Pathophysiology of Headaches Flashcards

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
Q

What is the evidence for the role of brainstem activation in migraine?

A

PAG, locus coeruleus, dorsal raphe nucleus, nucleus raphe magnus - activated on side ipsilateral to pain

26
Q

What is the evidence of the role of thalamus activation in migraine?

A

Seen in brain imaging of spontaneous and induced migraine attacks
May be caused by initial hypothalamic activation - causes progression from premonitory to headache phase