24. Headaches

The most common forms of benign headaches are tension-type headache (TTH), cervicogenic headache (CH), and migraine-type headache. For each headache type, basic epidemiology, pathophysiologic mechanisms, and clinical manifestations are reviewed in this chapter. The middle portion of the chapter describes mechanisms and clinical procedures applicable to the cervical spine that have implications for chiropractors and apply to all three headache types. These mechanisms and procedures form a coherent manual therapy approach to the understanding and assessment of these most common forms of headaches. The final portion of the chapter presents the available evidence from randomized controlled clinical trials of spinal manipulation/adjustment for these headache types.

TENSION-TYPE HEADACHE

TTH is the most prevalent form of benign, primary headache.¹²³^{and 4} The terminology of this category of headache has evolved from the earliest classification of the National Institutes of Health (NIH) Ad Hoc Committee. ⁵ It has been called “tension headache” and “muscle contraction headache.” The most recent definitions derive from the Classification of the International Headache Society (IHS), ⁶ where the term TTH was proposed. TTH has been described as a bilateral headache of mild-to-moderate intensity experienced with an aching, tightening, or pressing quality of pain; it may last from 30 minutes to 7 days, is not accompanied by nausea or vomiting, and either photophobia or phonophobia (but not both) may be experienced.

The IHS introduced two forms of TTH: (1) episodic and (2) chronic. The distinction between the two forms is based solely on the frequency of headache days. In episodic tension-type headaches (ETTHs), headaches are experienced no more than 180 days per year; in chronic tension-type headaches (CTTHs), headaches occur more than 180 days per year.

Epidemiology of Tension-Type Headache

Prevalence and Incidence

A small body of population-based studies on TTH exists, the most recent of these reporting on Canadian, ⁷ U.S., ⁸ Danish, ⁹ German, ¹⁰ and Finnish¹¹ populations. These studies have used various survey methods, including telephone interviews, ^7,⁸ subject interviews, ⁹ and mail surveys. ^10,¹¹ All but one of the most recent of these studies have used the IHS criteria for TTH described previously. With one exception, ⁹ these studies have involved large, randomly selected samples with good response rates (Table 24-1).

**Table 24-1** PREVALENCE OF TENSION-TYPE HEADACHE: RECENT STUDIES
Authors	Location	Survey Method	Sample Size	Prevalence Rate
HA, Headache; TTH, tension-type headache.
Pryse-Phillips et al, 1992⁷	Canada	Telephone	2905	Lifetime prevalence for HA, 58%; for TTH, 21%
Honskaalo et al, 1993¹¹	Finland	Mail	22,809	Prev. for once-weekly TTH, 7%-17%
Gobel, Peterson-Braun, and Soyka, 1994¹⁰	Germany	Mail	5000	Lifetime prevalence for TTH, 38.3%
Rasmussen et al, 1995⁹	Denmark	Interview	1000	Lifetime prevalence for all TTH, 66%; for once-weekly TTH, 20%-30%
Schwartz et al, 1998⁸	United States	Telephone	13,345	Lifetime prevalence for TTH, 38.3%

Several studies reported a slightly higher rate of TTH in females than in males⁷⁸⁹^{and 11} but Gobel, Peterson-Braun, and Soyka¹⁰ failed to confirm this. Similarly, some studies reported an increased prevalence in those aged 25 to 45, ⁷ whereas others found no increasing trend with age.⁸⁹¹⁰^{and 11} Schwartz and colleagues⁸ reported higher prevalence rates in whites and those with higher education.

In summary, the reported prevalence rates vary from approximately 10% to 65%, depending on the classification, description, and severity of headache features. In general, these rates derive from large, randomly selected, well-representative samples. The consistency of findings is notable, particularly among urban populations, leading to the conclusion that slightly more than one third of the adult population suffers from this problem.

Frequency of Tension-Type Headache

The findings of several studies, ^7,^10,¹¹ agree that only 3% of TTH sufferers experience headaches more than 180 times yearly, thus being classified as CTTH. Rasmussen⁹ reported that of this 3%, the percentage that suffers TTH more than once weekly (over 52 times per year) is 20% to 30%. Gobel, Peterson-Braun, and Soyka¹⁰ reported that only 28% suffer TTH more than 36 times yearly. Honskaalo and colleagues¹¹ reported an increasing yearly frequency with age, varying from 7.3 and 13.5 per year for males and females younger than 30 years of age to 27.7 per year for both genders older than 65 years. This increase appears to be linear from one decade of adulthood to the next.

Severity of Headaches

TTH is, by definition, a milder, less severely painful form of headache than migraine or other primary categories (i.e., cluster headache, CH). Gobel, Peterson-Braun, and Soyka ¹⁰ reported that in TTH sufferers, headache severity was mild in 22%, moderate in 68%, and severe in 10%. Rasmussen⁹ reported that 58% of subjects in a TTH sample had “mild, infrequent conditions.” Adding these subjects to the study produced the highest reported prevalence rate. Schwartz and colleagues⁸ used a pain-rating scale and reported mean (standard deviation) headache severities as 4.98 (1.99)/10 for ETTH and 5.55 (2.10)/10 for CTTH. In their sample, 62% were classed as moderately severe, whereas 25% were mild and 13% severe, closely matching Gobel, Peterson-Braun, and Soyka’s figures.

In summary, it appears that at least 50% of TTH sufferers rate their headaches as moderately or severely painful.

Psychosocial Influence

The psychosocial effects of all varieties of headache are substantial and highly relevant to patient management. In a follow-up study of the Canadian sample, Edmeads and colleagues¹² reported that a high proportion of TTH sufferers endured adverse effects on their relationships: 89% reported TTH adversely affected their families, 71% reported it adversely affected their friends and colleagues, and 80% reported it adversely affected their physical activities. The full range of psychosocial influence of TTH includes adverse disturbances of daily activities, disturbed quality of life, lost or disturbed workdays, as well as the costs of these disruptions. In Pryse-Phillips and colleagues’ study, ⁷ 44% of TTH sufferers reported a significant reduction in activities of daily living (ADL) because of headache (with a mean duration of 18 hours per year), whereas 8% reported taking at least 1 day off work because of their last TTH.

According to Rasmussen, ⁹ 60% of TTH sufferers reported an adverse effect on work capacities, with 12% missing 1 or more workdays per year. Nine percent (9%) of subjects had missed work in the previous year, with an interval of 1 to 7 days lost. They estimated a work-loss rate of 820 days/1000 people per year, for a total of 2,300,000 annual workdays lost in Danish society. In Schwartz and colleagues’ U.S. sample, ⁸ 8.3% of subjects reported lost workdays (with a mean of 9 days per year), whereas 43.6% reported “reduced effectiveness” days (mean: 5 days).

Treatment of Tension-Type Headache

Treatment of TTH varies widely within both medical and nonmedical circles. In addition, the patterns of health care use by TTH sufferers are variable. According to Edmeads and colleagues, ¹² 45% of their sample of TTH sufferers had consulted with a physician; 32% of these patients were subsequently referred to a specialist. These figures are lower than those for migraine sufferers. In contrast, the Danish results reported by Rasmussen⁹ are much lower, with only 14% attending a physician and 4% receiving specialist referrals. Cultural and psychosocial variables may have an influence on treatment-seeking behavior and therapy delivery in different countries.

Medical Approaches

Medications remain the mainstay of the medical approach to managing TTH. Two basic medication approaches exist: (1) symptom relief, or abortive therapy (given every time a headache occurs), and (2) prophylactic therapy (given on a regular basis for headache prevention). Edmeads and colleagues¹² reported that 90% of their TTH sample used over-the-counter (OTC) medications, typically analgesic or antiinflammatory drugs. Twenty-four percent (24%) used prescription medications, which typically include stronger doses of the OTC drugs, muscle relaxants, and combination drugs. Only 3% were on prophylactic medications, which include low-level antidepressants and serotonin-enhancing agents.

Wober-Bingol and colleagues¹³ reported on 210 headache sufferers referred to two Austrian specialist centers. Thirty-nine percent (39%) of subjects were on some form of prophylactic regimen; however, this was a medication regimen in only 9%. Of the 19 cases that were receiving antidepressants, 11 reported them to be effective.

Nonmedical Approaches

Considerable variety exists in the nonmedical approaches to the treatment of TTH. Edmeads and colleagues ¹² reported that 34% of their headache sample had used nonmedical forms of treatment, although these may have included a broad spectrum from psychology-based treatments to physical therapies to nonpharmacologic medications. Rasmussen⁹ reported that 5% to 8% of headache respondents had sought care from physiotherapists or chiropractors. Wober-Bingol and colleagues’ study¹³ of specialist-level patients reported that 29% had received prophylactic physiotherapy, with only one quarter reporting that it was effective. In an earlier study, Graff-Radford, Reeves, and Jaeger¹⁴ reported that 35% of their specialist level headache subjects (U.S. sample) had previously received chiropractic treatment.

The question of the percentage of chiropractic patients who complain of headache is an important one. Unfortunately, to date no study has accurately determined this percentage or used the IHS criteria to determine the percentage of TTH versus migraine sufferers. Several studies from chiropractic college clinics estimate that between 5% and 10% of patients report to chiropractors with a primary complaint of headache. ¹⁵ According to Kelner and Wellman, ¹⁶ 10% of the chiropractic patients in their small survey of alternative health practitioners (i.e., chiropractors, naturopaths, massage therapists, reflexologists, acupuncturists) reported that headache was their primary complaint. Interestingly, this figure was the largest among the five complementary/alternative medicine (CAM) practitioners surveyed and was considerably larger than the percentage reported for the family physicians who were also surveyed.

In a recent study by Hurwitz and colleagues, ¹⁷ only 2.3% of patients sought chiropractic treatment for headache; however, 13.5% sought treatment for neck pain that may have included headache.

Clinical trial evidence for the chiropractic treatment of TTHs is presented later in this chapter (see p. 509).

CERVICOGENIC HEADACHE

Description and Epidemiology

The role of the cervical spine in headache has become increasingly well acknowledged. Despite the wealth of writing in chiropractic, osteopathic, physiotherapy, and manual medicine circles¹⁸¹⁹²⁰²¹^{and 22} (see reviews in 18 19 20 21 and 22), as recently as the late 1980s CH was poorly recognized in orthodox medical circles. Although numerous labels for the condition already existed, such as “headache of cervical origin,” “cervical headache,” “vertebrogenic headache,” and “spondylitic headache,” Sjaastad²³²⁴^{and 25} coined the diagnostic label of cervicogenic headache (CH) in 1983.

As Pollmann, Keidel, and Pfaffenrath²⁶ and Vincent and Luna²⁷ have noted, reports dating from 1926 (with the cases of Barre) to those of Bartschi-Rochaix²⁸ and Hunter and Mayfield²⁹ in 1949 to Campbell and Hoyd³⁰ in 1954 likely involved cases of supposed CH. From 1983 to 1987 many researchers^23,^25,^31,³² expanded on the topic; they provided sufficient basis for the IHS classification⁶ to include CH as a distinct entity (category number 11). The criteria for this category, shown in Box 24-1, were broader and more inclusive than Sjaastad’s original description, because Sjaastad’s description was challenged by some¹⁸¹⁹³³³⁴^{and 35} as being so restrictive as to relegate this headache type to a rare variant. Recognizing this situation, Bogduk, one of the most prominent writers in this field, has proposed a new definition of CH, which has been adopted by the North American Cervicogenic Headache Society: “Referred pain perceived in any region of the head caused by a primary nociceptive source in the musculoskeletal tissues innervated by cervical nerves” (Bogduk N, personal communication).

Box 24-1

FEATURES OF CERVICOGENIC HEADACHE

1. Unilateral pain that does not change sides

2. Reduced range of neck motion

3. Provocation of pain by neck movements, awkward neck positions, or suboccipital pressure

4. Associated neck or nonradicular shoulder/arm pain

5. Pain radiates from neck to anterior head (particularly frontal and ocular)

6. Moderate pain intensity (no throbbing pain)

7. Varying durations of pain including continuous fluctuating pain

8. Minor associated symptoms and signs (which may or may not be present) including:

• Nausea, vomiting, dizziness

• Photophobia and phonophobia

• Difficulty swallowing

• Blurred vision in ipsilateral eye

Modified from International Headache Society: Classification and diagnostic criteria for headache disorders: cranial neuralgias and facial pain, Cephalalgia 8(suppl 7):1, 1988.

Furthermore, a recent classification from the International Association for the Study of Pain (IASP) ³⁶ adds the additional criterion of successful abolishment of headache by anesthetic blockade of the various upper cervical nerves as a diagnostic factor. The confusion in applying these various classification or diagnostic schemes is exemplified in two recent studies. Persson and Carlsson³⁷ reported on 81 subjects with cervical or radicular arm pain (or pain in both areas); 67% of these subjects also reported experiencing headache. When they applied the IHS criteria, 81% of these cases were classified as having CH. However, when using Sjaastad, Fredriksen, and Pfaffenrath’s 1990 criteria, ³⁸ only 28% received the same diagnosis. They concluded that “cervical headache has no unique features that differ from those of TTH, and it would perhaps be appropriate that the diagnosis of CH is incorporated in the diagnosis of TTH.”³⁷

Leone and colleagues³⁹ applied all of the differing classification schemes to 940 primary headache cases and found very few subjects who manifested any unique features of CH that could not be subsumed in either TTH or migraine diagnoses. In fact, the boundaries between CH, TTH, and migraine headache were and continue to be quite blurred, particularly on the issue of bilaterality. Another conundrum that confuses the diagnostic picture is that many of the features of CH cited in Box 24-1 are physical signs that the astute clinician must obtain from careful physical examinations.

If the headache pain pattern is not so distinct as to point to the diagnosis immediately (as in cluster headache or, perhaps, migraine with aura) and the less astute clinician does not include examination of the neck in the assessment, then those features critical to the CH diagnosis will be absent in the clinical equation. An erroneous diagnosis of tension-type or migraine without aura might then be imposed, and the opportunity to address the possible cervicogenic cause of the headache will be lost. In this way, the prevalence of CH is very likely underestimated.

Given the diagnostic confusion previously cited, it is understandable that studies of the prevalence of CH (in either the general population or in headache samples) are fraught with difficulties and variations. A wide range of frequencies is reported in the literature. As cited previously, Leone and colleagues³⁹ found CH in only 0.7% of their headache sample, whereas Pffafenrath and Kaube⁴⁰ found CH in 13.8% of their larger headache sample, with 6% suffering exclusively from CH. Using the IHS criteria, along with careful questioning about cervical dysfunction, Nilsson⁴¹ found an annual prevalence of CH in a Scandinavian population to be approximately 15%. This is roughly at the lower end of prevalence estimates for TTH^8,⁹ and is identical to the prevalence of migraine headaches cited in these reports. This is far from the rare variant that CH was judged to be in the early 1980s.

Mechanisms of Cervicogenic Headache

According to Bogduk³⁴ the cervical source of headache may lie in any of the structures innervated by the first three cervical nerves. As such, a thorough knowledge of upper cervical innervation patterns is required. Before considering these patterns, it is convenient to categorize these somatic tissues according to localization (see box, Structural Model of Cervicogenic Headache).

Clinical Mechanisms

Numerous mechanical and arthritic processes affect the region and may give rise to upper cervical pain (i.e., develop into a “pain generator”). This discussion will omit mention of the many pathologic processes that can afflict the region and give rise to pain.

STRUCTURAL MODEL OF CERVICOGENIC HEADACHE

EXTRASEGMENTAL STRUCTURES

Long occipitothoracic muscles are relatively superficial in the neck; they include trapezius, sternocleidomastoid, and splenius cervicis. The occipitofrontalis muscle is also an important consideration related to cranial pain. Other important structures lying extrasegmentally include the vertebral artery (implicated in the Barre-Lieou syndrome ^22,^42,⁴³ and vertebrobasilar ischemic syndrome), the ascending sympathetic chain, and the superior cervical ganglion. Older theories implicated compression or irritation of these sympathetic structures in the generation of cranial pain and cranial vasomotor dysregulation; these theories have fallen out of favor, having been replaced by sensorimotor theories of pain.

INTERSEGMENTAL STRUCTURES

These structures include the classic spinal joints and deep spinal muscles (i.e., the semispinalis occiput and cervicis, multifidus, and suboccipital muscles [posterior, lateral, and anterior]). The clinician should remember that no intervertebral disk exists between C0-C1 and C1-C2. The suboccipital articulations include the bilateral atlantooccipital joints, the bilateral atlantoaxial joints, the atlantodental joint, Joints of Luschka, and the C2-C3 intervertebral disk. The suboccipital region contains a large number of specialized ligamentous structures (see Kapandji⁴⁴ for an excellent review).

INTRASEGMENTAL STRUCTURES

This category involves the neural and vascular structures contained in the intervertebral environment of C1-C2 and the intervertebral foramina of C2-C3 (specifically, the anterior and posterior rami of C1 and C2, the C2 dorsal root ganglion, and the C3 posterior nerve root). Bogduk’s reviews of upper cervical anatomy^33,^34,⁴⁵ are particularly extensive.

INFRASEGMENTAL STRUCTURES

This category includes the spinal cord and lower brainstem. Of particular importance is the spinal tract of the trigeminal nerve, which contains descending afferents from the trigeminal sensory ganglion that terminate as far caudally as C3 in the spinal nucleus of the V nerve. The descending tract contains three components: (1) the pars oralis (upper), (2) the pars intermedialis, and (3) the pars or subnucleus caudalis (lowest). These afferent fibers terminate on the same second-order neurons as do the afferents from the upper three cervical roots. The second-order neurons form a continuous column of cells called the trigeminocervical nucleus by Bogduk and Marsland³³ and the medullary dorsal horn by Gobel. ⁴⁶ This neural anastomosis of converging afferents is the fundamental neuroanatomic basis by which painful structures in the upper cervical region might generate referred pain to the cranium (see following).

INNERVATION PATTERNS FOR CERVICAL HEADACHES

C1 and C2 Anterior Ramus:

• Deep anterior suboccipital muscles

• Posterior dura

• Posterior cranial vessels

The C2 anterior ramus contains the sensory fibers of the hypoglossal nerve that run in the ansa hypoglossus.

C1 Posterior Rramus:

C1 posterior ramus is very small, but Kerr⁴⁷ proved its existence decades ago.

C1 Anterior Ramus:

• Superior oblique muscle

C2 Posterior Ramus:

The C2 posterior ramus has two branches: (1) medial and (2) lateral. The medial branch becomes the lesser occipital nerve and innervates rectus capitis posticus major and minor and the medial C1-C2 joint and ligaments. The lateral branch is the largest posterior ramus of the spine and is also known as the greater occipital nerve (GON). The GON gives off an articular branch to the lateral C1-C2 joint and a muscular branch to the inferior oblique. It then courses posteriorly and superior to pierce between the semispinalis capitis and trapezius muscle insertions, where it becomes cutaneous and innervates the skin of the posterior skull to the midline.

Bogduk^33,³⁴ has called the C3 posterior ramus the “third occipital nerve.” It innervates the C2-C3 zygapophyseal joint (Z-joint) and deep muscles and provides a recurrent meningeal nerve that innervates the C2-C3 intervertebral disk (IVD).

Extrasegmental Processes

Postural strain and microtrauma or macrotrauma can create myofascial dysfunction. Trigger points in the large regional muscles have been charted by Travell and Simons⁴⁸ and create typical referred pain patterns. Stress and occupational repetitive strain can produce static overload of these muscles, predisposing to local and referred pain.

Intersegmental Processes

Painful disorders of the C0-C3 joint structures are currently thought to be the most common disorder in cervical headaches. Pain patterns, both local and referred, have been mapped by provocation and anesthetic procedures in humans for the C0-C1 joint by Dreyfuss, Michaelsen, and Fletcher⁴⁹ and the C1-C2 and C2-C3 by Feinstein and colleagues⁵⁰ (for both joints) and others.⁵¹⁵²^{and 53} Researchers^54,⁵⁵ have used double-blind anesthetic blockades to identify the C2-C3 zygapophyseal joint (Z-joint) as the primary pain generator in over 50% of a group of whiplash sufferers with headaches.

Trigger points have also been mapped in the deeper intersegmental and suboccipital muscles. Tenderness in the deep suboccipital muscles is the most commonly reported finding in the large number of clinical reports (see review by Vernon and colleagues²²). In a 1992 study⁵⁶ at least one tender point was identified in at least 84% of a sample of tension-type and migraine sufferers, with most having two or more. Sjaastad, Fredrickson, and Stolt-Neilsen²⁴ reported on the high prevalence of paraspinal tenderness at the C2-C3 level. This finding has eventually become a hallmark of CH. Bouquet and colleagues⁵⁷ reported on 24 CH sufferers, 21 of whom had an ipsilateral trigger point at C2-C3. They also commented on a frequently noted finding of what they called an “enlarged C2 spinous process.” The prominence of this spinous process was proposed to result from rotational misalignment at that level. In Jaeger’s report on 11 CH patients, ⁵⁸ tenderness and misalignment around the transverse process of C1 were the most frequently noted findings.

Several authors have reported on standardized methods of measuring tender points in the craniocervical region. In 1989, Langemark and colleagues⁵⁹ developed a method of rating manual palpation for muscular tenderness. Tender points are rated on a three-point scale to a standardized manual pressure. It was determined that the pressure sufficient to blanch the examiners thumbnail was sufficient to elicit tenderness, which is then rated as follows:

0—No reaction

1—Slight reaction, no vocalization indicating pain, no movement

2—Moderate reaction with vocalization

3—Severe reaction with vocalization and flinching or other movements

Scores for a variety of muscles are added up bilaterally for a Total Tenderness Score (TTS). TTS in 50 TTH subjects was found to be highly reproducible on two examinations separated by 3 weeks. Comparison of findings in 24 healthy controls indicated significantly higher TTS in headache subjects. Numerous replications of this methodology have verified its reliability and validity. ^60,⁶¹ Although the manual palpation method has been used in subjects with both neck pain and headache and has been found to be very reliable, no study has yet investigated the role of tenderness in cranial, suboccipital, and neck and scapular muscles in TTH sufferers. In an unpublished study, the author used pressure algometry, another method frequently reported to measure tender points,⁶²⁶³⁶⁴⁶⁵⁶⁶⁶⁷⁶⁸⁶⁹^{and 70} in a comparison of 14 headache and 14 control subjects. There was a significant trend toward multiple tender points to be found in headache subjects (four or more). Overall values for each of eight tender points were lower in the headache as compared with control subjects.

Intrasegmental Processes

Entrapment of the greater occipital nerve (GON) and its ganglion has long been purported to cause greater occipital neuralgia. Recent evidence by Bogduk^34,⁷¹ casts more doubt on this theory, because anesthetization of the GON would reduce pain from any of the tissues it innervates. Irritation of the sensory fibers in the anterior ramus of C2 by inflammation or osteophytic outgrowths from the C1-C2 lateral joint has been implicated as a cause of the uncommon “neck-tongue syndrome,”⁷² in which upper cervical pain is accompanied by “numbness” or shooting pains into one side of the tongue.

Infrasegmental Processes

Only two direct mechanisms related to mechanical disturbances have been identified for the upper cervical cord. The first concerns a controversial mechanism reported by Hack and Koritzer⁷³ (see Chapter 23, p. 486 for further details) involving a ligamentous connection between the rectus capitis posticus minor and the dural lining at the foramen magnum. In a small number of reported cases, surgical ligation of this ligament has resulted in improvement in headache.

The second mechanism involves a herniation of the C2-C3 intervertebral disk (IVD). This is relatively rare and until recently only Elvidge and Choh-Luh⁷⁴ had reported on it. Recently the use of C2-C3 discograms and disk fusion surgery has resurrected this idea.

The most important role for the spinal cord in CH lies in the phenomenon of afferent convergence of the upper cervical and trigeminal systems, as described previously. ^22,⁷⁵ This mechanism is undoubtedly the explanation for referred pain to the cranium resulting from upper cervical deep-tissue pain. It should be remembered that the same convergence phenomenon explains why posterior intracranial pathologies result in referred upper cervical pain. This may be one of the mechanisms underlying the creation of upper cervical pain and myofascial dysfunction in migraine. Painful and inflamed posterior cranial vessels can refer pain to the suboccipital region—one more cause of diagnostic confusion!

MIGRAINE HEADACHE

The topic of migraine headaches is so vast that only a summary of the essentials necessary for students or primary care practitioners will be given here. The reader is encouraged to delve more deeply into major texts and articles for more information on the many theories regarding the cause of migraines, the many clinical variants, and the many types of treatments, both acute and prophylactic.⁷⁶⁷⁷⁷⁸^{and 79}

Definitions and Classification

Since the 1960s, migraines had been understood according to the theory of Wolff, ⁸⁰ who proposed a two-phase vascular model. In the 1940s, Wolff had proposed that, in the first phase, vasoconstriction of the cerebral arteries produced cerebral ischemia that was the basis for the aura or premonitory (i.e., warning) phase of migraine that may include transient, nonpainful visual or sensory symptoms. The clinician then proposed that the autoregulatory mechanisms of cerebral blood flow would become hyperactive and a “rebound vasodilation” would occur, resulting in the stretching of the cerebral arteries with the typical pounding pain of migraine. As such, the NIH Ad Hoc Committee⁵ used the following classification for the two major types of migraine headaches: Classic migraine included the typical migraine headache with the premonitory aura; common migraine was defined as migraine headache without the aura.

In 1988 the IHS published a new classification of headaches and cranial pains. ⁶ The IHS promoted a simpler terminology that has since become widely accepted: migraine with aura (for classic migraine) and migraine without aura (for common migraine). The characteristics of these two migraine types, which together make up the vast majority of migraine diagnoses, are shown in Box 24-2.

Box 24-2

FEATURES OF MIGRAINE

A. Migraine without aura:

• At least five attacks lasting 4 to 72 hours

• Headache has at least two of the following characteristics:

Unilateral location

Pulsating quality

Moderate or severe intensity

Aggravation by routine physical activity

• At least one of the following during a headache:

Nausea and/or vomiting

Photophobia and phonophobia

• Normal neurologic examination and no evidence of organic disease

B. Migraine with aura:

• At least two attacks

• Aura must exhibit at least three of the following:

Fully reversible and indicative of focal cerebral cortical and/or brain stem dysfunction

Gradual onset

Duration less than 60 minutes

Followed by headache with a free interval of less than 60 minutes, or headache may begin before or simultaneously with the aura

• Normal neurologic examination and no evidence of any organic disease

Modified from International Headache Society: Classification and diagnostic criteria for headache disorders: cranial neuralgias and facial pain, Cephalalgia 8(suppl 7):1, 1988.

A common feature of migraine headache is that various factors appear to act as triggering mechanisms.⁸¹⁸²⁸³^{and 84} Often, individual patients will be able to identify which factors from the common group of triggers appear to affect them the most. These include biochemical factors, particularly from foods rich in tyramine such as chocolate, cheese, red wine, and possibly any sort of alcohol; environmental factors, such as changes in barometric pressure, ambient odors, loud or harsh sounds, and certain kinds of lighting; psychosocial factors, particularly those associated with stress and anxiety; and hormonal factors, where menstruation may aggravate migraine and pregnancy may relieve it.

Epidemiology

In 1975 a landmark study, the “Pontypridd Study,”³ confirmed several key features of the epidemiology of migraine in the Western world. Overall, the prevalence of migraine is about 15% of the population. A female-to-male ratio exists of between 2:1 and 3:1, depending upon age. Migraine headaches can begin in childhood and adolescence, peak in the third and fourth decades of life, and diminish thereafter. Table 24-2 gives data from the Pontypridd study on age and sex prevalence of migraines.

**Table 24-2** MIGRAINE PREVALENCE DATA FROM THE PONTYPRIDD STUDY
Modified from Waters WE: The Pontypridd headache survey, *Headache* 14:81, 1974.© 1974
Age	% Males	% Females
21–34	16.8	30.1
35–54	16.4	26.0
55–74	12.5	16.6
75 and older	4.9	10.3

In 1992, Rasmussen and Olesen⁸⁵ published an important study of the Danish population. Seventy-four percent (74%) of their random sample had headaches during the previous year, with 16% of these being migraines. This represented a total population prevalence figure of 12%. The gender differential was confirmed with 25% of the female population reporting migraine (in males only 8% did so). Over half (56%) of migraineurs had seen their general medical practitioner and 16% had seen a specialist. Only 7% confirmed that they had been prescribed prophylactic medication, meaning that the vast majority of migraineurs resorted only to abortive or symptomatic medications. A large percentage of migraineurs (43%) reported that they had missed 1 or more workdays in the past year because of migraine, resulting in a projected loss of 270 days/1000 people.

The most recent large-scale population-based study comes from the United States. In 2001, Lipton and colleagues ⁸⁶ reported on a very large sample of just fewer than 30,000 respondents. The prevalence of migraine in this sample was 18.2% for females and 6.5% for males. Of these, 53% confirmed that they had experienced substantial impairment or the need for bed rest with their condition, and 31% reported taking at least 1 day off work in the past 3 months because of a migraine headache.

With regard to the frequency and pattern of migraine headaches, these are remarkably individuated. Migraineurs typically report their own pattern of triggering, headache development, and its subsequent course. A thorough history from each patient will elicit these details as they pertain to the individual triggering factors, the timing of the attacks during the day, their relationship to many different environmental factors, their typical presentation (i.e., which side of the head; whether an aura or prodrome is present and how often; whether some of the less common features of migraine, such as dizziness, abnormal sensations, and motor weaknesses or gastric pains are present), their response to various medications and other nonmedical measures, and their typical course.

In Stewart and colleagues’ first large report, ⁸⁷ 59% of females and 50% of males reported one or more severe headaches per month. Typically, migraine headaches are less frequent than TTHs and CHs. In addition, the frequency can wax and wane throughout life, particularly when women experience hormonal changes, such as during pregnancy or when receiving hormonal treatments. Finally, migraine frequency and severity appear to diminish in the latter decades of life.⁸⁸⁸⁹⁹⁰^{and 91}

Pathogenesis

Ever since the work of Wolff, migraine has been thought to be a disorder related to the cerebral vasculature. Wolff’s theory emphasized vasomotor processes, including vasoconstriction, as the basis of the “aura” or prodromal phase and vasodilation as the basis of the headache phase. This latter mechanism appeared intuitively correct given that migraine headaches are so often described as “pounding” in character. However, this theory did not explain several important features, including the following: The majority of migraine sufferers do not experience an aura or prodromal phase; migraine is unilateral, and a vascular theory is difficult to apply to this feature; vasodilation of the external cerebral vessels is common in fever, yet is not accompanied by migraine headaches, per se. The typical accompanying features of nausea and vomiting are not accounted for in an exclusively vascular theory.

In the 1980s several attempts were made to develop a neuronal theory of migraine. These models focused on hyperactivation of several cerebral or brainstem centers. Using special imaging procedures, the phenomenon of “spreading depression,” originated by Leao, ⁹² was applied to the observation of spreading vasoconstriction from the occipital lobe of the cortex forward, particularly in time with the development of headache in migraineurs. ^93,⁹⁴ Other investigators focused on the role of the locus ceruleus, a brainstem nucleus associated with the central sympathetic system, as the “central generator” of the migraine cascade. ⁹⁵ Additional brainstem mechanisms associated with central antinociception and involving the periaqueductal gray (PAG) matter and the nucleus raphes magnus (RPM) have been proposed. The beneficial effect of various medications popular at that time, including methysergide and propranolol, were thought to point to these sort of central mechanisms. ⁷⁶

Most recently, with the work of Moskowitz and colleagues⁹⁶⁹⁷^{and 98} and others,⁹⁹¹⁰⁰¹⁰¹¹⁰²^{and 103} a combined “peripheral-central” mechanism has been advanced that has led to the development of the most powerful antimigraine medications currently available. These investigators have developed a model based on the “trigeminovascular reflex.” In this theory, antidromic stimulation from the trigeminal sensory ganglion, which provides the nociceptive (not the autonomic) innervation of the cerebral vasculature, is thought to stimulate the peripheral nociceptive terminals on these vessels, stimulating the release of serotonin and substance P (SP). These two neurochemicals, in combination with others subsequently released (particularly histamine), evoke a peripheral or “neurogenic” inflammatory response, producing both pain and vasodilation. This inflammation may be sustained by other local biochemicals, and nitric oxide is currently under intense investigation in this role. Once inflamed, these vessels are rhythmically irritated by the pulse wave, producing the pounding characteristic of migraine pain. Central synaptic connections with the locus ceruleus (and with nuclei in the vestibular system) appear responsible for the associated nausea, leading to vomiting. Precisely why this mechanism operates only unilaterally is still unclear. As in past theories, trigger factors such as stress, hormonal, barometric, and biochemical mechanisms can operate at various levels, including cortical and brainstem levels, to initiate the cascade of processes eventuating in a migraine headache. ⁹⁶

The success of medications that block a particular cerebral vascular serotonin receptor subtype, the 1Ad receptor, and which are known as the tryptans, underscores the validity of this theory. ^97,¹⁰²

Genetic predisposition has been a commonly recognized feature of migraine. This is particularly so through the maternal line. A number of genetic markers for various types of migraine in various population subgroups have been identified. ^104,¹⁰⁵ At present it appears that genetic factors likely interact with environmental factors, lowering the threshold for the incipient dysfunctions in pain modulation and cerebral vascular regulation that underlie the migraine phenomenon and that are based in potentially numerous neurologic foci.

Medical Treatment of Migraines

This section on medical treatment of migraine will focus on pharmacologic and psychologic therapies, emphasizing pharmacologic treatments. The purpose is to give the reader a cursory review of the major medications used by family doctors, headache specialists, and emergency room physicians in the management of both acute migraine attacks and the long-term condition of recurrent migraines. Evidence on the effectiveness of each of these medications should be sought in the clinical trial literature and in the many reviews of these studies in the literature. Clinical texts on the management of migraine are too numerous to mention; the reader is encouraged to use those that are most current, because migraine therapy is constantly changing. ^78,⁷⁹

The pharmacologic treatment of migraine headaches is essentially divided into three main approaches: (1) abortive, (2) analgesic, and (3) prophylactic. The goal of abortive therapy is to intervene as early as possible in the migraine episode so as to abort its eventual development.⁷⁹¹⁰⁶¹⁰⁷^{and 108} For many years, ergotamine tartrate was the drug of choice in this regard. Ergotamine is a powerful drug with the potential for many side effects and the potential to aggravate nausea, which can be counterproductive in the management of migraine headaches. It is contraindicated in numerous conditions, particularly those involving the cardiovascular system and during pregnancy. The effect of ergotamine may be enhanced by the use of caffeine. If so, the dose of ergotamine may be reduced so as to preclude the development of side effects. A safer form of ergotamine is dihydroergotamine (DHE). The side effects appear to be less severe, allowing for more potent dosing. Abortive medications are often used in the emergency room, where adjunctive therapies such as antinauseants, anxiolytics, and analgesics can be used as well.

In the last decade a new class of drugs (the triptans) has emerged that appears to target the peripheral neurogenic inflammation in the cerebral vasculature rather than induce vasoconstriction, such as ergotamine appears to do. ^78,^79,^97,¹⁰⁸ The first of the triptans to be made available was sumatriptan. Initially it was only available for parenteral use, as in hospital emergency rooms. In more recent years it (and other forms of the triptan family) have been made available in pill form for oral self-medication. The adverse effect of sumatriptan on the peripheral vascular system is much less than with ergotamine. The triptans have rapidly emerged as the most widely used medication for the abortive treatment of acute migraine headaches.

Analgesic therapies are probably the most commonly used medications for self-management of the majority of migraine attacks. Simple analgesics include aspirin, acetaminophen, and the nonsteroidal antiinflammatory drugs (NSAIDs) such as ibuprofen, naproxen, diclofenac sodium, and ketorolac. ^109,¹¹⁰ A more powerful class of analgesics is those given in combination with sedatives and caffeine, including fiorinal and esgic. More powerful narcotics can be used in more severe bouts of acute headaches; in addition to compounds with codeine, these include the following: propoxyphene (Darvon), oxycodone (Percodan, Percocet), and meperidine (Demerol). Each of these medications has powerful side effects and the potential for abuse and addiction.

The third class of medications is used for prophylaxis.^110,¹¹¹ Long-term, regular use of these medications may prevent migraine attacks from developing in the first place. These medications include beta-adrenergic blocking agents (e.g., propranolol), calcium channel blockers (e.g., verapamil, nifedipine), antidepressant medications (e.g., the tricyclics), monoamine oxidase (MAO) inhibitors, serotonin reuptake inhibitors, NSAIDs, and specialized medications (e.g., methysergide, lithium). Methysergide is thought to act at the same serotonin receptors as the triptans, only on a more long-term basis. ⁷⁹

Nonpharmacologic approaches to the management of migraine include self-help and lifestyle measures and specific nondrug therapies. ^112,¹¹³ Migraineurs often learn which of the typical triggering factors precipitate their headaches. Dietary changes to reduce the intake of trigger foods such as chocolate, red wine, or other foods containing aggravating substances can be helpful. Avoidance of environmental or lifestyle factors such as smoking, excessive exercise, stressful situations, and alterations in the sleeping pattern can all make a difference in individual patients’ conditions. Finally, awareness of the effects of various medications on a patient’s migraine pattern needs to be pursued.

Nonpharmacologic therapies for migraine include chiropractic, biofeedback (thermal and electromyographic [EMG]–based); relaxation training; psychotherapies including cognitive therapy; and physical therapies such as myofascial therapy, heat and ice therapy, postural exercising, and acupuncture.¹¹²¹¹³¹¹⁴¹¹⁵¹¹⁶¹¹⁷¹¹⁸^{and 119}

CHIROPRACTIC TREATMENT OF HEADACHE

Treatment for headaches was recognized by the earliest chiropractors, and statistics on the success of this treatment were compiled as early as the 1920s. Numerous case studies and case series were published in the chiropractic literature,¹⁸¹⁹²⁰²¹^{and 22} but as of the late 1970s more rigorous clinical trials have been conducted and reported in the English and non-English biomedical literature.

To describe more fully the mode of treatment of headache by the majority of chiropractors, Vernon and McDermaid¹²⁰ conducted a survey of Canadian chiropractic specialists, Fellows of the College of Chiropractic Clinical Sciences (FCCS). The overwhelming majority of these specialists endorsed the use of spinal adjustment/manipulation, along with soft tissue therapies and postural exercises as the most commonly used and most valuable therapies.

Table 24-3 provides the relevant data from the body of randomized clinical trials published since the late 1970s on the treatment of headache by spinal adjustment/manipulation. It should be noted that several studies of neck pain treated by spinal adjustment/manipulation have also reported relief of headaches in large percentages of the subjects.

**Table 24-3** EVIDENCE TABLE FOR STUDIES OF SPINAL ADJUSTMENT/MANIPULATION FOR HEADACHES
Authors	Headache Type	Sample Size	No of Times	Treatment Groups (n)	Results	Side Effects	Quality Scores
MANIP, Chiropractic spinal manipulation; MOB, mobilization; REST, rest; Tx, treatment; S, severity; STT, soft tissue therapy; F, frequency; IHS, inclusion based on criteria of the International Headache Society; AMIT, amitriptyline; SHAM, sham placebo treatment; CMT, chiropractic manipulative therapy; MT, manual therapy; DIS, disability; DUR, duration; Fl/up, follow-up; PLA, placebo.
Hoyt et al¹²¹	Muscle contraction	22	1	(1) MANIP, 10 (2) MOB, 6; (3) REST, 6	Post-Tx S: (1) −48%^‡ (2) 0 (3) 0	Not mentioned	56
Jensen, Nielsen, and Vosmar¹²²	Posttraumatic	19	2	(1) MANIP, 10 (2) Ice, 9	Post-Tx S: (1) −30.7/100^† (2) +6.7/100	Not mentioned	60
Nilsson¹²³	Cervicogenic	39	6	(1) MANIP, 20 (2) STT, 19	Post-Tx F: (1) −3.4 (−59%) (2) −2.1 (−45%) Post-Tx S: (1) −15 (−45%) (2) −10 (−24%)	Not mentioned	64
Nilsson, Christensen, and Hartvigsen¹²⁴	Cervicogenic	53	6	(1) MANIP, 28 (2) STT, 25	Post-Tx F: (1) −3.2^* (−69%) (2) −1.6 (−37%) Post-Tx S: (1) −17^* (−36%) (2) −4.2 (−17%).	Not mentioned	72
Boline et al¹²⁵	Tension-type headache (IHS)	126	12	(1) MANIP, 70 (2) AMIT, 56	Post-Tx F: (1) −3.8/28 (2) −4.0/28 Follow-up F: Only gold members can continue reading. Log In or Register to continue Share this: Click to share on Twitter (Opens in new window) Click to share on Facebook (Opens in new window) Related Related posts: 7. Vertebral Subluxation 16. Caring for Aging Patients 26. Comparative Safety of Chiropractic 23. Musculoskeletal Disorders Research 14. Reactivation and Rehabilitation 4. Spinal Anatomy Stay updated, free articles. Join our Telegram channel Tags: Fundamentals of Chiropractic Aug 22, 2016 \| Posted by admin in MUSCULOSKELETAL MEDICINE \| Comments Off on 24. Headaches Full access? Get Clinical Tree Get Clinical Tree app for offline access Get Clinical Tree app for offline access