Migraine Flashcards

1
Q

What are primary headaches and give examples

A
  1. Headaches not caused by another medical condition
  2. Examples:
    Migraine, Cluster Headache, Tension Type Headache, Other primary headaches
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2
Q

Who do migraines most commonly affect?

A

More common in women

Most productive years: 18 to 55 years

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3
Q

What do migraines with aura present with

A

Additional visual or sensory disturbances

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4
Q

What do migraines without aura present with

A

Most common
More debilitating
Higher attack frequency

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5
Q

What is the diagnostic criteria for a migraine

A
  1. At least FIVE headache attacks lasting between 4-72 hours (untreated or unsuccessfully treated)
2. Headache must have TWO of following: 
Unilateral Location: one position
Pulsating quality
Moderate or severe pain intensity
Aggravation by or causing avoidance of routine physical activity
  1. During headache: one of the following:
    Nausea and/or vomiting
    Photophobia and phonophobia
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6
Q

What is diagnostic criteria: migraine with aura? (10)

A
  1. At least TWO headache attacks lasting between 4-72 hours
  2. Patients must have no motor weakness and have aura consisting of:
    Fully reversible visual symptoms including positive features e.g. flickering lights, spots or lines

Fully reversible sensory symptoms including negative features e.g. loss of vision

Fully reversible sensory symptoms including positive features e.g. pins and needles

Fully reversible sensory symptoms including negative features e.g. numbness

Fully reversible dysphasic speech disturbance

Two of the following:
1. Visual symptoms and/or unilateral symptoms

  1. At least one aura symptom develops gradually over >5 minutes and/or different aura
  2. Each symptom lasting more than or equal to 5 and or less than or equal to 60

Migraine without aura can then follow

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7
Q

If a migraine starts, how can you rule out it is not a stroke

A

Status Migrainous: attack lasts more than 72 hours

Migrainous Infarction: aura lasts more than 1 hour

Persistant aura without infarction: aura lasts more than 1 week

Migraine aura triggers seizure

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8
Q

What is the migraine pathophysiology

A

Complex genetic disorder, likely a polygenic multifactorial inheritance

Present understanding from familial hemiplegic migraine (FHM): a rare monogenic, autosomal dominant form of migraine with aura

Three genes: ion channels, transporters

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9
Q

What is the current migraine theory

A
  1. Neurovascular disease
  2. Activation and sensitisation in the Trigeminovascular pain pathway: controls nerves in mouth and face
  3. Innervates cranial tissues: particularly meninges and large blood vessels
  4. Cortical spreading depression: neurophysical correlate of migraine aura: slowly propagating wave of strong neuronal and glial depolarisation
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10
Q

Describe the trigeminovascular pain pathway

A

An afferent pathway:

Dura and pia mater in cerebral cortex

Trigemina ganglion

Trigeminal nucleus caudal

Medulla

Hypothalamus, thalamus, hippocampus, corpus, cortex

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11
Q

What is familial hemiplegic migraine type 1

A

Mutation of neuronal Cav2.1 channels

Multiple mutations identified- gain a function increased open probability

Shifted activation to more negative voltages

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12
Q

What are the common prescriptions used for migraineurs

A

Hypertension
Beta blocker
Calcium Channel Blocker

Pain
Narcotic analgesics: codeine

Antidepressants
TCA
Monoamine oxidase inhibitor
SSRIs
SNRIs

Anti wrinkle
Botox

MIGRAINE
TRIPTANS

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13
Q

What is the main molecular mediator of a migraine and what did it lead to discover

A
  1. 5-HT: pathophysiology of migraine as levels decrease during attacks
  2. Slow IV of 5-HT can abort migraine
  3. Led to triptans discovered, 5-HT 1D/B/F receptor agonists like sumatriptan (1st gen), zolmitriptan, rizatriptan (2nd gen)
  4. Provides relief of migraines
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14
Q

What are the mechanism of actions of 5-HT 1B/D or F receptor agonists like triptans

A

Constriction of cranial arteries

Inhibitory actions on the CNS

Inhibition of presynaptic TG neurons (includes 5-HT1BDF)

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15
Q

What is contraindicated in triptans and what can overuse lead to

A
  1. Contraindicated: coronary or cardiovascular disease, hypertension, pregnant women
  2. Overuse: severe rebound attacks and headache
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16
Q

What are the acute treatments for a migraine

A

Simple analgesic: paracetamol and aspirin

Anti-emetics: metoclopramide

Ergots: partial agonists for 5-HT: Ergotamine and dihydroergotamine

Opioid: codeine: last resort if triptans inefficient

17
Q

When are prophylactic treatments for a migraine used and give examples of some (9)

A
  1. Patients suffering 4+ actions a month
  2. beta blockers: metoprolol or propranolol
  3. TCA: Amitriptyline and Nortriptylline: prevents reuptake of 5-HT and antagonist of 5-HT2 receptors
  4. Anti-convulsant: Sodium valproate, gabapentin
  5. NSAIDS: Naproxen
  6. Calcium channel blockers: verapamil
  7. Anti-serotonergic drugs: Pizotifen: antagonist of 5-HT receptors
  8. Methysergide: semi synthetic ergot alkaloid, administed under hospital supervision due to side effects
  9. Botulinum toxin A: licensed for treatment of chronic migraine: relaxes muscles and inhibits release of peripheral nociceptive neurotransmitters: CGRP
18
Q

What is the calcitonin gene related peptide and why is it important in migraine attacks

A

CGRP: alternative processing of calcitonin gene

Potent vasodilator: involved in neurogenic inflammation and nociception

Migraine attacks: Increased CGRP in serum and saliva

Injection of CGRP into migraineurs leads to delayed migraine like headaches

19
Q

What makes up the CGRP receptor and what does it lead to

A

CLR (calcitonin receptor like receptor)

RAMP (Receptor activity modifying protein 1)

Angiogenesis, Proliferation, vasodilation

20
Q

What are used to target CGRP receptors

A

Gepants: CGRP receptor antagonists

Example of first clinical trial: Oicegepant

Example of phase III clinical trial: Telcagepant

used to target episodic and chronic migraine through injection

21
Q

What are additional migraine treatment targets

A

gap junction blockers: tonaberset

Angiotensin II receptor antagonists: candesartan

TRPV1: transient receptor potential channel vanillin 1 antagonists