Friday, November 24, 2017

Patient describes treatment of her severe TMJ issues. She travels to Chicago for treatment.

Jen describes her treatment for chronic pain.

https://www.youtube.com/channel/UCk9Bfz6pklC7_UluWFHzLrg/videos

Ears ringing, Jaw Cracking, Jaw Pain, Myofascial Pain in head neck and ears, balance problems, tingling in my hands and feet,
I WAS PRETTY DESPERATE AND IN A LOT OF PAIN!
I saw several dentists and was searching everywhere for an answer, I found Dr Shapira and e-mailed some of his former patients.
I have had oral appliance 2-2 1/2 months and it has made a huge diffence. I don't even think about my jaw anymore.
Prior to appliance it was even hard to eat.

With the appliance my balance is getting better.

The Sphenopalatine Ganglion (SPG) aka the Pterygopalatine Ganglion and it’s role in Pain Syndromes


This paper was originally published on the website:  www.SphenopalatineGanglionBlocks.com


There are also over 100 patient testimonial videos on SPG Blocks, Neuromuscular Dentry and Dental Sleep Medicine at:   https://www.youtube.com/channel/UCk9Bfz6pklC7_UluWFHzLrg/videos

The Sphenopalatine Ganglion (SPG) aka the Pterygopalatine Ganglion and it’s role in Pain Syndromes


I am going to go thru this excellent review paper and add my personal opinions based on almost 40 years of helping patients with chronic pain.  MY COMMENTS WILL BE IN ALL CAPITAL LETTERS:    THE ORIGINAL ARTICLE IS AVAILABLE ONLINE.
The Pterygopalatine Ganglion and its Role in Various Pain Syndromes: From Anatomy to Clinical Practice.
Maria Piagkou, MD, MSc, PhD*; Theano Demesticha, MD, PhD†
; Theodore Troupis, MD, PhD*; Konstantinos Vlasis, MD, PhD*; Panayiotis Skandalakis,
MD, PhD*; Aggeliki Makri, MD*; Antonios Mazarakis, MD, PhD*; Dimitrios
Lappas, MD, PhD*; Giannoulis Piagkos, MD*; Elizabeth O Johnson, MD, PhD*
*Department of Anatomy, Medical School, University of Athens, Athens; †
Department of
Anesthesiology, Metropolitan Hospital, P. Faliro, Greece
Abstract: The postsynaptic fibers of the pterygopalatine or sphenopalatine ganglion (PPG or SPG) supply the lacrimal
and nasal glands.   ACTUALLY, THE AUTONOMIC FIBERS RUN THRU ALL BRANCHES OF THE TRIGEMINAL NERVE, BOTH SYMPATHETIC AND PARASYMPATHETIC.
The PPG (SPG) appears to play an important role in various pain syndromes including headaches, trigeminal
and sphenopalatine neuralgia, atypical facial pain, muscle pain, vasomotor rhinitis, eye disorders, and herpes
infection.
TRIGEMINAL NERVE FIBERS AFTER AMPLIFICATION IN RETICULAR ACTIVATING SYSTEM ACCOUNT FOR OVER 50% OF ALL BRAIN INPUT.
Clinical trials have shown that these pain disorders can be managed effectively with sphenopalatine
ganglion blockade (SPGB). In addition, regional anesthesia of the distribution area of the SPG sensory fibers for nasal
and dental surgery can be provided by SPGB via a transnasal, transoral, or lateral infratemporal approach.  IF INJECTIONS  TO THE SPG ARE TO BE DONE THE SUPRAZYGOMATIC APPROACH TO THE INFRATEMPORAL FOASSA IS MOST EFFICATIOUS.
To arouse the interest of the modern-day clinicians in the use of the
SPGB (SPHENOPALATINE GANGLION BLOCK)  the advantages, disadvantages, and modifications of
the available methods for blockade are discussed.
INTRODUCTION
Broad morphological and functional knowledge of the head anatomy is essential for neurology, neurosurgery,
and maxillofacial surgery practice. Nevertheless, there are areas and structures that still have not been
described or depicted sufficiently, owing to their small volume and complicated access. The pterygopalatine
ganglion (PPG), also known as sphenopalatine ganglion (SPG), Meckel’s or sphenomaxillary ganglion, OR THE NASAL GANGLION, OR SLUDER’S GANGLION is
located in the cranial section of the autonomic nervous System and bears unique characteristics favorable for
the treatment of many painful syndromes involving the face and head.1  THE GANGLIA IS LOCATED IN THE PTERYGOPALATINE FOSSA ON THE MAXILLARY DIVISION (V2) OF THE TRIGEMINAL NERVE.
SPG is located near important neuroanatomic structures for pain perception. Its proximity to multiple sensory facial and trigeminal branches.  THE SPG GANGLIA IS THE LARGEST PARASYMPATHETIC GANGLIA OF THE HEAD AND IT ALSO HAS SYMPATHETIC FIBERS RUNNING THRU IT.
Pain Practice 2011 World Institute of Pain, Pain Practice, Volume 12, Issue 5, 2012 399–41
PAI PRACTICE  suggests that SPG may be involved in persistent idiopathic facial pain (PIFP)2 and unilateral headaches.3 A
few motor nerves accompany the SPG sensory trunks.  THE AUTONOMIC NERVES RUN ALONG TRIGEMINAL NERVES.
An irritation of the SPG motor root may produce face and neck neuralgias by its connection
with the facial nerve (FN) , V7) lesser occipital and cutaneous cervical nervesN AND account for disturbances in the eye and mandible
region by its connections with the ciliary and otic ganglions and a variety of visceral symptoms by its connection with the vagus nerve.
EAR PAIN / OTALGIA THE AUTONOMIC NERVES  cause reflex otalgia by its connection with the
tympanic plexus.  THIS CONNECTION CAN ALSO CRERAT PAIN SYNDROMES EITHER PRODUCED BY SOUND OR NOISE OR WORSENED BY SOUND.  In addition, there may be motor phenomena of the soft palate related to the involvement of the motor
fibers to the levator palate and azygos uvulae muscles.  SPG has also been identified as the first relay station of
the autonomic fibers after emerging from the pons, suggesting that it may be used therapeutically in autonomic
imbalance situations.   SPG may play a critical role as a vasodilator to protect the brain against ischemia
in stroke or ischemia of migraine with aura.4  THE TRIGEMINAL NERVE IS RESPONSIBLE FOR CONTROLLING BLOOD FLOW TO THE ANTERIOR TWO THIRDS OF THE MENINGES OF THE BRAIN.  ALL HEADACHES AND MIGRAINES ARE PRODUCTS OF THE TRIGEMINAL NERVOUS SYSTEM.  V5 HEADACHES MIGHT BE AN ACCURATE DESCRIPTION OF ALL MIGRAINES
The SPG as a major source for postganglionic parasympathetic fibers to the vascular beds of the cerebral hemispheres
is involved in tone regulation of the cerebral vessels.5 SPG’s communication with the superior cervical ganglion (SCG) (through the internal carotid
plexus) and the intracranial portion of the internal carotidartery (through its fibers from SPG) is related to edema, pain, dilatation, and low-grade encephalitis.6,7
SPG’s superficial location in the pharynx may explain
its sensitivity to odors, chemicals, and air particles.  SPG’s connection to the vagus nerve and the innervation
of the saliva producing glands predicts many of the digestive symptoms observed in dysfunctional
states.  SWALLOWING BEGINS IN THE MOUTH AND CONTINUES AS A PERISTALTIC WAVE THROUGHOUT THE ENTIRE GI TRACK.  SWALLOWING IS VERY IMPORTANT FOR EQUALIZING EAR PRESSURE BY PROPER OPENING AND CLOSING OF EUSTACIAN TUBES.  8 Overall, the SPG is important for intraocular pressure balance  (INTRAOCULAR PRESSURE MAY BE POSSIBLE TO TREAT WITH SPG BLOCKS) and cerebral vasodilatation associated with vascular originated headaches.1 Recent research
has highlighted the important role of the SPG in cerebrovascular autonomic physiology, in pathophysiology of cluster and migraine headaches, and in conditions
of stroke and cerebral vasospasm.9  IT SHOULD BE NO SURPRISE
SPG BLOCKS ARE BECOMING A TREATMENT OF CHOICE FOR MIGRAINES AND CLUSTER HEADACHES. ANATOMY OF THE PTERYGOPALATINE
GANGLION (PPG OR SPG).
The SPG, as THE LARGEST parasympathetic ganglion OF THE HEAD  is a nervous
mass of nervous tissues found in the course of the greater petrosal nerve (GPN) located deeply in the
pterygopalatine fossa (PPF). It is a small triangular or heart-shaped structure located close to the sphenopalatine
foramen (SPF) posterior to the middle turbinate and maxillary sinus, anterior to the medial plate of the
pterygoid process, and inferior to the sphenoid sinus and maxillary nerve (MN). IT IS ATTACHED TO THE MAXILLARY BRANCH OF THE TRIGEMINAL NERVE.  THE RECESS IS CALLED THE PTERYGOPALATINE FOSSA.
The SPG is morphologically configured in the last trimester of fetal life, and
during this period, its structure is established to ensure the nervous signal transmission.10 The SPG, a complex
neural center with multiple connections to trigeminal, facial, and sympathetic systems, consists of somatosensory, THE SOMATOSENSORY FIBERS ARE TRIGEMINAL AND MANY ARE PROPRIOCEPTIVE PASSING ON TH MESENCEPHALIC NUCLEUS, sympathetic (FROM SUPERIOR CERVICAL GANGLIA) , and parasympathetic fibers (FROM SPG NERVE CELLS) and receives a sensory, motor, and sympathetic root. The SPG sensory root is derived from two pterygopalatine branches of the MN; their fibers pass directly into the palatine nerves, and a few enter the SPG constituting its sensory root. The sensory distribution to the nose, throat, and sinuses gives characteristic indications in these regions.11 The SPG motor root probably derived from the nervus intermedius (glossopalatinus or nerve of Wrisberg) through the greater superficial petrosal nerve (GSPN) and may consist of sympathetic efferent (preganglionic) fibers from the medulla. SPG motor fibers form synapses with neurons whose postganglionic axons are distributed with the deep branches of the trigeminal nerve (TN) to the mucous membrane of
the nose, soft palate, tonsils, uvula, roof of the mouth,
upper lip, and gums and to the upper part of the pharynx.12
The SPG autonomic innervation is more complex.
The SPG sympathetic root is derived from the
internal carotid plexus through the deep petrosal nerve
(DPN). The GSPN and the DPN join to form the nerve
of the pterygoid canal (vidian nerve) before entering
the SPG. The SPG parasympathetic root has its preganglionic
origin in the superior salivary nucleus. The preganglionic
fibers pass through nervus intermedius, FN,
geniculate ganglion, and greater petrosal nerve reaching
the ganglion via nerve of pterygoid canal. The
GSPN carries taste along with the presynaptic parasympathetic
fibers. The taste fibers pass through the
SPG to the soft palate, while the parasympathetic
fibers synapse in the SPG and postsynaptic fibers supply
the lacrimal gland, mucosa of the palate, nasopharynx,
and nasal cavity.13
The DPN, a branch of the internal carotid plexus
(the continuation of the cervical sympathetic trunk in
the cranium), carries postganglionic sympathetic fibers
from the SCG. The postganglionic sympathetic nerve
fibers pass through the SPG without synapsing and join
branches of the MN, which distributes to the nasal
400 • PIAGKOU ET AL.
cavity, palate, and upper pharynx. The GSPN and
DPN (join at the foramen lacerum to form the vidian
nerve) pass forward, through the pterygoid canal, with
the corresponding artery, and joined by a small
ascending sphenoidal branch from the otic ganglion.
Finally, vidian nerve enters the PPF and joins the posterior
angle of the SPG14 (Figure 1).
NERVE SUPPLY FROM THE PTERYGOPALATINE
GANGLION
The nerves of the SPG are predominantly composed of
MN sensory fibers. Several delicate orbital branches of
the pterygopalatine nerves enter the orbit via the inferior
orbital fissure to supply the orbital periosteum and
muscle, and the mucous membrane of the posterior ethmoid
and sphenoid sinuses. The three palatine nerves,
the one greater (anterior palatine nerve) (GPN) and two
lesser (middle and posterior) palatine nerves (LPN), exit
the SPG inferior surface to descend behind the perpendicular
plate of the palatine bone. The anterior or GPN
descends through the pterygopalatine canal (PPC)
accompanied by the descending palatine artery. Emerging
onto the oral palatal surface at the greater palatine
foramen (GPF), it passes anteriorly, medial to the alveolar
bone process giving branches to mucosa and glands
of the hard palate, as far as the incisor teeth. The GPN
communicates in the incisive canal region with a branch
of the nasopalatine nerve. Posterior inferior lateral
nasal branches of the GPN leave the nerve in the PPC
and enter the nasal cavity to supply the middle and inferior
meatuses and the inferior concha. Several posterior
superior lateral nasal branches of the PPG pass through
the SPF into the posterior part of the nasal cavity and
distribute to the superior and middle nasal conchae, the
posterior ethmoidal air cells, and the posterior part of
the septum. The middle and posterior or LPN penetrate
the hard palate via the lesser palatine foramina (LPF) to
supply the soft palate, uvula, and tonsils. In addition,
taste receptors of the palate are innervated by special
visceral afferent fibers of the FN that are carried by the
GPN and LPN, back through the PPG and the greater
petrosal nerve to the geniculate ganglion. The nasopalatine
nerve (the larger of the posterior nasal branches)
passes across the roof of the nasal cavity to the septum
and runs inferiorly and anteriorly on the inclined edge
of the vomer, supplying the septum. At the incisive
canal, the two nasopalatine nerves descend to the palate,
communicate with the terminals of the anterior palatine
nerves, and consequently participate in the
innervation of the upper central incisors. Finally, the
pharyngeal nerve leaves the SPG posterior part and
enters the pharynx via the palatovaginal canal with a
pharyngeal branch of the maxillary artery (MA) to
reach the sphenoid sinus and nasopharynx behind the
auditory tube15(Figure 2).
SPHENOPALATINE GANGLION BLOCKADE (SPGB)
Sphenopalatine ganglion blockade has been achieved
with a variety of methods, for various pain disorders,
when more conservative treatments have failed. In
1908, Sluder proposed that a high-grade inflammatory
reaction in the posterior ethmoid and sphenoid sinuses
may be involved in certain cases of unilateral facial pain
associated with lacrimation, rhinorrhea, and mucosal
congestion. These symptoms are associated with the
extension of inflammation or the transmission of toxins
into the SPG.16 Sluder reported that patients who had
refused surgery for an active ethmo-sphenoid inflammation
later developed sphenopalatine ganglion neuralgia
(SPGN). He also claimed success in relieving the symptoms
of facial neuralgia, asthma,17 earache,18 and
lower-half headache19 using ablation. Ruskin described
Figure 1. Parasympathetic preganglionic axons derived from
the facial nerve leave the main trunk of the nerve and course as
the greater superficial petrosal nerve. Sympathetic postganglionic
axons derived from cell bodies in the superior cervical ganglion
(SCG) course on the ICA surface and enter the skull with
the artery at the carotid canal. The sympathetic axons course
through the adjacent sphenopalatine ganglion (SPG) without
synapsing and are distributed with the nerve and arterial
branches emanating from it, to the nasal and pharyngeal
mucosa. The parasympathetic fibers entering the SPG synapse
there and distribute to glands in the same mucous membranes.
Some of the postganglionic axons pass to the lacrimal gland by
way of first the maxillary nerve, then 1 of its branches, the
zygomatic nerve, and finally by way of 1 of the branches of the
ophthalmic division of the trigeminal nerve, the lacrimal nerve.
Sources: Adapted from Basic Human Anatomy – O Rahilly, Muller,
Carpenter and Swenson (on line darmouth.edu).
PPG and its Role in Pain Syndromes • 401
the technique with cocaine for the treatment of chronic
muscle spasm,20 arthritis,21 and polyarthritis,22 and
Ruskin A.P. used pentocaine for a variety of other conditions.23
Barre24 described a SPGB method using a
dropper to instill local anesthetic into the nose, but
much of the anesthetic was absorbed throughout the
nasopharynx without reaching the SPG. Hardebo and
Elner25 reported that SPGB can be used as an abortive
agent for cluster headache (CH).  THE USE OF SPG BLOCKS FOR CLUSTER HEADACHES MAKE IT A FIRST LINE OF TREATMENT FOR CLUSTER HEADACHES Although SPGB was
historically employed for various pain syndromes,
many of these reports are anecdotal and remain controversial.6,26–28
INDICATIONS FOR SPGB
A NWER USE OF SPG BLOCKS IS TREATMENT OF PANIC ATTACKS AND PTSD.  THE STELLATE GANGLION BLOCK (SGB) IS ALSO USED TO TREAT PTSD AND A STUDY IS CURRENTLY BE DONE BY THE US MILITARY.  SOME OF THE SYMPATHETIC FIBERS THAT COME THRO STELLATE GANGLION PASS THRU SPG FIBERS
Diagnostic and therapeutic head and neck blocks can
also assist with the diagnosis and management of
many chronic pain conditions (pain of musculoskeletal,
vascular, and neurogenic origin).29 Currently
accepted indications for the SPGB include: SPG and
trigeminal neuralgia (TGN), PIFP (previously referred
to as atypical facial pain), acute migraine, acute and
chronic CH, herpes zoster involving the ophthalmic
nerve, and a variety of other facial neuralgias12,29–31
Sphenopalatine ganglion neuralgia or Sluder’s neuralgia
(SPGN) is a type of facial neuralgia, defined as a
symptom complex consisting of neuralgic, motor, sensory,
and gustatory manifestations.32 SPGN could be a
trigeminal autonomic cephalalgia (TAC), described as
unilateral facial pain in the orbital region that sometimes
spreads retro-orbitally toward the zygoma and
extends posteriorly to the mastoid and occiput.33
SPGN refers to intermittent episodes of vasomotor
hyperactivity causing conjunctival injection, lacrimation,
serous nasal discharge and unilateral nasal mucosal
inflammation, and sensory disturbances of the
palate and oropharynx with distorted gustatory sensations.
Occasionally, SPGN is a bilateral constant pain
with exacerbations or a pain that stopped and reappeared
cyclically or with stabbing sharpness. The pain
is typically associated with anesthesia of soft palate,
pharynx, tonsils and nose, and hyperesthesia along the
distribution of the TN. The parasympathetic signs are
ipsilateral lacrimation, conjunctival injections, nasal
obstruction, rhinorrhea, serious nasal discharge, or
mucosal congestion34,35 (Table 1).
Trigeminal neuralgia, also called ‘‘tic douloureux,’’
is a peculiarly painful paroxysmic disorder that undergoes
spontaneous remissions and recurrences. The
pain, subserved by large fibers, can be triggered from
outside the trigeminal territory and by other factors
than mechanical stimuli. There are strong autonomic
influences of the pain, and there is a cutaneous vasoconstriction
in the trigeminal territory in which it
Figure 2. The sphenopalatine ganglion and its connections—communications
of the PPF. SPF, sphenopalatine foramen;
FR, foramen rotundum; PhC, pharyngeal canal; PtC,
pterygoid canal; PPF, pterygopalatine fossa.
Source: Adapted from Google pictures database (95 1252 pair.-
com).
Table 1. Sphenopalatine ganglion blockade (SPGB) in the Treatment of Sluder’s Neuralgia
Authors Patients Technique Efficacy
Salar et al.35 7 Percutaneous radiofrequency thermocoagulation
(RFTC)
1/10 needed repeat lesioning
2/10 needed additional RFTC
Pollock and
Kondziolka36
1 Stereotactic radiosurgery targeted at the
SPG—repeated radiosurgery 17 months later for
partial pain recurrence
2 years pain-free (without nasal discharge or
eye irritation)
Puig and Driscoll37 8 13 occasions of SPG (88% phenol) intranasal 90% decrease in head and face pain (for an
average of 9.5 months). The recurrent pain
was less severe, less frequent and of shorter
duration
Olszewska-Ziaber
et al.38
3 4% xylocaine intranasally and intranasal
phenolization
Total relief of pain
Karas et al.33 1 SPG gamma knife radiosurgical ablation Total relief of pain
402 • PIAGKOU ET AL.
occurs.39 TGN manifests as severe disabling facial pain
unilaterally either episodic or chronic and is most common
in older people than 50 years of age and in
women.40,41 Pain paroxysms can be precipitated by
nonpainful stimuli (touch, movement, wind exposure,
chewing, brushing teeth, shaving, and swallowing) in 1
or more branches of the 5th cranial nerve.13,41 The
pain is of much shorter duration than that of CH, but
sometimes, it can be associated with CH giving rise to
a ‘‘cluster tic.’’ Atypical TGN encompasses various
facial pain syndromes including those arising from
dental or otorhinolaryngological disorders. Paroxysmal
hemicrania (PH) belongs to TACs with severe strictly
unilateral pain attacks localized to orbital, supraorbital,
and/or temporal sites accompanied by 1 or more
ipsilateral autonomic features.40,42 SPGB could be considered
a reasonable alternative in drug-resistant PH
cases where indomethacin is contraindicated. Several
treatment options are available (Table 2).
Cluster headache (CH) is relatively uncommon and
the most painful form of recurring primary neurovascular
headache. CH has been described with a variety
of names, including histamine cephalgia (Horton headache)
and paroxysmal nocturnal cephalgia.49 CH is a
severe, strictly unilateral head pain (ocular, frontal,
and temporal) in the territory of the TN distribution,
associated with autonomic manifestations homolateral
to the pain and usually follows circadian and circannual
patterns. The autonomic manifestations seem to be
both parasympathetic (lacrimation and rhinorrhea)
and sympathetic (ptosis and miosis). The periodicity of
the attacks and seasonal recurrence of the cluster periods
suggest the involvement of a biologic clock within
hypothalamus.50 CH is characterized by a constant
unilateral orbital location and tends to recur nightly at
the same time and last for 6 to 12 weeks, followed by
complete freedom from headache for months or even
years. The associated autonomic phenomena of a
blocked nostril, rhinorrhea, injected conjunctivae, lacrimation,
ptosis, miosis, and flushing of the cheek are
frequently present. This headache typically responds at
least initially to medication. The pathophysiology of
CH involves the activation of parasympathetic nerve
structures located within the SPG, which explains
many of the associated symptoms (conjunctival injection,
lacrimation, nasal congestion, rhinorrhea, forehead
and facial sweating, miosis, ptosis, or eyelid
edema).51 The prominent cranial autonomic symptoms
may be due to central disinhibition of the trigeminovascular
autonomic reflex by the hypothalamus,
possibly through direct hypothalamic-trigeminal
connections.42 Communication between the SPG and
the V2 TN has also been described as a mechanism
responsible for CH.52
The International Headache Society (HIS) divided
CH into groups according to they include: CH periodicity
undetermined; episodic; and chronic CH (unremitting
from onset or evolved from episodic)
(Headache Classification Subcommittee).53About 90%
of people with CH have the episodic form, but 10%
have chronic CH (the attacks occur for more than 1
year without remission or with remissions lasting
< 1 month).42 Attacks occur in CH which follows a chronobiological pattern that appears to coincide with the seasonal change in the length of day. During a cluster period, headaches occur 2 to 3 times daily for Table 2. Sphenopalatine ganglion blockade (SPGB) in the Treatment of Trigeminal Neuralgia Authors Patients Technique Efficacy Manahan et al.43 1 10 treatments (bupivacaine 0.5%) Pain-free for 30 months Spacek et al.44 39 17 patients (carbamazepine and apuncture therapy) (group A) 11 patients (carbamazepine local ganglionic opiod analgesia (GLOA) and apuncture therapy (group B) 11 patients carbamazepine and GLOA without apuncture (group C) GLOA was carried out with 0.045 mg buprenorphine at the superior cervical ganglion or at the SPG 8 patients of group A, 5 of group B, and 2 of group C remained pain-free Most patients with no improvement were from group C Saberski et al.45 1 11 times repeated therapy (transnasal approach) Bradycardia was resolved with successful alleviation of pain Gre´goire et al.46 1 3 separate CT-guided injections Pain-free Kanai et al.47 25 2 sprays (0.2 mL) of either lidocaine 8% or saline placebo in the affected nostril using a metered-dose spray. Intranasal lidocaine 8% spray decreased symptoms. Pain was described as moderate or better by 23 patients of the lidocaine spray and 1 of the placebo group. Zarembinski and Graff-Radford48 26 SPGB fluoroscopically on 12 patients that responded to stellate ganglion blocks and 14 additional patients 20 of 26 patients responding to SPGB (76.9%) PPG and its Role in Pain Syndromes • 403 45 minutes to 1 hour. The SPG seems to play a very important role in pathology. It is hypothesized that SPGB relieves headaches because it breaks the vicious autonomic cycle of pain within the facial and cranial area54,55 (Table 3). Migraine headache is an intensely unilateral, periorbital severe pain. The perception of migraine headache is formed when nociceptive signals originating in the meninges are conveyed to the somatosensory cortex through the trigeminal ganglion, medullary dorsal horn, and thalamus. Different migraine triggers activate a wide variety of brain areas that impinge on parasympathetic neurons innervating the meninges. Migraine triggers either activate or originate in a number of brain areas whose projections converge on the superior salivatory nucleus. The superior salivatory nucleus, in turn, activates postganglionic parasympathetic neurons in the SPG, resulting in vasodilation and local release of inflammatory molecules that activate meningeal nociceptors. Typically, migraine headache is a unilateral pain beginning most commonly in frontotemporal area that may involve whole hemicranium, alternating sides between or during an attack. It is associated with depression, stress, hunger, fatigue, sleepiness, anorexia, nausea, vomiting, photophobia, and phonophobia. Redness and swelling of the mucous membrane of the nose and conjunctival injection may also occur with migraine70,71 (Table 3). In recent years, SPG neurolysis after successful blockade has been utilized in such cases with varying success.34,51,57,58,72 SPG neurolysis is indicated for PIFP,2 previously known as atypical facial pain. PIFP is defined as a constant, deep, and pulling or crushing pain in the head or face, present all or most of the day, which may become more intense during exercise. Pain is most often localized to the maxilla and may extend to the region of the eyes, nose, cheek, and temple.73 Patients who have PIFP syndromes (after trauma, surgery, or on an idiopathic basis) are more difficult to treat than those with typical TGN.58 The pathophysiologic mechanism remains unknown, and the cause is likely to be multifactorial.57 Remick et al.74 reported a 68% incidence of psychiatric disorders in patients with PIFP, but PIFP cannot be related to a psychiatric disorder. If symptoms make it impossible to determine the pain origin or if they do not guide the clinicians toward any other facial pain syndrome, then the diagnosis is a PIFP.75 PIFP may have a sympathetic component, which makes neurolysis of the SPG ideal as the postganglionic sympathetic nerves pass through the ganglion. Pulsed radiofrequency (PRF) treatment of the SPG can be considered with a maximal temperature of 42C for 1 or for more times during a period of 120 seconds.2 Head, Neck, Shoulders Pain, and Complex Regional Pain Syndromes6 Because the C2, C3, and C4 cervical roots are connected to the SCG and through the DPN to the SPG, the SPGB is able to relieve pain not only from the head, face, neck, and upper back but also diminishes the symptoms from the head and face, which are attributed to the upper cervical spine. The first successful SPGB for myofascial pain originating in the trapezius and sternocleidomastoid muscles was reported by Ruskin.76 Since then, other authors have asserted potential applicability for SPGB in the treatment of myofascial pain and fibromyalgia77,78 while others question the therapeutic applicability of SPGB for myofascial pain (Table 4). Head and Neck Advanced Malignancies Pain resulting from head and neck cancer can be severe and difficult to manage. In certain patients, SPGB can be effectively self-administered at home to manage chronic pain.81 Prasanna and Murthy82 have been used SPGB as an adjunct therapy for immediate relief from pain in the ear arising from the floor of the mouth and extensive tongue lesions because of malignancy (Table 5). Recently, SPGB has been applied for the treatment of musculoskeletal pain, especially that of the neck and back.28,31Although various studies with SPGB for management of low back pain have used cocaine,21 pentocaine,27 and 4% topical xylocaine28 with some success, these conditions are not yet considered among the primary indications. TECHNIQUES FOR SPHENOPALATINE GANGLION BLOCKADE (SPGB) The techniques for SPGB range from superficial to highly invasive. The drugs frequently used are local anesthetics (4% cocaine, 2% to 4% lidocaine, or 0.5% bupivacaine), depot steroids, or 6% phenol. To prolong the SPGB, radiofrequency thermocoagulation (RFT) can be employed. PRF has gained interest as a method. Because it is delivered in pulses, followed by a silent period, allows adequate time for dissipation of heat and energy, resulting in less damage to surround- 404 • PIAGKOU ET AL. Table 3. Sphenopalatine ganglion blockade (SPGB) in the Treatment of Cluster Headache (CH) and Facial Pain Authors Patients Syndrome Technique Efficacy Devoghel54 120 CH Alcohol infiltration Relief of pain > 85%
Onofrio and
Campbell56
26 Chronic CH Posterior fossa trigeminal
rhizotomy or percutaneous
radiofrequency trigeminal
ganglion rhizolysis
54% excellent relief of pain, 15% fair
to good relief of pain, 31% poor relief
Cepero et al.57 12 Facial pain SPG neurectomy High incidence of pain recurrence
Stechison and
Brogan58
4 Post-traumatic PIFP Transfacial transpterygomaxillary
access to foramen rotundum,
SPG, and maxillary nerve
3 patients (complete pain relief)
1 patient free of pain for 12 months
1 patient free of pain for 5 months
Taha and
Tew59
7 Chronic CH Percutaneous stereotactic
radiofrequency rhizotomy
Long pain relief
Sanders and
Zuurmond51
66 Episodic CH (56 patients)
(ECH)
Chronic CH (10 patients)
(CCH)
Radiofrequency lesioning in the
SPG (infrazygomatic approach)
Complete relief of pain in 34 patients
of ECH (60.7%) and in 3 patients of
CCH (30%) and no relief in 8 patients of
ECH (14.3%) and in 4 of CCH (40%)
Maizels4 1 Recurrent headache
(migraine with aura)
Intranasal lidocaine 4% during
the aura phase
The headache following the aura was
prevented and remained successful on
all but 2 occasions over 1.5 years
Costa et al.60 15 Episodic CH (6 patients)
Chronic CH (9 patients)
10% solution of cocaine
hydrochloride or 10% lidocaine or
saline under anteriorrhinoscopy
All patients responded promptly to both
anesthetic agents, with complete
cessation of induced pain. In the case
of saline application, pain severity
increased
Krasuki et al.61 15 Severe headache
head trauma (7 patients)
dental work (2 patients)
herpes zoster (2 patients)
fibromyalgia (1 patient)
pharyngitis (1 patient)
migraine (1 patient)
unkown reason (1 patient)
SPGB with sterile cotton sticks,
soaked in 4% lidocaine, inserted
through the patient’s nose to the
back of nasopharynx for 10
minutes, daily for a week
In 12 of 15 patients, the pain was
reduced
Yarnitsky et al.62 Migraine SPGB by applying lidocaine
intranasally
Mean pain score was 7.5 of 10 during
untreated migraine and 3.5 of 10 after
the SPGB. Cutaneous allodynia
remained despite the pain relief
Shah and
Racz63
1 Post-traumatic headache SPG pulsed-mode radiofrequency
lesioning
Pain relief more than 17 months
Bayer et al.64 46 Chronic face and head pain
(various aetiologies)
SPG pulsed-mode radiofrequency
lesioning (procedure was repeated
in 20% of the patients)
65% mild-to-moderate pain relief 14% no
pain relief and 21% complete pain relief
De Salles
et al.65
5 Classic unilateral CH
(1 patient)
neuropathic pain
(2 patients)
bilateral migrainous
neuralgia (1 patient)
bilateral PIFP (1 patient)
Radiosurgery of the SPG with a
single maximal dose of 90 Gy with
a 5- or 7.5 mm circular collimator
Only the patient with CH experienced
lasting pain relief
Felisati et al.66 21 Chronic drug-resistant CH Endoscopic SPG via the lateral
nasal wall
Treatment was inapplicable a cause
nasal stenosis (1 patient)
complete disappearance of the attacks
(8 patients) a partial benefit (3 patients)
no response (9 patients)
Yang and
Oraee67
1 Chronic, left-sided CH Topical anesthesia to the nasal
mucosa, followed by a needle
insertion guided by its tailored
plastic cover-sheath for injecting
blocking agents
Pain-free for 1 week, 60% pain reduction
with less frequent episodes and easily
controlled with abortive medicine for
3 weeks
Tepper et al.68 11 Intractable migraine SPGB using the infrazygomatic
transcoronoid approach under
fluoroscopy guidance
2 patients—pain-free
3 patients—pain reduction
5 patients—no response
1 patient—was not stimulated
Narouze
et al.69
15 Chronic CH SPGB via infrazygomatic approach
under fluoroscopic guidance
3 patients—no response
7 patients—pain reduction
3 patients—pain-free
2 patients—complete relief of pain
PPG and its Role in Pain Syndromes • 405
ing structures.88,89 More recently, electromagnetic
field-pulsed radiofrequency lesioning (EMF) has been
used. The current hypothesis on the mechanism of
EMF action is that the nerve membrane has a capacitor
function and EMF creates a high electric field,
which punches holes in the capacitor, thus blocking
transmission of stimuli through A-delta and C-fibers.90
The Intranasal Approach
The intranasal application of topical anesthetic is the
simplest and most tolerable technique. Cocaine or lidocaine
is placed on the nasopharyngeal mucosa posterior
to the middle turbinate, using a cotton-tipped
applicator. The zygomatic arch is taken as a reference,
because it is parallel to middle turbinate. However, the
topical anesthetic diffusion to the SPG is unpredictable,
and the SPGB is not durable.67 Nose abnormalities
can make this route difficult, uncertain, and
sometimes dangerous.11 Several modifications of the
traditional intranasal technique have been described.
Mingi91 modified the technique by using an intratracheal
cannula, instead of a cotton applicator, for better
patient tolerance. Varghese et al.92 combined both the
Table 4. Sphenopalatine ganglion blockade (SPGB) in the Treatment of Myofascial Pain (Fibromyalgia and Pain from
the Area of Head, Neck, and Shoulders)
Authors Patients Technique Efficacy
Scudds et al.79 61 Insertion of 2 soaking pledgets (lidocaine 4%
or sterile water) under direct vision,
6 times over a 3-week period
21 patients (35%) decrease in pain (> 30% of their
baseline value). Of these 21, 10 had received lid
and 11 placebo 4% lid is no better than
placebo in the treatment of chronic muscle pain
Ferrante et al.6 23 4% lidocaine, then TPI with 1% lidocaine, and
finally SPGB with saline placebo
or SPGB with saline placebo, then TPI with 1%
lidocaine, and finally SPGB with 4% lidocaine
SPGB with 4% lidocaine is no more efficacious
than placebo and less efficacious than administration
of standard trigger point injections (TPI)
Quevedo et al.80 2 One culturette swab dipped in 4% tetracaine,
in each nare, is advanced gently under the
inferior turbinate until it reaches the area of
the branch of the SPG. After 10 to
15 minutes, the culturettes are removed
Both patients experienced a 50% reduction in pain
level
Table 5. Sphenopalatine ganglion blockade (SPGB) in the Treatment of Other Pain Syndromes
Authors Patients Syndrome Technique Efficacy
Slade et al.83 13 Tear secretion Topical anesthesia (proparacaine 0.5%,
followed by lidocaine 2%)
Tear secretion was reduced substantially or
stopped completely after SPGB
Hennerberg
et al.84
17 Nicotine addiction Intranasal application of bupivacaine,
cocaine, or saline
Significantly fewer symptoms of physical
discomfort in the anesthetic treatment
groups
Prasanna and
Murthy82
30 Chronic vasomotor
rhinitis
Bilateral SPGB 29 patients—no recurrence of symptoms
(follow-up 12 to 20 months)
1 patient—symptom-free (for 8 months)
Robiony et al.85 12 Skeletal transverse
discrepancy of the
maxilla
Transcutaneous truncal anesthesia of
the maxillary nerve in association with
transmucosal anesthesia of the SPG
(lidocaine-prilocaine cream)
The maxillary anesthesia facilitated the
operations and reduced the amount of
postoperative pain
Hilinsky et al.86 1 Post-traumatic
pseudocerebrospinal
fluid rhinorrhea
Restore the normal autonomic
homeostasis in the nasal cavity either
with topical medicines or with surgical
procedures aimed at disruption of
parasympathetic preganglionic fibers
proximal to or at the SPG
Varghese et al.87 22 Head & neck
cancer pain
Nasal endoscopically guided neurolytic
SPGB with 6% phenol
17 patients had good immediate relief,
1 patient had partial relief, and 4 patients
reported inadequate relief
Prasanna5 1 Hyperhydrosis 2 SPGB at weekly intervals 50% reduction in the sweating with the
first block, and 90% improvement with
the second block. In a follow-up of
12 months, there was no recurrence.
Windsor and
Jahnke30
1 Eye pain due to
herpes keratitis
The patient experienced a month of relief
before the pain returned
406 • PIAGKOU ET AL.
principles of external approach for neurolytic and surface
SPGB for pain owing to advanced head and neck
cancer. Windsor and Jahnke30 attempted to control
the medication amount reaching the posterior nasopharynx
as well as provide better needle guidance.67
The increased danger to the nasal mucosa during needle
insertion led to the development of the transnasal
endoscopic technique, where the needle is inserted
under direct vision, using rigid sinuscope. Recently, Felisati
et al.66 described an endoscopic SPGB technique
that approaches the PPF via the lateral nasal wall.
Overall, intranasal topical application is not invasive
and should be attempted before submitting patients to
more invasive surgical approaches. Once a patient
experiences good pain relief, repeat blocks are performed
before finally deciding on SPG radiofrequency
lesioning (RF). A RTFC or EMF procedure can be performed
for prolonged analgesia. The use of phenol for
neurolysis via this approach is not recommended
because of the possibility of inadvertent spread of the
phenol into surrounding tissues.13
The Transoral Approach (Greater Palatine Foramen
Approach)
Injection through the pterygomaxillary fissure has
been commonly used by dentists for tooth extractions
and routine periapical surgery in the anterior maxillary
region. The intraoral route is the most direct, dif-
ficult, uncertain, and occasionally impossible to reach
the SPG11 and exhibits the greatest complications. Via
this approach, a curved dental needle passes through
the GPF at the posterior portion of the hard palate
just medial to the gum line opposite the third molar
tooth to reach the superior aspect of the PPF67 where
the main trunk of the maxillary division of the TN
lays.93 Paresthesia may be induced because the MN is
just cephalad to the SPG. The SPGB via this route is
extremely painful for the patient because the needle
passes through the canal that contains a nerve trunk,
artery, and vein and the anesthetic solution is deposited
into a space that has very little compliance.94
Because of the high vascularity of the region, an intraorbital
hematoma may result from injecting local anesthetic
in the terminal branches of the MA,77 which
follow the distribution of the terminal branches of the
MN. Infiltration of the PPF through the GPF approach
may result in infraorbital nerve injury and anesthesia
or injury of the orbital nerves.93 Another significant
disadvantage may be the difficulty in correctly identifying
the GPF, as the needle may not stop automatically
on the sphenoid bone and pass beyond the
sphenoid buttress to anesthetize other structures.67
Because the GPC and hard palate form an angle of
approximately 60,
95 it has been suggested to bend the
needle 45 to facilitate the passage of the needle
through the GPC and to prevent it from penetrating
too far into the PPF. There is no data on standard radiofrequency,
EMF lesioning, or phenol injection of
the SPG via this approach.90
The Infrazygomatic Arch (Lateral Infratemporal)
Approach
The infrazygomatic approach is necessary to perform
the majority of neurolysis techniques. The infrazygomatic
approach has been commonly performed blindly,
without C-arm fluoroscopic guidance, but it is highly
recommended using fluoroscopy. The approach is carried
out by using C-arm fluoroscopic guidance and a
direct lateral approach to place a cannula into the
superior portion of the PPF without requiring local
anesthetic to diffuse across mucous and bony membranes
and does not rely on secondary spread via the
nerves of the GPC.3,67
A transfacial transpterygomaxillary technique in the
region of foramen rotundum can be used to block the
MN and the SPG. For this, a spinal needle is inserted
at the intersection site of a vertical line extending
along the lateral orbital wall and a horizontal line tangential
to the lateral aspect of the inferior surface of
the zygomatic process of the maxilla. The procedure is
guided by CT scan to confirm the final needle position
or to guide fine adjustments in position. The used CT
scan helps avoid inadvertent passage of the needle
through the inferior orbital fissure into the intraorbital
contents or even the globe. This technique is indicated
for PIFP in the MN distribution. The advantage is that
allows the needle to be oriented more closely to the
axis of the foramen rotundum and the MN.58
COMPLICATIONS
The intimate relationship between the SPG and traversing
second-division trigeminal branches explains
the majority of potential complications following SPG
lesioning. SPGB is not a benign procedure, and infection
is possible if proper aseptic technique is not followed.
Nasal epistaxis can occur if the practitioner is
not careful when placing the cotton-tipped applicators
PPG and its Role in Pain Syndromes • 407
into the nasal passageway or if too much pressure is
applied from the needle to the lateral nasal wall.13
Epistaxis occurs more often during winter months,
when forced air heating may cause drying the nasal
mucosa. Complications associated with any invasive
craniocervical procedure, include hemorrhage, failure
to relieve pain, worsening of pain, nontarget nerve
injury, blindness, paralysis, stroke, seizures, and death,
although the risk of devastating complications in experienced
hands is remote.3 The use of chemical, surgical,
cryolysis, and thermocoagulation neurolysis
methods may not be the ideal strategy to treat noncancer
pain, because of the possibility of damaging vital
tissue.92
In contrast to the neurolytic procedures, pulsed radiofrequency
lesioning (PRF) provides long-term pain
relief without destroying neural tissue and has been
incorporated into existing percutaneous techniques for
craniofacial pain syndromes.96 In PRF, the impact of
electric field on the neuronal cells is well accepted; the
high-density electrical field generated around the RF
electrode tip is hypothesized to induce changes in the
nerve cells responsible for an altered pain signal transmission.
In PRF where the electrical current is delivered
in pulses, the heat generated is desipated during
the silent periods, suggesting that local heat induction
may not play a significant role. On the other hand,
PRF was found to induce a significant transient inhibition
of evoked excitatory transmission, and PRF activity
appears to be selective for small diameter (C and
Ad) axons that play a primary role in nociception.88
Radiofrequency lesioning (RF) of the SPG is performed
for 70 to 90 milliseconds at 67 to 80C. The mechanism
of action of RF has not been completely resolved.
There is some evidence that a heating effect induced by
the current may be involved, at least, in a part.97 However,
there is also growing evidence suggesting that the
high-density electrical field generated around the electrode
may alter neuronal activity and subsequently
alter pain transmission. PF can result in permanent or
more commonly temporary hypoesthesia, dysesthesia,
or differentiation pain in the palate, maxilla, or posterior
pharynx.98,99 Hematoma formation can occur after
injury of the MA large venous plexus, which lies
within the PPF following intravascular injection.100
(Figure 3). Cheek hematoma and infection are always
a possibility especially if the oral or nasal mucosa was
accidentally penetrated. Attention must be paid to the
total dose of local anesthetic used if toxic effects are to
be avoided.101
Complications associated with SPGB or neurolysis
include injury to the MN and MA, perforation of the
nasal wall and orbit, bradycardia, hemodynamic instability,
toxicity, nasal bleeding, facial hematoma and
numbness of the upper teeth, hard palate, or pharynx.
Intranasal sensory changes are rarely noticed. These
complications may be minimized if sharp needles are
replaced with curved-blunt needles and standard neurolysis
is replaced with pulsed radiofrequency lesioning.63
Recently, it has been noted in some patients,
reflex bradycardia (referred to as the ‘‘Konen reflex’’)
has been observed during radiofrequency treatment of
the SPG. In these cases, the lesioning was halted and
the bradycardia resolved.13,102
SUMMARY
Sphenopalatine ganglion blockade has been performed
for the past 90 years. The role of the SPG in the pathogenesis
of pain still remains debatable. Although the
effectiveness and duration of SPGB can vary, usually
depending on the patient, SPGB can be rewarding,
safe, and lasting intervention in the treatment of a
wide range of environmental sensitivity disorders and
illnesses. A thorough understanding of the anatomy
allows clinicians to predict correct needle placement
and may reduce the incidence of complications. The
PPG MN
Gasserian ganglion
MA
Figure 3. Anatomical lateral view of the pterygopalatine fossa
(PPF), which houses the maxillary artery (MA), the sphenopalatine
ganglion, and the MN. The (PPG) lies deeply in the fossa.
The sphenopalatine artery (SPA) is the end artery of the MA
located within the PPF and passes through the sphenopalatine
foramen on lateral nasal wall. Nasal bleeding from this artery is
potentially life threatening and may urgently require endonasal
endoscopic occlusion.100
Source: Adapted from Google Database (on line darmouth.edu).
408 • PIAGKOU ET AL.
search for the precise technique continues, and the currently
available evidence should be completed with
well-designed trials.
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Thursday, September 28, 2017

Neuromuscular offers effective treatment for headaches and migraines: The FDA Scandal that threatened this valuable treatment.



The FDA Scandal That Tried to Destroy Neuromuscular Dentistry.

Many of the original documents that detail the illegal actions at an FDA Hearing designed to destroy Neuromuscular Dentistry have become impossible to attain on the Internet.  I will remedy this with links to some important documents later in this post.

Meuromuscular Dentistry is expanding in leaps and bounds around the world with large active groups associated with ICCMO; The International College of CranioMandibular Orthopedics.

There are large active groups treating patients and do research in Argentina where Neuromuscular Dentistry is integrated in all four years of dental school.  In Italy where amazing research on Autonomic effects of neuromuscular dentistry is being published on a regular basis, in France where a prosthodontic program is very invested in neuromuscular program.

Both German and Japanese sections have a long strong history of advancements in neuromuscular dentistry.  There are new growing sections of IOCCMO in Russia and in India.  The next International ICCMO meeting will be held in Russia.

The information is available at Sleep and Health Journal.  It will be expanded over time.

https://www.sleepandhealth.com/articles-on-fda-abuses-of-myotronics/

Read articles on FDA abuses of Myotronics   https://www.sleepandhealth.com/wp-content/uploads/2017/09/Articles-on-FDA-abuses-of-Myotronics.pdf


Additional Msaterial excerpted from Congressional Oversight Committee  https://www.sleepandhealth.com/wp-content/uploads/2017/09/Additional-info-for-immediate-release.pdf
posted by Ira Shapira DDS at 7:47 PM

DOES CHRONIC TMJ AND MYOFASCIAL PAIN ALTER THE BRAIN?

A REMARKABLE ARTICLE WAS JUST PUBLISHED IN PAIN "Pain. 2010 May;149(2):222-8. Epub 2010 Mar 16.
Chronic myofascial temporomandibular pain is associated with neural abnormalities in the trigeminal and limbic systems."

It concerns a study done at Stanford University School of Medicine, Department of Anesthesia, Division of Pain Management.


Pain. 2010 May;149(2):222-8. Epub 2010 Mar 16.
Chronic myofascial temporomandibular pain is associated with neural abnormalities in the trigeminal and limbic systems.

Younger JW, Shen YF, Goddard G, Mackey SC.
Stanford University School of Medicine, Department of Anesthesia, Division of Pain Management, 780 Welch Rd., Suite 208E, Palo Alto, CA 94304, USA. jarred.younger@stanford.edu
Abstract

Myofascial pain of the temporomandibular region (M-TMD) is a common, but poorly understood chronic disorder. It is unknown whether the condition is a peripheral problem, or a disorder of the central nervous system (CNS). To investigate possible CNS substrates of M-TMD, we compared the brain morphology of 15 women with M-TMD to that of 15 age- and gender-matched healthy controls. High-resolution structural brain and brainstem scans were carried out using magnetic resonance imaging (MRI), and data were analyzed using a voxel-based morphometry approach. The M-TMD group evidenced decreased or increased gray matter volume compared to controls in several areas of the trigeminothalamocortical pathway, including brainstem trigeminal sensory nuclei, the thalamus, and the primary somatosensory cortex. In addition, M-TMD individuals showed increased gray matter volume compared to controls in limbic regions such as the posterior putamen, globus pallidus, and anterior insula. Within the M-TMD group, jaw pain, pain tolerance, and pain duration were differentially associated with brain and brainstem gray matter volume. Self-reported pain severity was associated with increased gray matter in the rostral anterior cingulate cortex and posterior cingulate. Sensitivity to pressure algometry was associated with decreased gray matter in the pons, corresponding to the trigeminal sensory nuclei. Longer pain duration was associated with greater gray matter in the posterior cingulate, hippocampus, midbrain, and cerebellum. The pattern of gray matter abnormality found in M-TMD individuals suggests the involvement of trigeminal and limbic system dysregulation, as well as potential somatotopic reorganization in the putamen, thalamus, and somatosensory cortex.

Prolotherapy and TMJ: Strengthening the tissues of the TMJoint (TMJ) to promote healing and stability.

Wikipedia defines Prolotherapy as:  "Prolotherapy, also called proliferation therapy or regenerative injection therapy, was originally defined by George S. Hackett, M.D. in 1956, as “The rehabilitation of an incompetent structure by the generation of new cellular tissue”. He “applied the term prolotherapy from the word “proli’” (Latin) meaning offspring; “proliferate” -to produce new cells in rapid succession."

The basic premise is that you can strengthen ligaments and tendons by causing them to grow more collage or to regenerate. 

Prolotherapy is an important aspect of some patients TMJ Treatment.  Tightening of ligaments can aid in capturing a disc and preventing clicking and locking as part of neuromuscular treatment.

Chicago: Best TMJ Treatment

This was originally published as a blog on www.ThinkBetterLife.com

The Best treatment for a TMJ disorder is very dependent on the exact symptoms and causes of the TMJ disorder in a particular patient. Determining the best treatment for an individual patient is usually done during a face to face visit but I can give several guidelines here.
Night Guard Treatment:
If you only have pain at night or just after awakening you are probably a good candidate for a Bruxism Appliance. These are designed to protect the teeth during nocturnal grind or bruxism.
This type of appliance is very effective for people who grind their teeth but can frequently cause more pain in patients who clench because it can createmore forces during clenching.
Clenching and grinding of the teeth during sleep is often associated with Sleep Disordered Breathing, including Snoring, RERA, UARS or Upper Airway Resistance Syndrome, Hypopnea or Apnea. These are dangerous conditions that can be made worse in some patients by a typical night guard.
Morning Frontal Headache and daytime tiredness are associated with sleep disordered breathing. Dentists trained in treating sleep disordered breathing can be found at AADSM.org .I have taught hundreds of dentists the basics of sleep apnea treatment.  Ideally, a diplomate of the American Board of Dental Sleep Medicine is your first choice.
The NHLBI or National Heart Lung and Blood Institute considers Sleep Apnea to be a TMJ Disorder.
ACUTE CLOSE-LOCK
Patients who have an acute close-lock of one or both TMJoints are Emergency patients. The wrong treatment can lead to permanent disability and the development of chronic pain syndromes.  Short term treatment is described below, long term stabilization will be discussed later.
An acute close-lock of one or both TMJoints can be evident upon wakening or may occur during the day. This is a type of Internal Derangement of the TMJoint. Patients who have chronic clicking or popping of one or both joints can have the disk get stuck anterior to the condyle of the mandible.
The symptoms for a unilateral close-lock of the TMJoint is reduced opening and sharp pain in the joint on the locked side. Attempting to open further gives increased pain and the jaw deviates to the side of the lock. If clicking was present previously it usually will be gone on the effected side.
The disk or meniscus is displaced and the condyle is pressing on the very delicate Retrodiscal Laminate. Trying to force the jaw open can permanently damage this important tissue.
Emergency Rooms are notorious for forcing the jaw open and causing increased pain and damage. For several years I taught emergency room physicians how to reduce close-lock dislocations. It is essential to support the jaw and prevent full closure or even a properly reduced joint can easily relock.
Many dentists and oral surgeons will place patients on a soft diet and prescribe non-steroidal anti-inflamatories such as Advil, Alieve or Aspirin. This is extremely risky approach to treating a close-lock. The longer the lock continues the more likelihood of permanent joint damage to the disk and retrodiscal lamina and the development of chronic pain.
The best approach is to reduce the dislocation as soon as possible and immediately supporting the bite with a temporary support to prevent recurrent locking. Unfortunately most dentists have no idea how to reduce a locked joint.  The reduction can be done with jaw manipulation either awake or sedated.  Acute close-lock can often be reduced easily by stimulation of specific reflexes in the jaw and pharynx.
Various appliances can be used to prevent damage and ease the reduction of more difficult locks these include unilateral pivotal splints for a lock in just one joint or a Rocobado spring loaded appliance for bilateral locks
Acute Open-Lock Dislocation or Subluxation
This is caused by a hyperextension of the jaw during opening.  It can happen from a yawn or biting ito very thick sandwich.  It can also occur immediately following a motor vehicle accident, usually being rear-ended.  It can also happen after difficult dental procedures and/or extractions especially of lower molars.
The condyle of the mandible actually moves out of the norman joint position and extends past the eminence where it gets stuck.  The patient will usually notice pain on the effected side and only 1 or 2 back teeth will touch on closing.  This tends to be frightening initially.This is again an Emergency, however this is easily treated at the ER in the hospital.
Patients with open locks need to learn not to hyperextend and to control maximum opening.  Prolotherapy can be used to tighten up the ligaments and tendons for a more stable joint that cannot hyperextend.  Surgery is another option usually best avoided.
Cheerleaders Joint
This is another condition that occurs frequently in cheerleaders, hence the name.  Shouting and cheering for a long time hyperextends the joint and it can create an open lock situation described above.  Sometime this will self reduce but there can be tremendous pain with jaw movement.  This is primarily muscle overuse pain and rest, stretching and anti-inflammatory medications is the best road.  It is vitally important to rule out close-lock and open lock conditions to avoid problems.
Post Dental Treatment:  Medial Pterygoid Myositis, Myalgia/Myosits
These conditions can occur following dental work and can be secondary to injections, inflammation joint or muscle tearing or stretching etc.
There is very little opening similar to a close lock but this is due to tight shortened muscles.  Time and anti-inflamatories can help.    There are variations of what is the cause, Muscle Splinting is a normal physiologic process where the muscles tighten up to protect an injured area.  Unfortunately, this can become chronic muscle shortening with muscle tightness, taut bands and trigger points.   Muscle Spasm is usually very painful but short in duration.  It is like a "Charlie Horse" of the jaw muscles.  Myositis is the slowest to resolve and is related to inflammatory changes in the muscle and can be quite painful.  Time, anti-inflamatories and stretching while icing helps.
FIBROMYALGIA AND MYOFASCIAL PAIN AND DYSFUNTION are two specific groups of muscle pain that must be included in this discussion of what is the best treatment.
All of the above conditions respond extremely well to Ultra Low Frequency TENS (ULF-TENS)  There are two units available for ULF-TENS the Myomonitor from Myotronics and and the BioTens from BioResearch.  No other TENS should be utilized.
These conditions also respond well to physical therapy, massage therapy and other manual techniques as well as ultrasound, interferential and micro current.  An Aqualizer Appliance ™ can be excellent short term treatment.
It is essential to determine if a close-lock internal derangement is also present.  Delay can lead to permanent damage.
Long-Term Chronic TMJ Dysfunction
TMJ is often called the Great Imposter due to the many associated symptoms that accompany the TMD
There are numerous types of appliances available including centric occlusion, centric relation and neuromuscular orthotics.  There is a specialized type of appliance called an NTI which has specific though limited uses.  Appliance can be made for the upper or lower arch.  Ideally, an appliance should always look and feel comfortable for 24/7 wear including for using while eating even if it is not to be worn all the time.  Frequently separate appliances are needed to treat sleep disorders breathing.
Doctors treating difficult cases should have additional training and expertise in a wide range of fields.  I suggest visiting doctors who are a Diplomate of The  American Academy of Pain Management and the American Board of Dental Sleep Medicine.  Neuromuscular Dentists should be member of ICCMO, the International College of CranioMandibular Orthopedics.  Centric relation dentists should belong to The American Equilibration Society though the best dentists belong to both groups and look at all aspects of treatment.
There are treatments that are often essential elements of complete treatment including management of trigger points with Spray and Stretch Techniques, Trigger Point Injections and /or manual techniques, Utilization of SPG or Sphenopalatine Ganglion  Blocks, and coordination with Specialists in dealing with the Occipital-Atlas-Axis joints, usually Atlas-Orthoganol or NUCCA Chiropracters or Osteopaths.
Jaw problems are related to breathing, airway and posture so experience in DNA Appliances is very helpful for TMD dentists.  Ideally, dentists treating TMJ disorders have a method of non-invasively seeing jaw function with computerized mandibular scans from Myotronics or BioResearch.
An absolute requirement of any doctor treating TMJ disorders is one who sets up time for  a consultation reviewing your medical history, evaluating what has previously been done and how it worked.  Your doctor should be able to clearly explain how all the different symptoms are related.  The best TMJ doctors can usually relieve muscle and headache pain temporarily while you are in the office, welcome your questions make you feel comfortable and never talk down to you.
The best TMJ Dentists are people you feel comfortable talking to.  The first visit will usually start in the consult room not the dental chair.  Acute close locks will usually quickly move to treatment room.  It is vitally important that you do not feel intimidated by your doctor, the best results occur when the patient and doctor work as a team to address problems.
Ideally, no permanent changes are made initially but rather treatment begins with a diagnostic orthotic. The goal of initial treatment is to relieve symptoms as quickly as possible and to understand the underlying etiology of the problem.  Equilibration of the teeth is usually avoided until the patient is comfortable and a treatment plan is accepted.  Wanton grinding on teeth can create new problems and it is hard to "ungrind a tooth"  That said, brand new dental work that caused the problem sometime may need adjustment.  The safest area of adjust is on the front teeth if they hit first but a diagnostic orthotic is still the best starting point.
Long term treatment should be discussed at the initial consultation but is only considered after resolution of pain and dysfunction.

The TMJ Association and The TMD Alliance:

An open letter to the TMJ Association

Review of  the TMJ Association         
TMJ Association Ltd
13625 Bishop's Woods Ct # 101, Brookfield, WI

  I am currently Chair of the Alliance of TMD Organizations which represents multiple groups involved in treatment of TMD.  When we contacted the TMJ Association they had no interest in working with us to better the health of all TMD patients.  The following is directly from the website of the TMD Alliance.

Alliance of TMD Organizations Fundamental Principles

Founded in 1995 on behalf of patients’ well-being, the Alliance of TMD Organizations’ mission is to support and protect the right and freedom of clinicians to practice in the field of TMD within the scope of their care, skill, judgment, and scientific information.

The Alliance of TMD Organizations has been created to represent the broad interests of professional organizations and their member practitioners who understand the importance of effective diagnosis and treatment of cranio-oro-facial disorders.
1. The Alliance of TMD Organizations supports ethical and professional patient centered care.

2. Treatment should be based upon individual patient needs.

3. TMD and associated facial pain disorders/diseases may encompass physical, functional, cognitive, and psycho-social factors all of which may contribute to patient’s symptoms and complaints. Dental occlusion may have a significant role in TMD; as a cause, precipitating, and/or perpetuating factor. Any or all aspects may be taken into consideration when developing diagnoses and treatments accepting that TMD and associated co-morbidities including other pain disorders may be multi-factorial in nature.

4. Diagnoses and treatments should be based upon scientific information in conjunction with the skill, knowledge, and judgment of the providing clinician within the scope of their care.

5. Patient care should progress from initially minimally invasive treatment with gradations of increased intervention weighing risk versus benefit within reasonable standards of care.

6. The diagnosis and treatment of TMD should be considered an emerging science accepting that approaches for diagnoses and treatments may change based upon scientific evidence, clinical evidence. Reasonable standards of care should always be considered in the differential diagnosis of all head, neck and facial pain.

7. Efforts should be made to allow for continuity of care between multi-disciplinary health care providers.

8. Although not gender specific, TMD symptoms and associated pain disorders are gender biased and found to be reported predominately in females.

9. Since TMD and associated pain disorders are by nature gender biased affecting a significant portion of the female population, they should also be considered a women’s health issue.

10. Third party payers should not discriminate based upon gender, body part, location of symptoms, specific dysfunction, or professional degree of the licensed health care provider.

These 10 basic principles were developed by the majority of the representatives of TMD Alliance members.

I understand that Ms Cowley the founder of the organization was the victim of a surgical disaster but her organization actually disuades patients from care that could improve their quality of life.

I believe that if the TMJ Association is really vested in the best interest of all patients then  the TMJA should accept the offer to work with the TMD Alliance and its member organizations.

This is an open invitation to the TMJ Association it to work with the dentists who treat TMJ disorders, the individual groups that further the scientific aims of those groups and with the TMD Alliance that represents the intrests of patients with TMJ Dysfunction.

Ira L Shapira DDS, D,ABDSM, D,AAPM, FICCMO
Chair, Alliance of TMD Organizations