People have suffered with headaches for millennia. The first documented mention of headaches was found in the hieroglyphs of ancient Egypt. They believed that a headache was punishment from the Gods but by the time of the ancient Greeks, even Zeus, the leader of the Gods, suffered with headaches. Our understanding of headaches and its treatment has changed, since then, but headaches continue to be a major problem for many. In large scale epidemiological studies of health, headache was the more frequently reported symptom in the general population, then common colds. The incidence of headache varies amongst the studies, but range from 50-90% of the population. All the studies agree that the frequency of headaches is greater in females.1
There is abundant evidence of the comorbidity of headaches and temporomandibular disorders in many patients. In TMD clinics, 70% of patients have headaches, usually tension type, but migraine as well.2 In headache clinics 55% of patients had signs of TMD. Of those with severe, recurrent headaches 66% developed myogenous or arthrogenous types of TMDs which they had not noticed prior to the onset of those headaches.3 Both groups also complained of neck and shoulder pain, in varying degrees and both exhibited similar amounts of pericranial muscle tenderness.4 In fact, in those with internal derangements of the TMJ and increased masticatory muscle tenderness, there were “silent” cervical spinal disorders and significantly more pain with palpation of the neck muscles.5
Patients who suffer from persistent headache often have difficulty in obtaining a clear diagnosis. There are many possible sources of pain in the head and neck, and the referral of pain from distant sites is common. According to the International Headache Society, head and face pain not caused by disease or trauma, results from headaches or temporomandibular disorders.
TMD is the most frequently overlooked etiological factor in headache,6 because of the physician’s limited understanding of this condition. This is in spite of the fact most people in a general population show signs of TMD and 10-12% actually need treatment.7 The number requiring treatment increases significantly when there has been trauma to the head, neck or face. Because the diagnosis of TMD is ignored or delayed, as a source of the symptoms, the patient continues to suffer. Therefore, every patient with persistent headache,8 especially those with tension type and migraine or resulting from trauma, should have an assessment of the stomatognathic system.9 It should be conducted by a dentist who is experience in treating complex craniomandibular conditions.
HEADACHES
The International Headache Society has developed a classification of headaches which lists more than a hundred types. However, they include a disclaimer that, their diagnostic criteria are not specific enough to completely allow for evidence based treatment of the various headaches.
The primary headaches are tension type, migraine and other trigeminal autonomic cephalgias (cluster headache, paroxysmal hemicrania, short unilateral neuralgiform headache with conjunctival injection and tearing SUNCT). They are described as benign, vascular, dysfunctional headaches. They are not fatal, always involve activation of the trigemino-vascular system and are caused by dysfunction of structurally normal tissues.
Secondary headaches are classified as those caused by an underlying organic condition and are a symptom of a recognized process,10 i.e. tumor, stroke, trauma, TMD etc. In order for a diagnosis of secondary headache to be confirmed, it must be greatly improved with treatment of the causative disorder and within a specific period of time.
There are many examples of headaches either disappearing or being substantially reduced with the treatment of a concomitant temporomandibular disorders. In one study of patients with temporomandibular disc disfigurement and headache, the injection of 12.5 units of a type A, Botulism toxin into the joint, reduced both the jaw pain and the headache.11 In another, patients who underwent various arthroscopic surgeries, found relief of their complaints of headache, neck and shoulder pain within 24 hours.12 In a simultaneous study of patients with similar symptoms, who received an intraoral orthotic and conservative modalities, 31.8% had a similar result.13 These findings suggest that, through central neuronal processing, temporomandibular disorders play a substantial role in headache.
When a primary headache is exacerbated by another disorder a diagnosis of primary and secondary headache can be made.14 Temporomandibular Disorder Headache is most frequently associated with tension type headaches and to a lesser degree with migraine.
PATHOGENISIS OF HEADACHE
According to Edmeads,15 headaches occur when pain sensitive structures in the head (and sometimes in the neck) are disturbed by malfunction or disease. The pain sensitive structures in the head are the skin, muscles, nerves and blood vessels of the scalp, the eyes, sinuses, teeth, jaw joints and the meninges of the brain and their blood vessels. The brain tissue itself is not sensitive to pain. Pain in the head and neck is mediated by several nerves; the trigeminal, nervus intermedius, glossopharyngeal and vagus nerves and the upper cervical roots. The trigeminal plays the major role in headaches. It is one of largest and most complex nerves in the entire body and utilizes 40% of the brains processing capacity. It provides sensory innervation to most of the pain sensitive structures, mentioned, above and motor innervation to the masticatory muscles.
Primary headaches results from stimulation of the nociceptive a delta and c fibers of the meninges and their blood vessels. All three branches of the trigeminal innervate these structures. The middle meningeal, a branch of maxillary nerve, is the largest of the meningeal arteries and supplies the major blood supply to the dura mater of the middle cranial fossa.
The recurrent meningeal, a branch of the mandibular nerve, and a branch of the Vagus also innervates this area. The ophthalmic innervates both the intra and extra cranial, parietal and frontal tissue.16 The trigeminal also innervates the Circle of Willis and the extra cranial arteries that can carry pain from those structures.17 The C1-3 spinal nerves innervate the vertebral and internal carotid arteries and the dura of the upper spinal cord and posterior cranial fossa.18 The blood vessels supplying the meninges anastomose freely ipsa and contra laterally,19 allowing for the spread of the pain.
All of these nociceptive neurons project to the trigeminal spinal nucleus (TSN) that lies in the spine between the second and fourth cervical vertebrae, although some animal studies have shown it reaching farther down in the spinal cord.20 The convergence of the fibers of C 1-2 with the trigeminal nerve is so dense that they act together, as one functional unit, to process nociceptive information from the craniofacial and cervical tissues.21 This central mechanism at the second neuron level22 allows for the spread of pain between the head neck and face, and explains the comorbid symptoms often seen in headache and temporomandibular disorders.
Cranial nerves VII, IX, X, XI and XII also synapse in the trigeminal spinal nucleus. VII, IX and X also have synaptic connections with each other. This vast interneuron network expands the scope of pain referral and complicates the diagnosis of orofacial, cervical and headache complaints. For example, in a recent study at the University of Toronto, electrical stimulation of the hypoglossal nerve activated 50% of the C1-2 dorsal horn neurons, resulting in pain in the neck.23
From the TSN, all these nocicep
tive transmissions project to the hypothalamus and then to cerebral cortex, where the perception of pain is appreciated.
MIGRAINE AND TENSION TYPE HEADACHE
Many believe that migraine and tension type headaches are the same entity, but at opposite ends of the pain spectrum, with milder pain in tension type. Recent studies have shown that migraine and tension type headaches are initiated by altered function of higher brain centres.24 This alteration occurs from stimulation by a variety of catalysts. In acute and chronic migraine the mid brain pons25 and the periaquaductal gray play crucial roles.26 In tension type headache it is the posterior hypothalamus and the parasympathetic reflex. Other precipitating factors are abnormalities in central pain processing and descending pain modulation,27 and changes in brain chemistry.28
Once stimulated these brain centres release algogenic substances, like neurokinin A, CGRP, substance P, nitric oxide and others into the dura, that activate, or alter the perception of activation, of the trigeminal perivascular unmyelinated nerve axons. This results in a sterile neurogenic inflammation and vasodilation of the blood vessels and is considered to be the pivotal component of the pathophysiology of migraine.29
The presence of nitric oxide30 is also a significant factor. It is a powerful vasodilator and appears to be a crucial molecule in primary headaches.31 It has a direct effect on the perivascular nociceptors in the head, and enhances the vasodilation. It is the vasodilation that causes the headache and promotes the development of central sensitization in the nucleus caudalis32 of the TSN. The central sensitization causes allodynia (innocuous stimuli perceived as uncomfortable and painful) resulting in tenderness of the pericranial musculature that is always present in migraine and tension type headache.
This orthodromic (nociceptive transmission from the periphery to the central nervous system) stimulation of the TSN can result in antidromic (the reverse) activation causing algogenic and vasoactive substances to again be released from the perivascular nociceptive nerves. This continual feedback loop will perpetuate the headache for hours.
TENSION TYPE HEADACHE
Because tension type headache is the headache most affected by temporomandibular disorders33 it deserves special consideration in this discussion. There is a positive correlation between tension type headache oro-mandibular dysfunction, anxiety, stress, and disturbances of the masticatory muscles, from any cause, including bruxism, a blow to the head or “whiplash injury”.34 It is the most common and least studied headache, affecting 88% of females and 69% of males in Canada, with varying frequency and intensity.
There are two types of tension type headache, episodic, in which peripheral pain mechanisms play a role and chronic (more than 15 days/month) in which. Central mechanisms are at work. The most significant abnormal finding is tenderness with palpation of the pericranial muscles, that increases proportionately as the pain increases. Even in the headache free state these people have increased pericranial muscle tenderness.35 They are more likely to occur in older people and in women who have had previous migraine or tension type headaches and are the headache most frequently associated with whiplash injuries. Chronic tension type headache has a high socio-economic impact because it results in significant quality of life impairments.36
BRUXISM AND HEADACHE
In general, bruxers have increased levels of pain in their jaw, face, throat, back and shoulders. When bruxing, their neck muscle activity can be 1.4 – 3.3 times greater than in their resting state.37 Seventy percent of bruxers have headache.38
In all headache patients, bruxism and increased tongue pressure, against the teeth, is much more prevalent39 and plays a significant role in the onset and exacerbation of both migraine and tension type headaches. In migraineurs it was found, that in many, the jaw clenching muscles were 70% larger than controls. and with tension type headache the temporalis muscles contracts 14 times more often, then controls, while asleep.40
In a study of headache sufferers who clench, it was found that clenching for thirty minutes at 30% of the maximum biting force caused an immediate headache in 63% of migraineurs,41 and a headache, within 24 hours, in 69% of those with tension type headaches.42 It is thought that bruxism may be an important factor in converting episodic tension type headache to chronic.43 With the use an intra-oral stabilization occlusal splint the intensity of most headaches and frequency of tension type headache, can be reduced by 70 – 80%,44 both in the short and long term.45
THE EFFECT OF TEMPOROMANDIBULAR DISORDERS ON HEADACHE
The masseter muscles show an essential and significant relationship to frequent headache.46 Internal derangements in the TMJs will increase the activity in the masseter (and temporalis) muscles whenever the condyle slides over the posterior band of the disc. This is significant, especially with the masseter, because it shows an essential and significant relationship to frequent headaches. Deep pain in the TMJs will also contribute to headache pain.
It has been shown that masticatory muscle pain to palpation does have a distinct relationship to headaches47 and the greater the muscle pain, the greater the headache. Many trigeminal free small diameter afferent nerve endings respond to deep pain in the masticatory muscles and TM joints. When stimulated there is an afferent discharge to the TSN. The subnucleus interpolaris has been identified as the major recipient for trigeminal ganglionic input from the jaw muscles.48 It contains neurons with nociceptive properties similar to those of the nucleus caudalis.49 Masseteric inflammation induces c-fos expression at the trigeminal interpolaris/caudalis transition zone50 bilaterally and in the tractus soliterius, ventrolateral medulla and inferior olivary nucleus.51
Trigeminal neurons are bipolar, having terminations on the cranial vessels, meninges etc., and others on second order neurons in the dorsal horn of the spinal cord and medulla.52 Therefore, one could reasonably conclude that deep orofacial pain, of myogenous or arthrogenous origin, can induce antidromic stimulation of the perivascular nociceptors in the meninges and precipitate or perpetuate headaches.
CONCLUSION
The practice of modern medicine and dentistry is grounded upon evidence based diagnostic and treatment modalities. In my opinion, the scientific evidence provided here shows that temporomandibular disorders must be included in the differential diagnosis of persistent headaches. If this diagnosis is made early on, prolonged patient suffering may be reduced.
Dr. B.M. Laibovitz maintains a practice limited to orofacial pain & temporomandibular disorders. He is a Fellow Academy of General Dentistry; Fellow: Academy of Dentistry International Diplomate; American Academy of Pain Mgmt. Diplomate; American Board of Orofacial Pain.
Oral Health welcomes this original article.
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