Headache (Lecture 11) Flashcards
Types of headaches (HA). . . Most HA caused by muscle contraction or blood flow
problems. ..
1. ) Secondary Headache
2. ) Tension-Type Headache
1.) Secondary Headache: underlying pathological cause
› Head/neck trauma, cranial vascular disorder, psychiatric disorders, lumbar puncture, inflammation, hematoma
.
2.) Tension-Type Headache: Most common kind of HA
› Sustained contraction of scalp & neck muscles secondary to anxiety/stress
› Dull, aching head pain; sensation of tightness or pressure across forehead or on the side or back of head
› Patients rarely seek treatment unless occurrence is daily
› TX: NSAIDS, Acetaminophen, Muscle Relaxants, ASA…. Medication Overuse Headaches (formerly Rebound Headaches)
Types of headaches
3. Cluster headaches
Migraines . . . general info and 3 most predictive symptoms of
migraine. . .
› 1 in 5 women, 1 in 16 men affected
› Chronic condition involving brain hypersensitivity and lowered threshold for trigeminal vascular activation
.
1. Moderate/severe disability
2. Photophobia
3. Nausea/vomiting (Also pain upon exertion)
Migraine with Aura
Most commonly visual but can be any type of warning, 10-15 min before; cortical spreading depression
Migraine without Aura includes all other migraines . . . triggers
› menses, stress, changes in sleep or meal schedules, loud sounds, odors, flickering lights
› Foods: MSG, nitrites, tyramines (wine, cheeses), phenylethylamines (chocolate)
› Drug withdrawal: alcohol, caffeine
.
Often mistaken for tension or sinus headache
› 75% of tension & migraineurs have neck pain during & immediately post headache
International Headache Society Diagnostic Criteria for Migraine without Aura
Mechanism of migraine initiation
1. Cortical Spreading Depression (CSD)
- Cortical Spreading Depression (CSD)
› A depression of neuronal activity spreads across the cortex
› Most likely responsible for aura (if present)
Begins as focal stimulation in occipital region –> spreads toward frontal cortex in a slowly propagating wave of hyperactivity followed by a prolonged suppression in neuronal activity
Depressed neural activity is associated with a decreased cerebral blood flow
(vasoconstriction)
Mechanism of migraine initiation
1. Cortical Spreading Depression (CSD) . . . Mediators
› Initiate local neurogenic inflammation
› Trigger vasodilation
› Orthodromic stimulation of the trigeminal nerve terminals back into the brain
Mechanism of migraine initiation
1. Cortical Spreading Depression (CSD)
. . .At the other end of the trigeminal nerve
› Painful messages are transmitted toward central centers via the trigeminal nucleus of the brainstem
› Signals are transmitted up to the thalamus & cortex
› The sensation of central pain arises + nausea, vomiting & autonomic activation
Mechanism of migraine initiation
2. Trigeminovascular System
Trigeminovascular System . . .Release of Neuropeptides leads to
Release of Neuropeptides leads to › Painful meningeal neurogenic inflammation . Leads to › Mast cell degranulation › Plasma protein extravasation › Vasodilation › Activation of nociceptors
Trigeminal nerve pathway . . . first step. . . triggered to release neuropeptides . . .
Treatment: abortive therapy (for headache)
Successful treatment of migraine is defined as
› Complete pain relief & return to normal function
› Within 2 hours of taking medication
NSAIDS – first line treatment for all migraine
› Mechanism of action: inhibition of prostaglandin synthesis (Neurogenic Inflammation)
› Most consistent evidence exists for ASA, IBU, Naproxen, Tolfenamic Acid, Diclofenac and combination Acetaminophen + ASA + Caffeine
Ergot Alkaloids . . . general/ MOA
Ergot Alkaloids . . . drug example and adverse effects
Abortive/ acute treatment (tx) options (2)
Treatment: Triptans . . . general
Treatment: Gepants . . . general
Treatment: Ditans . . .general
Migraine prevention . . . (general 3)
- Onabotulinum Toxin A
- Monoclonal Antibody CGRP Antagonists
- CGRP antagonists
- Other
Migraine prevention: Onabotulinum Toxin A (Botox)
- For chronic migraine prevention in patients with >14 headache days/month
- Black box warning: effects of botulinum toxin may spread from area of injection to other areas of the body causing symptoms similar to botulism
- ————› Swallowing/breathing difficulties (life-threatening)
- Inhibits Acetylcholine release
- Administered SQ q 12 w as multiple injections around the head/neck
Monoclonal Antibody CGRP Antagonists
Bind to CGRP ligand › decrease neuropeptide release › Erenumab-aooe (Aimovig) › Fremanezumab-vrfm (Ajovy) › Galcanezumab-gnlm (Emgality) › Eptinezumab-jjmr (Vyepti) › Available as IV and/or SC for prevention of migraine
AAN Guidelines for Migraine prophylaxis
Levels of evidence suggesting efficacy in migraine – describe levels A,B,C
› Level A: strong evidence, established as effective and should be offered as treatment
› Level B: moderate evidence, probably effective and should be considered as treatment
› Level B Negative: probably ineffective and should not be considered for migraine prevention
› Level C: weak evidence, possibly effective and may be considered
› Level C Negative: possibly ineffective and may not be considered
› Level U: Evidence is conflicting or inadequate to support or refute the use for migraine prevention
