Departemen Ilmu Penyakit Saraf

Universitas Jenderal Soedirman

Rumah Sakit Margono Soekardjo
Purwokerto
 Definisi

Hemikrania Hemigrania Migraine

Migraine Types
 Kriteria diagnosis

Minimal lima serangan yang memenuhi kriteria A sampai D:

A. Serangan sakit kepala yang berlangsung 4 sampai 72 jam
B. Sakit kepala memiliki minimal dua dari karakteristik berikut:
1. Lokasi unilateral
2. Kualitas berdenyut
3. Intensitas nyeri sedang hingga berat
4. Memberat oleh ataupun menyebabkan penghindaran aktivitas fisik rutin (misalnya
berjalan atau naik tangga)
C. Selama sakit kepala minimal salah satu dari berikut:
1. Mual dan/atau muntah
2. Fotofobia dan fonofobia

D. Tidak berhubungan dengan gangguan lain

Kriteria diagnosis
Tanda dan gejala migren
Tanda dan gejala migren
Fase migraine
 Teori Migrain
1. Teori vaskular
– Iskemik diinduksi
vasokontriksi intrakranial →
aura
– Diikuti vasodilatasi dan
aktivasi saraf nosiseptif
perivaskular → nyeri kepala
Bukti teori
• Pembuluh darah ekstra kranial melebar dan
berdenyut selama serangan migren
• Stimulasi pada pembuluh darah intra kranial → nyeri
kepala
• Pemberian agen vasokontriktor (ergotamin)
meringankan nyeri kepala, dan vasodilator
(nitrogliserin) memprovokasi nyeri kepala
• However, this theory did not explain the prodrome and associated
features.
• Nor did it explain the efficacy of some drugs used to treat
migraines that have no effect on blood vessels and the fact that
most patients do not have an aura.
• Regional cerebral blood flow (rCBF) remains normal in the
majority of patients.
• Activation of Meningeal Nociceptors by Increased
Parasympathetic Activity
• Modulation of Nociceptive Signals from the Thalamus to
the Cortex and the Threshold Set by Cyclical Brainstem
Activity
• Alterations in sympathetic and parasympathetic tone can
be found from the premonitory phase through to
postdrome
• Migraine triggers, such as stress, awakening, or other
changes in physiological activate nociceptive pathways
through increased parasympathetic tone

corticotropin superior
Norepinephrine Pronociceptive kappa-opioid
releasing salivatory
release signaling system
hormone nucleus (SSN)
• Headache phase may also be determined by the current
circadian phase of cyclical brainstem activity
• If cyclical brainstem activity is high, the threshold is raised
for transmission of nociceptive trigeminovascular signals,
and nociceptive signals are inhibited.
• If cyclical brainstem activity is low, the threshold is
lowered for the transmission of nociceptive signals, and
thus a migraine headache may occur
Activation of meningeal nociceptors by increased parasympathetic tone. BNST: bed nucleus of stria
terminalis;LH : lateral hypothalamus; PAG : periaqueductal gray; Pir : piriform cortex; PVN : paraventricular
hypothalamic nucleus;SPG : sphenopalatine ganglion; SSN : superior salivatory nucleus; TCC : trigeminal
cervical complex; TG : trigeminalganglion
 PHASE 2: AURA
• Initiation and Propagation of Cortical Spreading
Depression (CSD)
– Propagating wave of depolarization in neuronal and glial
cell membranes that is followed by inhibition of cortical
activity, coinciding with the initiation and progression of
aura symptoms
– CSD associated with a wave of hyperemia, followed by a
prolonged phase of cortical oligemia
Cortical Spread Depression
 Cortical Spreading Depression (CSD)

Depolarization and
Disruption of
Elevations in repolarization
cell membrane
Influx of Release of
extracellular K of hyperexcitable
ionic gradients
Na and Ca glutamate
neurons
Cortical spreading depression. EEG : electroencephalogram; K: potassium
Aura
 PHASE 3: HEADACHE
• The Trigeminovascular Pathway
• Activation of the Trigeminovascular Pathway
• Peripheral Sensitization
• Central Sensitization
Trigeminovascular Pathway
Activation of the Trigeminovascular Pathway

Vasoactive
Arterial
Nociceptive neuropeptides
vasodilatation, mast
Activation of
neurons (ATP, glutamate, K,
hydrogen ions,
cell degranulation meningeal
(duramater) and plasma
CGRP, and nitrous extravasation nociceptors
oxide)
 Calcitonin Gene-Related Peptide (CGRP)
1. CGRP is a potent vasodilator, and is present in afferents
innervating meningeal blood vessels
2. CGRP is a neurotransmitter that can enhance synaptic
transmission mediated by glutamatergic signaling
3. Elevations of CGRP can be detected in jugular venous
blood during migraine attacks
4. Intravenous injection of CGRP triggers migraine in
patients with migraine
Calcitonin Gene-Related Peptide (CGRP)

Arterial Plasma Trigeminal Nociceptive

CRGP vasodilatation extravasation ganglion transmission
 Serotonin

Contraction of smooth
inhibiting CGRP and inhibition of glutamate
muscle cells and
substance P (SP) and CGRP release into
inhibition of endothelial
synthesis the synaptic cleft
NO synthase (eNOS)

vaso- modulate block pain

constriction exocytosis afferentation
Serotonin
 Photopobia
1. Light enhances the activity of thalamic trigeminovascular
neurons;
2. A subgroup of light/ dura-sensitive neurons located mainly in the
LP/Po area of the posterior thalamus receive direct input from
RGCs; and
3. The axons of these neurons project to cortical areas involved in
the processing of pain and visual perception.
Photopobia