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Flashcards in (29) Headaches Deck (36):
1

Defn of primary vs secondary headaches

primary = without IDable cause
secondary = with underlying metabolic/structural cause

2

3 most common types of primary headaches

tension, cluster, migrane

3

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

4

mechanical or electrical stimulation of the _____ in the brain stem will trigger a pain response

thalamus or trigeminal nucleus caudalis

5

What nerves transmit headache pain? Which ones in the anterior cranial fossa? middle? posterior?

Ant: CN V,

Posterior: VII, IX, V; C2-3

6

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

7

What are some distinguishing clinical features of migranes

pulsating
4-72 duration
nausea
photo or phonophobia

8

symptoms of a migrane prodrome

mood swings, odd food craving, malaise, muscle ache and stiffness

9

migranes caused by dominantly inherited gene at several loci

familial hemiplegic migrane

10

what is one loci that carries a gene for migranes

10q23

11

Trigeminovascular system involving CN ____ innervation of pain receptors in ....

CN V1 innervation of dura, meninges, and large/medium cerebral arteries and veins

12

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

13

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

14

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

15

What determines how the aura clinically manifests?

which anatomical parts of the brain are excited by/experience the aura

16

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)

17

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

18

What are the mediators of neurogenic inflammation

Substance P and ***CGRP** = vasodilate and mast cell degranulation

19

In terms of the pathogenesis of a migrane, what does CGRP mediate?

signlas inital hyperpolarization and then mediates secondary pain signal

20

triptans are ______ agonists. What is the efffect of activating this receptor?

5HT-1--> inhibits release GCRT (CGRP??)

21

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

22

What binds the CRL receptor?

CGRP

23

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

24

What is the acute treatment for cluster headaches?

prophylactic treatment for cluster headaches?

acute: Nasal O2, subcut Sumatriptan

prophylactic: CCBs, Li, prednisone, valproic acid

25

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

26

good summary slide for primary headaches

pg 39

27

failure to diagnose and treat idiopathic intracranial HTN can lead to

loss of vision

28

What are some clinical features of IIH

papilledema
enlarged blind spots
tinnitus
female > men
overweight persons

may see diplopia secondary to CN VI

29

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

30

etiologies of primary symptomatic IIH

abx (tetracycline)
hypervitaminosis A
steriod withdrawal

(others)

31

etiologies of secondary IIH

venous sinus thrombosis
chronic meningitis
chiari malformation

(others)

32

What is diagnostic of IIH

opening LP pressure of >250 mmH2O + nml MRI/MRV

33

What is used to measure treatment success or dz progression in IIH

visual field changes

34

treatment of IIH

**weight loss** and reduce CSF production with acetazolamide and furosemide

35

giant cell arteritis affects (elastic or inelastic) vessels

elastic

36

clinical features of GCA

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