Headache
By
Wael Hamdy Mansy, MD
Assistant Professor of Clinical Pharmacy
King Saud University
Classification of headaches
Primary headaches
 OR Idiopathic
headaches

– THE HEADACHE IS
ITSELF THE DISEASE
– NO ORGANIC LESION IN
THE BEACKGROUND
– TREAT THE HEADACHE!
Secondary headaches
 OR Symptomatic
headaches

– THE HEADACHE IS ON LY A
SYMPTOM OF AN OTHER
UNDERLYING DISEASE
– TREAT THE UNDERLYING
DISEASE!
History and examination should
clarify if
Type of hedeache (1ry or 2ry).
 Is any urgency?
 In case of 1ry headache only the headache
attacks should be treated “attack therapy, or
prophylactic therapy is also necessary.

SECONDARY, SYMPTOMATIC
HEADACHES

THE HEADACHE IS A SYMPTOM OF AN
UNDERLYING DISEASE, LIKE
–
–
–
–
–
–
–
–
–
–
–
Hypertension
Sinusitis
Glaucoma
Eye strain
Fever
Cervical spondylosis
Anaemia
Temporal arteriitis
Meningitis, encephalitis
Brain tumor, meningeal carcinomatosis
Haemorrhagic stroke…
Primary, idiopathic
headaches
 Tension
type of headache
 Migraine
 Cluster headache
 Other, rare types of primary
headaches
Tension headache
Renamed tension-type headaches by
the International Headache Society in 1988, are
the most common type of primary headaches.
 The pain can radiate from the neck, back, eyes,
or other muscle groups in the body.
 Tension-type headaches account for nearly 90%
of all headaches. Approximately 3% of the
population has chronic tension-type headaches

Tension –type headaches can be episodic
or chronic.
 Episodic tension-type headaches occur 15
days a month.
 Chronic tension-type headaches 15 days
or more a month for at least 6 months.
 Can last from minutes to days, months or
even years, though a typical tension
headache lasts 4-6 hs

Cluster headache
Nicknamed
"suicide
headache",
is
a
neurological disease that involves an immense
degree of pain.
 "Cluster"
refers
to
the
tendency
of
these headaches to occur periodically, with
active periods interrupted by spontaneous
remissions.
 The cause of the disease is currently unknown.
It affects approximately 0.1% of the population,
and men are more commonly affected than
women

Migraine Headache
Prevalence
Familial
 Young, healthy women; F>M: 3:1

– 17 – 18.2% of adult females
– 6 – 6.5% adult males
2-3rd decade onset… can occur sooner
 Peaks ages 22-55.
 ½ migraine sufferers not diagnosed.
 94% of patients seen in primary care
settings for headache have migraines


Common misdiagnoses
for migraine:
– Sinus Headache (HA)
– Stress HA

Referral to ENT for sinus
disease and facial pain.
The International Headache Society (IHS)
classifies migraine headache
 The IHS defines the intensity of pain with a
verbal, four-point scale:

Number
Pain
Annotations
0
NO
1
Mild
does not interfere with usual
activities
2
Moderate
inhibits, but does not wholly
prevent usual activities
3
Severe
prevents all activities
Migraine Definition

IHS criteria: Migraine/aura (3 out of 4)
– One or more fully reversible aura
symptoms indicates focal cerebral
cortical or brainstem dysfunction.
– At least one aura symptom
develops gradually over more
than 4 minutes.
– No aura symptom lasts more than
one hour.
– HA follows aura w/free interval of
less than one hour and may begin
before or w/aura.

IHS Diagnostic criteria: migraine w/o
aura
– HA lasting for 4-72 hrs
– HA w/2+ of following:
 Unilateral
 Pulsating
 Mod/severe intensity.
 Aggravated by routine
physical activity.
– During HA at least 1 of following
 N/V
 Photophobia
 Phonophobia
History, PE, Neuro exam show no other organic disease.
At least five attacks occur
Migraine mechanism

Neurovascular theory.
– Abnormal brainstem
responses.
– Trigemino-vascular system.
 Calcitonin gene related
peptide
 Neurokinin A
 Substance P
Extracranial arterial vasodilation.
– Temporal
– Pulsing pain.
 Extracranial neurogenic
inflammation.
 Decreased inhibition of central
pain transmission.
– Endogenous opioids.

Important role in
migraine
pathogenesis.
 Mechanism of action
in migraines not well
established.
 Main target of
pharmacotherapy.

Aura Mechanism

Cortical spreading depression
– Self propagating wave of neuronal and glial depolarization across the
cortex
 Activates trigeminal afferents
– Causes inflammation of pain sensitive meninges that generates
HA through central/peripheral reflexes.
 Alters blood-brain barrier.
– Associated with a low flow state in the dural sinuses.

Auras
– Vision – most common
neurologic symptom
– Paresthesia of lips, lower
face and fingers… 2nd most
common
– Typical aura
 Flickering uncolored
zigzag line in center and
then periphery
 Motor – hand and arm on
one side
 Auras (visual, sensory,
aphasia) – 1 hr

Prodrome
– Lasts hours to days…
MIGRAINE WITH AURA

DURING AURA:
– VASOCONSTRICTION
– HYPOPERFUSION

DURING HEADACHE
– VASODILATION
– HYPERPERFUSION
BUT: AURA SYMPTOM IS NOT CONSEQUENCE OF
VASOCONSTRICTION INDUCED HYPOPERFUSION
CUASE OF THE AURA: SPREADING DEPRESSION.
THE VASOCONSTRICTION AND HYPOPERFUSION ARE
CONSEQUENCES OF THE SPREADIND DEPRESSION
AURA
SPREADING DEPRESSION
VASOCONSTRICTION,
HYPOPERFUSION
IMPORTANT TO KNOW! MIGRAINE
WITH AURA

IS A RISK FACTOR FOR ISCHAEMIC STROKE
– THEREFORE PATIENTS SUFFERING FROM
MIGRAINE WITH AURA
 SHOULD NOT SMOKE!!!
 SHOULD NOT USE ORAL CONTRACEPTIVE DRUGS!!!

THE PROPROTION OF PATENT FORAMEN
OVALE IN PATIENTS WITH MIGRAINE WITH
AURA IS ABOUT 50-55%! (IN THE
POPULATION IS ABOUT 25%).
Is there a relationship between
aura and patent foramen ovale
?
Paradoxic emboli theory is not likely
Shunting of venous blood to the arterial side could
be the reason  no breakdown of certain
neurotransmitters (5HT) in the lung!
 Comorbidity could be also an explanation.



However, closure of patent foramen ovale
decreases the frequency of migraine attacks.
 BUT! Migraine is a benign disease. Please do not
indicate closure of patent foramen ovale just
because of migraine with aura!

Migraine Subtypes

Basilar type migraine
– Dysarthria, vertigo,
diplopia, tinnitus,
decreased hearing, ataxia,
bilateral paresthesias,
altered consciousness.
– Simultaneous bilateral
visual symptoms.
– No muscular weakness.

Retinal or ocular migraine
– Repeated monocular
scotomata or blindness < 1
hr
– Associated with or followed
by a HA
Migraine Subtypes
Menstrual migraine
 Hemiplegic migraine

– Unilateral motor and
sensory symptoms
that may persist after
the headache.
– Complete recover

Familial hemiplegic
migraine
Migrainous vertigo





Vertigo – sole or prevailing symptom.
Benign paroxysmal vertigo of childhood.
Prevalence 7-9% of pts in referral dizzy and migraine
clinics.
Not recognized by the IHS
Diagnosis (proposed criteria)
– Recurrent episodic vestibular symptoms of at least moderate
severity.
– One of the following:
 Current of previous history of IHS migraine.
 Migrainous symptoms during two or more attacks of vertigo.
 Migraine-precipitants before vertigo in more than 50% of
attacks.
– Response to migraine medications in more than 50% of
attacks
Clinical manifestations

Clinical manifestations
– Lateralized in severe attacks –
60-70%
– Bifrontal/global HA – 30%
– Gradual onset with crescendo
pattern.
– Limits activity due to its
intensity.
– Worsened by rapid head
motion, sneezing, straining,
constant motion or exertion.
– Focal facial pain, cutaneous
allodynia, GI dysfunction,
facial flushing, lacrimation,
rhinorrhea, nasal congestion
and vertigo…
Precipitating factors
stress
head and neck infection
head trauma/surgery
aged cheese
dairy
red wine
nuts
shellfish
caffeine withdrawal
vasodilators
perfumes/strong odors
irregular diet/sleep
light
Treatment

Abortive
– Stepped
– Stratified
– Staged

Preventive
Abortive Therapy



Reduces headache recurrence.
Alleviation of symptoms.
Analgesics
– Tylenol, opioids…

Antiphlogistics
– NSAIDs

Vasoconstrictors
– Caffeine
– Sympathomimetics
– Serotoninergics
 Selective - triptans
 Nonselective – ergots

Metoclopramide
Abortive care strategies

Stepped
– Start with lower level drugs, then switch to more specific drugs
if symptoms persist or worsen.




Analgesics – Tylenol, NSAIDs…
Vasoconstrictors – sympathomimetics…
Opioids (try to avoid) - Butorphanol
Triptans – sumatriptan (oral, SQ, nasal), naratriptan, rizatripatan,
zomatriptan.
– Limited by patient compliance.

Stratified
– Adjusts treatment according to symptom intensity.
 Mild – analgesics, NSAIDs
 Moderate – analgesic plus caffeine/sympathomimetic
 Severe – opioids, triptans, ergots…
– Severe sx treatment limited due to concomitant GI sx’s.

Staged
– Bases treatment on intensity and time of attacks.
– HA diary reviewed with patient.
– Medication plan and backup plans.
Preventive therapy








Consider if pt has more than 3-4
episodes/month.
Reduces frequency by 40 – 60%.
Breakthrough headaches easier to abort.
Beta blockers
Amitriptyline
Calcium channel blockers
Lifestyle modification.
Biofeedback.
Botox
51% migraineurs treated
had complete prophylaxis
for 4.1 months.
38% had prophylaxis for 2.7
months.
Randomized trial showed
significant improvement
in headache frequency
with multiple treatments.
Conclusions
Migraine is common but unrecognized.
 Keep migraine and its variants in the
differential diagnosis.

References
1.
2.
3.
4.
5.
6.
7.
8.
9.
10.
11.
Landy, S. Migraine throughout the Life Cycle: Treatment through the Ages. Neurology. 2004; 62
(5) Supplement 2: S2-S8.
Bailey, BJ. Head and Neck Surgery – Otolaryngology 3rd Edition. 2001. Pgs. 221-235.
Bajwa, ZH, Sabahat, A. Pathophysiology, Clinical Manifestations, and Diagnosis of Migraine in
Adults. Up To Date online. 2005.
Lipton, RB, Stewart, WF, Liberman, JN. Self-awareness of migraine: Interpreting the labels that
headache sufferers apply to their headaches. Neurology. 2002; 58(9) Supplement 6: S21-S26.
Cady, RK, Schreiber, CP. Sinus headache or migraine?: Considerations in making a differential
diagnosis. Neurology. 2002; 58 (9) Supplement 6: S10-S14.
Perry, BF, Login, IS, Kountakis, SE. Nonrhinologic headache in a tertiary rhinology practice.
Otolaryngology – Head and Neck Surg 2004; 130: 449-452.
Daudia, AT, Jones, NS. Facial migraine in a rhinological setting. Clinical Otolaryngology and
Allied Sciences. 2002; 27(6): 521-525.
Spierings, EL. Migraine mechanism and management. Otolarynogol Clin N Am 36 (2003): 1063 –
1078.
Avnon, y, Nitzan, M, Sprecher, E, Rogowski, Z, and Yarnitsky, D. Different patterns of
parasympathetic activation in uni- and bilateral migraineurs. Brain. 2003; 126: 1660-1670.
Stroud, RH, Bailey, BJ, Quinn, FB. Headache and Facial Pain. Dr. Quinn’s Online Textbook of
Otolaryngology Grand Rounds Archive. 2001. http://www.utmb.edu/otoref/Grnds/HA-facialpain-2001-0131/HA-facial-pain-2001.doc
Ondo, WG, Vuong KD, Derman, HS. Botulinum toxin A for chronic daily headache: a randomized,
placebo-controlled, parallel design study. Cephalalgia 2004 (24): 60-65.