distributions at the same time. There is usually a trigger zone in the trigeminal distribution which, when stimulated, can result in an excruciatingly painful attack. The pain attacks last seconds to minutes and numerous pain episodes can be present daily. TN commonly goes through periods of remission where the pain can remit for months or even longer.  MANY PATIENTS WHO ARE DIAGNOSED AS TRIGEMINAL NEURALGIA DO NOT HAVE AN ACTIVE TRIGGER AREA AND THE DIAGNOSIS IS QUESTIONABLE.  OFTEN THEY ARE DIAGNOSED (MISDIAGNOSED) AS ATYPICAL TRIGEMINAL NEURALGIA BUT FURTHER EVALUATION CAN SOMETIMES REVEAL MORE SPECIFIC ACTUAL CAUSES OF PAIN.

The etiology of TN is often related to vascular compression  that may result in focal demyelination.  The superior cerebellar artery compression on the trigeminal root has been shown to be responsible for attacks of TN pain;  THESE PATIENTS CAN BE SUCCESFULLY TREATED SURGICALLY IF NON-SURGICAL TREATMENT FAILS, OFTEN WITH A GAMMA KNIFE. however, nonvascular compression by a cerebellopontine angle neoplasm, such as acoustic neuromas, meningiomas, cholesteatomas, and neurofibromas, have also been shown to result in TN attacks. RULING OUT THESE POSSIBLY LIFE THREATENING DISORDERS IS ESSENTIAL  A cranial nerve exam can demonstrate other neural deficits that may be present due to a mass pressing on the trigeminal root. Therefore, magnetic resonance imaging (MRI) and computed tomography (CT) imaging of the brain should be requested in order to rule out any intracranial pathology. Furthermore, myelin loss due to multiple sclerosis has been shown to be a causative disorder related to the paroxysmal pain firing of TN attacks.

Antiepileptic medications are the drugs of choice for the management of TN. Carbamazepine, oxcarbazepine, and gabapentin are commonly used as first-line medications.  THESE DISORDERS ARE BEST TREATED BY NEUROLOGISTS NOT DENTISTS Carbamazepine, evaluated in a systematic review, has been shown to be the most effective treatment. If these medications are not effective, or if the therapeutic range cannot be achieved due to side effects, then doses should be lowered and second-line drugs, such as baclofen and lamotrigine,  may be added to reduce the pain attacks. It is best to reduce the pain attacks completely with multiple medications if necessary. After achieving pain-free status and monitoring for pain attacks for a minimum of 3–6 months, a slow taper off of medication will demonstrate if the TN has gone into remission. If pain attacks recur, then pharmacologic management should immediately be reinstituted. If medications are no longer effective or if unmanageable side effects develop, then neurosurgical options, such as microvascular decompression or gamma knife radiosurgery, may be considered.  THE SPHENOPALATINE GANGLION BLOCK IS , BY FAR, THE SAFEST METHOD OF TREATING TRIGEMINAL NEURALGIA WHEN IT IS EFFECTIVE.

Glossopharyngeal neuralgia

Glossopharyngeal neuralgia is a rare condition associated with pain in the area supplied by the glossopharyngeal nerve.  Painful sites may include the nasopharynx, posterior part of the tongue, throat, tonsil, larynx, and ear. This disorder presents shooting paroxysms of pain that can occur multiple times a day with stimulation of the oropharyngeal region.  Common triggers may include mechanical stimulation of the trigger zone as well as activities including chewing, swallowing, coughing, talking, and head movement. The painful episodes may continue for months and then spontaneously go into remission. Due to the proximity of the vagal sensory nerves, glossopharyngeal neuralgia may coincide with a cardiac dysrhythmia such as bradycardia, asystole, and syncope.  IT IS ALSO COMMONLY ASSOCIATED WITH GASTRIC REFLEX AND OBSTRUCTIVE SLEEP APNEA Diagnosis may be confirmed by blocking the tonsillar and pharyngeal region with topical or local anesthetics. Imaging with a CT scan of the head and a brain MRI should be conducted to rule out pathology related to the nerve compression and possible oropharyngeal carcinoma. Pharmacologic treatment of glossopharyngeal neuralgia is similar to that for TN and may include the use of antiepileptic medications.  If medication management fails, then surgical procedures may be considered, such as a microvascular decompression to remove pressure from the glossopharyngeal nerve, radiofrequency thermocoagulation, gamma knife radiosurgery, or rhizotomy.  Peripheral trigeminal neuropathic pain

Peripheral neuropathic pain can arise as a result of a traumatic nerve injury resulting in chronic aching, continuous burning-like pain at the site of the injury.When a nerve injury occurs, the transected nerve will sometimes attempt to restore itself through axonal sprouting, resulting in a traumatic neuroma.  Diagnosis can be made through tapping (Tinel’s sign) or lightly pressing on the suspected site of the neuroma. In addition, allodynia and hyperalgesia will often be present in the area of the nerve injury or adjacent to it.  THESE PROBLEMS OFTEN RESPOND WELL TO SPHENOPALATINE GANGLION BLOCK TREATMENT   It is recommended to perform a diagnostic block of the painful site with topical anesthetic first (eg, benzocaine) followed by a somatic block with local anesthetic (eg, lidocaine injection).  If either of these blocks reduce or alleviate the pain, then topical creams or ointments may be utilized to treat the pain. The use of topical medications for the management of neuropathic pain is a good modality that reduces potential side effects of the systemic route.  Capsaicin is a common locally acting pharmacologic agent that can be utilized in cream or gel form, normally at a concentration ranging from 0.025%–0.05%   mixed with benzocaine 20% and applied with the use of a stent that covers the affected area (neurosensory stent). Recently, 8% capsaicin has been approved in the US and Europe for application directly into the skin, and has proved to be effective in alleviating pain.  In addition, compounding pharmacies can create a cream that may include analgesics/sedatives such as ketamine, NSAIDs such as diclofenac, anticonvulsant drugs such as gabapentin and carbamazepine, and tricyclic antidepressant medications such as nortriptyline and amitriptyline.  COMPOUNDED CREAM WITH JUST TRICYCLICS SUCH AS AMITRYPTILNE CAN BE EXTREMELY EFFECTIVE

Centralized trigeminal neuropathic pain


Prolonged stimulation of peripheral nociceptors may eventually lead to central neural changes.  NOCICEPTION IS VERY COMMON FROM PERIODONTAL INPUT FROM OCCLUSAL DYSFUNCTION.  UTILIZATION OF AN AUTONOMIC BLOCK, EITHER SPHENOPALATINE GANGLION OR STELLEATE CAN BE EFFECTIVE IN BREAKING THE CYCLE.  THE SPG BLOCK IS SAFER AND EASILY ADMINISTERED BY A DENTIST WHERE THE STELLATE GANGLION BLOCK IS USUALLY PREFORMED BY NEUROSURGEON OR ANAETHESIOLOGIST.   The pain in these cases is described as continuous, aching, and burning, with evidence of hyperalgesia and allodynia.  Diagnostic local anesthetic blocking of the affected site usually does not alleviate the pain in centralized neuropathic pain, thus treatment is conducted with centrally acting systemic medications.  Antiepileptic drugs, such as gabapentin and valproic acid, in combination with tricyclic antidepressants such as amitriptyline, may reduce pain, but often treatment of this condition is difficult.

Atypical odontalgia

AO is a centralized trigeminal neuropathy often localized in a tooth or tooth area that is frequently misdiagnosed, leading to unnecessary dental treatments in attempts to relieve the pain.  I HAVE SEEN NUMEROUS PATIENTS PRESENTING WITH SEVERE TOOH PAIN THAT WAS RELIEVED BY SPRAY AND STRETCH OR TRIGGER POINT INJECTIONS.  IT IS ALWAYS BEST TO RULE OUT NEUROPATHIC AND REFERRED MYOFASCIAL PAIN PRIOT TO DOING PULPAL THERAPY OR EXTRACTIONS ON OTHERWISE HEALTHY TEETH.  A PERCENTAGE OF TEETH PRESENTING AS ATYPICAL ODONTALGIA ARE SOMETIMES VERTICALLY FRACTURED TEETH THAT REMAINS UNDIAGNOSED. AO is described as a persistent idiopathic pain that does not fulfill the diagnostic criteria for cranial neuralgias and which is not attributed to another disorder,  and can be throbbing and burning in nature.  The pharmacological management of AO may include topical and systemic medications. PRIOR TO BEGINNING MEDICATION RULING OUT REFERRED PAIN IS ESSENTIAL.  ONE POSSIBLE CAUSE OF REFERRED PAIN IS CARDIAC REFERRAL.  THIS WAS CLEARLY SHOW BY DR ANNIKA ISBERG WHOSE PUBLISHED DATA SHOWED CRANIAL FACIAL PAIN INCLUDING SINUS AND TOOTH PAIN USUALLY PRECEDED CARDIAC EVENTS  If the pain is localized to a peripheral origin and the diagnostic block gives an equivocal response but a decrease in pain, a topical medication can be used and a neurosensory stent can be fabricated. Systemic approaches, such as tricyclic antidepressants, calcium channel blockers (pregabalin and gabapentin), sodium channel blockers (carbamazepine), and antiepileptics such as topiramate, can be used for the management of this condition. AGAIN, MOST OF THESE DRUGS AND MEDICATIONS ARE BEST SUPPLIED BY NEUROLOGISTS RATHER THAN DENTISTS.  The management of AO is very challenging, and a multidisciplinary approach is necessary, which should include orofacial pain specialists and neurologists in addition to psychiatric and psychological evaluations in order to identify comorbidities with depression and anxiety.  WHILE OROFACIAL PAIN DIAGNOSIS CAN BE COMPLICATED CLARITY IS OFTEN OBTAINED WHEN PAIN RELIEF CAN BE ACCOMPLISHED DURING THE CONSULTATION APPOINTMENT.  I SAW A NEW CONSULT THIS MORNING WHO WAS 32 YEARS OLD AND HAS BEEN IN PAIN FOR OVER 25 YEARS.  IT WAS POSSIBLE TO ELIMINATE 90% OF HER PAIN DURING CONSULTATION UTILIZING TRAVELL SPRAY AND STRETCH TECHNIQUES.  THIS PATIENT HAS PREVIOUSLY HAD MRI AND CAT SCANS AND SEEN A WIDE VARIETY OF PRACTIONERS BUT SHE ACTUALLY HAD TYPICAL MYOFASCIAL PAIN PATTERNS.


Another source of nonodontogenic toothaches and orofacial pains may present as a disturbance of the trigeminovascular system. THE TRIGEMINAL SYSTEM SHULD BE CONSIDERED THE MOST LIKELY SOURCE OF ALL CRANIAL FACIAL AND OROFACIAL PAIN INCLUDING HEADACHES MIGRAINES AND THE AUTONOMIC CEPHALGIAS. Migraine is commonly thought of as a headache that is unilateral and that causes pain behind the eye, neck, and cranium; however, migraine headaches can also present in the lower part of the face, particularly in the teeth.  It is very important that the orofacial pain clinician is aware of the possibility of this localization in addition to the clinical features that a migraine presents to avoid misdiagnosis as an odontogenic toothache or other type of orofacial pain, leading to improper management.


Primary headaches, such as migraine and TTH, are also disorders mediated by the trigeminal system that can be chronic and disabling, affecting over 15% of the US population at any one time and costing the US economy over $19.6 billion a year. Migraine is a primary disorder of the brain explained as a TRIGEMINALLY INNERVATED neurovascular disorder in which neural events result in meningeal blood vessel dilation, which results in further nociceptive activation of the trigeminovascular system AND RELEASE OF VASOACTIVE NEUROPEPTIDES SUCH AS SUBSTANCE P NEUROKININ A  AND CGRP, CALCITONIN GENE RELATED PEPTIDE.   The pathophysiology of migraine is still not completely understood, but it is known that key anatomical peripheral and central structures are involved. The trigeminovascular system consists of the dura mater that surrounds the meninges and spinal cord, the dural meningeal blood vessels (cranial vasculature), and the innervations of these structures provided by the ophthalmic branch (V1) of the trigeminal nerve and its afferent connection to the trigeminal nucleus caudalis (TNC) in the central nervous system, in addition to a reflex connection from the trigeminal nucleus to the parasympathetic outflow to the cranial vasculature through the superior salivatory nucleus.

The nociceptive (pain) information of these structures convey information to the nucleus caudalis or TNC, brainstem, and higher processing centers. The TNC also receives cervical inputs. Stimulation of the dura mater extends to the C2 and C3 regions, and is collectively described as the trigeminocervical complex (TCC). This anatomical relationship may explain why a migraine headache can sometimes be felt in the neck area.

Primary headaches, particularly migraine, are believed to involve activation and sensitization of the trigeminovascular system, specifically the afferent meningeal nociceptor projections to the ophthalmic division of the trigeminal nerve, and this is thought to cause the release of vasoactive neuropeptides such as substance P (SP), neurokinin A (NKA), and calcitonin gene-related peptide (CGRP), which is elevated during a chronic migraine attack.  What drives the trigeminovascular activation is still not clear, but it has been hypothesized that a dysfunction within nuclei of the brainstem and diencephalon may contribute to activation of this system, thereby relaying nociceptive information to other central structures. NEUROMUSCULAR DENTISTS AND MOST CLINICAL DENTISTS WHO SUCCESSFULLY TREAT PATIENTS WITH MULTIPHARMACY  BELIEVE THAT THE NOCICEPTION IS SPECIFICALLY FROM THE PROPRIOCEPTIVE INPUTS TO THE TRIGAMINAL NERVOUS SYSTEM FROM THE JAW JOINTS, THE TEETH, THE PERIODONTAL LIGAMENTS AND THE MASTICATORY MUSCLES.  THE DYSFUNCTION.  Trigeminal nerve release of CGRP is known to aid in the process of neurogenic inflammation, facilitating pain transmission leading to allodynia and hyperalgesia.  These nociceptive mediators will induce edema, mast cell activation, and further sensitization of the trigeminovascular system.

Facial migraine

In the new International Classification of Headache Disorders 3rd edition (ICHD-3 beta version) in the comments to section 1.1 (“Migraine without aura”) facial migraine is mentioned as a subset of patients who present with the typical migraine headache, but localized in the face and not as a subtype.   Facial migraine may follow the diagnostic criteria of migraine without aura (ICHD-3 1.1), which is described as a recurrent headache of moderate-to-severe intensity that lasts from 4–72 hours, with a pulsating quality, which is unilateral in location, aggravated by routine physical activity, and associated with nausea and/or phonophobia and photophobia.


The ophthalmic division of the trigeminal nerve innervates most of the cranial structures: this could explain the reason why most migraine sufferers feel pain in the periorbital region and behind their eye. In facial migraine, however, the pain is localized in the lower part of the face. Migraine localized in the area of the maxillary branch distribution (V2) has been reported.  V2 gives rise to the nervus meningeus medius, which innervates the dura mater of the anterior floor of the middle fossa, and this may explain the localization of the pain in the maxillary area. Migraine symptomatology localized on the V3 territory has also been reported and this could be explained since it is well recognized that stimulation of the dura mater in animals during electrophysiological experiments, and in humans during neurosurgery, induces pain in any of the three divisions of the trigeminal nerve.  More detailed reviews on migraine pathophysiology can be found elsewhere.


The management of migraine comprises pharmacological and nonpharmacological approaches. It is imperative that the treatment approach of migraine always includes a complete medical evaluation performed by the neurologist to rule out a secondary cause of the headache, such as systemic disease, tumors, or cerebrovascular abnormalities.

Nonpharmacological approaches

Patients need to be educated about the pain they are experiencing. When the pain is localized in the lower half of the face and/or in a tooth/teeth area (facial migraine), the patient should be assured that, even though the experienced pain may be severe and throbbing, it is not a toothache or related dental problem. This is extremely important since it will prevent unnecessary dental procedures due to misdiagnosis as odontogenic toothache or other orofacial pain.

Facial migraine is the same migraine headache described in the ICDH-3 (beta version) but with a different localization, therefore requiring that the same management protocol be followed. It is recommended to have the patient identify any trigger factors that may start the migraine attack. THESE SHOULD INCLUDE MASTICATORY SYSTEM TRIGGERS.  A good method by which the patient can provide this information is with the use of a pain diary, in which the patient keeps a record of the characteristics of the headache episodes along with the circumstances that made them appear. As soon as the patient can identify the possible triggers, then they are instructed to avoid or address them by, for example, a change in diet, sleep hygiene, or stress management. This is a great opportunity for the patient to realize that lifestyle changes may greatly influence their headaches and subsequently feel more in control of the disorder.

Other nonpharmacological methods that have proved useful for migraine and TTH are biofeedback, relaxation techniques, hypnosis, and psychological therapies. MANY PATIENTS CAN REDUCE OR ELIMINATE EPISODES  AND SEVERITY BY THE USE OF DIAGNOSTIC NEUROMUSCULAR ORTHOTICS INITIALLY AND LONG TERM ORTHOTICS I SUBSTANTIAL RELIEF IS REALIZED.

Pharmacological approaches

As described above, the TNC is a crucial anatomical relay center for conveying sensory information, predominantly nociceptive, coming from the orofacial region, the head and its cranial vasculature, to higher pain processing centers in the brain; in addition, it gives and receives projections from the superior salivatory nucleus and structures from the descending inhibitory system, such as the ventrolateral periaqueductal gray and rostral ventromedial medulla.These anatomical connections have positioned the TNC as a therapeutical target to potentially decrease or inhibit trigeminovascular nociceptive activation and further sensitization.

The same medications used for the management of migraine are used for the management of facial migraine, since it is the same disorder and same pathophysiology but different headache localization (face). If the migraine attack occurs less than twice per month, then an abortive medication should be considered. If the migraine attack is more frequent, it is best managed with preventive medications.

Abortive medications

Abortive medications are the first line of treatment for the acute treatment of migraine. The use of NSAIDs, such as naproxen sodium and ibuprofen, has been shown to be probably effective in alleviating a headache attack; THE EFFECTIVENESS OF NSAIDS IN PREVENTING MIGRAINE SHOULD BE CONSIDERED AS EVIDENCE OF PERIPHERAL NOXIOUS INPUT BEING A MAJOR TRIGGER OF MIGRAINE OF ALL TYPES.  however, patients taking NSAIDs on a daily or regular basis are at risk of exacerbating their existent headache and developing medication overuse headaches OR NEW PERSISTENT DAILY HEADACHES.  AN EVEN GREATER RISK IS THE ESTIMATED 40,000 ANNUAL DEATHS RELATED TO NSAID USE.

Ergotamine derivatives, such as dihydroergotamine (DHE), have been used for years for the treatment of moderate to severe migraine; however, triptans, because of their better tolerability and pharmacological specificity, have replaced ergotamine derivatives in the majority of cases.  DHE is a 5-HT1B and 5-HT1D agonist,  as well as acting at other receptors, and is useful in patients who have not responded to triptan therapy. DHE is available in intranasal and injectable preparations, the latter in particular being popularly used as an abortive agent in the emergency room.  THE USE OF SPHENOPALATINE GANGLION BLOCKS IS THE SAFEST METHOD OF PREVENTING AND TREATING MIGRAINES IN PATIENTS WHO FIND IT EFFICATIOUS.  PREVENTION CAN BE ACCOMPLISHED BY SELF ADMINISTRATION OF BILATERAL SPG BLOCKS INTRANASSALLY BY THE PATIENT.  IT IS EXTREMELY COST EFFECTIVE ONCE THE PATIENT HAS BEEN TAUGHT THE TECHNIQUE COSTING LESS THAN$1.00 PER BILATERAL BLOCK AND THE SIDE EFFECTS OF REDUCED BLOOD PRESSURE, ANXIETY AND DEPRESSION ARE APPRECIATED BY PATIENTS.

Serotonin 5-HT1B/1D receptor agonists (triptans), such as sumatriptan, are newer established medications for the acute treatment of migraine.  Studies have shown that they affect neuronal activation, inhibiting the presynaptic release of CGRP at the TCC, and also act in the ventrolateral periaqueductal gray and the thalamus.  5-HT1B/1D receptors are localized on the trigeminal ganglion in humans and rodents and at the level of the TNC in humans.  5-HT1B receptors are localized on human intracranial arteries.  Sumatriptan has been shown to prevent central sensitization of TCC neurons, but not abort central sensitization.  This may explain why triptans are effective when they are taken at the first sign of a migraine.

In addition to oral dosing formulations, subcutaneous and intranasal formulations offer a fast onset of action and are a good alternative for patients who experience gastrointestinal effects. The different pharmacokinetics between triptans should be considered when choosing the appropriate one for a patient.

New combination preparations, such as sumatriptan with naproxen sodium, have shown additive effects in improving pain relief and migraine-associated symptoms, such as phonophobia, photophobia, and nausea, when compared with monotherapy, as well as good tolerability in the acute management of migraine.  IN GENERAL SINGLE DRUGS ARE LESS EXPENSIVE AND EQUALLY EFFICATIOUS WHEN USED IN COMBINATION OFFERING THE ADDITIONAL BENEFIT OF SERARATE MEDICATION TITRATIONS.

Triptans can induce cardiovascular and cerebrovascular effects because of their vasoconstrictor properties, therefore they are contraindicated in patients with disorders in these systems.  However, new medications in development such as CGRP receptor antagonists, including oral telcagepant, have shown to be a good migraine abortive without the vascular effects.  Evidence has shown that the 5-HT1F receptor is another promising new target in the treatment of migraine: lasmiditan, a 5-HT1Freceptor agonist, has shown good clinical efficacy for acute migraine treatment in doubleblind placebo controlled trials.


Patients who have frequent migraine attacks, such as 15 headache days per month, can benefit from preventive therapy. IF A LONG TERM NEUROMUSCULAR ORTHOTIC REDUCES OR ELIMINATES THE MIGRAINES IT IS THE SAFEST LONG TERM APPROACH TO CARE The mechanism of action of the current preventive medications is not, however, well understood. Medications that have proven beneficial are beta adrenergic blockers such as propranolol and atenolol; calcium channel blockers such as verapamil and flunarizine; tricyclic antidepressants such as amitriptyline; serotonin antagonists such as methysergide; and antiepileptics such as topiramate and valproate.

Newer treatment strategies have been shown to be promising. The use of botulinum toxin injections for migraine prophylaxis and the management of chronic migraine and TTH have been shown to be effective and well tolerated.  BOTULINUM TOXIN IS ANOTHER TREATMENT THAT PROVES THE PROBLEM IS RELATED TO NOXIOUS NOCICEPTIVE INPUT FORM THE TRIGEMINALLY INNERVATED MASTICAORY SYSTEM.  THE DIAGNOSTIC NEUROMUSCULAR ORTHOTIC CAN SHOW WHETHER THIS TREAMENT IS AN EFFECTIVE PREVENTIVE PRIOT TO MANUFACTURE OF A LONG TERM ORTHOTIC.  In addition, neuromodulative procedures, such as occipital nerve stimulation approaches,  ULF TENS UTILIZED IN NEUROMUSCULAR DENTISTRY have been shown to be effective in the management of refractory headaches such as chronic migraine and cluster headache in which pain-free periods (weeks) can be accomplished.   More comprehensive reviews of preventive options for migraine can be found elsewhere.

Tension type headache


TTH is the most common primary headache disorder in the general population.  Its pathophysiology remains unclear, but peripheral and central mechanisms are likely to be involved. THE TENSION HEADACHES THAT CAN BE RELIEVED BY TRIGGER POINT DEACTIVATION ARE UNQUESTIONABLY MYOFASCIAL IN NATURE.  THE LIMBIC SYSTEM IS WHERE WE EXPERIENCE EMOTIONS AND PAIN IS AN EMOTIONAL RESPONSE OF LIMBIC RESPONSE. TENSION HEADACHES ARE ONE OF THE EASIES TREATED HEADACHE TYPES BUT OFTEN INVOLVE BOTH DENTISTRY AND OTHER PROFESSIONAL TO ADDRESS CERVICAL COMPONENTS.  I HAVE SEEN TREMENDOUS RESULTS WITH THE INITIAL DIAGNOSTIC NEUROMUSCULAR ORTHOTIC APPROACHING UNIVERSAL POSITIVE EFFECTS. A model has been proposed in which interaction between the limbic system, the descending inhibitory system, and peripheral inputs, such as those coming from the intracranial vasculature and myofascial inputs, may result in TTH.

The patient may describe the headache as a tight headband compressing their head with a dull, non-pulsating quality. The headache is bilateral with a mild-to-moderate intensity and will not worsen with routine physical activity. It can present as episodic attacks, but can evolve to a more chronic state. Sometimes the headache can be associated with pericranial tenderness. Muscles that are tender to palpation include the temporalis muscle and cervical muscles, such as the splenius, sternocleidomastoid, and upper trapezius muscles.  THESE HEADACHES ARE MORE FREQUENT IN PATIENTS WITH FORWARD HEAD POSTURES OR MORE ACCURATELY FORWARD NECK POSTURE WITH POSTERIOR CRANIAL ROTATION AT THE FIRST AND SECOND VERTEBRAE AND HOINT WITH THE OCCIPUT.  THIS ASSOCIATION HAS BEEN DEFINED MATHEMATICALLY IN THE QUADRANT THEOREM OF GUZAY.  IT IS FREQUENTLY SEEN IN PATIENTS WITH UPPER AIRWAY NASO PHARYNGEAL AIRWAY RESTRICTIONS. Headache associated with myofascial trigger points can meet the criteria for episodic and chronic TTH.  THESE HEADACHES COULD BE DESCRIBED AS HEADACHES SECONDARY TO REPETITVE STRAIN OF CRANIAL AND CERVICAL MUSCULATURE DEFINING THE CAUSE OF MYOFASCIAL PAIN AS THE CAUSE OF THE HEADACHE SYMPTOM This is very important to note during examination, since treatment should be oriented to address the MFP condition. The use of physical therapy and trigger point injection therapy is useful.

The management of TTH involves nonpharmacological and pharmacological approaches, as observed for migraine. Changes in lifestyle such as sleep hygiene, EVALUATION AND TREATMENT OF SLEEP DISORDERED BREATHING INCLUDING SNORING, RERAs, UARS, HYPOPNEA AND SLEEP APNEA.  detection of triggers with a pain diary, as well as stress management and relaxation techniques, have been shown to be beneficial. Pharmacological approaches, such as the use of NSAIDs as well as tricyclic antidepressants in addition to botulinum toxin injections, have proved useful.

Headache and TMD

It is known that headache and orofacial pain disorders, such as TMD, are highly prevalent conditions in the general population.  THERE IS AN ENORMOUS OVERLAP OF THIS CATEGORY WITH ALL OF THE OTHER CATEGORIES OF HEADACHES DUE TO COMMON INVOLVEMENT OF THE TRIGEMINAL NERVOUS SYSTEM.  EXCELLENT Evidence suggests that a clinical comorbidity between primary headaches and TMD exists. Epidemiological studies have shown that TMD symptomatology is more common in patients with primary headaches such as migraine, episodic TTH, and chronic daily headache, where the prevalence of primary headache, particularly migraine, was increased in patients with TMD.  In addition, patients with headache and orofacial pain disorders of musculoskeletal origin also present a higher disability impact.   It can be hypothesized that extracranial trigeminal nociceptive inputs arising from the craniofacial structures as a result of a TMD may influence the activation of the trigeminovascular system, since these nociceptive inputs convey in TNC where intracranial inputs do. Existing TMD may, therefore, influence and/or exacerbate a headache disorder, and a headache disorder may exacerbate a TMD condition   It is very important, therefore, that, during treatment, such comorbidity is addressed. A relationship between the orofacial pain specialist and the neurologist (headache specialist) must be established, as management should be focused on addressing both, the headache and the TMD condition, since they considerably increase the prevalence of each other.  THE CONNECTIONS BETWEEN MEDICAL CONDITIONS AND TMD HAVE BEEN BEST SHOWN BY THE WORK OF SHIMSHAK ET AL WHO SHOWED THAT THERE IS A 300% INCREASE IN ALL FIELDS OF MEDICINE IN PATIENTS CARRYING TMD DIAGNOSIS OR CO-DIAGNOSIS.  THE CAUSE AND EFFECT HAS NOT BEEN CLEARLY SHOWN BUT MANY BELIEVE THE COMMON ELEMENT IS SLEEP.  THIS WAS CLEARLY SPELLED OUT BY THE NATIONAL HEART LUNG AND BLOOD INSTITUE IN THIS REPORT:



National Heart, Lung and Blood Institute (NHLBI)

NHLBI Division of Heart and Vascular Diseases (DHVD)

NHLBI National Center on Sleep Disorders Research (NCSDR)

Trigeminal autonomic cephalalgias (TACs)

Cluster headache, paroxysmal hemicranias, and short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing are severe headaches that are not as common as migraine and that are characterized for their notorious parasympathetic autonomic symptoms.  DUE TO THE PARASYMPATHETIC SYMPTOMS THEY ARE ESPECIALLY CONNECTED WITH THE SPHENOPALATINE GANGLION AND AN SPG  BLOCK SHOULD BE CONSIDERED.  The typical localization of these headaches are the orbital, temporal or supraorbital regions but they can be present in the orofacial region such as in the mandible, TMJ, and dental areas. These headaches require neurological evaluation and management; therefore, it is of fundamental importance to make an appropriate differential diagnosis to avoid unnecessary dental treatments or being misdiagnosed as other types of orofacial pains of non neurovascular etiology. Detailed reviews of trigeminal autonomic cephalalgias and their treatment can be found elsewhere.  A DIAGNOSTIC NEUROMUSCULAR ORTHOTIC CAN BE UTILIZED TO DECREASE NOXIOUS INPUT INTO THE SYSTEM AND MAY HELP LOWER THE INCIDENCE AND SEVERITY OF THESE TROUBLESOME HEADACHES.  AGAIN, ALL HEADACHES ARE PRODUCTS OF THE TRIGEMNAL NERVOUS SYSTEM AND NOXIOUS INPUT CAN BE A TRIGGER.


Orofacial pain management can be challenging and the clinician should be aware of the different etiologies and characteristics of the diverse disorders of the orofacial region. The orofacial pain specialist has the experience and the knowledge to provide a correct diagnosis and management of these conditions. A multidisciplinary approach is ideal in the management of orofacial pain disorders.

Understanding the pain neurobiology of the trigeminal system is key to the development of better and safer therapeutics. It is necessary to stress the need for randomized controlled clinical trials that evaluate the efficacy of current and new therapies for the management of orofacial pains. New and exciting discoveries from the bench to the bedside will hopefully put an end to the burden of chronic orofacial pain conditions in the near future.



urr Pain Headache Rep. 2010 Feb;14(1):33-40. doi: 10.1007/s11916-009-0085-y.

Chronic orofacial pain.

Benoliel R1, Sharav Y.


Chronic orofacial pain (COFP) is an umbrella term used to describe painful regional syndromes with a chronic, unremitting pattern.  THIS IS IMPORTANT, OROFACIAL PAIN IS DEFINED AS CHRONIC AND NON-REMITTING WHICH IS DIFFERENT THAN WHAT MOST PATIENTS PRESENT 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.  THE SHARED CHARACTERISTICS IS THE TRIGMENINAL NERVE (DENTISTS NERVE) AND THE FACT THAT NOXIOUS INPUT INTO THE TRIGEMINAL NERVE ESULTS IN MANY PAINFUL DISORDERS

AN ARTICLE IN Headache. 2014;54(1):22-39 GIVE US MORE INFORMATION ON OROFACIAL PAIN.  http://www.medscape.com/viewarticle/819418

PhysicianMartina K. Shephard, BDent(Hons), MBBS(Hons), FRACDS; E. Anne MacGregor, MD, FFSRH; Joanna M. Zakrzewska, MD, FDSRCS, FFPMRCA


Orofacial pain represents a significant burden in terms of morbidity and health service utilization. It includes very common disorders such as toothache and temporomandibular disorders, as well as rare orofacial pain syndromes. Many orofacial pain conditions have overlapping presentations, THIS IS AN EXTREMELY IMPORTANT ASPECT OF OROFACIAL PAIN and diagnostic uncertainty is frequently encountered in clinical practice. THIS UNCERTAINTY IS PARTIALLY DUE TO MULTIPLE  CONDITIONS IN THE SAME PATIENT, SOME ARE PREDISPOSING FACTORS THAT WERE PRESENT LONG BEFORE ACUTE PROBLEMS BEGAN   This review provides a clinically orientated overview of common and uncommon orofacial pain presentations and diagnoses, with an emphasis on conditions that may be unfamiliar to the headache physician. A holistic approach to orofacial pain management is important, and the social, cultural, psychological and cognitive context of each patient (AXIS 2) needs to be considered in the process of diagnostic formulation, as well as in the development of a pain management plan according to the biopsychosocial model. Recognition of psychological comorbidities will assist in diagnosis and management planning.


Orofacial pain may be defined as pain localized to the region above the neck, in front of the ears and below the orbitomeatal line, as well as pain within the oral cavity.  THIS DEFINITION CAN BE DETRIMENTAL TO PATIENT CARE AS THE SOURCE OF PAIN FREQUENTLY CAN BE OUTSIDE  OF THE AREA WHERE THE PATIENT PERCEIVES THE PAIN.  It includes pain of dental origin and temporomandibular disorders (TMDs), and thus is widely prevalent in the community. Up to a quarter of the population reports orofacial pain (excluding dental pain), and up to 11% of this is chronic pain.  TYPICALLY WHEN ACUTE PAIN BECOMES CHRONIC IT IS HARDER TO TREAT DUE TO NEUROPLASTICITY  Patients with orofacial pain present to a variety of clinicians, including headache physicians, dentists, maxillofacial surgeons, otolaryngologists, neurologists, chronic pain clinics, psychiatrists, and allied health professionals such as physiotherapists and psychologists.  Orofacial pain is associated with significant morbidity and high levels of health care utilization.  SHIMSHAK SHOWED IN HIS TWO LANDMARK STUDIES PUBLISHED IN CRANIO JOURNAL THAT PATIENTS WHO CARRY A TMD DIAGNOSIS  UTILIZE 300% MORE HEALTH CARE DOLLARS THAN PATIENTS WHO HAVE NOT HAD THAT DIAGNOSIS

This review presents a clinically orientated overview of orofacial pain presentations and diagnoses. The scope of orofacial pain includes common disorders such as dental pain and TMDs, as well as a number of rare pain syndromes. Pain in the orofacial region is derived from many unique tissues such as teeth, meninges, and cornea.  THE CORNEA IS EXTREMELY IMPORTANT SOURCE OF INPUT TO THE TRIGEMINAL NERVOUS SYSTEM.  ACCORDING TO WIKIPEDIA THE INNERVATION OF THE CORNEA: 

“The cornea is one of the most sensitive tissues of the body, as it is densely innervated with sensory nerve fibres via the OPTHALMIC DIVISION OF THE TRIGEMINAL NERVE by way of 70–80 long and short ciliary nerves.   Research suggests the density of pain receptors in the cornea is 300-600 times greater than skin and 20-40 times greater than DENTAL PULP BUT ARE FREE NERVE ENDINGS SIMILAR TO THE FIBERS IN DENTAL PULP. making any injury to the structure excruciatingly painful.


The ciliary nerves run under the endothelium and exit the eye through holes in the sclera apart from the optic nerve (which transmits only optic signals).  The nerves enter the cornea via three levels; scleral, episcleral and conjunctival. Most of the bundles give rise by subdivision to a network in the stroma, from which fibres supply the different regions. The three networks are, midstromal, subepithelial/sub-basal, and epithelial. The receptive fields of each nerve ending are very large, and may overlap.”

HEADACHE ARTICLE:  This results in several unique physiological mechanisms that have been well reviewed.   Because of these unique mechanisms and the requirement for specialist knowledge of the complex anatomy and physiology of the orofacial region, diagnosis may be difficult. Many patients have consulted multiple clinicians for their condition yet remain undiagnosed or with an incorrect diagnosis.  FREQUENTLY THERE ARE MULTIPLE CORRECT DIAGNOSIS EACH ADDRESSING ONLY A PART OF THE PROBLEM LEAVING FRUSTRATED PATIENTS MOVING ON TO OTHER TREATMENTS   Our aim is to provide the headache physician with a guide to orofacial pain presentations and diagnoses informed by our clinical experience in the fields of medicine as well as dentistry, and to review the literature relevant to these conditions. We provide an overview of the common presentations of orofacial pain including dental causes of pain, non-dental causes of intraoral pain, and extraoral facial pain syndromes, as the signs and symptoms of many of these conditions can overlap significantly, causing diagnostic difficulty.

We also present a discussion of history, diagnosis, and management considerations relating to the biopsychosocial model of diagnostic formulation and management. This approach is particularly relevant and important in the field of orofacial pain given the significant level of psychological distress and social dysfunction that is associated with these disorders.  WHILE THE BIOPSYCHOSOCIAL ISSUE  (AXIS 2) MAY BE SIGNIFICANT WHEN AXIS 1 IS IGNORED PATIENTS WILL SUFFER! As with other types of chronic pain, there is often a mismatch between the patient’s expectation of a cure for their pain, and the reality that for many types of chronic pain, a cure is seldom possible.   I CLEARLY EXPLAIN TO ALL PATIENTS THAT THERE ARE NO MAGIC CURES!   THE ONLY TRUE CURE FOR PATIENTS SUFFERING FROM CHRONIC PAIN FOR WEEKS, MONTHS, YEARS OR DECADES WOULD BE A DO-OVER OF ALL THE TIME THEY HAVE SPENT IN PAIN.  TO RECOVER ALL OF THE MULTITUDE  LOSSES THEY HAVE SUFFERED DUE TO THE PAIN AND DYSFUNCTION.   Medicine alone does not have the tools to manage a condition that has a neurophysiological cause but is also experienced emotionally, socially, financially, and spiritually. Recognition of psychological comorbidities is essential for appropriate diagnosis and successful pain management.

Types of Orofacial Pain

Dental Pain

There are few causes for dental pain; however, because of significant neural convergence THIS CONVERGENCE IS BECAUSE THE MASTICATORY SYSTEM IS THE OVERWHELMING PORTION OF INPUT TO THE TRIGEMINAL NERVOUS SYSTEM.  NOXIOUS INPUT IS ALMOST ALWAS FROM THE DENTIST’S NERVE   in the jaws and face, it may be referred, poorly localized, or misdiagnosed. The 4 major causes of dental pain are pulpitis, cracked tooth syndrome, dental abscess, and dentine sensitivity.   These are often acute conditions, but because they are common, they may coexist with other chronic pains.

Both the dental pulp and periodontal ligament contain nociceptors. Nociceptive output in these areas is triggered by changes in pressure and the effect of inflammatory mediators.  THERE ARE AT LEAS 29 TYPES  NERVOUS RECEPTORS IN THE PERIODONTAL LIGAMENTS ALONE


Pulpitis is the term used to describe pain because of inflammation of the dental pulp, and it is usually due to dental caries. Inflammation of the pulp leads to accumulation of extracellular fluid, inflammatory mediator release, and vasodilatation, which causes an elevation of pressure within the pulp chamber, which is a non-compliant space. The pressure increases further as venous stasis and eventually pulp necrosis occur, with release of inflammatory mediators and necrotic cell contents. Elevated pressure and inflammatory chemicals activate nociceptors in the pulp chamber causing pain.

Reversible pulpitis is defined as a transient pain in response to specific stimuli (hot, cold, sweet), which occurs when the pulp is inflamed. These symptoms resolve when the cause of the inflammation is treated. The pain of reversible pulpitis may be described as fleeting, shooting, stabbing, or sensitive.

Irreversible pulpitis is characterized by spontaneous pain, which may be worsened by or persist following the removal of a stimulus such as heat or cold. It is an indicator of incipient pulpal necrosis. The pain of irreversible pulpitis is often described as persistent, throbbing, dull, or aching. It may be worsened by physical activity and head movement.

Pulpal pain is often poorly localized as the inflammation is restricted to the pulp chamber and is thus not affecting proprioceptive nerve fibers, which are located in the periodontal ligament. It is common for patients to be unable to localize the exact source of the pain. Pulpal pain may respond to simple or opioid-based analgesics, but the pain of irreversible pulpitis will not resolve until pulpal necrosis has occurred or the pulpal tissue has been mechanically removed (by endodontic treatment).

If pulpal inflammation and infection reaches the base of the pulp chamber, an area known as the apex or root tip, it may extrude through the apical foramen into the periodontal space. This will cause pain due to stimulation of nociceptors in the periodontal ligament space, and the pain will be well localized due to involvement of periodontal ligament proprioceptive fibers. Extrusion of inflammatory fluid and necrotic cell products into the periodontal space causes pain because of pressure effects, and the tooth will become exquisitely tender to touch or biting. This leads to the pain becoming very well localized, and the source of pain may be readily identified by gentle tapping on the tooth. When inflammation and infection has progressed through the apical foramen, it is described as a periapical abscess.

Dental infection may progress into the bone, under the oral mucosa or into soft tissue spaces, and form an abscess or spreading infection, with resultant ongoing pain.

Cracked Tooth Syndrome

Cracked tooth syndrome occurs when a crack has occurred in the dental hard tissues and reaches the pulp chamber. The crack is usually not visible to the naked eye. Pain because of cracked tooth syndrome is classically intermittent, provoked on biting or releasing biting on a hard object, and is notoriously difficult to diagnose. It may be described as sharp or sensitive, and is usually related to mastication. The tooth may also become sensitive to hot and cold stimuli. It is thought that the pain is due to fluid shifts within the dentine tubules, which are generated due to pressure differences as the crack opens and closes during mastication. It can be extremely difficult to diagnose.

Dentine Sensitivity

Pain because of dentine sensitivity is classically stimulated by exposure to cold, heat, sweet foods/drinks, and mechanical trauma such as toothbrushing. The sensation is due to the movement of fluid in dentinal tubules in response to osmotic or temperature-related effects. Dentinal tubules contain the processes of cells residing in the dental pulp (odontoblasts), and fluid movement appears to trigger nociceptive output by mechanisms that are as yet unclear. Gingival recession can lead to exposure of the endings of dentine tubules, as can loss of enamel on the crown of the tooth. Dentinal sensitivity is described as very rapid, fleeting, shooting pain, or sensitivity, and is always in response to an identifiable stimulus.  THE INFORMATION IN THE PRECEDING SECTION IS BASIC DENTAL KNOWLEDGE.

Non-dental Intraoral Pain:


Intraoral pain may also arise from non-dental structures.   Oral mucosal malignancies such as squamous cell carcinoma or salivary gland carcinoma may be painful because of ulceration or perineural invasion.

Inflammatory oral mucosal diseases such as oral lichen planus, recurrent aphthous stomatitis, vesiculobullous diseases, and oral mucosal infections such as candidiasis or herpes viruses (herpes simplex, varicella zoster) may all cause significant oral pain. Patients with hematinic deficiencies, diabetes, hematological malignancies, HIV/AIDS, and Behçet’s disease may have significant oral mucosal pain and/or ulceration. Examination will usually reveal the associated oral mucosal abnormalities.

Pain may be experienced in the oral cavity, face, and neck because of salivary gland pathology. Blockage of a major salivary gland duct may be due to infection, mechanical obstruction by tumors, docholithiasis, or ductal strictures. Obstruction of the duct will lead to pain as the gland fills with saliva, which cannot be released. Pain due to chronic ductal obstruction typically worsens preprandially or during meal times. Infection of the salivary glands will result in gland swelling, pain, and erythema/warmth of the overlying skin.


Post-Traumatic Trigeminal Neuropathic Pain/Atypical Odontalgia


This definition encompasses intraoral pain that is localized to a non-diseased dentoalveolar structure, such as a tooth or an area of alveolar ridge from which a tooth has previously been extracted.   The pain is often described as “burning,” “shooting,” or “shock-like,” and there may be significant hyperalgesia and allodynia of the affected region, often with an associated area of hypoesthesia or dysesthesia. The pain is usually continuous, with some patients experiencing evoked severe episodes. The area is usually clearly defined with little radiation.   Patients have described it as “nails being hit the whole time” or “kicked in the face and left bruised and burning.”


Controversy remains about nomenclature and criteria for these conditions, and in this article, we differentiate them by the presence or absence of a precipitating event. THE PROBLEM MAY OR MAY NOT BE RELATED TO PERCIPTITATING EVENT WHICH OFTEN IS ASSOCIATED NOT WITH NEW SYMPTOMS BUT EXACERBAATION OF OLD SYMPTOMS. It has been proposed that formal neurophysiological testing would help distinguish those with neuropathic pain compared with inflammatory causes.   Patients with trigeminal neuropathic pain OFTEN BUT NOT ALWAYS have an identifiable traumatic episode preceding the onset of the pain. The precipitating event may include physical trauma such as facial fractures, iatrogenic trauma such as restorative, endodontic, or oral surgical procedures (apicectomy, extraction, implant placement), prolonged severe infection of dentoalveolar structures, or dental procedures carried out with ineffective anesthesia.  Trigeminal neuropathic pain is persistent and severe, and associated with a high level of psychological distress and a risk of further iatrogenic harm because of patients seeking ongoing dental or surgical interventions for relief of pain.  TRIGEMINAL NEUROPATHIC PAIN MAY RESPONT TO SPHENOPALATINE GANGLION BLOCKS

Atypical odontalgia or persistent dentoalveolar pain refers to a similar clinical presentation without a clear precipitating event.  “Persistent dentoalveolar pain” is an ontological definition describing the symptoms and signs without attributing a causation or mechanism. Such definitions are developed using analysis of patient interviews.  These conditions are usually managed along the same pathways as for other neuropathic pain.   Until there are internationally agreed diagnostic criteria based on case–control studies and more well-conducted trials have been carried out, treatment of these conditions can vary substantially between clinicians, leaving patients confused and continually consulting in hope that a “cure” will be found.  MANY TIMES THESE PROBLEMS ARE SECONDARY TO LONG TERM NOXIOUS TRIGEMINAL INPUT, PEPETITIVE STRAIN INJURIES AND OTHER AXIS 1 & 2 PROBLEMS.

Burning Mouth Syndrome


Burning mouth syndrome describes a collection of symptoms affecting the oral cavity, including a “burning” or painful sensation, often with an associated alteration in taste sensation and an altered perception of the quality and quantity of saliva. The symptoms are most commonly localized to the tongue.  On clinical examination, the oral mucosa appears entirely normal. The area of abnormal sensation does not typically follow anatomic boundaries, is usually bilateral, and is continuously present. Patients may describe their symptoms as “discomfort” rather than pain. One patient described their symptoms as a “Prickly feeling like an injection wearing off,” and when choosing photographic images as representative of their symptom, many choose images of fire.     Other causes of oral burning sensations such as hematinic deficiencies, diabetes, other systemic diseases, and oral infections should be ruled out. The condition is most common in perimenopausal or postmenopausal females, and is strongly associated with psychological comorbidities such as anxiety and depression.  TRICYCLIC ANTIDEPRESSANTS IN SYSTEM AND/OR TOPICAL APPLICATION ARE  OFTEN EFFECTIVE.  GELCLAIR IS A PRESCRIPTION PRODUCT USED TO TREAT ORAL MUCOSITIS AND STOMATITIS SECONDARY TO CHEMOTHERAPY AND RADIATION THERAPY.  THE ACTIVE INGREDINT IS HYALOURONIC ACID.  Patients often report that their symptoms are worsened during periods of psychological stress. The etiology of the condition is unclear, although recent studies have suggested the presence of a small-fiber sensory neuropathy, thus suggesting it is a form of neuropathic pain, but others propose a steroid dysregulation mechanism.  THESE ARE BOTH DISORDERS OF THE AUTONOMIC NERVOUS SYSTEM LEADING US TO BELIEVE  BURNING MOUTH SYNDROME  IS PROBABLY AN AUTONOMIC DYSFUNCTION AND IT  FREQUENTLY RESPONDS TO SPHENOPALATINE GANGLION BLOCKS. The condition can be difficult to manage, and a variety of RCTs have been reported, which include drug therapies and cognitive behavior therapy.   Research on this condition is difficult to conduct in part due to its rarity and a lack of animal models; however, studies are being undertaken that indicate evidence of central changes on functional magnetic resonance imaging (MRI), thus supporting the hypothesis that there are definite neurophysiological elements to this condition, rather than it being a psychosomatic condition as has been previously suggested.

Facial Pain With/Without Intraoral Pain


TMDs are the most common causes of orofacial pain, affecting 10–15% of the population.  THIS NUMBER CAN VARY WIDELY AND IS PROBABLY LOW..  MANY PHYSICANS AND DENTISTS DO NOT UNDERSTAND THAT TMD DOES NOT REQUIRE THE PRESENCE OF JOINT NOISES OR JOINT PAIN   A MORE PROPER DIAGNOSIS WOULD BE MASTICATORY SYTEMS DISORDERS BECAUSE THE MYOFASCIAL AND FUNCTIONAL COMPONENT OF TMD ARE OFTEN OVERLOOKED IN THE ABSENCE OF TMJOINT ISSUES.  Presenting features include pain localized to the pre- and post-auricular areas, the angle and ramus of the mandible, and the temporal region. There may be associated clicking, sticking, or locking of the temporomandibular joints. The pain may be intermittent or continuous, and is usually described as dull, aching, (MUSCLE) or throbbing, or in the words of patients: “weight on the side of the face getting heavier and heavier,” “pressure feeling,” “elastic band that is too tight,” or “needles digging in.” Some patients experience pain that is sharp or shooting in character, intermixed with dull continuous pain. The pain commonly radiates into the temporal or occipital regions into the neck and across the malar region of the face; it can be unilateral or bilateral, and of varying severity. There may be an associated bruxing or clenching habit. The pain is typically aggravated by opening the mouth wide, yawning, or chewing. There may be limitation of mouth opening.

TMD has historically been classified using the Research Diagnostic Criteria into myofascial pain, disc displacement, and other disorders,   as the International Classification of Headache Disorders (ICHD)-II of TMD was not useful in clinical settings.     Newer classification criteria refer to myalgia, myofascial pain with referral, and myalgia with disc involvement. THESE NEWER CLASSIFICATIONS ARE FAR MORE ACCURATE AND REFLECT MASTICATORY AND POSTURAL MUSCLE PAIN,  THE EFFECT OF THE JAW ON HEAD AND NECK POSTURE OFTEN RESULTS IN CERVICAL, UPPER BACK AND SHOULDER MUSCLES REFERRING PAIN TO THE HEAD AND NECK.  THE NHLBI ALSO PUBLISHED A REPORT ON THE CONNECTION OF TMD AND SLEEP APNEA AND OTHER SLEEP DISORDERS

A large prospective cohort study is currently underway in the USA investigating the prognostic factors related to the development of TMD.   Participants with and without TMD participate in a battery of psychometric, biometric, and genetic tests. Baseline data on the psychological characteristics of the TMD cases demonstrate that this population shows higher levels of distress, catastrophizing, and increased somatic awareness compared with non-TMD controls. A number of other studies have reported similar findings.  THE BIG QUESTION IS THE EFFECT ON THE TMD SYMPTOMS ON THE BIOMETRIC TESTING RESULTS.  DO PATIENTS  HAVE “higher levels of distress, catastrophizing, and increased somatic awareness” SECONDARY TO THEIR TMD ISSUES?

TMD has been linked with other psychological and chronic pain conditions, including fibromyalgia, back pain, headaches, chronic widespread pain, and hypermobility.  THIS MAY BE DO TO THE PHYSIOLOGICL EFFECTS OF HEAD AND JAW POSITION ON THE REST OF THE BODY.  THE CONNECTIONS TO CHRONIC PAIN MAY BE DUE TO POSTURAL CHAIN OF EFFECTS ON TOP OF EFFECTS OF PAIN THRU THE LIMBIC SYSTEM.  PAIN IS ACTUALLY AN EMOTIONAL RESPONSE TO A STIMULI  Degenerative temporomandibular joint disease is rare but may occur in rheumatoid arthritis. Interest has been raised recently in the possibility of TMD-related headache, which may involve aspects of peripheral and central sensitization.  ONE COULD SAY THAT ALL HEADACHES ARE RELATED TO TMD THRU THE TRIGEMINAL NERVOUS SYSTEM.   http://www.iccmo.org/all-migraines-come-from-trigeminovascular-system-or-why-physiologic-dentistry-and-spg-blocks-can-cure-or-eliminate-migraines/

Management of TMD is primarily conservative, as in the majority of cases, the disorder is self-limiting. THIS STATEMENT IS PROBABLY LUDICROUS WHEN ONE CONSIDERS THAT 10% GO ON TO DEVELOP DEBILITATING CHRONIC PAIN.    Careful explanations are crucial as it has been shown that patients experience a considerable amount of uncertainty both in terms of diagnosis and then management, as dentists also often find it difficult to manage.  MANY DENTIST WHO HAVE HAD ADVANCED TRAINING IN TREATING PAIN HAVE CONSIDERABLE EXPERTISE IN TREATING THESE DISORDERS AND CAN PREVENT THE PAIN BECOME WIDESPREAD   Approximately 10% of patients develop chronic pain, and this has been linked to fibromyalgia, depression, and chronic widespread pain.   Therapies used for TMD include simple analgesia, tricyclic antidepressants, occlusal splints or bite guards, diet modifications, physiotherapy, cognitive behavioral therapy, and surgery.   Evidence for the majority of these therapeutic options is poor, THIS IS NOT TRUE, ACTUALLY THERE IS EXCELLENT EVIDENCE  BASED ON CLINICAL CASE STUDIES BUT THERE IS LITTLE LONG TERM BLINDED AND RANDOMIZED STUDIES PRIMARILY BECAUSE THESE ARE ALMOST IMPOSSIBLE TO HAVE THESE STUDIES AND ETHICALLY DO YOUR BEST TO RELIEVE PATIENT SUFFERING.  DRUG AND PSYCHOSOCIAL STUDIES ARE EASIER TO PREFORM BUT CONTROL OF VARIABLES IS DIFFICULT IF NOT IMPOSSIBLE. and there remains considerable confusion about the best form of management.   Surgery is only indicated for TMD with significant functional limitation or in cases with associated degenerative joint disease or disc dysfunction.  SURGERY CAN COVER MANY PROCEDURES FROM SIMPLE ARTHROCENTESIS TO OPEN ARTHROTOMIES.   MINIMALLY INVASIVE PROCEDURE THAT ARE DONE WHILE STABILIZING THE BITE ARE FAR MORE EFFECTIVE THAN THE SAME PROCEDURES WITHOUT STABILIZATION.   Education, psychological support and self-management strategies are recommended as part of a multidisciplinary approach to the management of TMD, and these should be done early to reduce costs.    There remains considerable variation in the way TMD is diagnosed and managed partly due to conflicting evidence. It is anticipated that the large US-based Orofacial Pain: Prospective Evaluation and Risk Assessment (OPPERA) study will provide more robust evidence, as it is a prospective study that has enrolled asymptomatic participants.



Why Patients Are Forced To Live With Severe Pain and Migraines

Dr. Shapira Uncategorized 0 Comments

It is an unfortunate truth that headaches that are often easy to treat end up damaging patients quality of life for many years, often wrecking their entire lives.

I recently saw a patient who kept diaries in second grade and talked about her headaches every day. She has had constant pain for the last nine years.

We started treatment with a diagnostic physiologic orthotic and trigger point injections in her trapezius muscles and for the first time in nine years she was out of pain.

She had spent a week at Mayo Clinic where she was told she had migraines and to “get over it, its genetic” and told to just accept it.

Nothing like taking away a patients hope.

She has had an orthotic now for 24 hours anThis patient has a problem with pain from muscles but no particular problem with clicking or popping joints.d is astonished she is still pain free.

The Trigeminal Nerve is the center of all headaches and as everyone knows the Trigeminal Nerve is the Dentist’s nerve.…

Dentist Chicago | TMJ Chicago

What our clients say | Dentist Chicago

A scientific approach,
with a personal connection

ira2Dr. Ira Shapira: “I love science. Science provides the necessary facts, to better understand people’s issues as a healthcare provider. Applying these facts properly (recognizing that every individual deserves personalized focus, attention and treatment), is the key to Effective TMJ and Sleep Disorder Solutions.”

What is a TMJ disorder?

Everyone experiences the occasional headache, shoulder pain, or sore neck. Most of the time we can dismiss the cause as nothing more than stress or our busy lives, but, when pain becomes a daily occurrence or is accompanied by other symptoms, there could be something more going on.

Learn More

What is a sleep disorder?

If you find yourself constantly battling fatigue, feeling as if your sleep is disrupted on a nightly basis, or if your family complaints about your snoring, you could have an underlying sleep disorder. There are several, common sleep issues (e.g.: sleep apnea) that plague many individuals like you.

Learn More

Why Dr. Ira Shapira?

“I like to think of my patients as though they were members of my family. I want them to have the quality of care they can appreciate and that I would expect for myself or my family. That’s why I try to stay current with the latest findings in the field of Physiologic (TMJ) and Sleep Disorder dentistry.

Learn More

Like to know more? Download our FREE eBook

  • Preventive Care 3Sleep Disorder Treatment

    When you find it difficult to sleep or your sleep is disrupted night after night, we recommend you take steps to determine if you have a sleep disorder and seek an effective remedy.

    Free Sleep Disorder E-Book
  • Frequent headaches?

    It’s time to get rid of those headaches once and for all. Set up a consultation with us to discuss the connection between your chronic headaches and a potential TMJ disorder.

    Free TMJ Disorder E-Book
  • ZahnarztNeck & Back Pain

    Once relieved of your pain, you’ll be amazed at how good it feels to comfortably move in a pain free fashion again. Normal physiology and function promotes ongoing health and wellness.

    Free TMJ Disorder E-Book

Sick and tired of TMJ pain or sleep problems?


Meet Dr. Ira Shapira
at Think Better Life

Dentist Chicago | TMJ Chicago

What our clients say | Dentist Chicago

A scientific approach,
with a personal connection

ira2Dr. Ira Shapira: “I love science. Science provides the necessary facts, to better understand people’s issues as a healthcare provider. Applying these facts properly (recognizing that every individual deserves personalized focus, attention and treatment), is the key to Effective TMJ and Sleep Disorder Solutions.”

What is a TMJ disorder?

Everyone experiences the occasional headache, shoulder pain, or sore neck. Most of the time we can dismiss the cause as nothing more than stress or our busy lives, but, when pain becomes a daily occurrence or is accompanied by other symptoms, there could be something more going on.

Learn More

What is a sleep disorder?

If you find yourself constantly battling fatigue, feeling as if your sleep is disrupted on a nightly basis, or if your family complaints about your snoring, you could have an underlying sleep disorder. There are several, common sleep issues (e.g.: sleep apnea) that plague many individuals like you.

Learn More

Why Dr. Ira Shapira?

“I like to think of my patients as though they were members of my family. I want them to have the quality of care they can appreciate and that I would expect for myself or my family. That’s why I try to stay current with the latest findings in the field of Physiologic (TMJ) and Sleep Disorder dentistry.

Learn More

Like to know more? Download our FREE eBook

  • Preventive Care 3Sleep Disorder Treatment

    When you find it difficult to sleep or your sleep is disrupted night after night, we recommend you take steps to determine if you have a sleep disorder and seek an effective remedy.

    Free Sleep Disorder E-Book
  • Frequent headaches?

    It’s time to get rid of those headaches once and for all. Set up a consultation with us to discuss the connection between your chronic headaches and a potential TMJ disorder.

    Free TMJ Disorder E-Book
  • ZahnarztNeck & Back Pain

    Once relieved of your pain, you’ll be amazed at how good it feels to comfortably move in a pain free fashion again. Normal physiology and function promotes ongoing health and wellness.

    Free TMJ Disorder E-Book

Sick and tired of TMJ pain or sleep problems?


Meet Dr. Ira Shapira
at Think Better Life

CRPS Chicago: Complex Regional Pain Syndrome can respond to SPG Blocks

Dr. Shapira Unsorted 6 Comments

Complex Regional Pain Syndrome most frequently occurs following and injury but can also occur from long standing pain problems leading to central sensitization. CRPS is one of the most difficult disorders to treat.  Prior to discussing Sphenopalatine Ganglion Blocks in the treatment of CRPS it is important to understand the basics.

Patients with CRPS often experience Hyperalgesia or increased sensitivity to nociceptive input can be severe with even minimal noxious stimulation leading to severe or paroxysmal pain responses and Allodynia, the perception of pain from non-nociceptive input such as light touch.

Complex Regional Pain Syndrome is the current designation for what was previously called reflex sympathetic dystrophy (RSD) and /or causalgia
Another designation was reflex neurovascular dystrophy (RND) which is an amplified musculoskeletal pain syndrome (AMPS).

CRPS frequently is associated with systemic autonomic dysregulation with major effects on the CNS or Central Nervous System and resultant symptoms including neurogenic edema.

The International Association for the Study of Pain describes two types of CRPS: Type I previously designated as reflex sympathetic dystrophy (RSD) and Type 2 previously designated as Causalgia.

Type one is also referred to as Sludeck’s Atrophy, Reflex Neurovascular Dystrophy or Algoneurodystrophy. Type 1 is by far the most common type of CRPS . Nerve lesions have not yet been confirmed in type 1 CRPS.

Type 2 by contrast routinely has easily seen nerve damage which may be why it is more difficult to control. While Type 1 is often considered Idiopathic disease Type 2 has a presumed cause of obvious frank nerve damage.

Treatment is challenging in cases of CRPS and is often unsatisfactory especially after the condition has become advanced. The enormous degree of enhanced sympathetic activity causing secondary vasoconstrictionmake some believe there is an unidentified neurotransmitter involved.

My personal theory is a combination of Neural Plasticity causing severe Central Sensitization with increased afferent nociceptive sensitivity leading to storms of neurotransmitter release inside the brain and possible wide spread chages in Gap Junctions in the CNS which could explain the spread of CRPS in affected individuals. The communication could spread directly cell to cell and not synaptically. The Glial cells could be a likely suspect of transmitting this gap junction spread as would the Schwann Cells responsible for Myelin Sheath coverage of neurons.

Secondarily, there is a descending storm of efferent activity again leading to storms of neurotransmitter release as well as kinins and histamine that also may open up increased Gap Juntion spread of the disorder periferrally. The Afferent – Efferent spread will create an I/O error or input output error to the brain.. Computer experts would dub this
Garbage in – Garbage out.

In computers the tech would shut down the computer and reboot.  In humans this is a more difficult problem.  Ketamine has been used to treat CRPS but probably is most effective if used to prevent or reverse early CRPS.  Ketamine is effective in reducing opiod  use post-surgery.  Opiod use stimultes the Glial cell to break down opiods therefore decreaing the amount used to control pain is key.  Ketamine used to treat intractable neuropathic pain and is useful in preventing spinal sensitization, the wind-up associated with chronic pain.  By reducing neuroplasticity it may prevent development of CRPS and other disorders associated with Central Sensitization.

While this may help with pain it will not be an effective “reboot” of the system.  (below source wikipedia) The effect of Ketamine causes dissociation between the limbic and thalamoneocortical systems with intact ocular, laryngeal, and pharyngeal reflexes.  Ketamine is an antagonist of the glutaminergic N-methyl-D-aspartate receptor (NMDA-R), both centrally and in the spinal cord, prevents neuronal Ca2+influx, interference with neuronal plasticity, learning and memory, analgesia at central and spinal cord level, as well as interruption of the central sensitization core to chronic pain syndromes.

Ketamine could be used early to prevent Central Sensization but it has weak evidence in the literature.

Pain Med 2015 Jan 13. doi: 10.1111/pme.12675.  A systematic Review of Ketamine for Complex Rgional Pain Syndrome was a Cockchrane review that” yielded 262 articles, 45 of which met the inclusion/exclusion criteria. Of those included, 6 were reviews, 5 were randomized placebo-controlled trials, 13 were observational studies, and 21 were case reports.”  The conclusions were “there is no high quality evidence available evaluating the efficacy of ketamine for CRPS and all manuscripts examined in this review were of moderate to low quality. Therefore, we conclude there is currently only weak evidence supporting the efficacy of ketamine for CRPS, yet there is clearly a rationale for definitive study.”

This does not mean Ketamine is not effective in individual cases, it just cannot yet be considred a first line treatment.   I believe the reason Ketamine is only weak in response is that Ketamine doses are insufficient to reboot the system in both dosage and time of infusion.

The use of a Curare type anaesthesia is association with Ketamine may be the Reboot Mechanism that is necessary for severe CRPS.    Theis will reversibly inhibit the nicotinic acetylcholine receptor at the physiologic junction.  Curare was shown to effectively treat tetanus and strichnine poisoning by interfering with nerve conduction from motor neuron to muscle at the physiologic junction (think Botox).  This would require total life support including respiration.  While the patient is in the anaesthesized state Insulin Potentiation Therapy using a shocking dose of insulin could simultaneously be used to Reboot the system.  Hyperbaric Oxygen Therapy is currently under investigation for CRPS therapy and conceivably could be used in conjunction with Insulin Potentiation.  Insulin potentiation can also be used to move medications across cell membranes and /or the blood brain barrier.  This could allow targeted medication use to limit adverse side effects of the medications.  I first learned about Insulin Potentiation Therapy from a friend Dr Steve G Ayre a Canadian physician who worked with moving AZT across the Blood Brain Barrier in earl aids research.  I learned fro Steve about Insulin Potentiation and then used the addition of very small amounts of insulin to lidocine while doing trigger point injections.  Steve was conviced that Oxygen Potentiation held enormous benefits in  the future.

Insulin Potentiation may  become a treatment of choice for administering drugs to treat acquired Gap Junction Disease.

Cochrane reviews would never find evidence for drastic treatment of this type but considering the decrease in quality of life (QOL) in CRPS patients.  A study “Risk factors for suicidal ideation among patients with complex regional pain syndrome.” by Lee DH, Noh EC, Kim YC, et al. in Psychiatry investigation. 2014 Jan;11(1):32-8. reported 74% of patients were considered at high risk for suicide. (abstract below).

The severe nature of CRPS and effects on QOL or Quality of Life demands seeking answers for our patients.  Sympathetic Blocks including stellate ganglion blocks have had some success but there is little wrtten on the utilization of Sphenopalatine Ganglion Blocks for treating CRPS.  ”

I recently had a patient in my office for routine dental work but due to her severe CRPS we had anaesthesia with Ketamine to facilitate what otherwise would have been incredibly painful experience.  After the necessary dental work was done a bilateral SPG block was performed thru the greater palatine foramen intra-orally.  The patients husband the pain relief from the Ketamine infusion lasted longer than when she goes in for just Ketamine infusion.  These changes could be due to dosage and time of infusion or to addition of Parasympathetic Ganglion Block of the Sphenopalatine Ganglion.

I first began utilizing SPG Blocks in the 1980’s when a  TMJ/ Headache/ Migraine patient brought in the book “Miracles on Park Avenue” about an ENT physician who treated all matters of pain with Sphenopalatine Ganglion Blocks.  The patient wanted me to    help them find a doctor who would perform the block.   There were no doctors in greater Chicagoland area but a friend and mentor Dr Jack Haden in Kansas City taught me a simple method of doing SPG blocks transnasally.  The effect was life changing for my patient and I have been an advocate ever since.  There are numerous protocols for administering SPG Blocks including intra-oral and extra-cranial injections and transnasal approaches such as MiRx protocol with TX360 or use of Sphenocath.  I prefer the original method I learned for Jack Haden and the book “Miracles on Park Ave: Treatment of Arthritis andd other Chronic Pain” by Albert Benjamin Gerber.  The bibliography ain that book was my library index of articles I read to understand the SPG block.

The advantage to the original approach is that it can easily and safely  be self administered by patients at home one or multiple times daily and is extremely effective in eliminating and/or preventing pain in many patients.  It is a tool I use in treating TMD (TMJ) patients, Migraine , Chronic Migraine, Autonomic Cephalgia, Tension headache and Chronic Daily Headache patients.

Correcting underlying physiology is easier when patients are comfortable.

“Risk factors for suicidal ideation among patients with complex regional pain syndrome.”  Lee DH, Noh EC, Kim YC, et al.    Psychiatry investigation. 2014 Jan;11(1):32-8.

Objective: Chronic pain frequently coexists with psychiatric symptoms in patients diagnosed with complex regional pain syndrome (CRPS). Previous studies have shown a relationship between CRPS and the risk of suicide. The purpose of this study was to assess risk factors for suicidal ideation in patients with CRPS.

Methods: Based on criteria established by the International Association for the Study of Pain, 39 patients diagnosed with CRPS Type 1 or Type 2 were enrolled in this study. Suicidal ideation was assessed using item 3 of the Hamilton Depression Rating Scale (HAMD), and symptoms of pain were evaluated using the short form of the McGill Pain Questionnaire (SF-MPQ). Psychiatric symptoms were assessed in using the Structured Clinical Interview for DSM-IV Disorders (SCID-I, SCID-II), the HAMD, the Hamilton Anxiety Rating Scale (HAMA), the Global Assessment of Functioning Scale (GAF), and the Pittsburgh Sleep Quality Index (PSQI).

Results: Twenty-nine patients (74.4%) were at high risk and 10 (25.6%) were at low risk for suicidal ideation. Risk factors significantly associated with suicidal ideation included depression (p=0.002), severity of pain (p=0.024), and low scores on the GAF (p=0.027). No significant correlations were found between suicidal ideation and anxiety or quality of sleep.

Conclusion: Significant risk factors for suicidal ideation in patients with CRPS include severity of pain, depressive symptoms, and decreased functioning. These results suggest that psychiatric evaluation and intervention should be included in the treatment of CRPS.

***What follows is Reprinted from the National Institute of Neurological Disorders and Stroke*****


What is complex regional pain syndrome?

Complex regional pain syndrome (CRPS) is a chronic pain condition most often affecting one of the limbs (arms, legs, hands, or feet), usually after an injury or trauma to that limb.  CRPS is believed to be caused by damage to, or malfunction of, the peripheral and central nervous systems.  The central nervous system is composed of the brain and spinal cord, and the peripheral nervous system involves nerve signaling from the brain and spinal cord to the rest of the body.  CRPS is characterized by prolonged or excessive pain and mild or dramatic changes in skin color, temperature, and/or swelling in the affected area.

There are two similar forms, called CRPS-I and CRPS-II, with the same symptoms and treatments. CRPS-II (previously called causalgia) is the term used for patients with confirmed nerve injuries. Individuals without confirmed nerve injury are classified as having CRPS-I (previously called reflex sympathetic dystrophy syndrome).  Some research has identified evidence of nerve injury in CRPS-I, so the validity of the two different forms is being investigated.

CRPS symptoms vary in severity and duration. Studies of the incidence and prevalence of the disease show that most cases are mild and individuals recover gradually with time. In more severe cases, individuals may not recover and may have long-term disability.

Who can get CRPS?

Anyone can get CRPS. It can strike at any age and affects both men and women, although it is much more common in women. The average age of affected individuals is about age 40. CRPS is rare in the elderly. Children do not get it before age 5 and only very rarely before age 10, but it is not uncommon in teenagers.

What are the symptoms of CRPS?

The key symptom is prolonged pain that may be constant and, in some people, extremely uncomfortable or severe. The pain may feel like a burning or “pins and needles” sensation, or as if someone is squeezing the affected limb. The pain may spread to include the entire arm or leg, even though the precipitating injury might have been only to a finger or toe. Pain can sometimes even travel to the opposite extremity. There is often increased sensitivity in the affected area, such that even light touch or contact is painful (called allodynia).

People with CRPS also experience constant or intermittent changes in temperature, skin color, and swelling of the affected limb. This is due to abnormal microcirculation caused by damage to the nerves controlling blood flow and temperature. An affected arm or leg may feel warmer or cooler compared to the opposite limb. The skin on the affected limb may change color, becoming blotchy, blue, purple, pale, or red.

Other common features of CRPS include:

  • changes in skin texture on the affected area; it may appear shiny and thin
  • abnormal sweating pattern in the affected area or surrounding areas
  • changes in nail and hair growth patterns
  • stiffness in affected joints
  • problems coordinating muscle movement, with decreased ability to move the affected body part, and
  • abnormal movement in the affected limb, most often fixed abnormal posture (called dystonia) but also tremors in or jerking of the affected limb.

What causes CRPS

Doctors aren’t sure what causes some individuals to develop CRPS while others with similar trauma do not. In more than 90 percent of cases, the condition is triggered by a clear history of trauma or injury. The most common triggers are fractures, sprains/strains, soft tissue injury (such as burns, cuts, or bruises), limb immobilization (such as being in a cast), or surgical or medical procedures (such as needlestick). CRPS represents an abnormal response that magnifies the effects of the injury. In this respect it is like an allergy. Some people respond excessively to a trigger that causes no problem for other people.

Peripheral nerve abnormalities found in individuals with CRPS usually involve the small unmyelinated and thinly myelinated nerve fibers (axons) that carry pain messages and signals to blood vessels. (Myelin is a mixture of proteins and fat-like substances that surround and insulate some nerve fibers.) Because small fibers in the nerves communicate with blood vessels, small nerve fiber injuries may trigger the many different symptoms of CRPS. Molecules secreted from the ends of hyperactive injured small nerve fibers are thought to contribute to inflammation and blood vessel abnormalities. These peripheral nerve abnormalities in turn trigger abnormal neurological function in the spinal cord and brain, leading in some cases to complex disorders of higher cortical function.

Another abnormality in CRPS involves the blood vessels in the affected limb, which may dilate (open wider) or leak fluid into the surrounding tissue, causing red, swollen skin. The underlying muscles and deeper tissues can become starved of oxygen and nutrients, causing muscle and joint pain and damage. At times, the blood vessels may over-constrict (clamp down), causing cold, white, or bluish skin. The dilation and constriction of small blood vessels is controlled by small nerve fiber axons as well as chemical messengers in the blood.

CRPS also affects the immune system. High levels of inflammatory chemicals (cytokines) have been found in the tissues of people with CRPS. These contribute to the redness, swelling, and warmth reported by many patients. CRPS is more common in individuals with other inflammatory and autoimmune conditions such as asthma.

Limited data suggest that CRPS also may be influenced by genetics. Rare family clusters of CRPS have been reported. Familial CRPS may be more severe with earlier onset, greater dystonia, and more than one limb being affected.

Occasionally CRPS develops without any known injury. There may have been an internal injury caused by an infection, a blood vessel problem, or entrapment of the nerves, so careful examination is needed to determine the cause and treat it.

In many cases, CRPS is the result of multiple causes that act together to produce various symptoms.

How is CRPS diagnosed?

Currently there is no single diagnostic test to confirm CRPS. Diagnosis is based on the affected individual’s medical history and signs and symptoms that match the definition. But because several other conditions can cause similar symptoms, careful examination is important. Since most people improve gradually over time, diagnosis may be more difficult later in the course of the disorder.

Testing also may be used to help rule out other conditions, such as arthritis syndromes, Lyme disease, generalized muscle diseases, a clotted vein, or small nerve fiber polyneuropathies (such as from diabetes), because these require different treatment. The distinguishing feature of CRPS is usually a history of earlier injury to the affected area, as most of these other conditions are not triggered by injury. Individuals without a history of injury should be carefully examined to make sure that another treatable diagnosis is not missed.

Magnetic resonance imaging or triple-phase bone scans sometimes identify CRPS-characteristic changes in the bone metabolism. CRPS is often associated with excess bone resorption, a process in which certain cells break down the bone and release calcium into the blood.

What is the prognosis?

The outcome of CRPS varies from person to person. Almost all children and teenagers have good recovery. Occasionally individuals are left with unremitting pain and crippling, irreversible changes despite treatment. Anecdotal evidence suggests early treatment, particularly rehabilitation, is helpful in limiting the disorder, but this benefit has not yet been proven in clinical studies. More research is needed to understand the causes of CRPS, how it progresses, and the role of early treatment.

How is CRPS treated?

The following therapies are often used:

Rehabilitation therapy. An exercise program to keep the painful limb or body part moving can improve blood flow and lessen the circulatory symptoms. Additionally, exercise can help improve the affected limb’s flexibility, strength, and function. Rehabilitating the affected limb also can help to prevent or reverse the secondary brain changes that are associated with chronic pain. Occupational therapy can help the individual learn new ways to work and perform daily tasks.

Psychotherapy. CRPS and other painful and disabling conditions often are associated with profound psychological symptoms for affected individuals and their families. People with CRPS may develop depression, anxiety, or post-traumatic stress disorder, all of which heighten the perception of pain and make rehabilitation efforts more difficult. Treating these secondary conditions is important for helping people cope and recover from CRPS.

Medications. Several different classes of medication have been shown to be effective for CRPS, particularly when used early in the course of the disease. No drug is approved by the U.S. Food and Drug Administration specifically for CRPS. No single drug or combination of drugs is guaranteed to be effective in every person. Drugs to treat CRPS include:

  • non-steroidal anti-inflammatory drugs to treat moderate pain, including over-the-counter aspirin, ibuprofen, and naproxin
  • corticosteroids that treat inflammation/swelling and edema, such as prednisolone and methylprednisolone (used mostly in the early stages of CRPS)
  • drugs initially developed to treat seizures or depression but now shown to be effective for neuropathic pain, such as gabapentin, pregabalin, amitriptyline, nortriptyline, and duloxetine
  • botulinum toxin injections
  • opioids such as oxycontin, morphine, hydrocodone, fentanyl, and vicodin
  • N-methyl-D-aspartate (NMDA) receptor antagonists such as dextromethorphan and ketamine
  • nasal calcitonin, especially for deep bone pain, and
  • topical local anesthetic creams and patches such as lidocaine.

All drugs or combination of drugs can have various side effects such as drowsiness, dizziness, increased heartbeat, and impaired memory. Inform a healthcare professional of any changes once drug therapy begins.

Sympathetic nerve block. Some individuals report temporary pain relief from sympathetic nerve blocks, but there is no published evidence of long-term benefit. Sympathetic blocks involve injecting an anesthetic next to the spine to directly block the activity of sympathetic nerves and improve blood flow.

Surgical sympathectomy. The use of this operation that destroys some of the nerves is controversial. Some experts think it is unwarranted and makes CRPS worse; others report a favorable outcome. Sympathectomy should be used only in individuals whose pain is dramatically relieved (although temporarily) by sympathetic nerve blocks. It also can reduce excess sweating.

Spinal cord stimulation. Placing stimulating electrodes through a needle into the spine near the spinal cord provides a tingling sensation in the painful area. Typically the electrode is placed temporarily for a few days to assess whether stimulation will be helpful. Minor surgery is required to implant all the parts under the skin on the torso. Once implanted, the stimulator can be turned on and off, and adjusted using an external controller. Data shows that about one-fourth of individuals develop equipment problems that may require additional surgeries.

Other types of neural stimulation. Neurostimulation can be delivered at other locations along the pain pathway, not only at the spinal cord. These include near injured nerves (peripheral nerve stimulators), outside the membranes of the brain (motor cortex stimulation with dural electrodes), and within the parts of the brain that control pain (deep brain stimulation). A recent option involves the use of magnetic currents applied externally to the brain (called repetitive Transcranial Magnetic Stimulation, or rTMS). The advantage is that no surgery is required; the disadvantage is need for repeated treatment sessions.

Intrathecal drug pumps. These devices pump pain-relieving medications directly into the fluid that bathes the spinal cord, typically opioids and local anesthetic agents such as clonidine and baclofen. The advantage is that pain-signaling targets in the spinal cord can be reached using doses far lower than those required for oral administration, which decreases side effects and increases drug effectiveness. There are no studies that show benefit specifically for CRPS.

Emerging treatments for CRPS include:

  • Intravenous immunoglobulin (IVIG). Researchers in Great Britain reported that low-dose IVIG reduced pain intensity in a small trial of 13 patients with CRPS for 6 to 30 months who did not respond well to other treatments. Those who received IVIG had a greater decrease in pain scores than those receiving saline during the following 14 days after infusion. A larger study involving individuals with acute-phase CRPS is planned.
  • Ketamine. Investigators are using low doses of ketamine—a strong anesthetic—given intravenously for several days to either reduce substantially or eliminate the chronic pain of CRPS. In certain clinical settings, ketamine has been shown to be useful in treating pain that does not respond well to other treatments.
  • Hyperbaric oxygen. Several studies have investigated the use of hyperbaric oxygen therapy for chronic pain. Individuals lie down in a tank containing pressurized air, which delivers more oxygen to the body’s organs and tissues. Although research is still experimental, some researchers report hyperbaric oxygen can reduce swelling and pain, and improve range of motion in individuals with CRPS.

Several alternative therapies have been used to treat other painful conditions. Options include behavior modification, acupuncture, relaxation techniques (such as biofeedback, progressive muscle relaxation, and guided motion therapy), and chiropractic treatment.

What research is currently being done on CRPS?

The National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health (NIH), is the primary Federal supporter of research on the brain and central nervous system. Other NIH institutes also support research on CRPS and other painful conditions.

NINDS-supported scientists are studying new approaches to treat CRPS and to intervene more aggressively to limit the symptoms and disability associated with the syndrome.

Previous research has shown that CRPS-related inflammation is supported by the body’s natural immune response. Researchers hope to better understand how CRPS develops by studying immune system activation and peripheral nerve signaling using an animal model of the disorder. The animal model was developed to mimic certain CRPS-like features following fracture or limb surgery, by activating certain molecules involved in the immune system process.

Limb trauma, such as a fracture and then having the limb placed in a cast, is a common cause of CRPS. By studying an animal model, researchers hope to better understand the neuroinflammatory basis of CRPS and to identify the relevant inflammatory signaling pathways that lead to the development of post-traumatic CRPS. They also will examine inflammatory effects of cast immobilization and exercise on the development of pain behaviors and CRPS symptoms.

Peripheral nerve injury and subsequent regeneration often lead to a variety of sensory deficits. Researchers hope to identify specific cellular and molecular changes in sensory neurons following peripheral nerve injury to better understand the processes that underlie neuroplasticity (the brain’s ability to reorganize or form new nerve connections and pathways following injury or death of nerve cells). Identifying these mechanisms could provide targets for new drug therapies that could improve recovery following regeneration.

Children and adolescents with CRPS generally have a better recovery than adults and offer a unique model for the study of chronic pain reversal. Scientists studying children with CRPS are investigating neuroplasticity and the biological processes that cause CRPS to occur, in the hopes of developing more effective therapies and accelerated recoveries for adults and children.

New Article on Treatment of Chronic Cluster Headaches a Trigeminal Phenomenom

Dr. Shapira Unsorted 0 Comments

A New article “Neuromodulation in cluster headache” has just been published on Chronic Cluster Headaches Treatment. (See Pub Med Abstract below) I find it very interesting that while they describe Deep Brain Stimulation, Occipital Nerve Stimulation and various types of surgical intervention they do not discuss direct neurostimulation through the trigeminal nerve. It is a well known fact that almost 100% of headaches have a large trigeminal nerve component.

Various Surgical procedures of the trigeminal nerve and sphenopalatine ganglion are discussed but not the more effective and safer procedures of Sphenopalatine Ganglion blocks. The MiRx protocol has been shown to be extremely effective using the Tx360 device. The standard intranasal approach is extremely effective and has advantages of being the most cost effective method of SPG blocks and the only one patients can self administer to abort cluster headaches before they occur.

Physiologic Dentistry utilizes neurostimulation to relax muscles and eliminate noxious input into the trigeminal nervous system. It is a long term physiologic correction and can be used in conjunction with occipital nerve stimulation or Spenopalatine Ganglion Blocks for highly effective treatment.

High risk testament that is best avoided if possible is surgical treatment by radio surgery or ablation of the Sphenopalatine Ganglion.

The Treatment of Choice for Chronic Cluster Headaches that I recommend is non-invasive treatment utilizing an ULF TENS and a Physiologic Diagnostic Orthotic as the first step combined with safe effective and inexpensive SPG Blocks for the majority of patients. Both of these treatments have have efficacy and minimal risk. If additional relief is required occipital stimulation should be consider.


Another recent article  in Headache.  2014 Oct 23. doi: 10.1111/head.12458. on use of TX360 for Sphenopalatine Ganglion Blocks (SPG Blocks) for chronic migraine concluded “SPG blockade with bupivacaine delivered repetitively for 6 weeks with the Tx360® device demonstrates promise as an acute treatment of headache in some subjects with CM. Statistically significant headache relief is noted at 15 and 30 minutes and sustained at 24 hours for SPG blockade with bupivacaine vs saline. The Tx360® device was simple to use and not associated with any significant or lasting adverse events. Further research on sphenopalatine ganglion blockade is warranted.

Pub Med abstract

Adv Tech Stand Neurosurg. 2015;42:3-21. doi: 10.1007/978-3-319-09066-5_1.
Neuromodulation in cluster headache.
Fontaine D1, Vandersteen C, Magis D, Lanteri-Minet M.
Author information

Medically refractory chronic cluster headache (CH) is a severely disabling headache condition for which several surgical procedures have been proposed as a prophylactic treatment. None of them have been evaluated in controlled conditions, only open studies and case series being available. Destructive procedures (radiofrequency lesioning, radiosurgery, section) and microvascular decompression of the trigeminal nerve or the sphenopalatine ganglion (SPG) have induced short-term improvement which did not maintain on long term in most of the patients. They carried a high risk of complications, including severe sensory loss and neuropathic pain, and consequently should not be proposed in first intention.Deep brain stimulation (DBS), targeting the presumed CH generator in the retro-hypothalamic region or fibers connecting it, decreased the attack frequency >50 in 60 % of the 52 patients reported. Complications were infrequent: gaze disturbances, autonomic disturbances, and intracranial hemorrhage (2).Occipital nerve stimulation (ONS) was efficient (decrease of attack frequency >50 %) in about 70 % of the 60 patients reported, with a low risk of complications (essentially hardware related). Considering their respective risks, ONS should be proposed first and DBS only in case of ONS failure.New on-demand chronically implanted SPG stimulation seemed to be efficient to abort CH attacks in a pilot controlled trial, but its long-term safety needs to be further studied.…

What is TMJ?

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What is TMJ? Learn more about it!


Everyone experiences occasional headaches, shoulder pain, or sore neck. Most of the time we can dismiss the cause as nothing more than stress or our busy lives, but, when pain becomes a daily occurrence or is accompanied by other symptoms, there could be something more going on.

If you are suffering from undiagnosed, chronic pain, TMJ may be the reason. But what is TMJ, and why does it cause pain?

How does your TMJ work?

TMJ is an abbreviated term for the temporomandibular joint also known as your jaw joint. Other abbreviations; TMD for Temporomandibular Disorder and TMJD for Temporomandibular Joint Disorder, are also accepted and used interchangeably  to refer to the pain, disorder or dysfunction of this joint and other affected areas surrounding it.

Like all of the wonderfully complex parts of our bodies, the temporomandibular joint is designed for smooth, continuous and pain-free operation. These two essential joints work in unison to allow you to:

  • bite
  • speak
  • chew
  • sing
  • yawn
  • laugh
  • talk

In fact, for your jaw to do everything you need it to, it must be able to open close, move forward and back and from side to side.

The bones of your joints do not work alone. To move, each of your ball and socket jaw joints are cushioned by a disc and surrounded by the muscles, ligaments and nerves that make them work.

What causes jaw problems?

While TMJ causes are not always clear, they are often be related to specific events or life changes, including:

  • uneven dentistry
  • direct injury to the temporomandibular joint
  • ongoing stress resulting in bruxism and clenching of the jaw
  • shifting or missing teeth
  • a misaligned jaw or underdeveloped jaw due to genetics or childhood breathing problems
  • arthritis
  • sleep disorders, especially sleep disordered breathing

Where does the pain come from?

Since the TM joint consists of so many interdependent parts, if even one piece is out of commission, stressed or damaged in some way, the rest of the connecting parts are affected. This includes the part of our nervous system that is responsible for providing input to the brain for as much as 40 percent of the human head and face.

The nerve, specifically called the trigeminal nerve is of great interest to the physiologic dentist evaluating and treating TMJ disorders. As the name implies, there are three branches to this nerve, and they are connected with many of the functions of the TM joint, including:

  • Routine chewing functions of the upper and lower jaw
  • Swallowing
  • Breathing
  • Talking
  • Kissing
  • Eyes
  • Ears
  • Sinuses
  • Teeth

Even though TMJ pain directly communicates through the trigeminal nerve structures, it may also result in referred pain to certain locations in the head and neck.  Almost 100% of all headaches  and migraines, as well as sinus pain are mediated primarily by the trigeminal nerve.  Symptoms of referred pain may include the following symptoms:

  • Frequent morning headaches or migraines
  • Grinding, clicking or popping noise in the TM joints
  • Dizziness
  • Neck, shoulder or back pain
  • Tinnitus

Learn more about TMJ

DentistTMJ is a complex disorder. Effective treatment depends on an accurate diagnosis.

If you would like to find out if TMJ is at the root of your chronic pain, take our TMJ questionnaire or, better yet, come in for a consultation.

Copyright 2014 • Dr. Ira Shapira • ThinkBetterLife.com

For effective TMJ and Sleep Disorder solutions. 3500 Western Ave Suite 101 | Highland Park, IL 60035 | Phone: (847) 533 8313.

Dr Shapira is a licensed general dentist in Illinois

Serving the communities of Chicago, Deerfield, Evanston, Highland Park, Kenilworth, Lake Bluff, Lake Forest, Libertyville, Lincolnshire, Mettawa, Morthon Grove, Northbrook, Northfield, Skokie, Vernon Hills, Wilmette, Winnetka, Lake County

The information provided on this website is not intended to serve as medical advice. An appropriate diagnosis and treatment plan for any patient can be made only by a treating dentist, physician, or group of doctors. Think Better Life shall have no liability or responsibility to any person with respect to loss or damage caused or alleged to be caused directly or indirectly by the information contained in this website or obtained from other websites to which a visitor may connect and view

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