This document summarizes information about migraines including: - Migraines are recurrent headaches that are often preceded by prodromal symptoms like yawning or lethargy. They involve throbbing pain localized to one side of the head. - Migraines can involve an aura phase with neurological symptoms like visual disturbances or numbness before the headache. Different types of migraines are classified based on the presence and type of aura. - The pathophysiology of migraines involves cortical spreading depression triggering the release of vasoactive substances from nerves which cause vasodilation and sterile inflammation activating the trigeminal nerve. - Treatment involves managing triggers, medications like triptans for

1. Chair person-Dr Prakash Kori
Student-Dr Darshan.M

3.  Migrane is complex recurrent headache.
 The term migrane is derived from greek
word from hemikranios which means half
head.
 Migrane can occur at any age but intial
attack occurs during adoloscence.
 More common in females(18% in females
and 6% males).
 Family history in 90%.

4.  U/L throbbing or pulsatile localized in the
frontotemporal and ocular areas,moderate
to severe intensity,which tends worsen with
routine levels of physical activity.
 Patient prefer to lie in a dark room.

5. Prodrome
phase.
Aura Headache Postdrome

6.  Vague premonitory symptoms that begin 12
to 36 hrs before aura and headache which
lasts for 15 to 30 minutes.
 Symptoms include yawning,excitation or
depression,lethargy,hunger.

8.  Also known as common migrane.
 Type of headache that occurs without
transient neurological symptoms.
 It is usually preceded by prodromal
symptoms.
 The pain is usually unilateral
supraorbital,throbing which may become
genralised or spread to contralateral side.
 Pain increases on exertion,valsalva
manouver,during head low position.

9. Aura
 It is a complex neurological symptoms that
may precede or accompany headache.
 It usually develops over 5-20 minutes and
lasts less than 60 minutes.
 it may be
visual,sensory,language,brainstem,motor
and cerebellar.
 It may occur alone or sequentially.

10. Visual aura
 Scintillating scotoma highly characterstic of
migrane.
 most common.
 It usually begins as schimmering arc of
white light in the right or left visual visual
field ,the arc of light gradually expands,it
may have defnite zig-zag pattern.
 Originate in the calcarine cortex.

12.  Positive scotoma is usually followed
negative scotoma.
 Other visual symptoms
micropsia,macropsia,photopsia.

14. Sensory aura
 Second most common aura.
 Parasthesia involving face and hands lasts for 5
to 20 minutes or also known as cherio-oral
migrane.
 Numbness may be hemisensory,all four limbs
or it may be restricted to face,lips or cheeks.
 Latent period of 10 to 20 minutes b/w aura
and migrane

15. Guage aura
 Aphasia can occur as aura in migrane.
 It is mild and transient.
 It may receptive or expressive.
Alexia or agraphia can also occur as an Aura.

16.  Aura not followed by headache.
 a/k/o migrane equivalent.
 Patient will be having h/o migrane with aura
the past.

17.  Occurs in adoloscents and
teenagers,equally in males and females.
 Usually begins with typical aura which is
bilateral followed by severe occipital
headache
 a/w brainstem symptoms such as
vertigo,dizziness,nystagmus,ataxia,dysarthr
ia and tinnitus.

18.  Reticular formation disturbances in
brainstem leads to impaired level of
conciousness can be aroused,recovery is
followed by severe headache.
 Bassilar migrane is replaced by migrane
without aura as the age advances.

19.  Migrane a/w weakness of one half of the
body or one sided facial palsy.
HEMIPLEGIC
MIGRANE
FHM
SPORIADIC

20.  Unlike typical aura weakness is followed by
headache which persist during and after
headche subsides.
 It may persists for hours,days,even months.
 Pateient complains of heaviness of one half
of the body,but clincal examination is
normal.
 Recovery is usually complete.

21. FHM 1
•Mutations in CACNA1A gene located in chromosome
19p a/w with cerebellar ataxia and nystagmus
FHM 2
•Mutation in sodium channel gene ATP1A2 n
chromosome 3
FHM 3
•Mutations in a sodium channel alpha subunit coding
gene.
.

22.  Always occurs in teenagers.
 Unilateral retrorbital pain.
 Once headache subsides thre will be ptosis
with complete paralysis of 3rd nerve.
 Sometimes 4th and 6th nerve also involved.

23.  Retinal dysfunction such as unilateral
photopsia,scattered loss of visual field,altitudinal
defects or unilateral vision loss.
Probable migrane.
 Migrane like headache secondary to another
disorder

24. Neurovascular
 Migrane is primarily a neurogenic process with
secondary changes in perfusion.
Cortical spreading depression.
 It is a wave of of neuronal excitation in the
cortical grey matter that spreads from its site
of origin at the rate of 2-6mm/min.
 The cellular deplarization causes aura phase in
turn activates trigeminal fibres to cause
headache

25. VASCULAR THEORY.
 Vasoconstriction is responsible for aura and
vasodilatation is resoponsible fòr headcahe
in migrane.
Based on 3 observations.
 Extracranial vessel becomes dilated and
pulsatile during an attack.
 Stimulation of intracranial vessel causes
headache.
 Vc reduces headache and Vd stimulates
headcahe.

26. Vasoactive subastances and
neurotransmitter.
 Perivascular nerve activity results in release
of substances such as substance
p,neurokinin A CGRP and nitric oxide which
produces vasodilatation,protein
extravasation and sterile inflammation
stimulating trigeminocervical complex.

27. Dopamine pathway.
 Some of the symptoms assciated with
migrane such as nausea,vomiting
headche,yawning can be attributed to
dopaminergic pathway.

28.  Stress
 Sleep deprivation
 Medications(ocps and nitrates)
 Strong odours.
 Harmonal changes(pregnancy and lactation)
 Head trauma.
 Excersice.
 Cold stimuslus.
 Fod contaning tyramine and monosodium
glutamate.

29. 1)status migranousus.
2)Persistent aura without infarction.
3)Migranousus infarct.
4)Migranousus aura triggered seizures

30. At least 5 attacks fullfilling criteria B&D.
A. Headache attacks lasting for 4-72 hours.
B. Headache has atleast two of the following
characterstic.
1.unilateral in location.
2.pulsating or throbbing type.
3.moderate to severe.
4.aggrevated by routine physical activity
D. During haeadache one of the following
1.nausea or vomiting
2.phonophobia or photophobia.
E.Not attributed to other causes

31.  Cranial/cervical muscle tenderness.
 Horner syndrome.
 Tachycardia/bradycardia.
 High BP
 Conjunctival congestion.
 Hemisensory or hemipareitic neurological
deficits.

32. Migrane is a clinical diagnosis.
 I/s are required to exclude other
structural,metabolic and other causes of
headache.
 Rule out comorbid disease that could
complicate headache and its treatment.

33. Indications of neuroimaging.
 Onset of migrane after 50 years of age.
 Change in pattern of previous migrane.
 First severe headache.
 Headache with abnormal neurological
findings.
 Headache with fever.
 Migrane and epilepsy.
 Posteriorly located headaches in children.

34.  Visual field testing is performed if there is
persistent visual phenomenon.

35. Dietary and lifestyle modifications.
 Cessation of smoking.
 Reduce alcohol intoxication.
 Avoid stress and triggers.
 Avoid drugs that precipitate such as
nitrates,nifedepine,indomethacin,theophylli
ne.
 Food which contains nitrites and
monosodiumcglutamate.

37. Triptans
5HT1B
MEDIATES CEREBRAL
BLOOD VESSEL VESSEL
VASOCONSTRICTOIN
5HT1D
INHIBITS
INFLAMMATORY
MEDIATORS.
AGONIST
IT ALSO INHIBITS ACTIVATION F NEURONS IN TRIGEMINAL NUCLEUS CAUDALIS

38. Routes
Oral
25mg,50mg,100mg
upto maximum 0f 200
mg/d
Subcutaneous
6mg can be repeated
after 2 hours
Intanasally
5mg and 20 mg
Duration of action is 2 hrs

39.  Rizatriptan most efficacious,early onset of
action,5-10 mg tablet may repeat after 2hrs
maximum dose is 30 mg
 Side effects-Parasthesia,Flushing,heaviness of
chest and neck,decrease diameter of coranary
vessel.
 Containdications-Undiagnosed
HTN,PVD,preganancy and lactation,CAD.

40. Ergotamine.
 Both vasodilator and vasoconstrictor.
 Agonist activity at 5HT receptors.
 Better acting when given i.v or rectally.
 Dihydroergotamine 2mg rectally or orally.
 Reduces recurrence of headache in 24 hrs.
 S/E-nausea ,vomiting.
 Contra indications-CAD,undiagnosed
HTN,PVD, Pregnancy and lactation.

41. Other drugs.
 Magnesium sulfate infusion.
 Dexamethosne or predinsolone 20 mg
every 6hrs intially and tapered over 2-3days
for status migranousus
 Chlorperazine 5mg to maximum of 30 mg.
 Prochlorperazine and promethazine for
vomiting.
 Opiods-butrophenol nasal spray.

43. Indications of prophyalaxis.
 Frequency of migrane >2/months.
 Duration f individual attack is longer than 24
hrs.
 Headache which causes major disruption in
lifestyle.
 Symptomatic medications is ineffective.
 Use of abortive medications more than twice
a week.
 Hemiplegic migrane.

44. 5 principal class of drugs is used.
 Antiepileptics.
 Antidepressants.
 Antihypertensive.
 Sertonin agonist.
 NSIADS.

45. Antiepileptics
 Well tolerated.
 Valproic acid is the drug of choice 400-
600mg/day.
 Other drugs-
gabapentin,carbamazepine,topiramate.

46. Antihypertensive.
 B-blockers
Propranolol(80-240mg),Timolol.
 CCBS.
Diltiazem,Verapmil,Nimodepine,Flunarazine
Flunarazine are effective only in migrane
with aura.

47. Antidepressants.
 Tricyclic antdepressantsse.
Amitryptilline 10-75 mg at night.
 Selective sertonin receptors antagonist.
Fluxotine.
 Other-
buprapion,mirtazepine,trazodone,venlafexi
ne.

48. Sertonin agonist.
 Methylsergide.
 Reserved for intractable headache,given for 6
months
 Dose-2mg intially gradually increased upto
maximum of 8mg over period 7-10 days.
 It causes retroperitoneal fibrosis,heartvalve
fibrosis,Pulmonary fibrosis.
 Should be monitored frequently with ct
abdomen,2D ECHO,Serum creatinine.

49. Calcitonin gene related peptide
antagonist(gepants).
 It is a neurpeptide implicated in the
pathophysiology of migrane.
 It is the first specific non-
sertornergic,migrane specific drugs without
vasconstrictor actvity.
 Suitable for patients with CAD,PVD and
undiagnosed HTN.
S/E-hepatotoxicity.

50. Orexin receptors antagonist.
 Orexin A and B are neuropeptides that are
synthesized in hypothalmus.
 Plays a role in nocioceptioon.
 Filorexant orexin 1 and 2 receptor
antagonist orginall developed to treat
insomnia.

51. Neuromodulation
 Transcranial magnetic stimulation-uses
fluctuating magnetic field to induce
electrical current in the cortex that is
thought to depress cortcal spreading
depression

52. Neurostimulation.
1)Cefalay- It is a device with supraaorbital
transcutaneous stimulation used in
prevention of migrane,
 it is safe and well tolerated.

53. 2)Cerena transcranial magnetic stimulator.
 Hand held machine.
 Applies single pulses of TMS to the back of
head.
 Indicated in the treatment of acute migrane
with aura.
 Approved by FDA.

54. 3)Gamma core
 Hand held device.
 For acute and preventive treatment of
migrane.
 It generates electrical signal that stimulates
vagal nerve
 It inhibits glutamate in glutamate in
trigeminal nucleus caudalis.

55.  OTHER
Riboflavin 400 mg/day.
Magnesium 600 mg/day.
Botlinum toxin.
NSIADS-Aspirin,mefenamic acid,ibuprofen.

56.  Harrison 19 th edition.
 Bradley neurlogical examination in clinical
practice.