Headache Disorders
Adam Quick, MD
Department of Neurology
adam.quick@osumc.edu
Objectives
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At the end of the module,
you will learn to:
Be able to list the important questions to ask when taking a history from a
patient with recurrent headaches.
List the most important things to check on neurologic examination in a
patient with headaches.
Distinguish a dangerous headache (such as subarachnoid hemorrhage,
meningitis, expanding mass lesion or temporal arteritis) from benign/primary
headaches.
For each of the major primary headaches, describe the typical clinical
features: frequency, onset, location, duration, character, premonitory
symptoms, accompanying features, triggering or provocative features,
ameliorating features, family history.
Describe briefly current theories of altered neuronal activity in the etiology of
migraine and cluster headaches.
Describe the physiological and clinical manifestations of headaches
Headache
 Headaches are an extremely common problem
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Most people will experience a headache of some sort during their
lifetime
Primary headache disorders are headache syndrome that are not
caused by another medical problem – the headache syndrome IS
the disorder itself
 First purpose of history and examination is to distinguish
benign recurrent or primary headaches from secondary
headaches that suggest the possibility of a lifethreatening event or condition
History Taking
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Age of onset
Frequency – single vs recurrent
Onset, rate of progression
Character of pain: pressure, stabbing,
throbbing, pounding
 Location of pain
 Severity of pain
 Duration
Symptoms Suggestive of Primary HA Disorder
 Stable pattern of headache over time…even if the
current headache is a little atypical
 Follows pattern of a defined primary headache
 Positive family history
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Most common with migraine
 Headache improves with sleep
 Headache worsened during or just prior to menses in
women
 Normal physical and neurological examinations
Additional Headache history
 Premonitory symptoms - auras
 Associated symptoms such as nausea, vomiting,
photophobia, phonophobia, tearing, ataxia, visual
disturbances, numbness, other focal neurologic
symptoms
 Provocative and ameliorative symptoms
 And do you have several different types of headache
types?
 Important medications: oral contraceptives, analgesic
medications, anti-platelet agents
Headache Warning Signs
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First or worst headache of life
Abrupt new headache symptoms or clear change in
headache pattern
New onset headache after age 50
Headache that disrupts sleep or is present upon
awakening
Headache brought on by exertion or coughing
Headache with a significant positional component
New headache following head trauma
Signs/symptoms of systemic illness: fever, night sweats,
weight loss
Neck stiffness
Alterations in personality, behavior or consciousness
Abnormal neurologic exam
Physical Examination
 Vital signs: pulse, blood pressure, fever
 General systems examination: rash
 Pupils,visual fields and fundi (papilledema and retinal
hemorrhages)
 Localizing signs on neurologic exam
 Signs of meningeal irritation – meningismus or neck
stiffness
 Superficial temporal artery pulses
Diagnostic Testing
 Labs that may be useful include :CBC,
Erythrocyte sedimentation rate, Thyroid
Stimulating hormone level and
toxicology
 Lumbar Puncture
 Neuroimaging
Lumbar Puncture
 Crucial in several clinical situations
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First or worst headache of the patient’s life
Headache associated with altered mental status or fever
Progressively worsening headache
Postural headache
An atypical chronic and intractable headache
 Generally in a patient presenting with headache it is
reasonable to get imaging (CT) prior to LP
Indications for Neuroimaging
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Any unexplained objective abnormality
on neurological exam
Rapidly increasing headache frequency
History of being awakened by headache
New headache in patients with cancer or
immune deficiency
H/O IV drug use
Recent head trauma or history of falls
(especially in elderly)
New-onset HA after age 50
HA precipitated by coughing, sexual
activity, exercise
Fever, personality changes or altered
level of consciousness
Head CT has about a 95% chance of
finding sub-arachnoid hemorrhage within
the first 24 hours
Headache – Initial Impression
After taking the history and performing an exam, you
should be able to categorize the headache as most likely
a primary headache disorder such as migraine or tension
headache vs. a secondary headache from a process
such as meningitis or intracranial hemorrhage.
Life-Threatening Headache
Conditions
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Subarachnoid hemorrhage
Intraparenchymal hemorrhage
Meningitis/Encephalitis
Expanding mass (tumor, abscess)
Hypertensive crisis
Temporal arteritis
•PRIMARY HEADACHE DISORDERS
MIGRAINE
TENSION HEADACHE
CLUSTER HEADACHE
The word migraine is French in origin and
comes from the Greek hemicrania
(as does the Old English term megrim)
hemicrania means “half the head"
MIGRAINE
Migraine Headache
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Common disorder with peak prevalence in middle age
15-18% of females!!!!
6% of males
7% of children
Onset usually in 2nd or 3rd decade, prevalence increases
to age 40 and then declines
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Males more commonly have onset prior to puberty and frequently
improve in their late teens and 20’s
Females more commonly have onset during puberty and may see
a remission at menopause
Diagnostic Criteria for Migraine
Defined as at least 5 episodic attacks of HA lasting 4
to72 hr with two of the following symptoms:
 Unilateral pain
 Pulsating or throbbing type of pain
 Pain of moderate-severe intensity
 Aggravation with movement, or activity
And one of the following: nausea and/or vomiting;
photophobia or phonophobia
Migraine Aura
 Seen in about 30% of migraine patients
 Cortical spreading depression - a wave of oligemia
that passes across the cortex at the rate of 2-6 mm
per minute preceded by initial short phase of
hyperemia
 Oligemia is a response to depressed neuronal activity
and is still present with the headache begins
 Visual: scintillating scotoma (loss of portion of the
visual field), flashing lights, spots, colors, “fortification
spectra”
 Somatosensory: numbness, tingling
 Can occur before, during or after the headache
phase
Spreading cortical depression
Scintillating scotoma
More scintillating scotomata
Aura - Frequency in Migraineurs
 Frequency of migraine types:
64% - only w/o aura
18% - only with aura
13% - both with and w/o aura
5% - Aura without headache
 Therefore only 31% of patients with headache have aura
Diagnostic Criteria for Migraine with
aura
At least 2 attacks fulfilling criteria for migraine without aura plus:
 Fully reversible visual symptoms including positive features
(flickering lights or spots) and/or negative features (scotoma)
 Fully reversible sensory symptoms including positive features such
as “pins and needles” and/or negative features such as numbness
 Fully reversibe dysphasic speech
 And at least 2 of
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Homonymous visual symptoms 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 5-60 minutes duration
 Headache occurs during or within 60 minutes of aura
 Not attributable to another disorder
Interesting migraine variants
 Hemiplegic migraine – “stroke-like”
 Basilar migraine (brainstem findings such as vertigo,
ataxia, dysarthria, diplopia, confusion or alteration in
level of consciousness)- despite the name there is no
evidence that there is any involvement of the basilar
artery physiologically
 Retinal migraine – blindness in one eye
Migraine Pathogenesis
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Exact pathogenesis is not known
A current leading theory is that there is neuronal hyperexcitability of the
cerebral cortex (a decreased threshold for activation – perhaps via calcium
channel function abnormalities).
Excessive cortical neuron firing may then trigger cortical spreading
depression and activation of the trigeminovascular system- location of pain
sensitive structures
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When activated can cause the release of substance –P,CGRP
Local vasodilatation and plasma leakage
Neurogenic inflammation
Experimental evidence also shows dysfunction of brainstem pain and
vascular control centers: Locus ceruleus, raphe nuclei, periaqueductal gray.
The sensory component of trigeminal nerve (trigeminal nucleus caudalis) is
in a persistent hyper-excitable state
Suprachiasmatic nucleus may play a role
Migraine Triggers- these may alter cortical
excitability
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Fasting
Alcohol consumption
Oral contraceptives/HRT
Caffeine or caffeine withdrawal
Foods: chocolate, aged cheeses, MSG, nitrites,
dairy products
 Stress or release from stress
 Sleep – too little or too much
 Bright lights, loud noises
Acute Treatment of Migraine
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Analgesics/NSAIDs
Antiemetics for nausea/vomiting
Midrin
Ergots - potent vasoconstrictors
Triptans - serotonin 5-HT 1B/1D receptor agonists
Narcotics - try to avoid
Triptans
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Sumatriptan (Imitrex) - po, sq, pr, intranasal
Zolmitriptan - (Zomig)
Naratriptan – (Amerge)
Rizatriptan - (Maxalt)
Frovatriptan – (Frova)
Almotriptan – (Axert)
Migraine Prophylactic Treatment
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Beta-blockers: propanolol, metoprolol, nadolol, timolol
TCA - amitriptyline, nortriptyline
Calcium channel blockers: verapamil
Anticonvulsants: topiramate, valproate
Herbals: feverfew, butterbur
Adam Quick MD
TENSION HEADACHE
Tension Headache
 Thought to be the most common type of primary headache
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Lifetime prevalence of 30-78%
 Persistent non-pulsating band like pain
 Clinical Presentation
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Lasts 30 minutes to 7 days
2 of the following
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Bilateral location
Pressing/tightening (non-pulsating) quality
Mild or moderate intensity
Not aggravated by routine activity
Both of
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No nausea or vomiting
No more than one of photophobia or phonophobia
 Exact pathophysiology is unknown
Treatment of Tension Headache
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NSAIDs
Midrin
TCA
Non-pharmacological treatment
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Relaxation, exercise, stress management, good sleep hygiene
Adam Quick MD
CLUSTER HEADACHE
Cluster Headache
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Much less common than migraine or tension headache
Male to female ratio of 5:1
High prevalence between ages of 20-40
Occurs in clusters lasting weeks or months
Striking periodicity
Pathogenesis
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Less clearly understood than migraine headache
Involves hypothalamus which controls circadian rhythms
Functional hypothalamic dysfunction has been confirmed by abnormal
metabolism based on magnetic resonance spectroscopy and positron
emission tomography
Excessive discharge of cholinergic activity is prominent
Central disinhibition of nociceptive and autonomic pathways
Increase blood flow through the orbit
Abnormal metabolism on PET scan
Clinical Manifestations of Cluster
Headache
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Sudden, severe attacks of unilateral periorbital pain
 Almost always stays on the same side
Lasting from 15 minutes to 180 minutes
Conjunctival injection, lacrimation, ptosis and nasal congestion
Attacks occurs in clusters
 One headache every other day to >5 in one day
 2 weeks to 3 months 1-2 times/year
Commonly awakens person from sleep
Clusters of headache may last several weeks and remit for months or years
One of the worst pains known to humans
 Patients will roam around, bang their heads on walls, extremely
aggitated
 Some consider suicide
Treatment
 Acute Therapies
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High flow Oxygen
Ergotamine
Sumatriptan
 Preventative Treatments
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Verapamil
Prednisone
Lithium
Topamax
Methysergide maleate
Cyproheptadine
Valproic sodium
Medication-Induced Headache
 Very common problem in patients with frequent
headaches
 People with recurrent headaches who take analgesics
such as aspirin, acetaminophen, non-steroidal antiinflammatory medications or narcotics such as codeine
may transform their headaches into a chronic daily
headache through a poorly understood mechanism.
 The goal is to manage frequent headaches effectively
before this happens.
 Goal should be to limit acute treatment to 2 days per
week or less
 Patients must be weaned off the culprit medication to
see improvement
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Often done in conjunction with administration of a headache
preventative agent such as topiramate
Summary
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When taking a headache history and performing a physical exam, be certain
to focus on clinical features that can help you distinguish a primary
headache disorder from a more threatening secondary headache
Migraine headache
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Very common primary headache that affects women more than men and typically
produces unilateral or bilateral throbbing pain of moderate to severe intensity with
associate nausea/vomiting, light and sound sensitivity, worsened by activity.
Migraine aura affects a subset of patients with migraine and often produces visual
phenomenon or other neurological symptoms
Tension headache is another common primary headache characterized by
a aching, band-like pain
Cluster headache is one of a group of primary headache disorders known
as the Trigeminal Autonomic Cephalgias
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One of the worse pains known to humans
Seems to be associated with circadian rhythms and weather changes
Thank you for completing this module
Questions?
Adam.quick@osumc.edu
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