Headaches and Migraine Flashcards

1
Q

Primary care consultations (similar for specialists) for headache:
__% are primary
__% are secondary
__% medication over-use headaches.

A

80
12
6

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does the classification of primary and secondary headaches differ?

A

Primary - diagnosis made in the absence of physical signs

Secondary - diagnosis made in the presence of physical signs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Which type of primary headache is most common?
Tension-type
Migraine
Cluster headache

A

Tension-type headache (80%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What defines a ‘normal’/tension-type headache?

A

Disappear soon after the noxious or potentially noxious stimulus has ceased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe a tension-type headache.

A
Band-like, bilateral
Tightness/pressure/dull ache
Radiate to neck and shoulders
Mild to moderate
Not aggravated by movement
30 min to several day
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe a cluster headache. How are they treated?

Are they more common in men or in women?

A

Excruciating pain - they go on for 6-8 weeks, with about 6-8 attacks a day lasting 30 minutes to 3 hours.
Treat with 100% oxygen at 12-15L per minute, vasoconstrictors and triptans.
They are more common in men.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What are the criteria for migraine diagnosis?

A

A. At least five attacks in a lifetime fulfilling criteria B-D
B. Headache attacks lasting 4-72 hours
C. Headache has at least two of the following four characteristics:
1. Unilateral location
2. Pulsating quality
3. Moderate or severe pain intensity
4. Aggravation by or causing avoidance of routine physical activity
D. During headache, occurrence of at least one of following symptoms:
1. Nausea and/or vomiting
2. Photophobia and phonophobia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the five stages of a migraine?

A
Premonitory
Aura
Headache
Resolution
Recovery
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How many % of migraine attacks are without aura?

A

70-80%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can the pathophysiology of migraines be summarised in simple words? What about more scientifically?

A

Migraines are caused by triggers acting on an excitable brain, provoking a change in brain chemistry.
Triggers acting on an excitable brain cause:
Trigeminal vascular sensitization –> headache AND
–> vasodilation and central sensitisation (which –> headache)
They also cause:
Cortical spreading depression –> aura –> TGVS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is an aura? Describe it.

Where does it emanate from?

A

Visual (99%) and/or sensory and/or speech/language symptoms.
It develops gradually, with symptoms lasting 20-30 minutes each, and typically resolved before the onset of the headache.
Visual cortex (NOT THE EYES)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe the five stages of migraine - how long do they each last? What are the symptoms?

A
  1. Premonitory – 12-48 hours, food craving, tired, heightened perception, fluid retention
  2. Aura – less than an hour
  3. Headache – 4-72 hours, nausea, vomiting, lethargy, sensitivity to light/sound/smell, difficulty focusing, poor concentration
  4. Resolution – 2-12 hours, vomiting, deep sleep, medication
  5. Recovery – 2-24 hours, feel tired, hungover, limited food tolerance, diuresis. The brain has to reset itself - can’t have a migraine daily.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What does having an aura increase your risk of?

A

Ischaemic stroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cortical spreading depression causes an aura. What does this mean?

A

A transient and local suppression of the spontaneous electrical activity in the cortex which slowly moves across the brain.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Explain the headache section of the migraine.

A
  • Blood vessels in meninges become swollen/stretched and release neuro-inflammatory peptides.
  • This activates the nerves, which send a pain signal to the trigeminal ganglion. This is responsible for peripheral sensitisation (throbbing pain).
  • The trigeminal ganglion transmits to nucleus caudalis, which provokes central sensitisation (this prolongs/continues the attack = ALLODYNIA). This happens within 60 minutes of the onset of pain and can last up to 10 hours.
  • Pain impulses are then relayed to the thalamus.
  • Relayed from thalamus to cerebral cortex, where the impulses are decoded as pain.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is central sensitisation? What is it due to?

A

Neuronal hyperexcitability in the trigeminal nucleus caudalis, possibly due to increased CGRP, calcium ions and glutamate.

17
Q

What do preventative medications for migraines target?

A

Central sensitisation

Pain signal transmission

18
Q

What do acute medications for migraines target?

A

Neuropeptide release

Vasodilation