Headache Flashcards
How common is headache?
25% of referrals to neurology §
What is a feature of headache?
Sensitivity to light or sound
How many features does a tension headache have?
1 - either sensitivity to light or to sound
What features do migraines have?
Both sensitivity to light and sound
What are some examples of pirmary headache?
tension
migraine
cluster
What are some examples of secondary headache?
meningitis
What are the 3 headache classifications?
Primary, secondary and cranial neuropathies/other face pains
What types of pain are there?
nociceptive
inflammatory
neuropathic
Where do we feel pain?
Acute pain - modulation of nociception occurs via a series of ascending and descending neural networks which suppress or facilitate signals
Attention, context, emotion and mood affects the pain perception e.g. in the war - called the ‘pain matrix’
Brain network accessed during nociceptive processing imaged with fMRI
What was originally thought to be the aetiology of migraine?
Used to think it was vascular - early experiments stimulated vessels but no evidence of physiological changes in smooth muscle
Measuring blood flow during migraine attacks - migraine not temporally correlated with either hypo or hyperperfusion
What is migraine now considered to be caused by?
Migraine is now considered a disorder of brain excitability:
1/3 rd of patients don’t have throbbing pain
Lesions or electrodes cause pain without vasodilation
Stimulation of insular cortex also causes pain
What are some of the clinical features of migraine?
Most people have episodic migraine - pain for 4-72 hours with recurrent attacks
Pain often on one side
Often pulsing/throbbing
Worse when move around - people want to sit still during attack
Sensitivity to light and sound - want to lie down in a dark quiet room
Can also have sensitivity to touch e.g. glasses become too heavy
Can have nausea
Not attributed to another disorder
Can have aura or not - sometimes flashing lights, tingling in hand etc.
Prodrome - signs before migraine e.g. tired, craving food, fluid retention
Postdromes - signs after migraine
What are some of the theories as to how headaches start?
Central mechanism that activates peripheral nociception that initiates pain
Cortex activates trigeminal nerve afferents
Brainstem may be the migraine generator
Sterile neurogenic inflammation
Abnormal central interpretation of normal sensory input
Measuring cortical spreading of brain activity
Cortical spreading of depression
Potential that blood vessels are involved by releasing diffusible messengers that may influence the activity of neighbouring neurons and glial cells
How is the pain of headaches modulated?
The brain structure itself doesn’t feel pain
The meninges do feel pain
Trigeminal nerves and C2-C3 have sensory inputs to the trigeminal cervical complex which converge on the same second order neurons - explains why can feel pain at the front and back
Use electrodes to measure activity whilst stimulating different areas to see if you can modulate that activity
Plastic changes happen at trigeminal nociceptive terminals and TCC due to repeated stimulus - results in both peripheral and central activation and is thought to play roles in development of headache
TCC is modulated by ascending and descending pain modulating systems at cortical and subcortical level
What is CGRP?
CGRP is a peptide that is upregulated during migraine
Now clinical trials for drugs that modulate CGRP and found to be effective
