Headache
Paul G. Mathew, M.D.,1,2 and Ivan Garza, M.D.3
ABSTRACT
KEYWORDS: Primary headache, migraine, trigeminal autonomic cephalgias, cluster
headache, tension-type headache
EVALUATION The ï¬rst 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 speciï¬c 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: PMATHEW@partners.org).
1
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
Ofï¬ce-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:
https://dx.doi.org/10.1055/s-0031-1271313. 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-speciï¬c 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 Classiï¬cation
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.
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SEMINARS IN NEUROLOGY/VOLUME 31, NUMBER 1
2011
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
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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 classiï¬cation,
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-ï¬nding difï¬culties. 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,’’ ‘‘ï¬rst,’’ or ‘‘worst’’ headache, a
signiï¬cant 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 immunodeï¬ciency
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.
HEADACHE/MATHEW, GARZA
7
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 ï¬rst 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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Primary
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SEMINARS IN NEUROLOGY/VOLUME 31, NUMBER 1
2011
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 ï¬rst
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, ï¬ts 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 ‘‘ï¬rst’’ 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 Classiï¬cation of Headache Disorders 2nd Edition (ICHD-2) is the
current guideline that headache specialists use for the accurate classiï¬cation
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 classiï¬cation are available online at the
International Headache Society’s Web site (https://ihs-classiï¬cation.org/en).
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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HEADACHE/MATHEW, GARZA
9
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 ï¬ve attacks fulï¬lling 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 fulï¬lling 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 fulï¬lling criteria
B–D for migraine without aura begins during the aura or follows aura within 60
minutes E. Not attributed to another disorder
ABORTIVE MIGRAINE TREATMENT
Nonsteroidal anti-inflammatory medications (NSAIDs),antiemetics, triptans, and
dihydroergotamine are the mainstays of abortive treatment for migraine
headaches. Other commonly used nonspeciï¬c 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 speciï¬c 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 beneï¬cial, 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.
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SEMINARS IN NEUROLOGY/VOLUME 31, NUMBER 1
2011
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 MIGRAINE TREATMENT
Preventative medications should be considered in cases where migraines occur
with high frequency or signiï¬cantly 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 efï¬cacy. Propranolol, topiramate, divalproex sodium,
and amitriptyline have proven efï¬cacy and are considered ï¬rst-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
efï¬cacy 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 beneï¬t 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 beneï¬ts 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
HEADACHE/MATHEW,GARZA
11
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, speciï¬c 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 deï¬nition, 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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SEMINARS IN NEUROLOGY/VOLUME 31, NUMBER 1
2011
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 ofï¬ce 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 efï¬cacy be achieved. This
article provides a basic foundation in the essential elements of ofï¬ce based
headache management, and hopefully serves as a means to the advancement of
headache care in the setting of a highly underserved subspecialty.
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Table 12 Medication Overuse Headache Diagnostic Criteria5
A. Headache present on 15 days/month fulï¬lling criteria B and C B.
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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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2011
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