Migraine Ha Management

Front 1

Occurs more in women, highest incidence in ages 25-55. Most freq disabling condition in middle aged women. Are migraines more a neuronal activity problem or a vascular change?
- Is related to xs discharge from ___ system
- also related to itxn b/w ___ and cranial blood vessels- which leads to release of neuoropeptides which cause vasodilation and HA
- sets up __ inflam response in the arteries of scalp and possibly in dura

Back 1

1. neuronal activity
2. trigeminal system
3. brain stem
4. STERILE inflammatory response

Front 2

- Acitivity within the trigeminovascular system may be regulated in part by noradrenergic neurons but more importantly ___ neurons in the brain stem.

Back 2

1. serotonergic

Front 3

Migraine pathogenesis may be due to __ in levels of 5HT in blood and increase in excreted 5HT. IV administered %HT relieves sx of migraine

Back 3

1. decrease in plasma levels of 5HT

Front 4

What is considered a common migraine which affects 85% of pts?
What are some of sx that are seen w/ migraine?
What qualities do the HA usually present w/?
Is there any other disease related to the migraine HA?

Back 4

1. Migraine without aura
2. unilateral pain, throbbing or pulsating quality, pain of moderate to severe intesity, aggravation by movement or routine physical activity
- HA will also have N&V or photophobia or phonophobia and exquisite sensitivity to nociceptive input
- no other organic disease

Front 5

What is considered a classic migraine?

Back 5

Migraine with aura-- affects 15% of pts

Front 6

What are some common expression of aura in migraines?
How long do auras last?

Back 6

- visual aura, sensory paresthesias (marching paresthesias-cherioaural march), speech disturbance
- develop over 5-20 minutes but last less than an hour, they have a gradual evolving, onset instead of maximal simultaneous onset as w/ TIA

Front 7

What are some common triggers for migraines?

Back 7

1. change in routine especially w/ sleep and meals
2. physio or psychological stress
3. fatigue
4. change in sensory stimuli
5. food containing MSG, caffiene, red wine, nitrates

Front 8

For migraine tx should pts be started at lowest type of med? Triptans and DHE are 1st line for pts w/ ___ to ___ migraine or for pts w/ __ to ___ HA that response poorly to nonspecific analgesics

Back 8

No, pts should be given stratified care based on severity
- moderate to severe
- mild to moderate HA

Front 9

If pt has sig N&V what type of med should be given?

Back 9

- anti emetic such as metoclopramide
- also do not give med orally, instead give parenterally

Front 10

NSAIDs- MOA, AE

Back 10

inhibits the sterile inflammatory rxn in the trigeminovascular system through inhibition of PG synth
- AE: dyspepsia, infreq ass, w/ serious GI SE, caution in pts w/ htn, HF, previous ulcer disease, renal disease, or hypersensitivity to aspirin

Front 11

NSAIDs- general dosing

Back 11

- pts should be given higher doses so that NSAIDs have anti-inflammatory action

Front 12

Difference b/w ibuprofen and naproxen?

Back 12

- naproxen is much more rapid onset

Front 13

Ketorolac- PK, Dosing

Back 13

- ONLY PARENTERAL NSAID
- limit dosing to less than 3x a wk b/c of risk of nephrotoxicity

Front 14

NSAID- Use

Back 14

- DOC for mild to moderate migraine HA
- effective for both migraine and tension HA
- improves efficacy and prevents recurrence when added to triptan
- should be used EARLY in migraine attack- DO NOT give enteric coated NSAIDs

Front 15

DHE- MOA

Back 15

- Nonselective 5-HT1 receptor agonists that constrict intracranial blood vessels and inhibit the development of neurogenic inflammation in the trigeminovascular system
- Also effects α-adrenergic, β-adrenergic, and dopaminergic receptors

Front 16

DHE- Use, PK

Back 16

- effective for established migraine HA, useful for migraines that return w/ shorter acting agents, MOST IMPORTANTLY- for pts that experience rebound HA-- very low incidence of rebound HA
- rapid onset w/ LONG duration of action - 6-10 hrs
- no more than 8 sprays per wk

Front 17

- DHE- CI, AE

Back 17

CI- CAD, PVD, UNCONTROLLED HTN, pregnancy
AE: N&V, less than w/ ergotamine tartare, alteration of taste
MOA: works via 5HT1 agonism to cause vasoconstriction and to decrease neurogenic trigem inflammation- thus coronary and vascular SEs

Front 18

Triptans-MOA

Back 18

- structural analogs of 5HT, relief of migraine HA at 3 sites
- vasoconstriction of pain producing intracranial blood vessels
- inhibition of inflammatory vasoactive neuropeptide release
- interruption of pain signal transmission within the brain stem trigeminal nuclei

Front 19

5HT1 B- mediate contraction of
1.
2.
3.

Back 19

1. peripheral blood vessels
2. coronary blood vessels
3. meningeal blood vessels

Front 20

5HT1 D ___ activn of trigeminovascular afferents
- also ___ release of neuropeptides-- which decreases neurogenic inflammation and prevents sensitization of sensory afferents

Back 20

1. inhibit- stimulation inhibits pain signal transmission
2. decreases

Front 21

Which type of triptan formulation takes longer to provide relief?
Triptans- Use

Back 21

1. oral, injection and nasal spray formulations work in 10-15 minutes
- advantage over DHE b/c better tolerated and more effective, wider window of efficacy (i.e. even if given late still work), and work on ancillary migraine sx- i.e. photophono phobia, N&V

Front 22

Triptans- AE, CI

Back 22

-AE: N&V, chest pressure or tightness- mild and usually resolves in 2 hrs, but may very rarely be due to cardiac ischemia
- CI: chest SE very rare but very serious, so pts w/ CAD, uncontrolled HTN, peripheral or cerebral vascular dx, prinzmental angina, previous MI
- be cautious in pts w/ high risk- i.e. smokers, diabetics, high cholesterol, and category C for pregnant pts

Front 23

Triptans- DI

Back 23

DI: lithium, SSRI, other triptans, and MAO inhibitors-- due to serotonin syndrome
- ergotamine (DHE) and triptans should NOT be used within 24 hrs of each other
- propranolol increases serum levels of rizatriptan and zolmitriptan

Front 24

What are the long acting triptans?

Back 24

1. frovatriptan and naratriptan

Front 25

Naratriptan- PK

Back 25

- longer duration of action but delayed onset
- good for menstrual migraine

Front 26

What is a very fast acting triptan?

Back 26

Zolmatriptan-- nasal spray- works in 15 minutes

Front 27

How do you limit rebound HA w/ triptans?

Back 27

- try to limit use to less than 2 days per wk

Front 28

If 1st dose of triptan ineffective will 2nd dose be more or less likely effective?
If one triptan does not work does that mean all triptans will not work?

Back 28

Less likely to be effective
- no, if one triptan does not work another might still work

Front 29

Excederin migraine has ?
How does caffiene work, what is the caveat

Back 29

1. ASA
2. APAP
3. caffiene- works by increasing absorption by acidifying the duodenum but may increase incidence of rebound HA

Front 30

Butalbital/caffiene- Use, disadvantage

Back 30

Use: appropriate for pts w/o hx of substance abuse, who will lim use to less than 1/wk for HAs refractory to other safter meds
- disadvantage- sedating, abuse potential, rebound HA

Front 31

Butorphanol- MOA, Use, Disadvantage

Back 31

MOA- kappa receptor agonist/antagonist, reserved for recalcitrant HA
Use: short term use- last resort
Disadvantage- sig dependance and abuse potential

Front 32

Corticosteroids- MOA, Use

Back 32

- reduces PG release,
- Use: effective for short term tx of intractable HA due to high incidence of SE

Front 33

Metoclopramide- Use
Name some other meds of same class

Back 33

- antiemetic of choice
- other antiemetics-- chlorpromazine, prochlorperazine

Front 34

Medication Overuse Headache can occur when?
Tx for MOH?

Back 34

- most abortive agents greater than days per wk over 2-3 mos, cause daily or near daily dull HA-- happens especially w/ caffeine or barbituates
- Prophylactic medication

Front 35

Prophylactic tx- Use, Timing

Back 35

Use: To reduce frequency and severity
- increased responsiveness to abortive migraine therapies
- used for pts that have severe HA greater than or equal to twice per month
- pts in whom abortive therapies are contraindicated
Timing: must use 1-2 mos before effects are seen and used for at least 3-6 mos

Front 36

Beta Blockers- Use, MOA, Caution/CI

Back 36

Use: are prophylactic tx of choice, ideal for pts w. comorbid htn, post MI/angina, or anxiety
MOA: raise migraine threshold by modulating adrenergic or serotonergic neurotransmission in cortical or subcortical pathway
Caution- pts w/ asthma. COPD, depression, PVD

Front 37

Verapamil- Use, AE

Back 37

Use: most effect CCB but has only modest benefits-- less effective than beta blockers
AE: reserved for pts who have not benefited from DOC, constipation, bradycardia, worsening systolic CHF

Front 38

TCA- Use, MOA, AE

Back 38

Use: good for pts who have concomitant depression, tension HA, pts w/ neuropathic pain- diabetic neuropathy
- MOA- 5ht/NE reuptake inhibition
AE: sedation, wt gain, PROLONGATION OF QT interval, anticholinergic effects - thus contraindicated in pts w/ BPH, glaucoma

Front 39

TCA- CI

Back 39

- pts w/ CAD b/c will prolong QT interval
- caution in pts w/ BPH, dementia, or glaucoma

Front 40

Valproic acid (i.e. depakote)- Use, MOA, AE, CI

Back 40

Use: anti epileptic also approved for prevention of migraine HA
MOA: reduces high frequency neuronal firing and sodium dep action potentials and enhances GABA effects
AE: sig wt gain, N&V, tremor, hair loss, hepatotoxicity, PCOD
CI: EmBRYOCIDAL-- NTDS!

Front 41

Topiramate- Use

Back 41

Use: prophylaxis
AE: SIGNIFICANT wt LOSS, cog dysfx, and language difficulties

Front 42

Other prophylaxis

Back 42

Riboflavin- safe for pregnancy
Gabapentin- varying degrees of success, better tolerated than other antiepileptics
- estrogen gel, nsaids, montelukast, ace inh and arbs, botulinum toxin