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Migraines/HA Flashcards

1
Q

What causes an aura phase?

A

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

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2
Q

What causes migraines?

A

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

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3
Q

Are there any nociceptors in the brain?

A

No

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4
Q

What causes the release of neuropeptides in migraines?

A

Activation of the trigeminal sensory nerve

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5
Q

What neuropeptides are released during a migraine?

A

Calcitonin gene related peptide (CGRP)
Neurokinin A
Substance P

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6
Q

What do neuropeptides cause?

A

Vasodilation

Dura plasma extravasation

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7
Q

What parts of genetics can cause migraines?

A

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

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8
Q

What is premonitory sx?

A

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

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9
Q

What is an aura?

A

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

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10
Q

What are positive sx of an aura?

A

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

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11
Q

What are negative sx of an aura?

A

Scotoma (area of partial alteration in the field of vision)

Hemianopsia (decreased vision in half the field)

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12
Q

What are the sensory/motor sx of an aura?

A

Numbness in face and arms
Dysphasia
Weakness
Hemiparesis

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13
Q

What are the presentations of migraines?

A

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

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14
Q

What are common food triggers of migraines?

A 
Chocolate
Pickled foods
MSG
Aspartame
Tyramine
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15
Q

What environmental factors are triggers of migraines?

A 
Glare
Flickering lights
High altitude
Loud noises
Strong smells
Weather changes
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16
Q

What are behavioral factors that are triggers of migraines?

A 
excess or insufficient sleep
Fatigue
Menstruation
Sexual activity
Skipped meals
Prolonged exertion
Stress
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17
Q

What is a mild HA?

A

Aware of HA

Able to continue daily routine w/minimal alterations

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18
Q

What is a moderate HA?

A

HA inhibits daily activities

Not incapacitating

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19
Q

What is a severe HA?

A

Incapacitating

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20
Q

What patients should receive migraine tx?

A

Greater than 2 attacks/week

Attacks lasting longer than 48 hours

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21
Q

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

A

9 days/month

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22
Q

What is the most common cause of daily HA?

A

Medication overuse

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23
Q

What is the HA medication cycle?

A

HA returns as soon as medication wears off

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24
Q

What are non-pharm migraine tx options?

A

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

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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

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