Migraine is characterized by episodic headaches that are typically unilateral and associated with symptoms like nausea, visual disturbances, photophobia, and phonophobia. It is believed to originate from changes in brain nerve cell activity and blood flow which can cause visual symptoms prior to headache onset. Treatment involves identifying and avoiding triggers, using over-the-counter pain relievers during attacks, and preventive medications if attacks occur frequently. Triptans and ergotamine are prescribed for acute attacks while beta-blockers and antidepressants are common preventive options.

1. Migraine
Migraine
1

2. Migraine
• Characterised by episodic headache, typically
unilateral, associated with vomiting and visual
disturbance.
• Headache may be bitemporal and generalised
without focal visual or neurological
disturbance.
Migraine
2

3. The Headache Dilemma…
Migraine
Tension
Sinus
Treatment

7. HOW COMMON IS MIGRAINE
o
o
o
o
o
World- 15-20% of women
10-15% of men
In India 15-20% migraine
Adults-female: male ratio is 2:1
In childhood boys and girls are
affected equally until puberty when
predominance shifts to girls

8. Pathogenesis
• ↓ cerebral blood flow at the onset of an attack in migraine
with aura. During phase of attack, dilatation of extracranial
arteries related to fluctuations in blood 5-ht levels.
• Genetic predisposition.
• Chocolate, cheese, alcohol may precipitate attack.
• Episodes ↑ perimenstrually, at weekends or in women
taking oral contraceptives.
• Stress & anxiety may initiate an attack.
Migraine
8

9. 5-HT1D Agonist
5-HT2 Antagonist
Dilatation of B.V
5HT2receptor act
5-HT1D Agonist
Sensory nerve
discharge
Trigeminal Nerve
PG + kinin
release
NSAIDs
5-HT1D
Agonist
Neruogenic
Inflammation
(CGRP,SP release)
5-HT1D
Agonist
Perivascular
oedmea
Unknown abnormal
neuronal discharge
Spreading depression
+
Hypoperfusion
Directly
Aura
Aura
+
Pain
Pain

10. Release of CGRP, substance P &
Inflammatory Cytokines
1
2
3
4
5
6

11. PATHOPHYSIOLOGY
Vascular theoryo Intracerebral blood vessel constriction –
aura
o Intracranial/extra cranial blood vessel
vasodilatation-headache
Serotonin theoryo Decreased 5-ht levels linked with migraine
o Specific 5-ht receptors found in blood
vessels of brain

12. 3
4
Chemicals in the
brain cause blood
vessel dilation and
inflammation of the
surrounding tissue
Changes in nerve
cell activity and
blood flow
may result in visual
disturbance,
numbness or
tingling, and
dizziness.
5
2
Electrical impulses
spread to other
regions of the brain.
1
Migraine originates deep
within the brain
The inflammation
irritates the trigeminal
nerve, resulting in
severe or throbbing
pain

13. CLASSIFICATION
o Migraine with aura
o Migraine without aura
o Complicated migraine

14. PHASES OF ACUTE
MIGRAINE
o Prodrome
o Aura
o Headache
o Postdrome

15. PRODROME
o Vague premonitory symptoms that
begin from 12 to 36 hrs before the aura
and headache
o Symptoms include: Yawning
 Excitation
 Depression
 Lethargy
 Craving or distaste for various foods
o Duration- 15-20min

16. AURA
o Aura is a warning or signal before onset of
headache
o Symptoms include
 Flashing of lights
 Zig zag lines
 Difficulty in focussing
o Duration:15-30 min

17. HEADACHE
o Headache is generally unilateral and
is associated with symptoms like:
o Anorexia
o Nausea
o Vomiting
o Photophobia
o Phonophobia
o Tinnitus
o Duration:4-72 hrs

18. POSTDROME
Following headache, patient
complains of
o Fatigue
o Depression
o Severe exhaustion
o Some patients feel unusually fresh
o Duration: few hrs to 2 days

20. Clinical Features

Starts after puberty, continues till late midlife.

Attack may occur from a few days to several months.

Attacks may last for hours to days.

Premonitory symptoms – zig-zag lines, flashing, coloured lights,
defects in visual field & dysphasias with headache.

Headache localized to frontal region & spreads to whole of one
side of head – pain severe & throbbing associated with vomiting,
photophobia, pallor.

Patient is shifted to a bed in darkened room.
Migraine
20

21. MIGRAINE MANAGMENT
Non pharmacological treatment
o Identification of triggers
o Meditation
o Relax techniques
o Psychotherapy
Pharmacological treatment
o Abortive treatment
o Preventive treatment

22. ABORTIVE TREATMENT
Non specific treatmento Aspirin
o Paracetamol
o Ibuprufen
o diclofenac

23. ABORTIVE THERAPY
Specific treatmentErgot alkaloids:-ergotamine
dihydroergotamine
Triptans:- sumatriptan
rizatriptan
Antinauseant drugs:- metaclopramide
chlorpromazine
Triptans work best in 1st couple of hrs of attack
Ergotamine works at any time during the attack

24. Management

Avoid dietary and other precipitants.

Maintain a diary of attacks.

Stop oral contraceptives.

Soluble Aspirin (600-900 mg) or Paracetamol (1 Gm) with or
without Metoclopramide as antiemetic.

Ergotamine tartarate, 0.5-1.0 mg sublingually may abort
headache if taken as soon as visual symptoms are felt. No More
than 12 mg in a week. Excessive use may lead to vasospasm &
paradoxical headache. Contraindicated in pregnancy, IHD &
peripheral vascular disorders.
Migraine
25

25. …Management
• Serotonin agonist-triptans – Sumatriptan for acute attacks of
migraine (100 mg). No more than 300 mg per 24 hours or Inj.
Sumatriptan 6 mg SC. Not more than 2 injections per 24
hours. Highly efficacious.
• Prophylaxis if attacks occur weekly:
Propranolol : 40-80 mg 8 hrly.
Pizotifen
: 1.5-3 mg at night.
•
Amitriptyline
: 25-100 mg at night.
Migraine
26

26. Migraine & Oral Contraceptives
C/I migraine if there is typical aura, focal
features or if it is severe and lasts for
more than 72 hrs despite treatment
with ergotamine.
Migraine
28

27. Acute Migraine Attack
• It appears to begin in serotonergic (5-HT) and
noradrenergic neurons in the brain. These
monoamines affect cerebral & extracerebral
vasculature and cause release of vasoactive
substances such as H, PGs, neuropeptides
involved in pain, i.e. neurogenic inflammation
can be inhibited by antimigraine drugs.
• Migraine aura of visual or sensory disturbance
originates in occipital or sensory cortex.
• Throbbing headache is due to dilatation of
vessels – sensitive arteries outside the brain.
Migraine
29

28. Triggering Factors Avoidance
• Stress – exertion, anxiety, excitement, fatigue,
anger.
• Foods containing vasoactive amines –
chocolate, cheese.
• Bright lights, loud noise.
• Food Allergy.
• Hypoglycemia.
• Menstruation and oral contraceptives.
Migraine
30

29. Treatment – Stepped Approach
• Aspirin 600 mg oral dispersible (soluble) as
early as possible.
• Alternatives are Paracetamol, Ibuprofen,
Naproxen.
• Metoclopramide or Domperidone (dopamine
agonists) – antiemetics that promote gastric
emptying & enhance absorption of analgesic.
• Efficient use of analgesic & antiemetic is
adequate for majority of attacks.
Migraine
31

30. Stepped Treatment
 Severe migraine attacks should be treated with
triptans – Sumatriptan. Headache may return in
6-36h in 1/3rd patients. Use second dose.
 Ergotamine 1-2 mg used if other treatments
failed, but not within 12h of the last dose.
 Do not give triptans until 24h have elapsed after
stopping ergotamine.
Migraine
32

31. Triptans
 Selectively stimulate 5-HT 1B/1D – receptors found
in cranial blood vessels – vasoconstriction.
-Sumatriptan.
-Rizatriptan.
-Almotriptan.
-Naratriptan.
-Zolmitriptan.
Migraine
33

32. SUMATRIPTAN
•
•
•
•
Rapid oral absorption.
84% presystemic elimination.
SC bioavailability 96%.
Oral 50-100 mg, maximum 300 mg in 24h,
Repeat 2h.
• Intranasal 20 mg, maximum 40 mg in 24h,
Repeat 1h.
• SC 6 mg, 12 mg in 24h, Repeat 1h.
Migraine
34

33. Sumatriptan - ADRs
•
•
•
•
Malaise, fatigue, dizziness, vertigo, sedation.
N,V.
Feelings of chest pressure, tightness and pain.
Cardiac arrhythmias, MI.
Migraine
35

34. Sumatriptan – C/I
 Prophylaxis of migraine

MI
 IHD
 Variant angina
 Uncontrolled HT
 Concomitant ergotamine
 Within 2 wks after stopping MAOIs
Migraine
36

35. RIZATRIPTAN
• C/I: HT, IHD, Prinzmetal’s angina, Lactation,
Within 2 wks of MAOIs, Within 24 hrs of
treatment with another 5-HT agonist or
ergotamine.
Tab. Rizact 5 mg
Rs 30/-
10 mg
Rs 50/Migraine
37

36. ERGOTAMINE
 Partial agonist at α-adrenoceptors
(vasoconstrictor).
 Partial agonist at serotonergic receptors.
 Constricts all peripheral arteries.
 Effect persists for 24h, repeated doses cause
cumulative toxicity.
 Tablets 1 mg crushed before swallowing.
 Initially 1-2 mg, maximum 4 mg in 24h.
 Not more than 8 tablets in a week.
 Rectal suppositories of 2 mg preferred.
Migraine
38

37. …ERGOTAMINE
 CONTRAINDICATIONS:
Vascular & Valvular disease.
Pregnancy.
-Collagen diseases.
-Prophylaxis.
 ADRs:
-Muscle cramps.
-Stiffness.
-Tiredness.
-N,V,D.
 ERGOTISM: Severe peripheral vasoconstriction,
hypertension, gangrene of extremities, anginal pain.
Migraine
39

38. Drug Prophylaxis
• More than 2 attacks per month.
• Propranolol, Atenolol, Metoprolol.
• Verapamil, Flunarizine.
• Pizotifen, Cyproheptidine.
• Amytriptyline.
• Methysergide.
Migraine
40

39. THANK YOU
Migraine
41