MIGRAINE

∞ Core features - Unilateral headache, occasionally throbbing.

∞ Nausea, sensitivity to light, sound and exacerbations on head
movement.
∞ Considered to be a vascular disorder – now disproved by modern
imaging.
AETIOLOGY:
 Genetic predisposition
C/F:
 F>M
 Often develops in first 3 decades of life.
 Presents as an episodic headache, often associated with
nausea and vomiting.
 Episodes may occur at any time, but more frequently in the
morning.
 Gradual onset, peaks and subsides.
 Adults: 4-72 hrs; Children: 2-4 hrs
 Pain may be mild to severe.
 Mild – constant, tight (or) band-like pain.
 Severe – throbbing pain, may move from one part of head to
another, may even radiate down to neck and shoulder.
 Photophobia, phonophobia and osmophobia.
 May be preceded by aura of neurologic dysfunction – Visual
disturbances, vertigo numbness or weakness.
 Scalp tenderness during headache – 2/3rd patients.
  Trigger factors – Physical activity, alcohol, menses, weather
changes, irregular sleep pattern, certain food.
POSTULATED THEORIES:
∞ Three factors considered: Familial/genetic, Vascular,
Neuronal
∞ Familial evidence of migraine is high. Concordance in
monozygotic twins > dizygotic twins
∞ VASCULAR THEORY:
 Throbbing caused by cerebral vasoconstriction and
headache caused by reactive vasodilatation
 Migrainous fortification spectra – Aura consisting of
zigzag figures of bright luminous geometric lines &
shapes
 Even though cerebral flow abnormalities are seen in aura,
they aren’t significant enough to cause focal neurologic
symptoms
 But vascular theory doesn’t explain migraine without aura
where flow abnormalities are absent
 Hence, aura is now believed to be caused by neuronal
dysfunction
 Aura > Cortical changes in metabolism that begin in the
visual cortex > Spread across the cortex and continue >
Headache phase begins
 Headache may last upto 72 hours.
∞ NEURONAL THEORY AND THE TRIGEMINOVASCULAR
SYSTEM:
 Dysregulation of normal neuronal function causes an
increase in the metabolic activity, leading to a slow-moving,
spreading depression of cortical activity.
 The trigeminal nerve which innervates the meninges is
intricately involved.
 Association of a meningeal vessel nociceptor is considered.
 Activation of the trigeminal vascular system results in
vasoactive polypeptide release, including substance P and
calcitonin gene-related peptide(CGRP).
 These neuropeptides and other cytokines interact with vessel
walls and cause vasodilatation, plasma protein extravasation
and platelet activation.
 Leads to sterile inflammation that activates trigeminal nerve
nociceptive afferents that causes further pain production.
 Biologic, genetic and pharmacological evidence available to
prove that dopamine can induce most migraine symptoms,
there is dopamine receptor hypersensitivity in migraine, and
that dopamine receptor antagonists are effective in treating
migraine.
PATHOPHYSIOLOGY OF MIGRAINE:
∞ Migraine is associated with the trigeminovascular(TGV)
system as all pain-sensitive structures are innervated by it.
∞ The TGV system is stimulated by both neural(electrical) and
chemical(neurotransmitters) activators.
CASCADE OF EVENTS WHICH RESULT IN MIGRAINE

Stimulation

C-fibres antidromically release

tachykinins such as substance P,
calcitonin gene related peptide(CGRP)
into dural and meningeal blood vessels

Degranulation of mast cells to release

histamine

Vasodilatation and plasma

extravasation into the tissues

Release of substance P causes

inflammation & swelling of BV walls

Release of serotonin from platelets

further compounding the condition

Orthodromic signals sent to spinal tract

nucleus, resulting in pain
∞ Attacks of migraine without aura show an increase in
electromyographic(EMG) activity in pericranial muscles. It’s
largely muscular pain and responds to muscular relaxation
techniques.
∞ Masticatory muscle pains occur frequently with migraine
headaches.
∞ Serotonin receptors(5-HT) have subtypes of which 5 are
implicated in the pathophysiology of migraine.
∞ These receptors are involved in the constriction of cerebral BV
and AV anastomoses. They can also stimulate production of
prostacyclin and other products of arachidonic acid metabolism
in smooth muscle cells.
∞ Antagonists to them can block TGV neurogenic inflammation
but not that caused by substance P. They also inhibit serotonin
from inducing an arachidonic acid-derived inflammatory state.

Early stages of migraine there is patchy areas of

increased cerebral blood flow prior to a decrease in
systematic blood flow

Dimuntion of the flow starts in occipital region and

spreads forward - Spreading Oligemia

Progresses over the cortex and stops short of the

sulci

Reaches sensorimotor area only after the focal

neurologic symptoms(assoc. with diminished cortical
perfusion) begin. Lasts for several hours

Followed by delayed hyperemia

∞ Spreading depression of Laeo – Spreading oligemia slowly
progresses as a wave over the cortex, starting in the posterior
region and migrating anteriorly.
∞ Cortical blood flow doesn’t always dictate the presence or absence
of a headache, but dilation of middle cerebral and other
intracranial arteries may contribute to the perception of pain.

OTHER SYSTEMS INVOLVED IN MIGRAINE:

∞ The ANS as well as several brainstem structures also affect
cranial vessel function and have been implicated in migraine
pain.
∞ The parasympathetic fibres which arise in the superior salivatory
nucleus and accompany the facial nerve are thought to
contribute to migraine by the release of substances such as ACh,
vasoactive intestinal polypeptide and peptide histidine
isoleucine.
∞ Sympathetic fibres ascend from superior cervical ganglion to
form a plexus in the walls of both ICA and ECA. They contribute
to migraine by releasing norepinephrine, neuropeptide Y and
peptide YY.
∞ Locus ceruleus – located in the wall of 4th ventricle in the upper
pons. It’s a nucleus made up of cells that contain the highest
amount of noradrenaline in the brain.
∞ It receives afferent fibers from areas which relate to the internal
and external sensory stimuli (or) to the affective state. It also
projects out to the geniculate nuclei, thalamus, facial nerve &
trigeminal spinal tract nucleus.
∞ It directly affects the intracranial Bv and also stimulated the
release of norepinephrine from the adrenal gland, which in turn
 causes a platelet release reaction, thus augmenting the afferent
inflow through the trigeminal nerve and the cascade of
migraine.

PHASES OF MIGRAINE:
∞ 4 phases:
1. The premonitory phase/ Prodrome
2. The aura
3. The headache
4. Post-drome
∞ PRODROME: The period of time that occurs hours or even days
before the headache is felt.
∞ Any of the following symptoms may be present.
PSYCHOLOGIC NEUROLOGIC GENERAL
1. Depression Photophobia Stiff neck
2. Hyperactivity Hyperosmia Food cravings
3. Euphoria Dysphasia Anorexia
4. Talkativeness Phonophobia Sluggishness
5. Irritability Yawning Diarrhoea/Constipation
6. Drowsiness Difficulty in Thirst
7. Restlessness concentration Urination
Fluid retention

∞ 2 types of prodrome:
1. Non-evolutive – Up to 48hrs prior
2. Evolutive – Approx. 6hrs prior
 ∞ AURA: A complex of focal neurologic symptoms that
immediately precedes the headache. Usually develops in 5-20
min and lasts up to 1hr.
∞ Characterized by visual, sensory (or) motor phenomena and
may even include language disturbances.
VISUAL SENSORY MOTOR
1. Photopsia – unformed Paresthesia - Focal fatigue (or)
flashes of light numbness starting difficulty with speech
2. Scotoma – partial loss of from fingers, to Difficulty in
sight arms, to involve face, understanding
3. Teichopsia – zigzagging, lips and tongue language
flashing, coloured
phenomena that migrates
across the visual field
∞ After headache, there may be “postdrome” in which the pt. feels
tired, irritable, listless and generally washed out.
∞ Some migraineurs experience nasal stuffiness whereas others
experience profuse nasal secretions.
∞ Nausea is typical and vomiting is frequent.
∞ Most of the aforementioned characteristics are commonly seen.
∞ Some individuals feel unusually rested or euphoric after an
attack.
CLINICAL FINDINGS:
∞ 2 types of migraine:
1. Migraine without aura (common migraine) – MA
 Recurring headache disorder manifesting in attacks
lasting 4-72 hrs.
 IHS criteria:
1. At least 5 headache attacks fulfilling criteria 2-4.
 2. Headache attack lasts 4-72 hrs (untreated or
treated).
3. Headache has at least 2 of the foll. char. –Unilateral
location, pulsating quality, moderate to severe
intensity, aggravated by (or) avoidance of routine
physical activity.
4. During the headache, at least 1 of the foll. occurs:
Nausea and/or vomiting, photophobia, phonophobia.
5. The headache can’t be attributed to any other
disorder.
2. Migraine with aura (classic migraine) – MIA
 Recurring headache disorder manifesting with attacks
of reversible focal symptoms that usually gradually
develop over 5-20 minutes and last for less than 60
minutes.

 IHC criteria:
1. At least 2 attacks fulfilling criteria 2 to 4.
2. An aura consisting of atleast one of the foll. but
no motor weakness: (1) Fully reversible visual
symptoms, (2) Fully reversible sensory
symptoms, (3) Fully reversible dysplastic speech
disturbance.
3. Atleast one of the foll. 2 char.: (1) Homonymous
visual symptoms and/or unilateral sensory
symptoms (2) Gradual development of atleast one
aura over 5 minutes (or) more and/or different
symptoms occurring in succession over 5 min (or)
more (3) Each symptom lasts longer than 5 min
but not more than 60 min.
 4. The headache fulfills criteria 2 to 4 for MA.
5. The headache can’t be attributed to any other
disorder.
MANAGEMENT:
∞ Divided into 3 types:
1. Patient education and trigger avoidance
2. Non – pharmacologic methods:
 Maintain a regular schedule of daily events
 Avoid schedule changes
 Maintain healthy sleep hygiene and avoid any
change in sleeping hours
 Regular exercise, good health practices, regular
mealtimes
 Relaxation training, biofeedback, hypnosis,
cognitive-behavioral therapy, psychotherapy
3. Pharmacologic methods:
 Abortive therapy - < 1 time a week attacks
 Preventive therapy - >1 time a week attacks
 Abortives – NSAIDS, Ergotamines, Triptans,
Dopamine antagonists
 Preventive meds – Beta blockers, CCBs, 5HT1
antagonists, TCAs
∞ Mild to moderate/Excedrine migraine = Acetamenophine +
Aspirin + Caffeine