Headache
Abera kuma(MD)
Neurologist
INTRODUCTION
• Headache is defined as pain in the head or
upper neck.
– It is one of the most common locations of pain in the body
and has many cause.
– Diagnosis and management is based on a careful clinical
approach that is augmented by an understanding of the
anatomy, physiology, and pharmacology of the nervous
system pathways that mediate the various headache
syndromes.
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Introduction
• More than 300 different types and causes of headache
• Huge global burden-- missing working and school
days==the tremendous direct and indirect cost to
individuals, family and society
• Unrecognized and under diagnosed, mismanaged
• Barriers to the care and diagnosis –health workers,
patients, governments
Headache epidemiology
• 90% - at least once per year
• severe disabling -40% worldwide
• usually benign
• serious headaches-SAH, brain tumors, meningitis, giant
cell arteritis
• emergency serious- 5% of headaches
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Anatomy and Physiology of Headache
• Pain usually occurs when peripheral nociceptors are
stimulated in response to tissue injury, visceral distension, or
other factors.
• Pain can also result when pain-producing pathways of the
peripheral or central nervous system (CNS) are damaged or
activated inappropriately.
• Headache may originate from either or both mechanisms.
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• Relatively few cranial structures are pain-producing; these
include
– The scalp
– Middle meningeal artery
– Dural sinuses
– Falx cerebri
– Proximal segments of the large pial arteries
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• The key structures involved in primary headache appear to be
The large intracranial vessels & dura mater
The peripheral terminals of the trigeminal nerve that innervate
these structures
The caudal portion of the trigeminal nucleus, which extends into
the dorsal horns of the upper cervical spinal cord & receives
input from the first & second cervical nerve roots (THE
TRIGEMINOCERVICAL COMPLEX)
The pain modulatory systems in the brain that receive input from
trigeminal nociceptors
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Pathogenesis and Pathophysiology of
Headache
• Headache results from:
Distension, traction or dilation of intracranial or extra-cranial
arteries
Traction or displacement of large intracranial veins or their
dural veins
Compression, traction or inflammation of cranial and spinal
nerves = neurovascular inflammation
Spasm, inflammation or trauma to cranial and cervical muscles
Meningeal irritation & increased ICP
Activation of brain structures
Cortical spread depression
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PRINCIPLES OF THE HEADACHE
EVALUATION
• Evaluating a patient with new onset headache pain can be
challenging.
• It requires a systematic approach based upon an understanding
of the common headache syndromes.
• Making a correct diagnosis is the first and foremost step in the
proper management of headache patients.
• A systematic case history is the single most important factor in
establishing a headache diagnosis & determining the future
work-up and treatment plan.
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A Systematic Case History
Age at onset
Presence or absence of aura and prodrome
Frequency, intensity and duration of attack
Number of headache days per month
Time and mode of onset
Quality, site, and radiation of pain
Associated symptoms and abnormalities
Family history
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Precipitating and relieving factors
Response to any previous treatment
Any recent change in vision
Association with recent trauma
Any recent changes in sleep, exercise, weight, or diet
State of general health
Change in work or lifestyle (disability)
Change in method of birth control (women)
Possible association with environmental factors
Effects of menstrual cycle and exogenous hormones (women)
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Diagnostic Instruments
• A four question version adopted by the AAN
includes the following questions:
1. How often do you get severe headaches (ie, without
treatment it is difficult to function)?
2. How often do you get other (milder) headaches?
3. How often do you take headache relievers or pain pills?
4. Has there been any recent change in your headaches?
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Headache Red Flags
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Worrisome Headache Red Flags “SNOOP”
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Physical Examination
Obtain blood pressure and pulse
Listen for bruit at neck, eyes, and head for clinical signs of
AVM
Palpate the head, neck, and shoulder regions
Check temporal and neck arteries
Examine the spine and neck muscles
A functional neurologic examination including getting up
from a seated position without any support, walking on
tiptoes and heels, cranial nerve examination, fundoscopy and
otoscopy, tandem gait and Romberg test, & symmetry on
motor, sensory, reflex and cerebellar (coordination) tests.
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Diagnosis and Testing
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When to consider neuroimaging
• TEMPORAL PROFILE AND HEADACHE FEATURES:
1. The first or worst headache (thunderclap headache)
2. Subacute headache with increasing frequency or severity
3. Progressive or new daily persistent headache
4. Chronic daily headache
5. Side-locked
6. Headache not responding to treatment
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• DEMOGRAPHICS:
1. New headache in patient with cancer or HIV
2. New headache age > 50
3. Headache and seizures
• ASSOCIATED SYMPTOMS AND SIGNS:
1. Fever, stiff neck, nausea and vomiting
2. Focal neurological symptoms or signs
3. Papilledema, cognitive impairment or personality change
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Lumbar Puncture (if CT is normal)
The 1st unusually severe headache
Thunderclap headache with
negative CT head
Subacute progressive headache
Headache associated with fever,
confusion, meningism, or
seizures
High or low CSF pressure
suspected (even if papilledema is
absent)
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Sudden Onset Headache
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Headache classification
• HEADACHE
• Part I: The Primary Headaches
• Part II: The Secondary Headaches
• Part III: Cranial Neuralgias, Central and Primary Facial Pain
And Other Headaches
PRIMARY HEADACHE
1.Migraine
2.Tension-type headache (TTH)
3.Cluster headache and other trigeminal autonomic
cephalalgias(TAC)
4.Other primary headaches
SECONDARY HEADACHE
1.Post traumatic Headache
2.Vascular Headache of cranial or cervical origin
3.Non vascular headache intracranial origin
4.Post infective headache
5.Headache due to substance abuse/withdrawal
6.Headache due to disorder of homoeostasis
7.Headache due to non cranial causes
8.Headache attributed to psychiatric disorders
Migraine headache
1.Migraine without aura
2.Migraine with aura
3.Childhood periodic syndromes
4.Retinal migraine
5.Complications of migraine
6.Probable migraine
Epidemiology
• The prevalence up to 17 % of women and 6 % of men each
year.
• common aged 30 to 39
• 3x common in women than men
• Tends to run in families.
• Migraine without aura is the most common type, accounting
for approximately 80 % of cases.
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How Migraine Works
3
4
Changes in nerve
Chemicals in
cell activity and
the brain
blood flow
cause blood
may result in
vessel
visual
dilation and
disturbance,
inflammation
numbness or
of the
tingling, and
surrounding
dizziness.
tissue
2 5
Electrical The
impulses inflammation
spread to other irritates the
regions of the trigeminal
brain. 1 nerve,
Migraine originates resulting in
deep severe or
Premonitory Symptoms
• Precede a migraine attack by several hours to one or two days.
– Typical symptoms include :
• fatigue, concentration difficulty, neck stiffness, sensitivity to
light or sound, nausea, blurred vision, yawning, or pallor
– These may occur alone or in combination.
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Clinical Manifestations
• Commonly begins early in the morning but can occur at any
time.
• Lateralized during severe migraine attacks in 60 to 70 percent
of patients;
• Bifrontal or global headache occurs in up to 30 percent.
• Occasionally, bioccipital headaches.
Gradual in onset, following a crescendo pattern with
gradual but complete resolution.
The headache is usually dull, deep, and steady when mild
to moderate; it becomes throbbing or pulsatile when severe.
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Migraine Aura
• Complex of neurologic symptoms that accompanies migraine
headache.
• An aura presents as a progressive neurologic deficit or
disturbance with subsequent complete recovery.
– Auras are thought to be caused by CSD occurring in regions of
the cortex that correspond to the clinical manifestations of the
aura.
– This is associated with a decrease in cortical blood flow.
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• Typical auras may involve any of the following manifestations :
• Visual Disturbances
• Sensory Symptoms
• Motor Weakness
• Speech Disturbances
• Visual disturbances are the most common type of aura.
• Numbness and tingling of the lips, lower face, and fingers of
one hand (cheio-oral) is the 2nd most common type of aura.
• Some patients have several types of aura symptoms that vary
with attacks.
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Types of Migraine Treatment
• Acute
– Taken during an attack
– Reduces pain, associated symptoms and disability
and stops progression
• Preventive
– Taken daily for months to years
– Reduces frequency, severity, and duration
– Used in addition to acute treatments
Acute migraine treatment principles
• Treat early
• Use correct dose and formulation
• Limit to 2 days per week (with exceptions)
• If has early or severe nausea and vomiting, or if severe
headache develops rapidly use parenteral meds
• Assess patient’s side effect propensity
• Some patients respond to one drug and not another, try drug
with 2 headaches before moving on
Acute treatment options
• Specific
Nonspecific
– ergotamine/DHE
NSAIDs
– triptans
simple analgesics
– combination analgesics
– antiemetics/neuroleptics
– opioids
Acute Treatment - Triptans
• Mechanism of action • Precautions
• 5HT-1B/1D agonists • Ischemic heart dz or stroke
• Inhibit release of CGRP & • High risk for CAD
substance P • Pregnancy
• Inhibit activation of the • Hemiplegic or basilar
trigeminal nerve migraine
• Inhibit vasodilation in • Ergots
the meninges • Use w/ SSRIs?
Indications for a Preventive Agent
• Migraine-related disability > 3d/month
• Migraines last over 48 hours
• Acute treatments are contraindicated, ineffective, or overused
• Migraines cause profound disability or prolonged aura
• Patient preference
Preventive therapy
• Propranolol
• Amytriptyline
• Anti-epileptic –valproate, topiramate
• CCBs-verspamil
Tension Type Headache
• Occurs in up to 80% of the population
• Most patients treat with OTCs and do not seek medical
attention
• Pathophysiology unclear
– Theory of increased muscle tension is unproven
• Pain characteristics
– Bandlike, bilateral
– Extends form forehead to sides of temples
– Involves posterior neck muscles in cape-like distribution
Acute Treatment (Episodic TTH)
• First line: OTC analgesics (APAP, NSAIDs)
• Second line: ASA+APAP+caffeine, butalbital
containing products
• High risk of rebound headaches
• Limit acute treatment to 2-3 days per week
Preventive Treatment (Chronic TTH)
• Non-Pharmacologic • Pharmacologic
• Proper sleep hygiene • TCAs (best efficacy)
• Stress management • SSRIs (better tolerated)
• Acupuncture
• Biofeedback **Consider for patients with
• Physical therapy >15 headaches per month**
3.Cluster headache and other trigeminal autonomic cephalalgias
3.1 Cluster headache
3.2 Paroxysmal hemicrania
3.3 Short-lasting unilateral neuralgiform headache attacks with
conjunctival injection
and tearing (SUNCT)
3.4 Probable trigeminal autonomic cephalalgia
3.1 Cluster headache
A. At least 5 attacks fulfilling criteria B-D
B. Severe or very severe unilateral orbital, supraorbital and/or
temporal pain lasting 15-180 min if untreated
C. Headache is accompanied by 1 of the following:
1. ipsilateral conjunctival injection and/or lacrimation
2. ipsilateral nasal congestion and/or rhinorrhoea
3. ipsilateral eyelid oedema
4. ipsilateral forehead and facial sweating
5. ipsilateral miosis and/or ptosis
6. a sense of restlessness or agitation
D. Attacks have a frequency from 1/2 d to 8/d
E. Not attributed to another disorder
Cluster Headache Abortive Treatment
• Inhalation of 100% oxygen up to 15 L/min
• Sumatriptan (Imitrex) 4-6mg subQ or 20 mg nasally
Zolmitriptan (Zomig) 5-10 mg nasally or PO
• Dihdroergotamine (Migranal) 1 mg nasally up to 3 mg in 24
hours
• Prednisone 40-100 mg burst and taper
Cluster Headache Prevention
• Verapamil 120-360 mg PO daily
• Lithium 300 mg PO BID to TID
• Divalproex 500-1500 mg PO daily to BID
• Topiramate 50-200 mg PO divided BID
Symptom MIGRAINE TENSION CLUSTER
HEADACHE HEADACHE HEADACHE
Location Unilateral in 60 to 70 per Bilateral Always unilateral,
cent, bi-frontal or global usually begins around
in 30 per cent the eye or temple
Characteri Gradual in onset, Pressure or Pain begins quickly,
stics crescendo pattern; tightness which reaches a crescendo
pulsating; moderate or waxes and within minutes; pain
severe intensity; wanes is deep, continuous,
aggravated by routine excruciating, and
physical activity explosive in quality
Patient’s Patient prefers to rest in Patient may Patient remains active
attitude a dark, quiet room remain active or
may need to rest
Duration 4 to 72 hours Variable 30 minutes to 3 hours
Associated Nausea, vomiting, None Ipsilateral lacrimation
symptoms photophobia, and redness of the
phonophobia; may have eye; stuffy nose;
aura (speech or motor rhinorrhoea; sweating
deficits)
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Trigeminal Neuralgia
• Describes paroxysmal pain felt within the distribution of one
or more divisions of the trigeminal nerve, most common in
the V2 &V3 division of the nerve but V1 extremely rare.
• The pain is described as electric shock-like, shooting, or
lancinating.
• Each attack lasts only seconds, but the pain may be repetitive.
• The pain is often triggered by a sensory stimulus to the skin,
mucosa, or teeth within the area innervated by the ipsilateral
trigeminal nerve.
• The trigger could be chewing, teeth brushing, talking, and
even cool breeze striking the face.
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• Mostly unilateral and rarely bilateral
• Onset: after the age of 40 years in 90% of patients.
• It is slightly common in women.
• Coarse: exacerbating and remitting course over many
years & spontaneous remission may occur
• Normal neurologic examination
• Most cases have long been idiopathic – vascular cross
compression of trigeminal nerve may be the most
common idiopathic form
• Multiple sclerosis, cerebellopontine angle tumors,
schwannomas, and other local lesions account for a
very small proportion of cases
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ICHD-3 Diagnostic criteria
• A. Recurrent paroxysms of unilateral facial pain in the
distribution(s) of one or more divisions o the trigeminal nerve,
with no radiation beyond, and fulfilling criteria B and C
B. Pain has all of the following characteristics:
1. lasting from a fraction of a second to two
minutes
2. severe intensity
3. electric shock-like, shooting, stabbing or
sharp in quality
C. Precipitated by innocuous stimuli within the
affected trigeminal distribution
D. Not better accounted for by another ICHD-3
diagnosis
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Treatment Of Trigeminal neuralgia
• Carbamazepine is the drug of choice, response in
75% of patients
• Second-line options include:
– gabapentin, pregabalin, phenytoin and baclofen,
lamotrigine, oxcarbazepine, valproate, clonazepam,
and topiramate
• Refractory to medical therapy - Surgical procedure
– percutaneous procedures the trigeminal nerve or
Gasserian ganglion (rhizotomy),
– Gamma Knife radiosurgery and microvascular
decompression.
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