2. List of contents
• Introduction
• Classification
• Pathophysiology
• Symptoms of migraine HA
• Trigger of migraine
• Diagnosis
• Treatment
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3. Headache
• Headache(HA) is a symptom that can be caused by many
disorders for example” traction, inflammation of pain-sensitive
structures within the head” or it can be due to disorders of
extracranial structures such as the eyes, ears, or sinuses.
• HA can be categorized on the basis of the underlying etiology
into one of two major types (primary and secondary).
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4. Classification
• Primary headache disorders are characterized by
the lack of an identifiable and treatable underlying
cause. Migraine, tension-type, and cluster
headaches are examples of primary headache
disorders.
• Secondary headache disorders are those
associated with a variety of organic causes such as
trauma, cerebrovascular malformations, and brain
tumors.
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8. Primary Headache Disorders
• Migraine Headaches
• It is usually develop over a period of minutes to
hours, progressing from a dull ache to a more
intense pulsating pain that worsens with each
pulse.
• The headache usually begins in the front temporal
region and may radiate to the occiput and neck; it
may occur unilaterally or bilaterally.
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9. Cluster Headaches
• Recurrent headaches that are
separated by periods of remission that last from
months to even years. During those periods the
headaches usually occur at least once daily. The
headache generally is unilateral, occurs behind the
eye, reaches maximal intensity over several minutes,
and lasts for <3hrs
• Unilateral lacrimation, rhinorrhea, and facial flushing
may accompany the cluster headache.
• Precipitated by alcohol, naps, and vasodilating drugs.
• More common in males than females.
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10. Tension-Type Headaches
• It is the most common type of primary headache and is
more common in women than men. Pain is usually mild
to moderate and non pulsating. It is also described as
dull, persistent headache, occurring bilaterally in a hatband
distribution around the head. The headache may fluctuate in
intensity throughout the day.
• Tension-type headaches often occur during or after
Stress.
• Skeletal muscle over contraction, depression, and
occasionally nausea may accompany the headache.
• Mild photophobia or phonophobia occur in some patient.
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11. Classification of secondary Headache
• Headache Associated with Head Trauma
• Headache Associated with Vascular Disorders
• Headache Associated with Metabolic Disorder
• Miscellaneous Headaches Unassociated with
Structural Lesion
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12. Pathophysiology
• Intracranially, only a limited number of structures are
sensitive to pain.
• Headache may result from dilation, distention,
or traction of the large intracranial vessels.
• The brain itself is insensitive to pain. Whereas
scalp arteries and muscles are capable of
registering pain and have been implicated in
the pathophysiology of migraine and tension-type headache.
• Extracranially, most of the structures outside
the skull (e.g., eye, ear, teeth, skin, deeper
tissues) have pain afferents.
13. Migraine headache
Symptoms
• It is characterized by recurring episodes of throbbing
head pain, frequently unilateral. It can be severe and
associated with nausea, vomiting, and sensitivity to
light, sound, and/or movement.
• The migraine headache may occur at any time of day
or night but usually occurs in the early morning hours
on awakening.
• Pain is usually gradual in onset, peaking in intensity
over minutes to hours, and lasting between 4 and 72
hours untreated. Pain is typically reported as
moderate to severe and most often involves the
frontotemporal region.
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14. • A migraine aura
• Experienced by approximately 31% of sufferer. The
aura typically evolves over 5 to 20 minutes and lasts
less than 60 minutes. Headache usually occurs
within 60 minutes of the end of the aura.
• Visual auras can include both:
• * positive features (e.g., scintillations, means
experience flashing lights, , photopsia means light
stimuli that observed when the eyes are closed ,
teichopsia, the appearance of zigzag lines before
the eyes)
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15. • * negative features (e.g., scotoma, notice a
black spot at the corner of the eye which
impedes peripheral vision, hemianopsia,
decreased vision or blindness takes place in half
the visual field of one or both eyes. ).
• There are sensory and motor symptoms such
as paresthesia or numbness of the arms and
face, dysphasia or aphasia and weakness may
also occur.
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19. • DIAGNOSIS
• • In the headache evaluation, diagnostic alarms should
be identified, including:
• “first” or “worst” headache ever,
• onset of the headache
• Is it associated with systemic illness ( fever, nausea,
vomiting & stiff neck)
• focal neurologic symptoms or papilledema,
• positive family history for migraine,
• presence of food triggers,
• menstrual association,
• long-standing history,
• improvement with sleep,
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20. Check for abnormalities:
• vital signs (fever, hypertension),
• funduscopy (papilledema, hemorrhage, and exudates),
• trigger points
• neurologic examination (abnormalities or deficits in mental
status)
• Neuroimaging computed tomography (CT) or magnetic resonance
imaging (MRI) should be considered in patients with unexplained
findings on the neurologic exam & those with additional risk
factors
• LABORATORY TESTS
• • In secondary headache presentation, serum chemistries,
and other blood tests, such as a complete blood count,
antinuclear antibody titer, ESR and antiphospholipid antibody
titer as well as thyroid function tests may be considered.
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21. • TREATMENT
• Nonpharmacologic Treatment
• Identification and avoidance of factors that provoke
migraine attacks.
• Application of ice to the head and periods of rest or
sleep, usually in a dark, quiet environment, may be
beneficial.
• Behavioral interventions (relaxation therapy ,
cognitive therapy) are preventive options for
patients who prefer nondrug therapy or when drug
therapy is ineffective or not tolerated.
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22. Pharmacologic Treatment of Acute Migraine
• Acute migraine therapies are most effective when
administered at the onset of migraine.
• The frequent or excessive use of acute migraine
medications can result in a pattern of
increasing headache frequency and drug
consumption phenomena known as medication-overuse
headache.
• This occurs commonly with overuse of simple or
combination analgesics, ergotamine tartrate,
opiates and triptans. This may be avoided by
limiting use of acute migraine therapies to 2 or 3
days per week.
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23. • 1-Pretreatment with antiemetics
(prochlorperazine, metoclopramide)
• Given 15 to 30 minutes prior to administering oral
acute migraine therapy.
Non oral treatments (rectal suppositories, nasal
spray or injections) may be advisable when nausea
and vomiting are severe.
• In addition to its antiemetic effects,metoclopramide
helps enhances absorption of oral medications.
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24. • 2-Analgesics and Nonsteroidal Antiinflammatory
Drugs
• Simple analgesics and (NSAIDs) like Aspirin, ibuprofen,
naproxen sodium are effective as
first-line treatment for mild to moderate migraine
attacks
• The combination of acetaminophen plus
aspirin with caffeine or with short-acting
barbiturate (butalbital) are also effective.
• In general, NSAIDs with a long half-life are
preferred as less frequent dosing is needed.
• Rectal suppositories and intramuscular ketorolac
are options for patients with severe nausea and
vomiting.
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25. • 3- Ergot Alkaloids and Derivatives
• • Ergot alkaloids are useful for moderate to severe
migraine attacks. They are nonselective 5HT1 receptor
agonists. Venous and arterial constriction will occurs.
• • Ergotamine tartrate is available for oral, sublingual,
and rectal administration.
• Oral and rectal preparations contain also caffeine to
enhance absorption and potentiate analgesia.
• Because oral ergotamine undergoes extensive first-pass
hepatic metabolism, rectal administration is
preferred.
• Dosage should be titrated to produce an effective but
sub-nauseating dose.
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26. • • Dihydroergotamine (DHE) is available for
intranasal and parenteral (IM, IV & SC)
administration.
• • Nausea and vomiting are common adverse
effects of ergotamine derivatives. Pretreatment
with an antiemetic should be considered with
ergotamine and IV DHE therapy. DHE does not
appear to cause rebound headache.
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27. • 4-Serotonin Receptor Agonists (Triptans)
• Sumatriptan, zolmitriptan, naratriptan, rizatriptan,
Almotriptan , etc. are appropriate first-line therapies
for patients with moderate to severe migraine or as
rescue therapy when nonspecific medications are
ineffective.
• These drugs are selective agonists of the 5HT1B
and 5HT1D receptors. Relief of migraine headache
results from normalization of dilated intracranial
arteries.
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28. • Sumatriptan is available for oral, intranasal, and SC
administration.
• When compared with the oral formulation, SC
administration offers enhanced efficacy and a more
rapid onset of action (10 vs. 30 minutes).
• Intranasal sumatriptan also has a faster onset of effect
(15 minutes) than the oral formulation.
• Second-generation triptans (all except sumatriptan)
have higher oral bioavailability and longer half-lives
than oral sumatriptan.
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29. • 5- Opioids
• • Opioids and derivatives therapy should be closely
supervised. It includes:
• meperidine, oxycodone, hydromorphone
• All should be reserved for patients with :
• moderate to severe infrequent headaches in whom
conventional therapies are contraindicated or as
• rescue medication after failure to respond to
conventional therapies.
• 6- Glucocorticoids
• • Corticosteroids may be an effective rescue therapy for
status migrainosus, which is a severe migraine that may
last up to 1 week.
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30. • Pharmacologic Prophylaxis of Migraine
• administered on a daily basis to reduce the frequency, severity,
and duration of attacks.
• Prophylaxis should be considered in the:
• * patient with recurring migraines
• * frequent attacks requiring symptomatic medication more
than twice per week
• * symptomatic therapies that are ineffective, contraindicated,
or produce serious side effects
• * when headaches recur in a predictable pattern (e.g.,
exercise-induced or menstrual migraine).
• Attacks occur >2-4 times per month
• Disability occurs > 3 days per month
• Duration of attack > 48 h
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31. • 1) β-Adrenergic Antagonists
• β-Blockers (propranolol, nadolol, timolol, atenolol
& metoprolol) are the most widely used treatment
for prevention of migraine.
• Bronchoconstrictive and hyperglycemic effects
can be minimized with β1- selective β-blockers.
• β-Blockers should be used with caution in patients
with asthma, heart failure, peripheral vascular
disease, atrioventricular conduction disturbances,
depression and diabetes.
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32. • 2) Antidepressants
• Amitriptyline appears to be a tricyclic
antidepressant (TCA) of choice, but imipramine,
doxepin,nortriptyline, and protriptyline have also
been used.
• TCAs are usually well tolerated at the lower doses
used for migraine prophylaxis, but anticholinergic
effects may limit use, especially in elderly patients
or those with benign prostatic hyperplasia or
glaucoma. Evening doses are preferred because of
sedation.
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33. • 3) Anticonvulsants
• Valproic acid and divalproex sodium can reduce the frequency,
severity, and duration of headaches by at least 50%.
• The extended release formulation of divalproex sodium is
administered once daily and is better tolerated than the enteric-coated
formulation.
• Topiramate is recently approved by the FDA for migraine prophylaxis.
4) Calcium Channel Blockers
• Verapamil provided only modest benefit in decreasing the frequency
of attacks. It has little effect on the severity of migraine attacks. It is
generally considered a second- or third-line prophylactic agent.
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34. • 5) Methysergide
• Methysergide is a semi synthetic ergot alkaloid
that
is a potent 5HT2 receptor antagonist.
• Its use is limited by the occurrence of potentially
serious retroperitoneal, endocardial, and
pulmonary fibrotic complications that have
occurred during long-term uninterrupted use.
• It is reserved for patients with refractory
headaches that do not respond to other preventive
therapies.
• Methysergide is best tolerated when taken with
meals.
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35. • 6) A prophylactic use of Nonsteroidal
Antiinflammatory Drugs
• • NSAIDs are modestly effective for reducing
the frequency, severity, and duration of
migraine attacks, but potential GI and renal
toxicity limit daily or prolonged use.
• They may be used intermittently to prevent
headaches that recur in a predictable pattern
(e.g., menstrual migraine). Treatment should
be initiated 1 to 2 days before the time of
headache
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Historically, the primary headache disorders have
been thought to be related either to vascular
disturbances (migraine and cluster headache) or
muscular tension (tension-type headache).
• However, a neurovascular hypothesis proposed
that headache is triggered by disturbances in
central pain processing pathways leading to the
release of serotonin, a vasoactive neurotransmitter
which plays a role in migraine pathogenesis.
• That is why, drugs that alter serotonergic function
are highly effective for the symptomatic treatment
of migraine and cluster headache.
Such headaches may develop suddenly, over a
period of hours to days (acute headache), or more
gradually over days to months (subacute headache) .
Pain as pulsing and throbbing in one area of the head.
Very sensitivity to light and sound
N&V.
Seeing flashing lights or zigzag lines or temporarily lose their vision .
Prodrome
One or two days before a migraine, you may notice subtle changes that signify an oncoming migraine, including:
Constipation
Depression
Food cravings
Hyperactivity
Irritability
Neck stiffness
Uncontrollable yawning
Aura
Aura may occur before or during migraine headaches. Auras are nervous system symptoms that are usually visual disturbances, such as flashes of light. Sometimes auras can also be touching sensations (sensory), movement (motor) or speech (verbal) disturbances. Most people experience migraine headaches without aura. Each of these symptoms usually begins gradually, builds up over several minutes, and then commonly lasts for 20 to 60 minutes. Examples of aura include:
Visual phenomena, such as seeing various shapes, bright spots or flashes of light
Vision loss
Pins and needles sensations in an arm or leg
Speech or language problems (aphasia)
Less commonly, an aura may be associated with limb weakness (hemiplegic migraine).
Attack
When untreated, a migraine usually lasts from four to 72 hours, but the frequency with which headaches occur varies from person to person. You may have migraines several times a month or much less often. During a migraine, you may experience the following symptoms:
Pain on one side or both sides of your head
Pain that has a pulsating, throbbing quality
Sensitivity to light, sounds and sometimes smells
Nausea and vomiting
Blurred vision
Lightheadedness, sometimes followed by fainting
Postdrome
The final phase, known as postdrome, occurs after a migraine attack. During this time you may feel drained and washed out, though some people report feeling mildly euphoric.
CONSISTENCY
timing of meals, balance of diet –- don’t skip meals, mix of different food groups
sleep --- don’t oversleep or undersleep
caffeine – “minimum daily dose” of caffeine on a daily basis
exercise – the more aerobic exercise the better
Anti dopamine
Inhibit prostaglandin synthesis in cns
Stimulate a receptor to vasoconstrict vessels.
• Symptoms of severe peripheral ischemia (ergotism) include
cold, numb, painful extremities; continuous paresthesias;
diminished peripheral pulses; and claudication.
• Contraindications include renal and hepatic failure;
coronary, cerebral, or peripheral vascular disease;
uncontrolled hypertension; and women who are pregnant
or nursing.
• Clinical response to triptans varies among individual patients,
and lack of response to one agent does not preclude effective
therapy with another member of the class.
• Side effects of triptans include paresthesias, fatigue, dizziness,
flushing & warm sensations.
• Up to 15% of patients report chest tightness, pressure,
heaviness, or pain in the chest. Although the mechanism of
these symptoms is unknown, a cardiac source is unlikely in
most patients.
• Contraindications include ischemic heart disease,
uncontrolled hypertension, cerebrovascular disease, and
hemiplegic migraine.
• Triptans should not be given within 24 hours of ergotamine
derivative administration.
A. The present attack in a patient with Migraine without aura is typical of previous attacks except for its duration.
B. Headache has both of the following features:
Unremitting for more than 72 hours
Severe intensity
C. Not attributed to another disorder
• drug selection is based on side-effect profiles and
conditions of the patient, a trial of 2 to 3 months
duration is necessary to judge the efficacy of each
medication.
• Only propranolol, timolol, valproic acid & topiramate
(anticonvulsant) are approved by the FDA for migraine
prevention.
• Prophylaxis should be initiated with low doses and
advanced slowly until a therapeutic effect is achieved
or side effects become intolerable.
• Prophylaxis is usually continued for at least 3 to 6
months after headache frequency and severity have
diminished, and then gradually tapered and
discontinued, if possible.
Arterial vasoconstriction and turnning off generator that cause migraine
