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Paul G. Mathew, M.D.,1,2 and Ivan Garza, M.D.3


KEYWORDS: Primary headache, migraine, trigeminal autonomic cephalgias, cluster headache, tension-type headache

EVALUATION The first major step that a neurologist must take when evaluating a headache patient in an outpatient neurology practice is to establish whether the headache is a ‘‘primary’’ or ‘‘secondary’’ type of headache. Primary headaches are those that cannot be attributed to an underlying disorder, whereas secondary headaches are due to a specific underlying cause or disorder. In the case of secondary headaches, addressing the underlying disorder can often, but not always, lead to resolution of the headaches. Some of the common causes of secondary headaches are listed in Table 1.

History The most fundamental and essential component in the evaluation of headaches is a thorough history. Table 2 summarizes the important elements of a headache hisDepartment of Neurology, Brigham and Womens Faulkner Hospital, John R. Graham Headache Center, Jamaica Plain, Massachusetts; 2 Division of Neurology, Cambridge Health Alliance, Cambridge, Massachusetts; 3Department of Neurology, Mayo Clinic, Rochester, Minnesota. Address for correspondence and reprint requests: Paul G. Mathew, M.D., John R. Graham Headache Center, 1153 Centre Street, Suite 4970, Jamaica Plain, MA 02130 (e-mail:


tory. The history should be chronological, and should document the evolution of all associated symptoms. It is vital to have the patient recall when the headaches began, and whether there were any triggeringevents around the time of onset. Events such as head trauma, the presence of infectious diseases or inflammatory processes, and other neurologic disorders can all be associated with the development of headaches. Other details that should be elicited include the location, radiation, quality, frequency, and duration of pain. For female patients with headaches, seeking any prior or current association with menstruation, pregnancy, and/ or hormone therapy can be useful. In addition, assessing the presence of photophobia, phonophobia, osmophobia, nausea, vomiting, cutaneous allodynia, unilateral runny/stuffy nose, monocular tearing, monocular eye redness, and unilateral eyelid ptosis can be helpful in classifying headaches. Patients
Office-Based Neurology; Guest Editor, Devon I. Rubin, M.D. Semin Neurol 2011;31:5–17. Copyright # 2011 by Thieme Medical Publishers, Inc., 333 Seventh Avenue, New York, NY 10001, USA. Tel: +1(212) 584-4662. DOI: ISSN 0271-8235.


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Headache is one of the most common complaints among patients presenting to an outpatient neurology practice. The evaluation, diagnosis, and treatment of headache can be rather cumbersome and at times quite challenging for even the most seasoned neurologist. Many complex issues that although not causative, can play an exacerbating role in the genesis of headaches. In this article, the authors review some of the essential elements that are part of headache evaluation including headache-specific history, physical examination,warning signs of secondary headache disorders, and when to consider further studies. They then provide a brief review on the diagnosis of primary headache disorders according to the International Headache Society’s International Classification of Headache Disorders, 2nd Edition (ICHD-2), and treatment strategies of the more common primary headache disorders with a focus on migraine, trigeminal autonomic cephalalgias, tension-type headache, and chronic daily headache.




Table 1 Causes of Secondary Headache
Cause Cerebrovascular diseases Altered CSF dynamics Intracranial space-occupying lesion Infection Trauma Musculoskeletal Medications
CSF, cerebrospinal fluid.

Examples Carotid or vertebral artery dissension, cerebral venous sinus thrombosis, arteriovenous malformations, subdural hematoma, giant cell arteritis Idiopathic intracranial hypertension, hydrocephalus, spontaneous CSF leak Neoplasm, abscess Meningitis, encephalitis, abscess, sinusitis Cervical spine disorders, temporomandibular joint disorders Medication overuse headache

Table 2 Essential Elements of a Headache History
Age of onset Frequency Duration Time of onset Time to maximum intensity Characteristics – location, quality, severity Associated symptoms and signs – before, during, and after headache Precipitating factors Aggravating factors Relieving factors Previous treatments Review of systems Past medical history Family history Social history – occupation, habits, etc. Emotional state

Downloaded by: World Health Organization ( WHO). Copyrighted material.often deny many of these features, but the presence of these features can be assessed by asking about typical pain behaviors during more severe headaches. For example, migraine patients often deny photo- or phonophobia, but will admit to the preference of a dark, quiet room. Establishing the presence of a visual, sensory, language, or motor aura can be useful in migraine headache classification, but determining whether a symptom is a true aura or secondary to another cause can often be challenging. Common aura pretenders include blurred vision secondary to an ophthalmologic cause, tingling due to a peripheral nerve disorder such as carpal tunnel, and concentration issues rather than true aphasia due to chronic pain or sleep issues. Several factors can help delineate true aura from symptoms from another cause. A true aura typically occurs before or during the early portion of the pain phase of migraine headaches. Auras tend to have a gradual progression over minutes, such as enlarging scotomas, or a marching progression of numbness, weakness, and/or tingling

through an extremity. True language auras will manifest as the inability to name objects, read, write, understand others, and/or carry out simple conversation, rather than vague word-finding difficulties. Accompanying family members or friends can help to clarify features of language involvement. Classic visual auras consist of flashing or scintillating lights in the periphery of the vision, rather than just blurry vision, which is a common complaint, but not a true aura. Sleep is another behavior that should be scrutinized routinely during aheadache history because poor sleep hygiene can worsen headaches. Total hours of sleep, sleep interruptions and awakenings, the presence of snoring, restlessness, waking up feeling poorly rested, and excessive daytime sleepiness are all aspects of sleep that should be analyzed. Triggering or worsening of headaches with position changes, physical activity, coughing, sneezing, talking, chewing, and/or popping or clicking of the jaw are important details, especially when considering secondary causes of headaches. The clinician should remain vigilant of the ‘‘red flags’’ that could suggest a secondary headache rather than a primary headache disorder. These include age of headache onset >50 years, a ‘‘new,’’ ‘‘first,’’ or ‘‘worst’’ headache, a significant change in the characteristics of prior headaches, a headache always on the same side, increasingly worsened frequency and/or severity of headache, headache not responding to treatment, known systemic illnesses that predispose to secondary headaches (e.g., cancer or human immunodeficiency virus [HIV]), signs of systemic illness (e.g., fever, weight loss), posttraumatic headache, neurologic symptoms not consistent with typical aura (e.g., seizures), or an abnormal neurologic examination. Table 3 lists disorders that should be considered when certain ‘‘red flags’’ are present. Finally, a detailed history should also include past medical history, surgical history, social history, family history (especially of headaches), medication history, and procedural history. Medication history is of particular importance, and this should include the medicationdose, length of treatment, outcome, and adverse effects.



Table 3 Headache Red Flags and Diagnostic Considerations
Sign/Symptom ‘‘Thunderclap headache’’ is a sudden onset severe headache, maximum in intensity immediately, or in less than 60 seconds. Possible Causes Secondary Subarachnoid hemorrhage Other intracerebral hemorrhage Carotid/vertebral dissection CNS angiopathy Intracranial aneurysm CSF leak Pituitary apoplexy Third ventricle colloid cyst Ischemic stroke Cerebral venous sinus thrombosis Hypertensive crisis Reversible cerebral vasoconstrictive syndrome Primary orgasmic headache Migraine Primary thunderclap headache During or after physical exertion Secondary causes (43% had structural lesions in one series) Subarachnoid hemorrhage Intracranial neoplasm Third ventricle colloid cyst Arterial dissection Pheochromocytoma Cardiac ischemia Primary causes Migraine Primary exertional headache Nocturnal, wakening from sleep Secondary Intracranial space-occupying lesions Raised intracranial pressure Idiopathic intracranial hypertension (pseudotumor cerebri) Medication overuse headache (‘‘rebound headache’’) Obstructive sleep apnea Cervicogenic Primary Hypnic headache Cluster headache Migraine Orthostatic (worse while standing) CSF leak Secondary (following lumbar puncture, ENT surgery, neurosurgery, etc.) With papilledema Spontaneous (no clear cause) Secondary Intracranial space-occupying lesions Cerebral venous sinus thrombosis CT brain without contrast (acute setting) MRI and MRV brain Lumbar puncture with opening pressure – only if no intracranialspace-occupying lesions found MRI head with gadolinium if spontaneous CSF leak suspected ENT or neurosurgery referral MRI brain with contrast Cervical spine X-ray or MRI Possibly overnight oximetry Acute setting or with first occurrence: CT head Consider CSF MRI brain with gadolinium and MRA head/neck Testing to Consider CT in the acute setting MRI with gadolinium MRA head and neck MRV CSF if imaging normal Pheochromocytoma evaluation

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Table 3 (Continued )
Sign/Symptom Possible Causes Intracranial hemorrhage Primary Idiopathic intracranial hypertension (IIH or ‘‘pseudotumor cerebri’’) –Tend to be young, obese women –Transient visual obscurations During sexual activity and increases with sexual excitement At orgasm, typically an ‘‘explosive’’ or ‘‘thunderclap’’ Secondary causes Subarachnoid hemorrhage Arterial dissection CSF leak Primary orgasmic headache if other causes ruled out Brief headache with coughing, sneezing, straining, or Valsalva Secondary causes (50% have structural disease) Posterior fossa lesions (e.g., tumor) Arnold-Chiari malformation CSF leak Intracranial aneurysms Primary cough headache
CNS, central nervous system; CSF, cerebrospinal fluid, CT, computed tomography; ENT, ear, nose, throat; MRA, magnetic resonance angiography; MRI, magnetic resonance imaging; MRV, magnetic resonance venography.

Testing to Consider Ophthalmology exam required

Primary preorgasmic headache

Less worrisome for secondary cause when compared withorgasmic headache On first onset, it is mandatory to exclude a subarachnoid hemorrhage and arterial dissection Nonacute setting: MRI brain with gadolinium and MRA head/neck MRI brain with gadolinium Possibly MRA head

Physical Examination and Diagnostic Testing All patients that present with a chief complaint of headaches should have a thorough physical examination and neurologic examination, which should always include funduscopy to assess for papilledema or signs of increased intracranial pressure. For headache patients, additional examination maneuvers should be considered as a supplement to the neurologic examination to help identify certain etiologies. Palpation of the head and neck can be useful in assessing for cutaneous allodynia, temporal arteritis, and muscular tension. Examination of the temporomandibular joint can be helpful, as pain associated with popping and clicking of this joint can exacerbate headaches. Percussion over the occipital nerves (Tinel sign) may often reproduce a painful neuralgic paroxysm in occipital neuralgia. In addition, assessing neck stiffness on active and passive range of motion can suggest a cervicogenic component or meningismus. Imaging studies, and the type of imaging obtained, should be considered on an individual case basis. In general, imaging studies should be pursued in newonset headaches, worsening headaches with changes in character, headaches with focal neurologic signs, and any time the patient claims to be having the worse headache of his or her life. In patients with typical migraine headaches, imaging is seldom needed, but should beconsidered when the headache is associated

with a protracted or atypical aura, occurs after trauma, occurs after age 50 years, fits a basilar-type or hemiplegic form (see ICHD-2), is associated with increasing frequency, quality, or severity, or if a patient is in status migrainosus. Additionally, if the patient presents with their ‘‘first’’ or ‘‘most severe’’ migraine, imaging should be considered. Table 3 reviews suggested neuroimaging studies that should be performed in certain circumstances.

PRIMARY HEADACHE DIAGNOSIS Once the clinician has ruled out a secondary headache, making an accurate primary headache diagnosis is critical because each type of primary headache disorder has known treatment options that differ among the different primary headaches. The International Headache Society’s International Classification of Headache Disorders 2nd Edition (ICHD-2) is the current guideline that headache specialists use for the accurate classification of primary headache disorders. Since its publication in 2004, it has undergone minor revisions and is expected to continue to evolve through time.1 The diagnostic criteria and classification are available online at the International Headache Society’s Web site ( Although a detailed discussion of all primary headache disorders is beyond the scope of this article, here we will review the diagnosis and management of

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several of the more common primary headache disorders presenting to an outpatient neurology practice.Table 4 The International Classification of Headache Disorders, 2nd Edition (IHCH-2) Migraine Diagnostic Criteria1
Migraine without aura A. At least five attacks fulfilling criteria B–D B. Headache attacks lasting 4–72 hours (untreated or unsuccessfully treated) C. Headache has at least two of the following characteristics: Unilateral location Pulsating quality Moderate or severe pain intensity Aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs) D. During headache at least one of the following: Nausea and/or vomiting Photophobia and phonophobia E. Not attributed to another disorder Migraine with aura A. At least two attacks fulfilling criteria B–D B. Aura consisting of at least one of the following, but no motor weakness: Fully reversible visual symptoms including positive features (e.g., flickering lights, spots or lines) and/or negative features (i.e., loss of vision) Fully reversible sensory symptoms including positive features (i.e., pins and needles) and/or negative features (i.e., numbness) Fully reversible dysphasic speech disturbance C. At least two of the following: Homonymous visual symptoms and/or unilateral sensory symptoms At least one aura symptom develops gradually over 5 minutes and/or different aura symptoms occur in succession over 5 minutes Each symptom lasts 5 and 60 minutes D. Headache fulfilling criteria B–D for migraine without aura begins during the aura or follows aura within 60 minutes E. Not attributed to another disorder


Nonsteroidal anti-inflammatory medications (NSAIDs),antiemetics, triptans, and dihydroergotamine are the mainstays of abortive treatment for migraine headaches. Other commonly used nonspecific analgesics include acetaminophen, aspirin, cyclooxygenase 2 inhibitors, opiates, and combination analgesics that vary in content. Of the various medications used for migraine headaches, only triptans and dihydroergotamine are specific for migraines. Several different triptans are available for treatment of migraines (Table 5). All oral triptans can be effective and relatively well tolerated. As a class of medications, the differences between oral triptans are generally relatively small, but the effects can vary among individual patients.6 One of the factors for initial consideration in choosing a triptan is cost and formulary coverage of an individual’s insurance plan. Sumatriptan is currently the only generic triptan on the market. If sumatriptan is tolerated, but only somewhat beneficial, it can be combined with an NSAID and/or an antiemetic such as promethazine. In cases where sumatriptan is ineffective, switching to a different triptan or formulation would be reasonable. In addition to oral formulations, triptans are available as orally dissolving, intranasal, and injectable preparations. These routes of administration that may be particularly useful for these migraine patients with early and prominent vomiting. It is essential to warn patients that triptans often induce transient side effects including chest or throat

tightness, flushing, a heat sensation, dizziness, nausea, drowsiness, and tingling. Warning patients of these transient side effects canprevent patient anxiety related to the future triptan use and even emergency room visits for what patients confuse to be an anaphylactic reaction. Triptans should be avoided in patients with a history of coronary artery disease, stroke or transient ischemic

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Migraine Migraine is the most common primary headache disorder for which patients present for evaluation and treatment. In U.S. population studies, the prevalence of migraine is 18% in women and 6% in men.2–4 Migraine is divided into migraine with and migraine without aura. The ICHD-2 criteria for migraine are listed in Table 4. ‘‘Chronic migraine’’ is diagnosed when the migraine headache frequency is greater than 15 days per month (tension-type and/or migraine) and when 8 of those days involve headaches that satisfy criteria for migraine and that respond to treatment with triptans or ergots for greater than 3 months.5 Medication overuse headache (previously called ‘‘rebound headache’’) must be excluded when a diagnosis of chronic migraine is considered (see chronic daily headache section). If a patient is using acute headache treatments more than 2 days a week on average, the clinician should suspect medication overuse headache.




Table 5 Formulations and Half-Lives of Triptan Medications6
Generic Name Almotriptan Eletriptan Frovatriptan Naratriptan Rizatriptan Sumatriptan Zolmitriptan Brand Name Axert1 Relpax1 Frova1 Amerge1 Maxalt1 Imitrex1 Zomig1 Half-Life (Hours) 3–4 4 26 6 2–3 2.5 3Administration and Dose Oral 6.25, 12.5 mg Oral 20, 40 mg Oral 2.5 mg Oral 1, 2.5 mg Oral 5, 10 mg ODT 5, 10 mg Oral 25, 50, 100 mg Intranasal 5, 20 mg Subcutaneous 4, 6 mg Oral 2.5, 5 mg ODT 2.5, 5 mg Intranasal 5 mg
Adapted from Ferrari MD, Goadsby PJ. Triptans (serotonin, 5-HT1B/1D agonists) in migraine: detailed results and methods of a meta-analysis of 53 trials. Cephalalgia 2002;22(8):633–658.


Preventative medications should be considered in cases where migraines occur with high frequency or significantly interfere with the patient’s daily routines. Preventatives should also be considered when abortive treatments are contraindicated, have failed, have adverse effects, or are being overused. Preventative treatments for migraine span several different classes, including b-blockers (propranolol, atenolol, nadolol, metoprolol, timolol), calcium-channel blockers (verapamil), anticonvulsants (topiramate, divalproex sodium, gabapentin), and tricyclic antidepressants (amitriptyline, nortriptyline, protriptyline) (Table 6). There are several factors to be considered when choosing a preventative medication. A medication should be chosen that has proven efficacy. Propranolol, topiramate, divalproex sodium, and amitriptyline have proven efficacy and are considered first-line medications. The presence of a comorbid condition, such as hypertension or seizures, may lead to choosing a medication that may treat the condition as well as the migraine headaches. In some cases, a medication may be initiated for the comorbid condition in a patient whose headaches may not havenecessarily warranted a preventative medication, such as in a patient with infrequent headaches in whom a b-blocker is initiated for hypertension. As a

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attacks, and peripheral vascular disease. Other relative contraindications include uncontrolled blood pressure, smoking, hormone replacement, pregnancy, and breastfeeding. Concomitant use of selective norepinephrine reuptake inhibitors (SNRIs) or selective serotonin reuptake inhibitors (SSRIs) and triptans carry a very low risk of serotonin syndrome, and should not prevent appropriate patients from receiving treatment with triptans.7 Patients, however, should be warned of the symptoms of serotonin syndrome, and should seek medical attention immediately if those symptoms occur. In patients that fail to respond to over-the-counter analgesics and triptans, dihydroergotamine is a reasonable next option. Dihydroergotamine has similar contraindications to triptans.

general guideline, all preventative medications should be started at low doses and titrated slowly until the minimum effective dose is reached. A reasonable goal of prophylaxis is not to eliminate headaches but to decrease their frequency and intensity. All preventative medication trials should have a duration of at least 3 months at a therapeutic dose before a decision regarding efficacy can be made. It is important to realize that adequate doses and durations of medications may cause some level of mild improvement in headache frequency and intensity that does not meet the expectations of the patient and at timesthe provider. A preventive medication should be considered successful if it decreases headache frequency by 50%. Although monotherapy is preferred, in clinical practice some patients with refractory headaches may receive additive benefit from combinations of preventative treatments.8 Botulinum toxin type A injections may be an effective preventative treatment for certain migraine patients.9 This treatment is usually selected in patients with prophylactic medication failure, medication intolerance, limiting comorbidities, and/or poor compliance. If botulinum toxin type A is found to be effective, the benefits of botulinum toxin can be as short as 2 months and as long lasting as 4 months, and repeating injections at 3-month intervals is usually required.10 Figure 1 illustrates common injection sites utilized for botulinum toxin type A injections for migraine treatment. Infrequently, patients can develop neutralizing antibodies to botulinum toxin. This risk can be limited by minimizing the frequency of dosing to no more than every 3 months, and using the lowest effective dose.11,12 Based on negative trials and a recent evidence-based review, episodic migraine does not appear to be a good indication for botulinum toxin type A injections.13 Recent randomized, double-blind, parallel-group, placebo-controlled phase followed by open-label phase trials involving over 1200 subjects have yielded encouraging results for the use of botulinum toxin A in chronic migraine and suggested that botulinum toxin A is an effective, safe, and well tolerated treatment for chronic migraine.14,15



Table 6 Commonly Used Migraine Prophylactic Medications
Initial Dose (mg) 10 10 25–500 40–60 25 80–160 300 15–25 Typical Total Daily Dose Range (mg) 25–150 25–150 750–1500 40–240 50–100 160–480 900–2400 75–200 Adverse Effects Common Weight gain, constipation, sedation Nortriptyline Divalproex sodium Propranolol Atenolol Verapamil Gabapentin Topiramate Same as above Alopecia, weight gain, nausea, tremor Depression, fatigue Same as above Edema, constipation Edema, sedation, fatigue, dizziness Paresthesias, fatigue, weight loss Acute angle glaucoma, hyperthermia, metabolic acidosis, nephrolithiasis
Reprinted from Garza I, Swanson JW. Prophylaxis of migraine. Neuropsychiatr Dis Treat 2006;3(1):281–291. Copyright (2006), with permission from Dove Medical Press Ltd.

Drug Amitriptyline

Serious Cardiac dysrhythmias Same as above Pancreatitis, liver failure, thrombocytopenia Bradyarrhythmia Same as above Hypotension, dysrhythmias

There is a frequent association between migraines and menstrual periods in women with migraine headaches. If migraines occur only during their menstrual period, the label of ‘‘pure menstrual migraine’’ is applied. If they tend to have increased frequency and/or intensity of their migraines around the time of their menstrual periods, but also have migraines outside of their menstrual periods, the label of ‘‘menstrually associated migraine’’ is applied. In either case, specific prophylactic strategies can be applied around the time of menstrual periods and used in addition to more continuous preventative treatment. One strategy is the use oflongeracting triptans, such as frovatriptan or naratriptan, taken twice a day on a standing basis starting 2 days prior to the onset of menses, and continuing for 3 days into menses.16,17 Another strategy for menstrual migraine is

administration of a nonsteroidal anti-inflammatory medication, such as naproxen sodium, twice a day on a standing basis starting 2 days prior to the onset of menses, and continuing for 3 days into menses.18,19

Trigeminal Autonomic Cephalgias Trigeminal autonomic cephalgia (TAC) is a category of headaches that manifests as unilateral head pain associated with ipsilateral autonomic features. By definition, individual attacks can only occur on one side of the head, but infrequently sufferers can have attacks on the other side of the head. However, TACs never present as bilateral pain during an individual attack. Autonomic features include lacrimation, conjunctival injection, ptosis, and/or rhinorrhea that are ipsilateral to the pain.20

Figure 1 Common botulinum toxin type A injection sites for chronic migraine. (From Garza I, Cutrer F. Pain relief and persistence of dysautonomic features in a patient with hemicrania continua responsive to botulinum toxin type A. Cephalalgia 2010; 30(4):500–503. Reprinted with permission from Mayo Foundation for Medical Education and Research. All rights reserved.)

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Table 7 Trigeminal Autonomic Cephalgias20
Hemicrania Sex Frequency (per day) Length (min) Circadian/circannual Episodic:Chronic NauseaPhotophobia/phonophobia Agitation/restlessness Triggers Alcohol Cutaneous Treatment effects Oxygen Sumatriptan, 6 mg Indomethacin 70% 90% No effect No effect 20% 100% No effect 3 months C. At least two of the following pain characteristics: Bilateral location Pressing/tightening (nonpulsating) quality Mild or moderate intensity Not aggravated by routine physical activity such as walking or climbing D. Both of the following No more than one of photophobia, phonophobia or mild nausea Neither moderate or severe nausea nor vomiting E. Not attributed to another disorder2

CONCLUSION The management of headaches can be a complex and challenging task for the office based neurologist. It cannot be stressed enough that only through a thorough evaluation, and the establishment of the correct primary or secondary headache diagnosis can therapeutic efficacy be achieved. This article provides a basic foundation in the essential elements of office based headache management, and hopefully serves as a means to the advancement of headache care in the setting of a highly underserved subspecialty.

1. Headache Classification Subcommittee of the International Headache Society. The International Classification of Headache Disorders: 2nd edition. Cephalalgia 2004;24(Suppl 1): 9–160 2. Lipton RB, Stewart WF, Simon D. Medical consultation for migraine: results from the American Migraine Study. Headache 1998;38(2):87–96 3. Lipton RB, Stewart WF, Diamond S, Diamond ML, Reed M. Prevalence and burden of migraine in the United States: data from the American Migraine Study II. Headache 2001; 41(7):646–657 4. LiptonRB, Diamond S, Reed M, Diamond ML, Stewart WF. Migraine diagnosis and treatment: results from the American Migraine Study II. Headache 2001;41(7):638– 645 5. Olesen J, Bousser MG, Diener HC, et al; Headache Classification Committee. New appendix criteria open for a broader concept of chronic migraine. Cephalalgia 2006;26(6): 742–746 6. Ferrari MD, Goadsby PJ, Roon KI, Lipton RB. Triptans (serotonin, 5–HT1B/1D agonists) in migraine: detailed results and methods of a meta-analysis of 53 trials. Cephalalgia 2002; 22(8):633–658 7. Wenzel RG, Tepper S, Korab WE, Freitag F. Serotonin syndrome risks when combining SSRI/SNRI drugs and triptans: is the FDA’s alert warranted?. Ann Pharmacother 2008;42(11):1692–1696

that medication overuse headache has a prevalence of 1 to 1.4% in the general population, and women in their 50s have the highest subset prevalence of 5%.61 In the setting of medication overuse, both abortive and preventative treatments tend to be less effective.
Table 12 Medication Overuse Headache Diagnostic Criteria5
A. Headache present on 15 days/month fulfilling criteria B and C B. Regular overuse for 3 months of one or more acute/ symptomatic treatment drugs as defined under sub forms of 8.2 Ergotamine, triptans, opioids, or combination analgesic medications on 10 days/month on a regular basis for >3 months Simple analgesics or any combination of ergotamine, triptans, analgesics, opioids on 15 days/month on a regular basis for >3 months without overuse of any single class alone C. Headache has developed or markedly worsened during medication overuse

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Table 11 The International Classification of Headache Disorders, 2nd Edition (IHCH-2) New Daily Persistent Headache Diagnostic Criteria1




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