Headaches Revisited

Andrea M. Trescot, M.D.
Andrea Trescot, M.D. is a Pain Management Specialist with The Pain Center in Orange Park.

More than 20 million people in the US suffer from severe headaches, and the annual prevalence has increased nearly 60% since 1980. Nearly 80 percent of these patients report headache-related disability that may result in missed work. In fact, nearly 50 percent of headache sufferers are moderately or severely disabled by a headache attack or "migraine" and lose an estimated 13 workdays and 8 leisure days each year.1 "Migraine" is a term of much confusion in the lay public's mind. Physicians use the term migraine to mean a specific intracranial vascular headache. Patients usually use the term to mean a "sick headache" or a throbbing headache. Pain management doctors treating headache patients are beginning to realize that the symptomatic diagnosis of migraines (unilateral throbbing headache associated with photophobia, phonophobia and emesis) does not distinguish between intracranial and extracranial causes of headaches. In this article I will discuss some of the most common causes we have found to be associated with migraines and intractable headaches.

Supraorbital Neuralgia

Entrapments of the first division of the trigeminal nerve can cause unilateral or bilateral throbbing headaches, often just before menses or triggered by bright lights that cause squinting. Supraorbital neuralgia can be mistaken for frontal sinusitis. It can be caused by trauma to the face such as when the head hits the windshield or after a punch to the face. The headache might not present for many years until the scar cicatrix tightens enough around the nerve to finally cause entrapment. There can be auras, unilateral or bilateral throbbing, as well as photophobia, phonophobia, nausea and vomiting, and meet all the International Headache Society criteria for migraines. Fluid retention, such as before menses or with salt indiscretion (perhaps with red wine, MSG, or cheeses) can trigger these "migraines". We have also seen patients with "classic" cluster headaches (male, sudden onset, rhinorrhea, scleral injection, cyclic pattern) who have had instant and complete relief of their headaches with small (0.5cc volume) of local anesthetic. Treatment (and diagnosis) involves injection of local anesthetic with steroid. Cryoneuroablation can give long term relief by freezing the nerve at the Supraorbital notch. Plastic surgeons using botox for forehead wrinkles noted a dramatic decrease in "migraines" in treated patients, suggesting that muscle entrapment of the supraorbital and supratrochlear nerves may be a common pathology.

Infraorbital Neuralgia

This second division of the trigeminal nerve is also associated with headaches, often misdiagnosed as maxillary sinusitis. Like the supraorbital nerve, it can be injured years before the headaches start, and can present as menstrual headaches or classical/common migraines.

Auriculotemporal Nerve

Temple headaches are often due to entrapment of the auriculotemporal nerve, a third division trigeminal nerve which leaves the foramen ovale and then travels in front of the TMJ (innervating the joint as it goes by) to pierce the temporalis muscle. This is a common headache site (visualize all the headache patients rubbing or pressing their temples for relief). Patients will awaken with a headache at three or four o'clock in the morning secondary to bruxism during the lightest plane of sleep (i.e. early in the morning). The headache can be unilateral or bilateral, and throbbing in nature because of the proximity of the temporal artery. In fact, tenderness of the "temporal artery" has been used as supporting evidence of the vascular nature of migraines instead of recognizing that the ATN is possibly the true pathology. Teeth clenching with stress, prolonged talking or chewing and "TMJ" pathology (which may be actually ATN irritation) can all trigger these headaches.

Zygomatic Facial Nerve

Although the facial nerve is usually considered a pure motor nerve, there are sensory fibers across all the branches. The most common entrapment site we see is the zygomatic branch as it crosses the zygomatic arch. Edentulous patients will have the coronoid process move cephalad which catches the nerve in the arch. The pain can mimic the pattern seen by either the ATN or maxillary nerve, made worse in the early morning after the dentures have been removed the night before and the body tries to "find" the previous "natural" site of dental occlusion.

Posterior Auricular Nerve

Ear pain and parietal headaches can be caused entrapment of the posterior auricular nerve by the sternocleito-mastoid muscle. This can occur during flexion/extension injuries, especially if the head was turned at impact. Blows to the side of the head can also present as posterior auricular entrapment years later. There can be persistent "fullness" or decreased hearing as well as tinnitus and vertigo. These symptoms may be difficult to differentiate from SCM pathology (see SCM).

Greater And Lessor Occipital Nerve

The occipital nerve is made up of the dorsal rami of C2 and C3 (see cervical facets).2 The classic occipital neuralgia causes pain in the back of the head. However, because the ganglion interconnects with the trigeminal ganglion in the brain stem,3 occipital neuralgia will refer to any of the branches of the trigeminal nerves, especially the retroorbital area. These nerves pierce the nuchal fascia at the base of the skull and are therefore prone to trauma from flexion/extension injuries as well as entrapment by spasm of the trapezius muscle. There is a frequent association with throbbing (because of the proximity of the occipital artery) as well as nausea and vomiting. If the head were turned at impact, there would be a unilateral pain, which would then meet IHS criteria for migraines. There is usually also temporary relief with triptans, presumably because the occipital artery is constricted by the medicine, temporarily reducing the entrapment of the occipital nerve. However, as soon as the medicine wears off (usually about 8 hours) the headache comes right back. A prospective study of patients presenting to the ED with unilateral occipital headaches found 42% of the patients complained of nausea, dizziness 50%, and tinnitus 33%, with visual disturbances in 67%.4

Masseter Muscle

Chronic stress leading to teeth clenching, bruxism, dental malocclusion, and TMJ pathology can all cause spasm of the masseter muscle, which will refer pain to the temples, jaw, and over the eye.5

Sternocleidomastoid Muscle

This muscle will refer pain to the ear, temple and face, especially over the eye.5 Patients often complain of fullness in the ear with decreased hearing, leading to unnecessary ENT evaluations. There can also be tinnitus and vertigo, mimicking vestibulitis. Since flexion/extension injuries will traumatize the SCM, what has been considered coup-contracoup brain injuries are now being recognized as myofascial pain.

Trapezius Muscle

"Tension headaches" is a term that seems to trivialize the intractable occipital and retroorbital headaches that are caused by trapezius spasm.5 The pain can be caused by stress, chronic postural problems (for instance with prolonged neck flexion for reading), or flexion/extension injuries.

Cervical Facet Pathology

Although cervical facet pathology can obviously cause neck pain, the upper cervical facets are innervated by the dorsal rami that make up the occipital nerves.6 Therefore, C2 and C3 facet pathology will refer to the occipital nerve. In a similar way, pathology of the cervical discs can cause cervicogenic headaches. This is a common cause of headaches in the elderly because of the predominance of cervical arthritis. However, flexion/extension injuries will also cause cervical facet pathology, unilateral if the head was turned on impact.7

Interspinous Ligament

In 1954, Feinstein, et al8 followed up on work done by Kellgren9 in 1939 which showed that irritation of the cervical ligaments can refer pain to the head and face as well as the extremities. These cervical ligaments are also traumatized in flexion/extension injuries but also can occur with chronic low grade trauma. The subsequent ligament laxity no longer allows support of the 30 pound head, and the cervical muscles will go into spasm to hold the head up. This ligament pathology results in a straightening of the cervical lordosis. Thus, the common X-ray diagnosis of "loss of cervical lordosis secondary to spasm" is actually the reverse — contraction of a muscle above and below the lordosis must cause more lordosis if the muscles are the pathology.

Conclusion

In conclusion, many of the assumptions we have made regarding headaches and migraines are changing. This has important implications for the patient since extracranial headaches do not respond to standard intracranial treatment. Instead, diagnosis is made by palpation followed by injection of local anesthetic. Treatment is directed at reversing the underlying pathology, so that entrapments are treated with injectable antiinflammatories, muscle spasms treated with muscle relaxants or possibly botox, and ligament pathology treated with stimulated ligament repair. Cryoneuroablation, radiofrequency lesioning, disc annuloplasty, and subcutaneous nerve stimulation are all now being used with good success for chronic intractable headaches. The axiom "you can't treat what you can't diagnose" has never been more true than in the treatment of headaches and migraines.

REFERENCES

  1. Prevalence of chronic migraine headaches - United States, 1980-1989. MMWR. May 1991;40:331, 337-338.
  2. Bogduk N. The anatomy of occipital neuralgia. Clin. Exp. Neurol. 1981; 44:202-208.
  3. Kerr FWL. Structural relation of the trigeminal spinal tract to upper cervical roots in the solitary nucleus in the cat. Exp Neurol. 1961;4:134-148.
  4. Kuhn WF, et al. Occipital neuralgia: clinical recognition of a complicated headache. A case series and literature review. J Orofac Pain. 1997; 11(2):158-165.
  5. Travell JG, Simmons DG. Myofascial Pain and Dysfunction, 1983, Chapter 8, Williams & Wilkins.
  6. Bogduk N. The clinical anatomy of the cervical dorsal rami. Spine. 1982; 7:319-30.
  7. Keith WS. "Whiplash" injury at the second cervical ganglion and nerve. Can J Neurol Sci. 1986; 13:133-137.
  8. Feinstein MD, et al. Experiments on pain referred from deep somatic tissues. J Bone and Joint Surgery. 1954; 36A:981-997.
  9. Kellgren JH. On the distribution of pain rising from deep somatic structures with charts of segmental pain areas. Clin Science. 1939; 4:35-46.
Jacksonville Medicine / April, 2000

 

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