everything about migrain. pain management.

1. MIGRAINE
DR. RAVI SHANKAR SHARMA
FELLOW (DARADIA)
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2. DEFINITION
“Migraine is a familial disorder characterized by
recurrent attacks of headache widely variable in
intensity, frequency and duration. Attacks are
commonly unilateral and are usually associated
with anorexia, nausea and vomiting”
-World Federation of Neurology
2

3. EPIDEMIOLOGY
Migraine is (16%) of PRIMARY headaches, 10-20% of the general
population
Initial attack start mostly in adolescents
less frequent in old age group.
predominance in female 2:1
Evidence of positive family history is present in >90% cases.
NEJM 2002; 346(4): 257-269; XI Congress of the IHS, 2004
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4. CLASSIFICATION
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5. CLASSIFICATION ICHD-3rd ed (Beta version)
1. Migraine
1.1 Migraine without aura
1.2 Migraine with aura
1.2.1 Migraine with typical aura
1.2.1.1 Typical aura with
headache
1.2.1.2 Typical aura without
headache
1.2.2 Migraine with brainstem
aura
1.2.3 Hemiplegic migraine
1.2.3.1 Familial hemiplegic
migraine (FHM)
1.2.3.1.1 Familial
hemiplegic migraine type 1
(FHM1)
1.2.3.1.2 Familial
hemiplegic migraine type 2
(FHM2)
1.2.3.1.3 Familial
hemiplegic migraine type 3
(FHM3)
1.2.3.1.4 Familial
hemiplegic migraine, other
loci
1.2.3.2 Sporadic hemiplegic
migraine
1.2.4 Retinal migraine
1.3 Chronic migraine
1.4 Complications of migraine
1.4.1 Status migrainosus
1.4.2 Persistent aura without
infarction
1.4.3 Migrainous infarction
1.4.4 Migraine aura-triggered
seizure
1.5 Probable migraine
1.5.1 Probable migraine without
aura
1.5.2 Probable migraine with
aura
1.6 Episodic syndromes that may
be associated with migraine
1.6.1 Recurrent gastrointestinal
disturbance
1.6.1.1 Cyclical vomiting
syndrome
1.6.1.2 Abdominal migraine
1.6.2 Benign paroxysmal vertigo
1.6.3 Benign paroxysmal
torticollis
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7. MIGRAINE
Migraine Without Aura Migraine With Aura
No aura or Prodrome Aura or prodrome is present
Unilateral throbbing headache
may be accompanied by nausea
and vomiting
Unilateral throbbing headache
and later becomes generalised
During headache, patient
complains of phonophobia and
photophobia
Patient complains of visual
disturbances and may have
mood variations
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8. COMMONCAUSES OF HEADACHE
• PRIMARY HEADACHE:
• Migraine
• Tension type headache
• Cluster headache
• Trigeminal autonomic cephalgia
• SECONDARY HEADACHE:
• Infection (Systemic or brain infection)
• Injury (head injury)
• Ischaemic or haemorrhagic stroke
• Tumour (brain tumours)
• Lumbar puncture headache
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9. CLINICAL FEATURES
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10. PHASES OF ACUTE MIGRAINE
Prodrome
Aura
Headache
Postdrome
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11. 1- PRODROME
Vague premonitory (early) symptoms that begin from 12 to 36 hours
before attack in 25% of patients and last for 15 to 20 min
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Prodromal
symptoms include
Lethargy
Craving for food
Distaste for foods

12. 2- AURA
Aura is a warning or signal before onset of headache
last for 15-30 min
1. Visual aura: is the most common symptoms and occurs as
visual disturbance known as Flashing of lights, Zig-zag lines or
difficulty in focusing
2. Sensoriel aura is the second most common and occurs as
paraesthesia followed by numbness.
3. Lagunage aura is a mild confusion and difficulty in
concentrating or may be sever like alexia or agraphia.
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13. EXAMPLE OF VISUAL AURA

14. 3- HEADACHE
• Headache is generally unilateral and is associated
with:
Anorexia
Nausea
Vomiting
Photophobia
Phonophobia
Tinnitus
• Duration is 4-72 hrs
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15. 4- POSTDROME (Resolution phase)
Duration: Few hours - 2 days
Complains of:
• Fatigue
• Depression
• Severe exhaustion
• Some patients feel unusually fresh
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16. TRIGGERS OF MIGRAINES
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17. TRIGGERS
Visual stimuli
Flashing Lights
Anxiety, Stress and
Physical exertion
Lack of Sleep
Hormonal Changes Headache Foods Tyramine
Caffeine:
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Drugs
Weather changes
Psychological factors
Disturbed sleep
pattern
Auditory stimuli Olfactory stimuli
Hunger

18. RECORD OF
PERSONAL
WARNING AND
TRIGGERS
This information may
help the patient to
avoid future attacks.
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19. PATHOPHYSIOLOGY
19

20. 20
Pain sensitive structures in the head:
1. Scalp,
2. Aponeurosis,
3. Meningeal layers:
(Dura mater)
4. Blood vessels
(Meningeal arteries)

21. The pathophysiology of migraine is very complicated and
has many mechanisms, so to understand it we have to
consider the following essential roles of factors:
1. Serotonin role:
2. Calcitonin gene-related peptide (CGRP) role:
3. Genetic role:
4. Vascular role
5. Cortical spreading depression (CSD) of Leão.
6. Trigeminovascular system activation.
Pathophysiology

22. Serotonin ( 5- hydroxytryptamine), may be an important mediator of
migraine by the following observations:
Serotonin role:
 Serotonin causes:
• vasodilation in large artery
• vasoconstriction in small artery and capillary

23.  a potent vasodilater of cerebral and dural vessels.
It may mediate trigeminovascular pain transmission and the
vasodilatory component of neurogenic inflammation.
Calcitonin gene-related peptide
(CGRP) role:

24. The genetic basis of migraine is likely to be
complex-familial hemiplegic migraine
FHM1,2 gene
Genetic role:

25. Vascular theory
Intracerebral blood vessel vasoconstriction – aura
 Intracranial/Extracranial blood vessel vasodilation – headache
25
SUPPORT- Vascular theory
Radioactive xenon cerebral blood flow studies show
significantly reduced regional blood flow through
cortex during aura stage of migraine.

26. DIAGNOSIS
26

27. DIAGNOSIS
Medical History
Headache diary
Migraine triggers
Investigations (only to exclude secondary causes)
EEG
CT Brain
MRI
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28. MIDAS headache score
Migraine disability assessment(questionnaire)
Some doctors like to
estimate how much
migraines disrupt normal
activities before treatment
begins.
A questionnaire is given to the
patient to estimate how often
they miss various functions
(school, work, family activities)
because of migraines.
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29. DIAGNOSTICCRITERIA

30. DIAGNOSTICCRITERIA

31. DIAGNOSTICCRITERIA

32. MEDICAL IMAGING
(ONLY TO EXCLUDE SECONDARY CAUSES)
• Neuroimaging used in some cases to exclude secondary causes
of headache or ischemic complications.
• CT SCAN is of extremely low yield
• CT Perfusion may be very useful to analyze acute attacks
perfusion regional changes.
• MRI: It is more sensitive than CT in the detection of an
intracranial abnormality
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33. DIFFERENTIAL DIAGNOSIS
Mild to moderate
headache
associated with muscle
contraction leads to
headache.
Headache quality is of a
tightening (non-pulsating)
Severe headache
associated with lacrimation,
nasal congestion, rhinorrhea,
facial sweating or eyelid
edema.
Pain lasts for 15 to 180
minutes.
More common in male33
Moderate to Severe
headache
associated nausea,
vomiting, photophobia,
phono phobia
More common in female

34. MANAGEMENT
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35. MANAGEMENT
Non-pharmacological management
Pharmacological
Abortive management
Preventive management
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36. Non pharmachological treatment
Reducing the attack frequency and severity by avoiding triggers
Lifestyle modifications
Diet therapy:
Exercise therapy:
Meditation
Relaxation therapy (yoga):
Alternative Therapy: Acupuncture:
Psychotherapy
Biofeedback techniques:
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to reduce migraine triggers like stress and
early symptoms such as muscle tension

37. Pharmacological treatment
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38. TRIPTANS
Mechanism of action:
selective agonistic activity on 5-TH-Receptors.
5-HT1B-Receptor agonist causes vasoconstriction,
5 HT1D-Receptor agonist inhibits sensory neuropeptide release from perivascular trigeminal afferents.
It act at central and peripheral components of the trigeminal vascular system by activation of both types
of serotonin Receptors there so it attenuate the excitability of cells in the TNC (Trigeminal Nucleus Caudalis),
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Side effects:
1. Nausea and dizziness,
2. Paresthesia: (tingling or flushed sensation).
3. chest pain or unpleasant heaviness
4. minor coronary spasm
Contra indications:
1. hypertension,
2. heart disease
3. stroke
New class of antimigraine drugs are the most commonly prescribed

39. ERGOTAMINESDerivatives
Side effects:
nausea, dizziness, muscle pain,
or an unusual or bad taste in
the mouth
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Mechanism of action: agonistic activity on 5 HT receptors
Have both vasodilator and vasoconstriction effects depending on
dose and resting tone of target vessels.
usually not as effective as triptans.
Mode of administration : oral, parenteral, nasal, rectal.
Dose: 2 mg s/l repeated in 30 minutes if needed.
If more than 6 mg of ergotamine is required per week, use an
alternative preparation.
Contraindication
1. Coronary artery disease, hypertension,pvd
2. pregnancy
3. Hemiplegic migraine, basilar-type migraine or prolonged aura
4. Neurologic deficit.

40. CGRP Antagonist
Calcitonin Gene-Related Polypeptide
Gepants
A novel CGRP antagonist is currently undergoing evaluation in human trials.
Actions: has little vasoconstrictive effect on vascular smooth muscle,
So it benefit patients in whom
•triptan and ergotamine use is CI or has a lot of SE
•comorbid coronary artery disease.
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41. Preventive management
41
80% of migraineurs may
require prophylaxis

42. 1. Frequency of attack > 2 /week
2. Duration of attack > 2 days
3. severity is extreme
4. Presence of prolonged aura
5. If acute migraine treatment
1. Present unacceptable adverse effects
2. Contraindication to use
3. Not effective (patient can’t perform his daily routine)
6. Special circumstances such as
 hemiplegic migraine or
 attacks with a risk of permanent neurologic injury
7. Patient preference
Indications:-
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43. 1- Β-Adrenergic blockers: Propranolol, Timolol
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Propranolol is the ‘gold standard’ in migraine prophylaxis,
especially if patient has hypertension or anxiety co-exist.
Mechanism of action: Vasoconstriction, Anxiolytic action and Decreased
sympathetic activity
Limitations ; Short t½ of 3-5 hrs so patient will need multiple daily dosing
Propranolol long-acting preparations: Starting dose; 40-80 mg once daily
and max. (max 240 mg).
Side effects: Lethargy, depression, hypotension, bradycardia, impotence,
insomnia, and nightmares.
Contraindication: Asthma, severe depression and DM (it may mask the
adrenergic symptoms of hypoglycemia).

44. 2-Antidepressants
Amitriptyline Dosage : 10 to 50 mg at night
Mechanism of action:
1. Blockade of noradrenaline uptake at catecholamine terminals
2. Inhibition of serotonin reuptake may be related,
Side effects: (anticholinergic SE)
If tolerated, give the tricyclic agents a trial of at least 3 months after reaching a
therapeutic dose.
The optimal dose is determined by titration to the effective or maximum
tolerated dose within the therapeutic range (usually 40-320 mg qid) 44
Amitriptyline, Imipramine,
Desipramine, Nortriptyline,

45. 3-calcium channel blockers
Mechanism of action: Prevent vasoconstriction and platelet
aggregation and alterations in release and reuptake of serotonin.
Verapamil in doses of 80 to 160 mg 3 times, not as useful in
migraine without aura.
Flunarizine is weak drug as it reduce the frequency of attacks, but
the intensity and duration is less documented.
Side effect: sedation, constipation, dryness of mouth, hypotension,
flushing, weight gain, rarely extra-pyramidal symptoms.
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Verapamil, Flunarizine,
Nimodipine

46. 4- Anticonvulsants
Mechanisms of action unknown.
Side effect:
Sedation, dizziness, increased appetite,
increased bleeding time, increased
fragility of hair, and an asymptomatic
increase in liver function test values.
Contraindication:
pregnancy.
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Gabapentin: is effective in the
reduction of migraine incidence
The usual therapeutic dose range for
gabapentin is 900 to 3600 mg/day.
Valproic acid: given in the form
of divalproex sodium,
Dose range of 500 to 1750 mg/day
taken in divided doses.

47. 5- Serotonergic agents
Cyproheptadine is a peripheral serotonin antagonist.
It has weak anti-bradykinin activity and prevents platelet
aggregation.
it is more effective in children.
Side effect:-it causes drowsiness and significant weight gain.
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48. 6- Other prophylactic agents
Riboflavin administered orally in a dose of 400 mg/day has
been shown to be effective in migraine prophylaxis in a
prospective randomized controlled study
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49. 49
Topiramate
Mode of action: effects not only on γ-aminobutyric acid (GABA) but also on
non-NMDA glutamate and carbonic anhydrase activity.
Side effects :It may have prominent sedating and cognitive side effects.
paresthesia and weight loss, mildly increased risk for kidney stones.
Dosage: Slow gradual titration of the drug (15-25 mg/wk initially) to the
therapeutic range of 75 to 200 mg/day the most successful strategy.

50. BOTULINUM TOXIN FOR CHRONIC MIGRAINE
Two randomized, placebo-controlled studies
of onabotulinumtoxinA injections (12 weeks
apart) for the prevention of chronic migraine
headaches, with follow-up for 24 weeks (679
and 705 subjects),
revealed no change in frequency, but fewer headache days and migraine days com
pared to placebo,
Most common adverse effects with Botox injections were neck pain, muscle
weakness, eyelid ptosis, myalgia, and muscle stiffness, as well as, paradoxically,
worsening migraine.
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51. Botulinum toxin for chronic migraine
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52. NERVE BLOCKS FOR HEADACHE RELIEF
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26-gauge, 1/2” needle introduced
medial to the external occipital
protuberance.
Needle advanced to periosteum,
then withdrawn 1-2 mm.
Mixture of bupivacaine (Marcaine)
0.5%, 1-2 ml, and triamcinolone
(Kenalog) 40 mg/ml, 0.5 ml,
injected slowly in 0.5 cc aliquots,
with aspiration prior to each
injection.
Occipital nerve block

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