(29) Headaches Flashcards
Defn of primary vs secondary headaches
primary = without IDable cause secondary = with underlying metabolic/structural cause
3 most common types of primary headaches
tension, cluster, migrane
What are the pain sensitive structure in the head?
NOT the brain parenchyma
dura and meninges large arteries (at base of brain) venous sinuses periostium of the skull scalp muscles skin (of face) eyes teeth nasal sinuses
mechanical or electrical stimulation of the _____ in the brain stem will trigger a pain response
thalamus or trigeminal nucleus caudalis
What nerves transmit headache pain? Which ones in the anterior cranial fossa? middle? posterior?
Ant: CN V,
Posterior: VII, IX, V; C2-3
WHere is the 1st and 2nd synapses for the painfibers in the head?
1st= trigeminal nucleus caudalis and dorsal horn of upper spinal cord
2nd= VPL and VPM
What are some distinguishing clinical features of migranes
pulsating
4-72 duration
nausea
photo or phonophobia
symptoms of a migrane prodrome
mood swings, odd food craving, malaise, muscle ache and stiffness
migranes caused by dominantly inherited gene at several loci
familial hemiplegic migrane
what is one loci that carries a gene for migranes
10q23
Trigeminovascular system involving CN ____ innervation of pain receptors in ….
CN V1 innervation of dura, meninges, and large/medium cerebral arteries and veins
What CN and nuclei is responsible for the vasodilation and parasympathetic symptoms assc with headaches
afferents come in on CN V to the superior salivary nucleus where they synapse with CN VII efferents which mediate the vasodilation and parasymp shit assc with migranes
descrie the pathogenesis of a migrane
trigger stimulates the brain stem. Brainstem stims cortex which initiates the aura. The aura stimulates neurogenic inflammation of meningeal vasculature. This inflammation excites the already hyperexcitable (due to genetic predisposition) peripheral and central pain pathways
How is the pathogenesis of a migrane different in people that do not have an aura
the trigger or central generator (i.e. brainstem) directly activates neurogenic inflammation
What determines how the aura clinically manifests?
which anatomical parts of the brain are excited by/experience the aura
describe the changes that occur as the cortical spreading depression moves along the cortex?
it moves along at a rate of 2-5 mm/min bringing a wave of excitation and increased blood flow (hyperemia) with the excitation. as it moves, the excitation gives way to a period of more prolonged depolarization (i.e. that area becomes non-functional) which is assc with decreased blood flow (oligemia)
describe the changes that occur as the cortical spreading depression moves along the calcrine cortex
multicolored scintillations (excited) to scotoma (depolarized state) until the neurons recover
What are the mediators of neurogenic inflammation
Substance P and *CGRP = vasodilate and mast cell degranulation
In terms of the pathogenesis of a migrane, what does CGRP mediate?
signlas inital hyperpolarization and then mediates secondary pain signal
triptans are ______ agonists. What is the efffect of activating this receptor?
5HT-1–> inhibits release GCRT (CGRP??)
serotonin receptor subtype found in…
- vasculature
- peripheral trigeminal N
- central synapse of trigeminal N
serotonin receptor subtype found in…
- vasculature = 5HT-1B
- peripheral trigeminal N = 5HT-1D
- central synapse of trigeminal N = 5HT-1B, D, F
What binds the CRL receptor?
CGRP
Clinical features of cluster headaches
pain is usually unilateral, frontall, retro-orbital
unilateral rhinorrhea, conjunctival injection, horner’s syndrome, and lacrimation
non-pulsating
daily attacks to weeks/months; remission for yrs
Men > women
triggers are alcohol and tobacco
duration mins to 3 hrs
What is the acute treatment for cluster headaches?
prophylactic treatment for cluster headaches?
acute: Nasal O2, subcut Sumatriptan
prophylactic: CCBs, Li, prednisone, valproic acid
clinical features
is usually bilateral and bandlike
(no V/V, photo or phonophobia)
duration mins to 3 hrs
*chronic and episodic forms! – greater and less than 15 days
good summary slide for primary headaches
pg 39
failure to diagnose and treat idiopathic intracranial HTN can lead to
loss of vision
What are some clinical features of IIH
papilledema enlarged blind spots tinnitus female > men overweight persons
may see diplopia secondary to CN VI
Primary idiopathic vs primary symptomatic vs secondary IIH
Primary idiopathic = unknown cause
primary symptomatic = cause that alters CSF production or reabs
secondary = obstruction in CSF circulation/absorption
etiologies of primary symptomatic IIH
abx (tetracycline)
hypervitaminosis A
steriod withdrawal
(others)
etiologies of secondary IIH
venous sinus thrombosis
chronic meningitis
chiari malformation
(others)
What is diagnostic of IIH
opening LP pressure of >250 mmH2O + nml MRI/MRV
What is used to measure treatment success or dz progression in IIH
visual field changes
treatment of IIH
weight loss and reduce CSF production with acetazolamide and furosemide
giant cell arteritis affects (elastic or inelastic) vessels
elastic
clinical features of GCA
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