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Although episodic migraine is highly prevalent in the headache

population, chronic daily headache, especially that of long duration, can

pose an even more significant burden on individuals, their families, and

society. Chronic daily headache sufferers approach nearly 5% of the

population. Addressing the disability caused by the condition represents

an important public health challenge because these individuals

demonstrate an even lower quality of life on standard HRQL measures

than migraine patients. As the leading problem in headache practice,

chronic daily headache is a great challenge to physicians. Successful

treatment offers enormous scientific, clinical, and public health

opportunities.

Meletiche DM, Lofland JH, Young WB. Quality-of-life differences between patients

with episodic and transformed migraine. Headache. 2001;41(6):573-578.

Despite these shortcomings, the IHS division of all headaches into 2 major

groups is a simple, intuitive, and clinically applicable approach to headache

diagnosis. Indeed, the distinction between primary and secondary headaches

is, in reality, the first objective of every headache evaluation.

Primary headache types (shown in red here) are by definition benign, relatively

few in number and, fortunately, represent the vast majority of headache types

seen in clinical practice. Secondary headaches (shown in gold here), on the

other hand, occur as a symptom of any of a long list of possible underlying

diseases.

1. Classification and diagnostic criteria for headache disorders, cranial neuralgias and

facial pain. Headache Classification Committee of the International Headache Society.

Cephalalgia. 1988;8; (suppl 7):1-96.

The cause or type of most headaches can be determined by a careful history

and physical examination. The clinical imperative is to recognize the warning

signals that raise red flags and prompt further diagnostic testing. In the

absence of worrisome features in the history or examination, the task is then

to diagnose the primary syndrome based upon the clinical features. If atypical

features are present or the patient does not respond to conventional therapy,

the diagnosis should be questioned and the possibility of a secondary

headache disorder should be revisited (1,2).

Because migraine and tension-type headache (TTH) account for over 90% of

the primary headache disorders in clinical practice, this discussion will focus

on their clinical features, the warning signals of serious secondary headaches,

and the role of diagnostic testing in the evaluation of headache (3).

1. Silberstein SD, Lipton RB, Goadsby PJ. Headache in Clinical Practice. London,

England: Martin Dunitz; 2002.

2. Olesen J, Tfelt-Hansen P, Welch KMA. The Headaches. 2nd ed. Philadelphia, PA:

Lippincott, Williams & Wilkins; 2000.

3. Rasmussen BK, Jensen R, Schroll M, Olesen J. Epidemiology of headache in a

general population – a prevalence study. J Clin Epidemiol. 1991;44:1147-1157.

An attempt to elicit these worrisome features should be part of every

new headache evaluation because their presence may signify an

underlying pathological condition for which diagnostic testing is

obligatory.

Systemic symptoms, such as fever, malaise, or weight loss, should

suggest an underlying infectious or systemic inflammatory disorder.

Newly acquired neurologic signs or symptoms should always raise

concern.

The mode of onset is perhaps the most important characteristic of a

headache to be delineated. Those patients who have a sudden or

abrupt headache that peaks in seconds or minutes require careful

assessment to exclude causes such as subarachnoid hemorrhage

(SAH) venous sinus thrombosis, arterial dissection, or raised

intracranial pressure.

Any new or progressive headache that begins in middle age or any

headache that deviates significantly from a previous pattern should be

investigated further.

If these features are addressed, the chance of overlooking a sinister

cause for headache are greatly diminished.

This slide summarizes the 1-year prevalence of some common primary

headache disorders. By far, the most common headache disorder in the

general population is episodic tension-type headache, which affects 40%

of the population. These are the bilateral, pressing or squeezing

headaches of everyday life that do not have many accompanying features.

Migraine also is a common primary headache disorder, affecting 18% of

women and 6% of men.

Chronic daily headaches occur 15 days per month and affect 5% of

women and 2.8% of men. The two most common headaches are chronic

tension-type headache and transformed/chronic migraine, which will be

discussed within the context of chronic daily headache.

1. Lipton RB, Stewart WF, Diamond S, et al. Prevalence and burden of migraine in

the United States: data from the American Migraine Study II. Headache.

2001;41(7):646-657.

2. Schwartz B, Stewart WF, Simon D, Lipton RB. Epidemiology of tension-type

headache. JAMA. 1998;279:381-383.

3. Scher AI, Stewart WF, Liberman J, Lipton RB. Prevalence of frequent headache

in a population sample. Headache. 1998;38:497-506.

The term chronic daily headache (CDH) has not been formally accepted

worldwide and continues to generate scholarly debate as to its validity

and precise criteria. The term is best considered an umbrellaconcept

under which several related or unrelated headache disorders may

reside.

The International Headache Society (IHS) has not completely

addressed the classification of very frequent primary headache. For the

purpose of this presentation, we will define CDH of long duration as a

broad group of primary headache syndromes, not related to structural

or systemic illness, that occur more frequently than 15 days per month

and have a duration of longer than 4 hours per day.

Silberstein SD, Lipton R, Solomon S, Mathew N. Classification of daily and near

daily headaches: proposed revisions to the IHS classification. Headache.

1994;34(1):1-7.

The current IHS classification system does not comprehensively

address the classification of very frequent headache. As currently

defined, many patients with frequent headache cannot be classified, or

when they can be classified, they are often placed in the CTTH group.

Silberstein and colleagues have recommended a revision or

modification of the IHS criteria for frequent primary headache disorders

and proposed adding several new headache types to the current IHS

criteria. These changes would include a subdivision of daily headache

into TM/CM, CTTH, NDPH, and HC.

In their study of 150 consecutive outpatients with CDH, Silberstein and

colleagues applied the current IHS criteria for frequent headache as

well as their proposed revisions. Diagnosis of chronic daily headache or

near-daily headache was based on the presence of pain lasting more

than 4 hours a day for at least 15 days per month.

Under the current IHS criteria, 43% or close to half of the patients could

not be classified. Using newly proposed criteria, all patients in the study

were classified, with 78% as TM/CM, 15% as CTTH, and 7% as NDPH

or hemicrania continua.

Silberstein SD, Lipton RB, Sliwinski M. Classification of daily and near-daily

Migraine with aura has been referred to as classic migraine. References to

headache have been recorded as early as 3000 BC. Hippocrates, in 400 BC,

described the visual aura of migraine preceding headache as a shining light,

usually in the right eye, followed by violent pain in the temple that eventually

reaches the head and neck area.Because aura is such a classic migraine

phenomenon, its presence is nearly always diagnostic of this condition.

Only about 1 migraine patient in 8 ever experiences an aura. These people

tend to have auras with some headaches, but not with all.

The migraine aura is a complex array of symptoms that reflect focal cortical or

brain stem dysfunction. The aura develops gradually, over a 5–20 minute time

period, usually lasts for less than 60 minutes, and is accompanied or followed

by a headache. In some instances, particularly in late life, the aura may occur

without an associated headache. The migraine aura is most commonly visual,

although the aura may present as a sensory, motor, brain stem or language

disturbance.

1. Classification and diagnostic criteria for headache disorders, cranial neuralgias and

facial pain. Headache Classification Committee of the International Headache Society.

Cephalalgia. 1988;8; (suppl 7):1-96.

2. Silberstein SD, Saper JR, Freitag FG. Migraine: diagnosis and treatment. In:

Silberstein SD, Lipton RB, Dalessio DJ, eds. Wolffs Headache And Other Head

The challenges in sorting through the overlapping features and making a

migraine diagnosis are illustrated in this chart.

The American Migraine Study II, published in 2001, replicating a survey

conducted a decade earlier, questioned 29,727 respondents about their

headaches. Individualsself-reported symptoms were assessed to determine

whether they met the IHS diagnostic criteria for migraine. In addition to IHSdefined

status, self-reported physician diagnosis was determined. Individuals

were assigned to self-reported categories of physician diagnosis based solely

on their reported diagnosis and whether they met IHS criteria for migraine (1).

Forty-one percent of male and 51% of female respondents reported receiving

a physician diagnosis of migraine. This chart shows the percentage of

respondents who met the IHS criteria for migraine who reported receiving a

diagnosis other than migraine. Thirty-two percent of undiagnosed migraine

respondents reported a diagnosis of TTH. Forty-two percent reported a

diagnosis of sinus headache (2). The prevalence in the population of TTH is

78%, and sinus headache is 15% (3).

1. Lipton RB, Stewart WF, Diamond S, et al. Prevalence and burden of migraine in the

United States: Data from the American Migraine Study II. Headache. 2001;41(7):

646-657.

2. Lipton RB, Diamond S, Reed M, et al. Migraine diagnosis and treatment: Results from

the American Migraine Study II. Headache. 2001;41(7):638-645.

The pain process is a combination of direct factors, such as activation of the nociceptors of pain-producing intracranial structures combined with reduced function of the endogenous pain-control pathways that normally gate the pain.

1. Raskin NH. Headache. 2nd ed. New York: Churchill Livingstone; 1988.

2. Barbanti P, Fabbrini G, Pesare M, Cerbo R. Neurovascular symptoms during migraine

attacks. [abstract] Cephalalgia. 2001;21(4):295.

3. Kaniecki R. Migraine headache exacerbation with sumatriptan injection: a sign of supratherapeutic dosing? [abstract] Cephalalgia. 2001;21(4):413.

Although research demonstrates that some criteria are more predictive of migraine tan others, no single criterion is sufficient. Likewise, no single criterion is essential to confirm a diagnosis of migraine.

A common misconception is that aura is the telltale sign of migraine. Eighty-five percent of migraine patients do not experience aura. Many, but not all, patients have other symptoms

that they recognize as premonitory. Common amongst these are: tiredness, stiff neck, craving for sweets, and yawning.

Although nausea is very common in migraine patients, vomiting occurs much less frequently. Most migraine patients experience nausea with a large proportion of their headaches, vomiting with a few of their headaches, and neither symptom with some of their headaches. Many migraine patients report never having vomited in association with

their headaches.

Unilateral pain is a common characteristic of migraine and can be a key symptom in making the diagnosis. However, many migraine patients report headaches that begin

bilaterally and then settle on one side or headaches that remain bilateral throughout, but

nonetheless meet the other criteria for migraine.

Similarly, pulsating or throbbing pain is a common characteristic of migraine but just as

many migraine patients will report a penetrating, boring, or stabbing pain.

Because approximately 80% of migraine patients also have other headaches and may

have more than one headache type at the same time, parsing out migraine symptoms can

be challenging. Headache specialists widely believe that moderate to severe, recurrent

headache is migraine until proven otherwise.

1. Pryse-Phillips WEM, Dodick DW, Edmeads JG, et al. Guidelines for the diagnosis and

management of migraine in clinical practice. Can Med Assoc J. 1997;156(9):1273-1287.

2. Russell MB, Rasmussen BK, Fenger K, Olesen J. Migraine without aura and migraine with

aura are distinct clinical entities: a study of four hundred and eighty-four male and female

More than in any other headache disorder, migraine sufferers identify

triggers. Stress is the trigger most commonly listed by patients. Dietary

factors are also frequently reported triggers, although few have been

scientifically validated. Although the impact of food triggers probably is

not great for the population, their impact could be for the individual.

Oversleeping and sleep deprivation are commonly recognized triggers.

Patients should maintain a routine bedtime and avoid sleeping in.

Hormonal headaches are triggered by variations in female estrogen

levels and possibly other hormonal factors. Noise, bright lights, and

fumes are commonly identified migraine triggers. Physical exertion can

cause headache of the subtype, exercise-induced migraine.

1. Silberstein SD, Saper JR, Freitag FG. Migraine diagnosis and treatment. In:

Silberstein SD, Lipton RB, Dalessio DE, eds. Wolffs Headache and Other

Head Pain. 7th ed. Oxford, England: Oxford University Press; 2001:121-237.

2. Silberstein SD, Lipton RB, Goadsby PJ. Headache in Clinical Practice.

Oxford, England: Isis Medical Media; 1998.

Treatment can be acute, preemptive, or preventive.

Acute treatment is initiated during an attack to relieve pain and disability

and to stop progression of the attack.

Preemptive treatment is used when a known headache trigger exists,

such as exercise or sexual activity, and for patients experiencing a timelimited

exposure to a trigger, such as ascent to a high altitude or

menstruation.

Preventive treatment is maintained for months or even years to reduce

attack frequency, severity, and duration.

Patients taking preventive medication can also use acute and

preemptive medication.

1. Silberstein SD. Preventive treatment of migraine: an overview. Cephalalgia.

1997;17(2):67-72.

2. Silberstein SD, Saper JR, Freitag FG. Migraine diagnosis and treatment. In:

Silberstein SD, Lipton RB, Dalessio DE, eds. Wolffs Headache and Other

Head Pain. 7th ed. Oxford, England: Oxford University Press. 2001:121-237.

A number of medications are available to treat migraine, and choice

depends on the severity and frequency of headaches. These categories

of medications include nonspecific and specific treatments.

Nonspecific treatments are those effective for any pain disorder and

include nonsteroidal anti-inflammatory drugs (NSAIDs), combination

analgesics, opioids, neuroleptics/antiemetics, and corticosteroids.

Specific therapies, such as ergotamine-containing compounds, DHE,

and triptans, are effective only for the treatment of migraine and related

disorders.

1. Diener HC et al. A practical guide to the management and prevention of

migraine. Drugs. 1998; 56(5):811-824.

Drugs useful in the prevention of migraine are often useful in the treatment of CDH. The following drugs are particularly valuable:

Antidepressants, which also treat often accompanying depression and

sleep disturbance. Tricyclics, such as amitriptyline, nortriptyline, and

doxepin, are generally considered first-line treatments. SSRIs may have

value for particular individuals. MAOIs may be useful for difficult cases.

Beta-adrenergic blockers are appropriate in those patients who are likely

to benefit and tolerate beta-adrenergic blockade.

Sodium valproate is particularly useful in the presence of varying

comorbidities, including rapid mood changes, seizure-like events, and in

patients who cannot tolerate or benefit from antidepressants or betaadrenergic

blockers.

Calcium channel antagonists as well as daily use of ergot derivatives, such

as methysergide, occasionally are required.

Monotherapy is preferred. Combination use of these medications must be

carried out cautiously, but various combinations of medication (known as

rational copharmacy) have proven useful, especially in resistant cases.

Rational copharmacy is the use of more than one agent at a time to enhance

treatment efficacy. Useful combinations may include a tricyclic antidepressant

and a beta-blocker, a beta-blocker and sodium valproate, or methysergide

and a tricyclic antidepressant.

Silberstein SD, Lipton RB, Goadsby PJ. Headache in Clinical Practice. 2nd ed. London,

England: Martin Dunitz; 2002.

A number of medications are available to treat migraine, and choice

depends on the severity and frequency of headaches. These categories

of medications include nonspecific and specific treatments.

Nonspecific treatments are those effective for any pain disorder and

include nonsteroidal anti-inflammatory drugs (NSAIDs), combination

analgesics, opioids, neuroleptics/antiemetics, and corticosteroids.

Specific therapies, such as ergotamine-containing compounds, DHE,

and triptans, are effective only for the treatment of migraine and related

disorders.

1. Diener HC et al. A practical guide to the management and prevention of

migraine. Drugs. 1998; 56(5):811-824.

An effective migraine management plan is based on establishing a therapeutic

partnership with the patient. Therapy can be optimized through a management

program that encompasses education and behavioral treatments as well as

pharmacologic therapy.

Educating patients on the nature and mechanism of their illness will help encourage

dialogue and empower the patient to actively participate in his or her own headache

management program.

Patients should be encouraged to keep a headache diary for both diagnostic and

treatment purposes. Review of the diary may yield previously unrecognized patterns

of headache, including migraine triggers. Work with the patient to identify possible

triggers, and discuss possible strategies to avoid or minimize exposure.

Behavioral strategies should be initiated, which include establishing more regular sleep

patterns, improvement in diet, and an exercise program. Patients should be

encouraged to participate in behavioral modification programs that have been proven

to be successful. These include cognitive-behavioral therapy, stress management,

relaxation training, and biofeedback therapy. Although active participation in

nonpharmacologic treatment may produce a slower response than pharmacologic

treatment, it encourages an active role for patients. These strategies are particularly

important when pharmacologic interventions are limited (eg, comorbid conditions

precluding specific migraine drugs).

Pharmacologic treatment of migraine can involve both acute and preventive

interventions. Patients with frequent headache may require both approaches. Acute

treatment is aimed at aborting the headache, whereas preventive treatment is geared

toward reducing the frequency and severity of anticipated attacks.

In summary, education, behavioral management, acute therapy, and preventive

The diagnosis must be properly established by ruling out organic disease.

A wide range of treatments is available and needed to effectively treat this

patient population. Acute treatment for CDH is directed at the acute

migraine or migraine-like events, including the standard abortive

medications for migraine.

Attempt to limit use of medication to no more than two headaches per

week and two doses per headache. In the presence of medication overuse

or rebound, these medications must be discontinued. Use of acute

medications that do not cause rebound is essential.

If the patient is rebounding, inpatient management or ambulatory infusion

treatment may be required. An escalation of acute pain is likely during this

period of medication overuse withdrawal. Aggressive, innovative pain

control methods must be used to maintain patient compliance.

If medications implicated in rebound are given again (which is

discouraged), they should be given no more than one to two days per

week on a regular basis. Nonmedical treatment, as well as aggressive

preventive and acute pharmacotherapy, are required. Reduction of

traditional headache (migraine) provoking factors, such as smoking and

stress, is worthwhile.

Often critical to outcome is the treatment of neuropsychiatric, comorbid,

and behavioral disturbances. The latter group of conditions often interferes

with headache treatment, frustrating both the physician and the family.

The source of pain in CDH is unknown: although several theories have been

proposed. These include the following:

Abnormal excitation of peripheral, nociceptive, afferent fibers from repetitive

peripheral input

Enhanced responsiveness of the nucleus caudalis neurons from repetitive,

central peripheral stimulation

Intrinsic dysnociception, perhaps genetically predisposed

Induction through medication overuse

Extrinsic factors of physical/psychological stress/infection/trauma that excite

the nervous system; stress also can reduce endogenous antinociception

Changes that can occur within the nervous system as a result of repetitive

attacks of migraine.

Particularly intriguing is the genetic predisposition possibility, which would render the

individual more vulnerable to extrinsic and intrinsic provocation. Central sensitization

and windup, among other neurobiological phenomena, might explain the basis for

induction progression in patients with frequent and repetitive migraine attacks.

Other concepts that have been forwarded in the literature regarding the possible

mechanism of chronic daily headache, as well as chronic migraine, include central hyperexcitability of pain systems, low serotonin with receptor upregulation, NMDA receptor dysfunction, low beta endorphin levels and viral provocation.

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