Migraines Flashcards

(65 cards)

1
Q

What are migraines?

A

An episodic neurologic disorder characterized by headaches lasting 4–72 hours

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2
Q

Diagnostic criteria for migraines (pain features)

A

Must have ≥2: unilateral head pain; throbbing pain; worsens with activity; moderate to severe pain

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3
Q

Diagnostic criteria for migraines (associated symptoms)

A

Must have ≥1: nausea/vomiting; photophobia (light sensitivity); phonophobia (sound sensitivity)

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4
Q

What is photophobia?

A

Sensitivity to light; patients prefer dark rooms and may wear sunglasses

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5
Q

What is phonophobia?

A

Sensitivity to sound; normal sounds feel loud and irritating

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6
Q

Migraine classifications

A

With aura; without aura (most common); chronic migraines

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7
Q

Definition of chronic migraines

A

≥15 days/month for ≥3 months

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8
Q

How do chronic migraines typically develop?

A

Start as episodic and increase in frequency over time

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9
Q

Primary risk factor for migraines

A

Family history

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10
Q

Hormonal influence on migraines

A

Associated with estrogen and progesterone

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11
Q

Who is more susceptible to migraines and why?

A

Females due to hormonal involvement

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12
Q

When are migraines more frequent hormonally?

A

Before and during menstruation

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13
Q

When do migraines often decrease?

A

During pregnancy and menopause

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14
Q

Proposed hormonal trigger mechanism

A

Cyclical withdrawal of estrogen/progesterone during menstrual cycle

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15
Q

Other contributing factors for migraines

A

Genetic and environmental factors

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16
Q

Common migraine triggers

A

Fatigue;
sleep disturbances (too little or too much sleep)
missed meals;
overexertion;
weather changes
stress; hormonal changes
alcohol (especially red wine)
bright lights
strong smells

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17
Q

Example of environmental trigger example

A

Strong smells (e.g.

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18
Q

Is migraine pathophysiology well understood?

A

No

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19
Q

Key pathophysiologic associations

A

Changes in brain metabolism and blood flow

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20
Q

Proposed migraine mechanism

A

Neurotransmitter changes and altered blood vessel tone

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21
Q

Neuronal activity in migraines

A

Increased depolarization → hyperactivity

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22
Q

Effect of excitatory neurotransmitters

A

Activate vascular system → vasodilation → migraine

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23
Q

Four phases of a migraine

A

Premonitory; Aura; Headache; Recovery

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24
Q

Premonitory phase timing

A

Hours to days before headache

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25
Premonitory phase prevalence
Occurs in about one-third of patients
26
Premonitory phase symptoms
Fatigue; irritability; loss of concentration; stiff neck; food cravings
27
Aura phase prevalence
Occurs in about one-third of patients
28
Aura phase duration
Up to ~1 hour
29
Types of aura symptoms
Visual; sensory; motor
30
Examples of visual aura symptoms
Shimmering lights; flashing spots; blind spots
31
Examples of sensory aura symptoms
Numbness; tingling; pins and needles
32
Examples of motor aura symptoms
Weakness; speech difficulty; coordination issues
33
Headache phase characteristics
Throbbing pain starting unilateral then spreading
34
Headache phase duration
4–72 hours
35
Headache phase associated symptoms
Fatigue; nausea; vomiting; dizziness; scalp sensitivity
36
Recovery phase symptoms
Irritability; fatigue; depression
37
Recovery phase duration
Hours to days
38
What is abortive therapy?
Symptomatic treatment of migraine attacks
39
When is abortive therapy most effective?
When given early in the headache course
40
First-line treatment for mild–moderate migraines
Basic analgesics (aspirin
41
Why are basic analgesics used first?
Effective
42
Next step if analgesics fail
Add or use a triptan
43
Benefit of combining triptans with analgesics
More effective than either alone
44
Treatment for moderate–severe migraines (no N/V)
Oral migraine-specific agents (triptans)
45
Example combination therapy
Sumatriptan + naproxen
46
Alternative for patients who cannot take triptans
CGRP antagonists
47
Treatment for migraines with severe nausea/vomiting
Add antiemetics (ondansetron
48
What are triptans?
Serotonin 5-HT1B/1D receptor agonists
49
Mechanism of triptans
Promote vasoconstriction of intracranial vessels; suppress inflammatory neuropeptides; block pain pathways
50
Routes of administration for triptans
Subcutaneous (SQ); oral (PO); intranasal
51
Which triptan route works fastest?
Subcutaneous
52
Which route has fewer side effects?
Intranasal
53
PO triptan side effects compared to SQ
Similar but less frequent
54
Common side effects of triptans
Injection site reaction; chest pressure; flushing; weakness; headache; bad taste (nasal)
55
Why do triptan side effects occur?
Due to vasoconstriction effects
56
Contraindications for triptans
Ischemic stroke; coronary artery disease; heart disease; angina
57
What are CGRP antagonists?
Migraine drugs used when triptans are ineffective or contraindicated
58
Example CGRP antagonist
Rimegepant (Nurtec)
59
Route of CGRP antagonist
Oral (PO)
60
Side effects of CGRP antagonists
GI upset (abdominal pain
61
Metabolism concern with CGRP antagonists
CYP substrate → caution with inhibitors/inducers
62
When is preventative therapy indicated?
>4 migraines/month OR migraines lasting >12 hours
63
Classes used for migraine prevention
Beta blockers; tricyclic antidepressants; antiepileptics; estrogen
64
Examples of preventative medications
Propranolol; amitriptyline
65
Goals of preventative therapy
Reduce frequency