Headache and Migraine Flashcards
Primary headache
Diagnosis made on history in absence of physical signs
Treating headache, not thing that may be causing it
Secondary headache
Diagnosis made on history in presence of physical signs
Underlying cause treated
Primary headache types
Tension type
Migraine
Cluster
Tension-type headache facts
80% primary headaches
F>M
Migraine facts
15% primary headaches
F>M
Cluster headache facts
0.2-0.3% primary headaches
M>F
Tension type headache
Disappear soon after noxious stimulus stops Band-like, bilateral Tightness, pressure, dull ache Mild to moderate Not aggravated by movement Treatment- acute, prophylactic
Cluster headache
Treatment- high flow O2- constricts blood vessels 6-8 weeks Extreme pain Unilateral 30 mins --> several hours Usually couple of hours after go to sleep No cure Strong link to smoking
Migraine without aura diagnostic criteria
At least 5 attacks fulfilling:
- Headaches 4-72 hours
- Headache 2/4 characteristics of: unilateral, pulsating, moderate/severe pain, aggravated by physical activity
- During headache at least one of: nausea and/or vom, photophobia + phonphobia
Migraine diagnostic
Light bothers you Headaches limit ability to work/study Feel nauseated or sick --> 2 positive answers- 93% --> 3 positive answers- 98%
Migraine pathophysiology
Triggers –> (Cortical spreading depression –> aura –> ) Activation/sensitisation of TGVS –> headache
Types of migraine
Without aura: 70-80%
With aura: 20-30%
Migraine aura
Visual 99%
Gradual development
Duration of each symptom typically 20-30 mins
Complete reversibility
Typically resolves before onset of headache
No motor weakness
When does migraine start
Chemical changes start 24 hours before headache - Premonitory phase
5HT
Monoamine neurotransmitter
Vasoconstrictor and/or vasodilator
Increase during migraine
Drugs that deplete serotonin trigger migraine
Serotonin infusions help relieve migraine
Triptans
Acute
5HT 1d/b agonists
Methysergide
Prophylactic
5HT2b antagonist
Reserpine
Depletes serotonin
–> triggers migraine
Aura
Originates from visual cortex Still persists when eyes closed Unilateral May resolve before onset of headache Less than an hour Consequence of CSD Gets bigger as CSD spreads across cortex
Cortical spreading depression
A transient and local suppression of spontaneous electrical activity in cortex with moves slowly across the brain
3mm a minute
Aura is consequence of CSD
Thought to be caused by constriction of BVs by serotonin, reducing blood flow
Serotonin effects
Causes meninges on outside of brain to dilate
Once dilated, release of other inflammatory neuropeptides- CGRP
CGRP
37 AA neuropeptide Potent vasodilator Widely distributed in CNS + PNS Levels rise spontaneously during migraine attacks Decreases after triptans CGRP infusions trigger migraine
Trigeminal ganglion (in roof of mouth)
Neuropeptides activate nerve pathways
Nerves send pain signals to trigeminal ganglion
Trigeminal ganglion transmits pain impulses to trigeminal nucleus caudalis in brainstem
Relays pain to thalamus
Thalamus –> cerebral cortex
Triptans
5HT 1d/b agonists Acute treatment Sumatriptan Zolmitriptan Naratriptan
CGRP monoclonal antibodies
Prevention
Erenumab
Fremanezumab
Eptinezumab