Pathophysiology of Headaches Flashcards

(26 cards)

1
Q

What is hyperalgaesia?

A

Decreased pain threshold - nociception hypersensitivity

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2
Q

What is allodynia?

A

Innocuous stimuli perceived as noxious

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3
Q

Which nerve is involved in headaches and what does it innvervate?

A

Trigeminal (VI) nerve

Jaw and brain vasculature

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4
Q

Which brain areas cause descending pain inhibition?

A

PAG and RVM

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5
Q

What are the symptoms of a tension-type headache?

A
Bilateral pressure
Not affected by movement
No nausea/photophobia/phonophobia
Pericranial muscle tenderness
No pericranial muscle inflammation
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6
Q

What is the cause of episodic tension-type headache?

A

Peripheral neuron sensitised - more central neuron activation - stops without input from peripheral neuron

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7
Q

What is the cause of chronic tension-type headache?

A

Central neuron sensitised - remains active without input from peripheral neuron

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8
Q

What are the 3 types of trigeminal autonomic cephalagies and what are their characteristics?

A

SUNCT - short, very frequent
Paroxysmal hemicrania - moderate duration, moderate frequency
Cluster headache - long, infrequent

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9
Q

What are the symptoms of cluster headache?

A

Stabbing pain on one side of face
Autonomic features on one side of face - weeping eye, facial sweating, eyelid oedema
Bursts of attacks - divided by remission periods

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10
Q

What is the cause of TACs?

A

Hypothalamic malfunction

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11
Q

What are the symptoms of a migraine?

A
Aura/no aura
Unilateral throbbing pain
Nausea
Photophobia/phonophobia/osmophobia
Pain worsened by movement
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12
Q

What are the triggers of migraine?

A

Missing meals
Missing sleep
Hormones - in females
Stress

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13
Q

What are the phases of a migraine attack and what do they involve?

A

Premonitory - craving, yawning, heightened perception
Aura
Headache - nausea, hypersensitivity, poor concentration
Resolution - deep sleep, vomiting
Recovery - tired, hungover

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14
Q

Which condition is used to study migraine genetics?

A

Familial hemiplegic migraine

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15
Q

What is the overall effect of the genetic mutations involved in familial hemiplegic migraine?

A

Neuronal hyperexcitability

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16
Q

What is FHM1 and what is the effect of its mutation?

A

Ca2+ channel gene

Increased presynaptic Ca2+ influx

17
Q

What is FHM2 and what is the effect of its mutation?

A

Na+/K+ ATPase gene

Decreases K+ and glutamate uptake into glia

18
Q

What is FHM3 and what is the effect of its mutation?

A

Na+ channel gene

Increases high frequency discharges

19
Q

What is the evidence for the hyperexcitability migraine theory?

A

Increased plasma and CSF glutamate in sufferers

Lower threshold for visual cortex excitation in sufferers

20
Q

What type of brain activity occurs in the premonitory phase of migraine?

A

Increased hypothalamic activity

21
Q

What is an aura?

A

Transient sensation - e.g. visual blindspot, tingling limbs

22
Q

What type of brain activity occurs in the aura phase of migraine?

A

Cortical waves of spreading depression - initial excitation leaves wave of spreading depolarisation
Move at slow rate
Do not cross cerebral hemispheres or spread to deeper brain areas
Could release mediators - inducing headache

23
Q

What is the effect of meninge stimulation?

A

Headache pain

24
Q

What is the evidence for the role of the trigeminovascular system in migraine?

A

Calcitonin gene-related peptide (CGRP) increased in cranial circulation during migraine - may be trigeminal origin
NO and CGRP infusion causes vasodilation of intracranial blood vessels and headache in all - also delayed migraine only in sufferers

25
What is the evidence for the role of brainstem activation in migraine?
PAG, locus coeruleus, dorsal raphe nucleus, nucleus raphe magnus - activated on side ipsilateral to pain
26
What is the evidence of the role of thalamus activation in migraine?
Seen in brain imaging of spontaneous and induced migraine attacks May be caused by initial hypothalamic activation - causes progression from premonitory to headache phase