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Flashcards in Migraines/HA Deck (105):
1

What causes an aura phase?

Reduction in cerebral blood flow that beings in the occipital region and moves across the cerebral cortex

2

What causes migraines?

From fibers in the intracranial extra cerebral blood vessels, dura mater, and large venous sinuses
Could be related to dysregulation of serotonin release
Genetics

3

Are there any nociceptors in the brain?

No

4

What causes the release of neuropeptides in migraines?

Activation of the trigeminal sensory nerve

5

What neuropeptides are released during a migraine?

Calcitonin gene related peptide (CGRP)
Neurokinin A
Substance P

6

What do neuropeptides cause?

Vasodilation
Dura plasma extravasation

7

What parts of genetics can cause migraines?

Cause imbalances of the CNS which have a lower threshold for pain
Abnormalities in Ca and Na channels responsible for neurotransmitter
Low levels of serotonin, dopamine, and increased levels of glutamate

8

What is premonitory sx?

Occurs in the hours or days before the onset of the HA
Can vary greatly between individuals, but is consistent w/in the individual
Generalized throughout the body
Bothersome but not debilitating
Could be caused from something other than a migraine

9

What is an aura?

A complex of positive and negative focal neurologic sx that precedes or accompanies an attack
Evolves over 5-20 minutes
Lasts less than 60 minutes
Most often visual and affects half of visual field
Most often debilitating

10

What are positive sx of an aura?

Scintillations
Photopsia (flashes of light)
Teichopsia (shimmering colors)
Fortification spectrum (arc of light)

11

What are negative sx of an aura?

Scotoma (area of partial alteration in the field of vision)
Hemianopsia (decreased vision in half the field)

12

What are the sensory/motor sx of an aura?

Numbness in face and arms
Dysphasia
Weakness
Hemiparesis

13

What are the presentations of migraines?

Aura
Premonitory sx
Gradual onset, peaking in minutes, lasting 4-72 hours
Pain in face and head, most common in frontotemporal region
Unilateral initially, can become bilateral throughout the attack
Throbbing and pulsating
Common: nausea, GI SEs

14

What are common food triggers of migraines?

Chocolate
Pickled foods
MSG
Aspartame
Tyramine

15

What environmental factors are triggers of migraines?

Glare
Flickering lights
High altitude
Loud noises
Strong smells
Weather changes

16

What are behavioral factors that are triggers of migraines?

excess or insufficient sleep
Fatigue
Menstruation
Sexual activity
Skipped meals
Prolonged exertion
Stress

17

What is a mild HA?

Aware of HA
Able to continue daily routine w/minimal alterations

18

What is a moderate HA?

HA inhibits daily activities
Not incapacitating

19

What is a severe HA?

Incapacitating

20

What patients should receive migraine tx?

Greater than 2 attacks/week
Attacks lasting longer than 48 hours

21

What is the maximum amount of days that HA medications should be taken?

9 days/month

22

What is the most common cause of daily HA?

Medication overuse

23

What is the HA medication cycle?

HA returns as soon as medication wears off

24

What are non-pharm migraine tx options?

Track HA/activities/triggers/sx to avoid/decrease potential

25

What are the most effective OTC analgesics for migraine?

NSAID or ASA/APAP/Caffeine

26

Which medications have higher risks of rebound HA?

Combination

27

When is APAP recommended?

HA monotherapy

28

Which NSAIDs have the most demonstrated benefit for migraines?

ASA
Ibuprofen
Naproxen
Tolfenamic acid

29

How do NSAIDs work in migraines?

Inhibits inflammation and pain by inhibiting PGs

30

What is the MOA of barbiturates in migraines?

Depresses the sensory cortex
Decreased motor activity
Altered cerebellar function
Drowsiness and sedation
Respiratory depression

31

What are the concerns of butalbital use in migraines?

Overuse
Abuse
WD

32

What is midrin?

APAP
Isometheptene
Dochloraphenazone

33

What is the MOA of isometheptene?

Sympathomimetic that reduces stimuli leading to vascular HA via constriction of dilated cranial and cerebral arterioles

34

What is the MOA of dichloraphenazone?

Sedative and antipyrine that reduces the emotional response to painful stimuli

35

What is midrin useful for?

Mild to moderate HA

36

What is the MOA of butorphanol?

Mixed opioid agonist

37

How is butorphanol supplied?

Nasal spray

38

What are the ergot alkaloids?

Ergotamine
Dihydroergotamine

39

What is the MOA of ergot alkaloids?

Partial agonist and/or antagonist activity on a variety of receptors to cause constriction of peripheral and cranial blood vessels and inhibit inflammation

40

What are DDIs of ergot alkaloids?

Strong 3A4 inhibitors
Azoles, PI, macrolides

41

What are the AEs of ergot alkaloids?

Cardiac valvular fibrosis (avoid in patients w/AFib or valve disease)
Vasoconstriction
Most common: N/V/D, ab pain, weakness, fatigue, sweating, chest tightness

42

Which medication is not commonly recommended in the elderly for migraines?

Ergot alkaloids

43

What can enhance the absorption and potency of ergot analgesia?

Caffeine

44

What are ergot alkaloids used for?

Moderate to severe HA

45

What should not be used within 24 hours of ergot alkaloids?

Triptan

46

What are contraindications for ergot alkaloids?

Renal/hepatic failure
Coronary cerebral or peripheral vascular disease
Uncontrolled HTN
Sepsis
Pregnancy

47

What is the MOA of triptans?

Selective agonists of the 5-HT1b and 5-HT1d receptors
Normalization of dilated intracranial arteries by vasoconstriction, neuronal inhibition, and inhibition of transmission through trigeminocervical complex

48

Which medication is an appropriate first line choice for mild to severe migraines?

Triptans

49

What are AEs of triptans?

Paresthesias
Fatigue
Dizziness
Flushing
Warm sensations
Somnolence
Chest pain

50

What are contraindications for triptans?

IHD
Uncontrolled HTN
Cerebrovascular disease

51

How does botulinum toxin work in migraines?

Significant decrease in number of days

52

What is petasites derived from?

Butterbur plant

53

What is the use of petasites in migraines?

Decrease frequency

54

What is the use of histamines in migraines?

Decreased attack frequency
Decreased intensity
Decreased rescue medication use

55

What is the use of Co-Q10 in migraines?

Reduced attack frequency
Water soluble

56

When are opioids used in migraines?

Reserved for patients with mod-severe sx whom have failed above treatments or contraindications to treatment

57

What are drawbacks to using opioids for migraines?

Dependency and rebound HAs

58

What is the most common anti-emetic for migraines?

Metoclopramide - can increase absorption of migraine medication

59

When are corticosteroids used for migraines?

Status migrainous
Continuous migraine for up to 1 week

60

Which medications are used for migraine prophylaxis?

B-blockers
Antidepressants
Anticonvulsants
CCBs

61

How long can a prophylactic dose change take to reach maximal effectiveness?

2-4 weeks

62

How long should monitor max doses to make sure the dose has had time to work before adding on additional medications?

4 weeks

63

When do we give prophylactic migraine medications?

Substantial impact on daily life
Do not respond well to acute care
Frequency is great enough that acute care may lead to rebound HAs

64

How do BB work in migraines?

Reduce frequency

65

When are BB not effective for migraine prophylaxis?

With intrinsic sympathomimetic activity

66

What is the most common antidepressant used for migraine prophylaxis?

Amitriptyline

67

Which antidepressants should not be used for migraine prophylaxis?

SSRIs

68

Which anticonvulsants have demonstrated efficacy in migraine prophylaxis?

VPA
Divalproex
Topamax
Gabapentin

69

What is the MOA of anticonvulsants in migraine prophylaxis?

Enhancement of GABA inhibition
Modulation of glutamate
Inhibition of sodium and calcium ion channels

70

When are anticonvulsants useful in migraine prophylaxis?

Comorbid conditions
Seizures
Anxiety
Manic-depressive disorder

71

How do we monitor VPA?

Best tolerated
Monitor liver function

72

How do we monitor Divalproex?

Wt gain

73

What are AEs with divalproex/VPA?

Pancreatitis
Liver failure
Teratogenic risk

74

When are CCBs used in migraine prophylaxis?

2nd or 3rd line
Verapamil is the most common

75

How long until verapamil is effective?

8 weeks

76

When should women start prophylaxis of migraines?

2-3 days prior to menses or usual start of HA

77

How dow contraceptives work in migraines?

Decrease duration and severity

78

When should contraceptives be avoided for migraine prophylaxis?

Aura
2-4 times more likely to have a stroke

79

What is a cause of a tension HA?

Least studied
Thought to originate from myofascial factors and sensitization of nociceptors

80

What are stimuli of tension HA?

Mental stress
Non-physiologic motor stress
Local myofascial release of irritants

81

What is the presentation of tension HAs?

No premonitory sx/aura
Dull, non-pulsatile tightness or pressure
Bilateral pain is most common
Frontal or temporal pain most common regions
Mild photophobia or phonophobia may be reported

82

How can tension HA be classified?

Episodic or chronic

83

What are types of tx for tension HA?

Most are treated OTC by the patient, relatively poorly studied
Behavioral therapy
Non-pharm
Non-opioid analgesics

84

What are behavioral therapies for tension HA?

Stress management
Relaxation
Counseling
Can reduce sx

85

What are non-pharm tx for tension HA?

Heat or cold packs
Ultrasound
Stretching
Exercise
Massage
Acupuncture
Ergonomic instruction
Trigger point injections

86

How long can non-opioid therapy be used for tension HAs?

No more than 9 days per month to stop overuse/rebound HAs

87

What is the most severe of the primary HA disorders?

Cluster HA

88

What are the characteristics of cluster HAs?

Severe, unilateral head pain in series lasting for weeks or months separated by remission periods lasting months or years

89

Are men or women more likely to have cluster HAs?

Men

90

What is the pathophysiology of cluster HAs?

Cyclic nature implicates a pathogenesis of hypothalamic dysfunction with resulting alterations in circadian rhythms

91

What hormones are out of sync in cluster HAs?

Cortisol
Prolactin
Testosterone
Growth hormone
Luteinizing hormone
Endorphin
Melatonin

92

How long can cluster HAs occur?

2 weeks to 3 months followed by pain free intervals (2 years)

93

When is the most common time for cluster HA?

At night during season change

94

What is the onset and duration of cluster HA?

Suddenly and last 15-180 minutes

95

Which HA do not present with auras?

Cluster
Tension

96

What is the pain like in cluster HAs?

Excruciating
Penetrating
Boring in intensity

97

What are the locations of pain in cluster HAs?

Orbital
Supraorbital
Temporal unilateral locations

98

What are cluster HAs accompanied by?

Conjunctival injection
Lacrimation
Nasal stuffiness
Eyelid edema
Sweating
Miosis/ptosis
Restlessness
Agitation

99

How often may cluster HA occur during an attack?

Once every other day to 8 times a day

100

What positions might a patient with a cluster HA be in?

Sitting and rocking or pacing clutching their head

101

Patients with cluster HA may use what?

Alcohol
Nicotine
Coffee

102

What are the treatments of cluster HAs?

Oxygen
Ergotamine derivatives
Triptans

103

What forms of triptans are most effective for cluster HAs?

SQ
Intranasal formulations

104

What medications are used for cluster HA prophylaxis?

Verapamil (preferred)
Lithium (can be added to verapamil)
Ergotamine (prophylactis or abortive)
Corticosteroids (relief after 1-2 days)

105

What is the monitoring for cluster HAs?

Number of HA
AE
HA cycle patterns
Triggers