(29) Headaches

Question 1

Defn of primary vs secondary headaches

Answer 1

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

Question 2

3 most common types of primary headaches

Answer 2

tension, cluster, migrane

Question 3

What are the pain sensitive structure in the head?

Answer 3

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

Question 4

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

Answer 4

thalamus or trigeminal nucleus caudalis

Question 5

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

Answer 5

Ant: CN V,

Posterior: VII, IX, V; C2-3

Question 6

WHere is the 1st and 2nd synapses for the painfibers in the head?

Answer 6

1st= trigeminal nucleus caudalis and dorsal horn of upper spinal cord

2nd= VPL and VPM

Question 7

What are some distinguishing clinical features of migranes

Answer 7

pulsating
4-72 duration
nausea
photo or phonophobia

Question 8

symptoms of a migrane prodrome

Answer 8

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

Question 9

migranes caused by dominantly inherited gene at several loci

Answer 9

familial hemiplegic migrane

Question 10

what is one loci that carries a gene for migranes

Answer 10

10q23

Question 11

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

Answer 11

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

Question 12

What CN and nuclei is responsible for the vasodilation and parasympathetic symptoms assc with headaches

Answer 12

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

Question 13

descrie the pathogenesis of a migrane

Answer 13

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

Question 14

How is the pathogenesis of a migrane different in people that do not have an aura

Answer 14

the trigger or central generator (i.e. brainstem) directly activates neurogenic inflammation

Question 15

What determines how the aura clinically manifests?

Answer 15

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

Question 16

describe the changes that occur as the cortical spreading depression moves along the cortex?

Answer 16

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)

Question 17

describe the changes that occur as the cortical spreading depression moves along the calcrine cortex

Answer 17

multicolored scintillations (excited) to scotoma (depolarized state) until the neurons recover

Question 18

What are the mediators of neurogenic inflammation

Answer 18

Substance P and *CGRP = vasodilate and mast cell degranulation

Question 19

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

Answer 19

signlas inital hyperpolarization and then mediates secondary pain signal

Question 20

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

Answer 20

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

Question 21

serotonin receptor subtype found in…

• vasculature
• peripheral trigeminal N
• central synapse of trigeminal N

Answer 21

serotonin receptor subtype found in…

• vasculature = 5HT-1B
• peripheral trigeminal N = 5HT-1D
• central synapse of trigeminal N = 5HT-1B, D, F

Question 22

What binds the CRL receptor?

Answer 22

CGRP

Question 23

Clinical features of cluster headaches

Answer 23

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

Question 24

What is the acute treatment for cluster headaches?

prophylactic treatment for cluster headaches?

Answer 24

acute: Nasal O2, subcut Sumatriptan
prophylactic: CCBs, Li, prednisone, valproic acid

Question 25

clinical features

Answer 25

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

Question 26

good summary slide for primary headaches

Answer 26

pg 39

Question 27

failure to diagnose and treat idiopathic intracranial HTN can lead to

Answer 27

loss of vision

Question 28

What are some clinical features of IIH

Answer 28

papilledema
enlarged blind spots
tinnitus
female > men 
overweight persons

may see diplopia secondary to CN VI

Question 29

Primary idiopathic vs primary symptomatic vs secondary IIH

Answer 29

Primary idiopathic = unknown cause
primary symptomatic = cause that alters CSF production or reabs
secondary = obstruction in CSF circulation/absorption

Question 30

etiologies of primary symptomatic IIH

Answer 30

abx (tetracycline)
hypervitaminosis A
steriod withdrawal

(others)

Question 31

etiologies of secondary IIH

Answer 31

venous sinus thrombosis
chronic meningitis
chiari malformation

(others)

Question 32

What is diagnostic of IIH

Answer 32

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

Question 33

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

Answer 33

visual field changes

Question 34

treatment of IIH

Answer 34

weight loss and reduce CSF production with acetazolamide and furosemide

Question 35

giant cell arteritis affects (elastic or inelastic) vessels

Answer 35

elastic

Question 36

clinical features of GCA

Answer 36

add in