Headache (Lecture 11)

Question 1

Types of headaches (HA). . . Most HA caused by muscle contraction or blood flow

problems. ..
1. ) Secondary Headache
2. ) Tension-Type Headache

Answer 1

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)

Question 2

Types of headaches

3. Cluster headaches

Answer 2

Question 3

Migraines . . . general info and 3 most predictive symptoms of
migraine. . .

Answer 3

› 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)

Question 4

Migraine with Aura

Answer 4

Most commonly visual but can be any type of warning, 10-15 min before; cortical spreading depression

Question 5

Migraine without Aura includes all other migraines . . . triggers

Answer 5

› 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

Question 6

International Headache Society Diagnostic Criteria for Migraine without Aura

Answer 6

Question 7

Mechanism of migraine initiation

1. Cortical Spreading Depression (CSD)

Answer 7

1. 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)

Question 8

Mechanism of migraine initiation

1. Cortical Spreading Depression (CSD) . . . Mediators

Answer 8

› Initiate local neurogenic inflammation
› Trigger vasodilation
› Orthodromic stimulation of the trigeminal nerve terminals back into the brain

Question 9

Mechanism of migraine initiation
1. Cortical Spreading Depression (CSD)
. . .At the other end of the trigeminal nerve

Answer 9

› 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

Question 10

Mechanism of migraine initiation

2. Trigeminovascular System

Answer 10

Question 11

Trigeminovascular System . . .Release of Neuropeptides leads to

Answer 11

 Release of Neuropeptides leads to
› Painful meningeal neurogenic inflammation 
.
 Leads to 
› Mast cell degranulation
› Plasma protein extravasation
› Vasodilation
› Activation of nociceptors

Question 12

Trigeminal nerve pathway . . . first step. . . triggered to release neuropeptides . . .

Answer 12

Question 13

Treatment: abortive therapy (for headache)

Answer 13

 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

Question 14

Ergot Alkaloids . . . general/ MOA

Answer 14

Question 15

Ergot Alkaloids . . . drug example and adverse effects

Answer 15

Question 16

Abortive/ acute treatment (tx) options (2)

Answer 16

Question 17

Treatment: Triptans . . . general

Answer 17

Question 18

Treatment: Gepants . . . general

Answer 18

Question 19

Treatment: Ditans . . .general

Answer 19

Question 20

Migraine prevention . . . (general 3)

Answer 20

• Onabotulinum Toxin A
• Monoclonal Antibody CGRP Antagonists
• CGRP antagonists
• Other

Question 21

Migraine prevention: Onabotulinum Toxin A (Botox)

Answer 21

• 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

Question 22

Monoclonal Antibody CGRP Antagonists

Answer 22

 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

Question 23

AAN Guidelines for Migraine prophylaxis

Levels of evidence suggesting efficacy in migraine – describe levels A,B,C

Answer 23

› 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