MIGRAINE AND PRIMARY
HEADACHES
DR FADIMATU KABIR SAAD
NEUROLOGIST/SENIOR LECTURER FTHG/GSU
INTRODUCTION
• Headache disorders are neurologic conditions characterized by
recurrent head pain.
• Broadly categorized into TWO main categories:
• PRIMARY disorders like migraines, tension headaches, and cluster
headaches.
• SECONDARY disorders which are symptoms of underlying medical
issues.
• Painful cranial neuropathies and other facial pain syndromes.
• Understanding the headache type is the first step towards effective
management and relief.
EPIDEMIOLOGY
• Globally approximately 40% of the population, or 3.1 billion people
are affected.
• Commoner in females than males
• Affects people of all races, income levels and geographic areas.
• Not only painful but they are disabling and impose a burden on
individuals that can include impaired quality of life and financial cost.
MIGRAINE
• Complex disorder characterized byrecurrent episodes of headache,
mostly unilateral with associated visual or sensory symptomscollectively known as AURA. (preceed headache).
• Common in women with strong genetic component.
• usually episodic and is thought to result from release of pain
producing inflammatory substances around nerves and blood vessels
of the head.
• Identified triggers include alcohol, sleep disruption, stress, lack of
exercise, medications e.g histamine, nitroglycerine, estrogen. etc
Signs and symptoms
• Typical symptoms include;
• Headache lasts 4-72hrs
• Unilateral and localized pain in the frontotemporal and ocular area
but may be felt anywhere around the head and neck.
• Throbbing or pulsatile, with moderate to severe pain that worsens
with physical activity.
• Nausea and vomiting
• Sensitivity to light and sound.
contd
• Conjuctival injection
• Cranial/cervical muscle tenderness
• Tachycardia or bradycardia
• Hypertension or hypotension.
• Features of migraine aura• May preceed or accompanyheadache phase
• Develops over 5-20 mins and lasts less than 60 mins
• Commonly visual but can be sensory, motor or any combination.
• Scintillating scotoma is most common visual, or glittering zigzag.
Diagnostic criteria
• At least 5 headache attacks that lasted 5-72hrs( untreated or unsuccessfuly
treated) with at least 2 of thefollowing
• Unilateral location
• Pulsating quality
• Moderate or severe intensity
• Aggravation by routine physical activity.
• And at least 1 of the following
• Nausea and/ or vomiting
• Photophobia and phonophobia
• Must not be attributable to another disorder.
classification
• 1.1 migraine without aura
• 1.2 migraine with aura
• 1.3 chronic migraine
• 1.4 migraine complications
•
status migrainosus
•
migrainous infarction
• 1.5 probable migraine
• 1.6 hemiplegic migraine
• Migraine with brainstem aura.
PHASES OF MIGRAINE
• four phases are recognised
• 1- premonitory phase - fatigue, food cravings, yawning, and mood
changes
• 2- aura phase - reversible visual disturbances eg- zigzag lines, blind
spots, sensory changes or speech difficulties
• 3.- headache phase• 4- postdrome phase- post-migraine hangover, exhaustion, cognitive
sluggishness or mild head soreness.
PATHOPHYSIOLOGY
• Regarded as a primary brain disorder driven by cortical
hyperexcitability, trigerminovascular activation, and neuropeptide
signalling esp CGRP.
• hours to days before the headache, the hypothalamus and brainstem
become hyperactive.
• this is followed by a wave of neuronal depolarization which sweeps
slowly across the cerebral cortex, followed by prolonged suppression
of neuronal activity and massive efflux of potassium with influx of
calcium and sodium into neurons.
• this triggers the activation of the trigerminal nerve fibres that
innervate the pain sensitive blood vessels and meninges.
contd
• the trigerminal nerve releases vasoactive neuropeptides- primarily
CGRP, SUBSTANCE P,NEUROKININ A. Which causes vasodilation of
meningeal blood vessels, and plasma protein extravasation leading to
sterile inflammation.
• these signals travel to the trigerminal nucleus caudalis and higher
cortical pain centers resulting in central sensitization.
• later in the postdrome phase, the inflammation subsides but altered
excitability in the cns lingers as the brain returns to normal.
treatment
• acute relief and preventive therapies
• first line acute treatments include• NSAIDS( ibuprofen or naproxen),
• triptans ( sumatriptan, rizatriptan,
• CGRP ANTAGONISTS- GEPANTS ( rimegepant, zavegepant)
• metoclopramide ( anti- nausea)
preventive treatments
• to reduce frequency of headaches
• 1- beta- blockers( propranolol and calcium channel blockers)
• 2- antidepressants- tricyclics ( amitriptylline etc)
• 3- anti seizure drugs e.g topiramate
• 4- injectables; CGRP inhibitors ( AIMOVIN OR BOTOX.
LIFESTYLE CHANGES
• TEMPRATURE therapy- cold packs or ice to head and neck for
numbing effect
• caffeine in small amounts
• sleep schedules, regular meals, staying hydrated.
OTHER PRIMARY HEADACHES
• 1- TENSION TYPE
• 2- CLUSTER HEADACHE
• 3-TACS ( SUNA, SUNCT, PH)
• 4. LOW CSF PRESSURE HEADACHES
• 5- COLD STIMULUS HEADACHE
• 6- NUMULAR HEADACHE
• 7-DRUG OVERUSE HEADACHE.
•
THANK YOU