Migraine Flashcards

Question

Acute treatment of migraine - Why triptans > ergots

Answer 1

1. Ergots have not shown relationship with CGRP and central pain process involvement. While Triptans can inhibit vasoactive peptide release (e.g., CGRP) and normalize elevated CGRP levels. 2. Better SE profile of Triptans

Answer 2

Powerful vasoconstrictor effects - use cautiously in cardiovascular pathologies CI in arterial hypertension, coronary heart disease, Raynaud's disease, hist of ischemic stroke

Answer 3

Sumatriptan: - Pregnancy: not first line, possible **incr in rate of preterm birth**, caution use - Lactation: (SubQ) excreted into breastmilk, minimize infant exposure by **avoiding breastfeeding for 12h** after treatment (*Lactmed: 8h, U2D: 12h, PIL:24h*)

Answer 4

- do not use within 2 weeks after MAOi discontinuation (serotonin syndrome) - do not use within 24h of ergot/other triptans (vasospastic rxn)

Answer 5

- MOA: tonic action on vascular smooth muscles in the external carotid network, leading to vasoconstriction by stimulating alpha-adrenergic and 5-HT receptors (esp 1B and 1D), prevent release of neuropeptide and inflammatory mediators - Inferior to triptan therapy on the outcome of headache relief at 2h - CI: CVD, CHD, cerebrovascular disease, uncontrolled HTN

Answer 6

- Not recommended by some guidelines as **non-specific to migraine** + **abuse potential** - more commonly able to cause **MOH** - indiscriminate activation of opioid signaling can have **adverse effects such as hyperalgesia, allodynia, worsening of nausea** - however, for pt who do not respond to migraine-specific agents, opioids may be indicated intermittently during acute episodes

Answer 7

Antiemetics (e.g., Metoclopramide) - improve N/V symptoms, esp when combined with analgesics

Answer 8

AHS: based on number of headache days per month + degree of disability caused by the attacks EHF: impair QoL + not controlled with acute therapy, risk of overuse of acute therapy

Answer 9

Reduce **frequency, duration, severity** of attacks, esp if QoL impaired

Answer 10

- Attacks significantly interfere with pt daily routine despite acute treatment s - Frequent attacks (.=4MHDs) - CI to / failure of / overuse of acute treatment - Adverse effects with acute treatment - Patient preference - cost, lifestyle, SEs

Answer 11

- Anticonvulsants: Sodium valproate, Topiramate - Beta-blockers (B1 antagonist shown to reduce HA attacks): Propranolol (non-selective), Metoprolol (selective B1) - CGRP monoclonal antibodies (mAbs) Others: - Neuromodulation devices - Neurotoxins - ARBs - Triptans *Pharmacologic, interventional, biobehavioral, neurostimulation, nutraceuticals, lifestyle modifications

Answer 12

CGRP is a nociceptive vasodilative peptide released from trigeminal neurons. CGRP release triggers a cascade of central pain spreading, central pain amplification process. => pain transmission, vasodilation of cerebral blood vessels, neurogenic inflammation In migraine, CGRP levels are elevated Therefore, drugs that inhibit CGRP activity are effective in treating migraine

Answer 13

1. Erenumab (anti-CGRP receptor antibody) - targets CGRP receptors 2. Anti-CGRP antibodies - targets CGRP proteins 3. Gepants - small molecules that antagonize CGRP receptors

Answer 14

Not just brain, also found in external jugular veins and throughout the body

Answer 15

- 2nd order neuron (1st oder trigeminal neurons release CGRP to 2nd order neurons => nociception) - smooth muscle cells (vasodilation of cerebral blood vessels) - mast cells (trigger neurogenic inflammation)

Answer 16

CGRP has been hypothesized to act as a vasodilator safeguard during ischemia Hence, if inhibited long-term, may worsen mild and transient ischemic events, could possibly worsen HTN control

Answer 17

- Expensive ($2000/month) - SubQ injection monthly - Clinical benefit within 3 months - Not yet approved for use in pt <18yo - Lack of long term safety data

Answer 18

4-7 monthly migraine days and both: - inability to tolerate, or inadequate response to 8-week trial of two prior treatment classes - at least mod diasbility (MIDAS >=11, HIT-6 >50) 8-14 monthly migraine days and: - inability to tolerate, or inadequate response to 8-week trial of two prior treatment classes Chronic migraine and either: - inability to tolerate, or inadequate response to 8-week trial of two prior treatment classes OR - inability to tolerate, or inadequate response to a minimum of two quarterly injections (6 month) of onabotulinumtoxinA

Answer 19

Either of the 2 criterias are met: 1. Reduction in mean monthly headache days or headache days of at least mod severity of >=50% relative to the pretreatment baseline 2. Clinically meaningful improvement in ANY of the following validated migraine-specific patient-reported outcome measures: MIDAS (reduction of >=5 points when baseline 11-20, >=30% when baseline >20), MPFID (reduction of >= 5 points), HIT-6 (reduction of >= 5 points)

Answer 20

- headache diary (frequency, severity, acute meds use, symptoms, SEs, adherence) - PRO tools - disability assessments (e.g., MIDAS) - adverse effects from meds

Answer 21

I: 0-5 (little to no disability) II: 6-10 (mild disability) III: 11-20 (mod disability) IV: >20 (severe disability)

Answer 22

AHS guidelines recommend - every 3 months after starting monthly tx - every 6 months after starting quarterly tx Assess change in frequency and severity of attacks, evaluate migraine-related symptoms, identify and address adverse events to the treatment, monitor med use, ensure adherence

Answer 23

- 50% reduction in frequency - sig dcr in attack duration (defined by pt) - sig dcr in attack severity (defined by pt) - improved response to acute tx - reduction in migraine-related disability - improvement in QoL

Migraine Flashcards

(47 cards)