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 “umbrella” concept
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. Wolff’s 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. Individuals’ self-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. Wolff’s 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. Wolff’s 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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