Chronic Head and Neck Pain is difficult and frequently disabling but sometimes the answers are easy with the right combination of treatment. To understand what goes wrong with treatment you need to understand the basic principles that determine success. There are over 100 different types or groups of headaches. (reference below). There is excellent evidence that Migraine in women requires multiple treatments. (abstact below)
All headaches and migraines are mediated by the trigeminal nervous system and to treating and eliminate these types of pain you must address the trigeminal nervous system.
Patient Testimonial Videos: https://www.youtube.com/channel/UCk9Bfz6pklC7_UluWFHzLrg/videos
The second essential aspect of treating head and neck pain is to understand, map out and treat the myofascial aspects of head and neck pain. These include taut muscle bands, trigger points and most important the referral patterns of active trigger points. These myofascial trigger points are connected to the multiple Cranial nerves including the Trigeminal Nerve, the Facial Nerve and the Accessory nerves. (see abstract below “Self Reported Migraine and Chronic Fatigue Syndrome are More Prevalent in People with Myofascial…..Temporomandibular Disorders)). There are studies that show conbined treatment of TMJ disorders and Migraines give far better results in resolving migraines.
Unfortunately very few professionals address both Nervous and myofascial aspects of these underlying sources of chronic head and neck pain. Most physicians have never become comfortable recognizing which issues require input from dental professionals, the exception being ENT’s who are the physicians most in tun to recognizing TMJ disorders. Costen, an ENT in St Louis made the original description of TMJ disorders which were initially called Costen’s Syndrome.
There is another extremely important piece to resolving head and neck pain and that is the Autonomic Nervous System. The Autonomic nervous system has two components, the Sympathetic nervous system and the Parasympathetic nervous system. The autonomic nervous system is an essential key to successful treatment. This is a chronic pain patient who just received a SPG Block for migraine. https://www.youtube.com/watch?v=DCPLDRJ2twg
Most long term and chronic pain pain is mediated and maintained by the Sympathetic nervous system. This is especially true of head and neck pain. There is an extremely important structure called the Sphenopalatine Ganglion(SPG) that is located on the maxillary branch of the trigeminal nerve. The SPG is the largest Parasympathetic Ganglia of the head but it also has sympathetic fibers than run thru it from the superior cervical chain.
The Sympathetic Nervous System also controls the “Fight or Flight Reflex”, which is a survival reflex. If we are in imminent danger it prepares us to fight or to run. It is a perfect response to acute stress with high risk. Unfortunately , this same reflex wreaks havoc with chronic stress and often leads to myofascial pain issues, TMJ disorders, Jaw Pain, Tension headaches and migraines.
The Parasympathetic nervous system is the opposite of the sympathetic response. It controls the “Feed and Breed” or “Eat and Digest” reflexes. these are the feelings we feel when we play with babies, puppies or kittens and this turns off the fight or flight reflex.
The autonomic nervous system in disarray can create sleep and anxiety problems, depression and panic attacks and in general leads to higher levels of head and neck pain. This is a video of a patient who received first SPG Block for Anxiety. https://www.youtube.com/watch?v=0FUxuBO4YEI
The Sphenopalatine Ganglion Block is an amazing procedure that can reset the Autonomic Nervous System and is extremely effective at preventing and treating all types of headaches and Migraines especially the Autonomic Cephalgias and is considered the treatment of choice for cluster headaches. There are multiple avenues available for blocking the SPG. The most effective method is self administered SPG Blocks that patients can give themselves as needed. The cotton-tipped nasal catheters are a godsend to many patients. The Sphenocath, Allevio and TX360 are usually administered in physicians offices but patients can be taught to self administer those as well.
SPG Blocks also turn off anxiety and depression and instill a general feeling of well being. They have also show effectiveness for a wide variety of disorder, including Fibromyalgia . This is a video of a Fibromyalgia Patient after her first SPG Block. https://www.youtube.com/watch?v=A5xUFtuZe_Y
SPG Blocks were first described by Sluder in 1908. His description of “Sluder’s Neuralgia” is often thought to be an early description of TMD, Migraine or Cluster headache. I have been using this amazing block for over 30 years. The next video is a patient who became a physician after experiencing relief from an SPG Block. He found out on the day of the video that the treatment that changed his life forever was a SPG Block. https://www.youtube.com/watch?v=Sn46l_nH9-A
The Trigeminal Nerve, often called the Dentist’s nerve is best addressed by a neuromuscular dentist who understands the neurophysiology of the entire system. It is the single largest neural input to the brain and after amplification in the Reticular Activating System accounts for over 50% of all input to the brain. It is important to understand the structures that this nerve innervates to understand why treatment that does not focus on neural input from the masticatory system are almost doomed to fail. The Trigeminal Nerve ges to the Jaw Muscles, The Jaw Joints or TemporoMandibular Joints (TM Joints or TMJ), the dental pul, the gingiva and mucasa of the mouth (the gums) the anterior 2/3 of the tongue, the lining of the sinuses, the lining of the nose, the tensor of the ear drum (tensor veli tympani muscle) and the muscle that opens and closes the eustacian tubes (the tensor veli palatini) that also helps in swallowing and preventing food from entering the nose. More important is the proprioceptive input through the periodontal ligaments of the teeth which has at least 29 different neural receptors and is the largest proprioceptive input into the brain via the mesencephalic nucleus. The contribution to headaches, migraines and autonomic cephalgias is because the trigeminal nerve controls the blood flow to the anterior 2/3 of the meninges of the brain. The connections between TMJ disorders and jaw disorders are very well known. This is a patient whose neck pain was relieved thru TMJ treatment. https://www.youtube.com/watch?v=qQpDZtztgFc
There is excellent research in Orofacial Pain showing that migraine does not improve unless TMJD is also treated. See the abstact below on Comorbid Migraine and Temporomandibular Disorders the concludes “In women with TMD and migraine, migraine significantly improved only when both conditions were treated. The best treatment choice for TMD pain in women with migraine is yet to be defined.”
Suffering from Chronic Head and Neck Pain? There are over 100 additional patient testimonial videos at my toutube channel:
The Trigeminothalamic pain network is the central hub of headache disorders as outlined in the excellent article. “Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, cortical spreading depression, sensitization, and modulation of pain.” (PubMed Abstract below) This apatient is a Doctor who had a Sphenopalatine Ganglion Block done by me at one of my lectures and experienced dramatic pain relief.
TMJ disorders and Sleep Disorders are also associated with the same complex of nerves and tissues. Sleep disorders increase pain, anxiety and depression. Every single patient who has head and neck pain should read the report “Cardiovascual and Sleep Related Consequences of Temporomandibular Disorders. https://www.nhlbi.nih.gov/files/docs/workshops/tmj_wksp.pdf
All of the vascular and neuronal spread of headaches begins with nociception into the Trigeminal Nervous System which is addressed by neuromuscular dentistry. In addition the Myomonitor, the ULF-TENS device utilized in Neuromuscular Dentistry also acts as a Sphenopalatine Ganglion Stimulator. The neuromuscular approach to craniomandibular disorders addresses all of the relevant issues needed to treat and eliminate a large majority of head and neck pain problems.problems.
The International Classification of Headache Disorders, 3rd edition (beta version).
Migraine pathophysiology: anatomy of the trigeminovascular pathway and associated neurological symptoms, CSD, sensitization and modulation of pain.
Scientific evidence support the notion that migraine pathophysiology involves inherited alteration of brain excitability, intracranial arterial dilatation, recurrent activation and sensitization of the trigeminovascular pathway, and consequential structural and functional changes in genetically susceptible individuals. Evidence of altered brain excitability emerged from clinical and preclinical investigation of sensory auras, ictal and interictal hypersensitivity to visual, auditory and olfactory stimulation, and reduced activation of descending inhibitory pain pathways. Data supporting the activation and sensitization of the trigeminovascular system include the progressive development of cephalic and whole-body cutaneous allodynia during a migraine attack. Also, structural and functional alterations include the presence of subcortical white mater lesions, thickening of cortical areas involved in processing sensory information, and cortical neuroplastic changes induced by cortical spreading depression. Here, we review recent anatomical data on the trigeminovascular pathway and its activation by cortical spreading depression, a novel understanding of the neural substrate of migraine-type photophobia, and modulation of the trigeminovascular pathway by the brainstem, hypothalamus and cortex.
Self-Reported Migraine and Chronic Fatigue Syndrome Are More Prevalent in People with Myofascial vs Nonmyofascial Temporomandibular Disorders.
To compare the number of comorbidities and the prevalence of five specific comorbidities in people who have temporomandibulardisorders (TMD) with or without myofascial pain.
This cross-sectional study included 180 patients seeking TMD treatment in Boston and Montreal hospitals. A self-administered questionnaire was used to collect information on sociodemographic and behavioral factors, as well as the presence of the following five comorbidities: migraine, chronic fatigue syndrome, irritable bowel syndrome, interstitial cystitis, and restless leg syndrome. TMD was diagnosed using the Research Diagnostic Criteria for TMD. Chi-square and Student t tests were used for categorical and continuous variables, respectively, to test for differences between myofascial (n = 121) and nonmyofascial (n = 59) TMD groups. Multiple logistic regression analysis was used to compare the type and number of self-reported comorbidities in both groups, controlling for confounding variables.
The following were found to be significantly higher in the myofascial TMD group than in the nonmyofascial TMD group: self-reported migraine (55% vs 28%, P = .001), chronic fatigue syndrome (19% vs 5%, P = .01), and the mean total number of comorbidities (1.30 vs 0.83, P = .01).
Individuals with myofascial TMD had a higher prevalence of self-reported migraine and chronic fatigue syndrome than those with nonmyofascial TMD.
Treatment of comorbid migraine and temporomandibular disorders: a factorial, double-blind, randomized, placebo-controlled study.
To investigate the effectiveness of single and concomitant treatment of migraine and temporomandibulardisorders (TMD) in women with the comorbidity.
Eligible female patients met International Classification of Headache Disorders, second edition (ICHD-2) criteria for migraine with or without aura and the Research Diagnostic Criteria for myofascial TMD (Grade ll or lll). After a run-in period (30 days), women with both migraine and TMD were enrolled into a four-arm, double-blind, placebo-controlled, factorial study testing the separate and joint effects of a migrainetreatment (propranolol 90 mg) and a TMD treatment (stabilization splint [SS]) in four groups of patients. The four treatment groups were propranolol and SS (n = 22); propranolol placebo and SS (n = 23); propranolol and non-occlusal splint (NOS) (n = 23); and propranolol placebo and NOS (n = 21). The primary endpoint for migrainewas change in headache days from baseline to the third month, and the secondary endpoint was change in days with at least moderate headache in the same period. The TMD endpoints included pain threshold and mandibular vertical range of motion. Data were analyzed using analysis of variance (ANOVA, Dunn’s post-hoc test) or Kruskal-Wallis test.
For the primary endpoint, in intention-to-treat (ITT) analyses (n = 94), propranolol and SS were associated with a nonsignificant reduction in the number of headache days, relative to all other groups. For per-protocol (PP) Completer analyses (n = 89), differences in the number of headache days reached significance (P < .05). The propranolol and SS group was significantly superior to the other groups on all other headache endpoints and in disability, in both ITT and PP analyses. No significant differences among groups were seen for the TMD parameters.
In women with TMD and migraine, migraine significantly improved only when both conditions were treated. The best treatment choice for TMD pain in women with migraine is yet to be defined.