Headaches and Migraines Flashcards

1
Q

What is the difference between a primary and secondary headache?

A
Primary = absence of physical signs 
Secondary = presence of physical signs (headache due to an underlying condition)
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2
Q

Describe normal/tension-type heaches.

A

Will disappear soon after noxious stimulus has ceased (can last 30 mintues to several days)
Pain is band-like, bilateral (tightness, pressure, dull ache)
Treated with general painkillers, can also use prophylactics

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3
Q

Describe cluster headaches - how long do they last, treatment etc.

A

Very extreme and painful type of headache
More likely to occur in men
Can last 6-8 weeks, with each attack lasting 20 minutes to 3 hours
For acute attacks, treat with 100% oxygen for ~20 minutes
Use verapamil

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4
Q

Migraines are the result of central neuronal hyperexcitability. What are the causes of this hyperexcitability?

A

Abnormality of calcium channels - mutant voltage gated P/Q type calcium channels - this influence presynaptic NT release
Could also be due to genetic abnormalities - these might reduce the threshold of response to triggering factors

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5
Q

What % of migraine attacks are accompanied by an aura?

A

20-30%

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6
Q

How long does each stage of a migraine attack last?

A
  1. 12-48 hours
  2. <1 hour
  3. 4-72 hours
  4. 2-12 hours
  5. 2-24 hours
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7
Q

What is the 1st stage of a migraine attack, what are the signs?

A
Premonitory 
Signs:
- food cravings 
- yawning 
- neck pain
- heightened perception
- fluid retention
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8
Q

What is the 2nd stage of a migraine attack, what are the signs?

A

Aura
Signs:
- visual (99%) and/or sensory and/or speech/language symptoms
- duration of each symptom is approx. 20-30 minutes

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9
Q

What is cortical spreading depression (CSD)?

A

a transient and local suppression of spontaneous electrical activity in the cortex which moves slowly across the brain resulting in an aura
(rate of spread is ~3 mm/min)

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10
Q

What is the 3rd stage of a migraine attack, what are the signs?

A
Headache
Signs:
- anorexia
- N+V
- malaise
- lethargy
- sensitive to light/sound 
- heightened sense of smell 
- difficulty focusing/concentrating
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11
Q

Explain what the trigeminovascular pathway is in relation to migraines/pain.

A
  • Blood vessels vasodilate (induced by neuropeptides)
  • This causes further release of inflammatory peptides
  • Neuropeptides activate the nerve pathways - nerves send pain signals to the trigeminal ganglion
  • Peripheral sensitisation mediates throbbing pain
  • Trigeminal nerve transmits pain impulses to the SpV (spinal trigeminal nucleus caudalis) in the brainstem
  • SpV relays these impulses to the thalamus
  • Information passes from the thalamus to the cortex
  • Cortex then decodes information into our experiences of pain
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12
Q

What is CGRP and how is it related to migraines?

A

CGRP = calcitonin gene-related peptide
It is a 37 amino acid neuropeptide and a potent vasodilator
CGRP increases during spontaneous migraine attacks
CGRP decreases after effective symptomatic treatment with triptans
CGRP infusions TRIGGER migraines
Migraine drugs include CGRP receptor antagonists

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13
Q

What is the 4th stage of a migraine attack, what are the signs?

A

Resolution
Signs:
- vomiting
- deep sleep

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14
Q

What is the 5th stage of a migraine attack, what are the effects on the body after a migraine attack?

A
Recovery 
After migraine:
- limited food tolerance
- tiredness
- feel hungover
- diuresis
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15
Q

What preventative medications are there for migraines and how do they work?

A
  1. 5-HT1D receptors = trigeminal inhibition
  2. CGRP monoclonalantibodies = prevent vasodilation
    (includes erenumab, fremanezumab, eptinezumab, galcanezumab)
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16
Q

What acute medications are there for during a migraine attack?

A
  1. 5-HT1D receptors
  2. 5-HT1B receptors = target vasoconstriction (after vessels have dilated)
    (include sumatriptan, zolmitriptan, naratriptan, eletriptan etc.)
17
Q

Which of the following can lead to an aura?

  1. cortical spreading activation
  2. cortical spreading depression
  3. activation of trigeminovascular system
  4. inhibition of trigeminovascualr system
A

cortical spreading depression