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Neurology > Migraines and Headache > Flashcards

Migraines and Headache Flashcards

1
Q

Primary Headaches

A
  • Tension headache
  • Cluster headache
  • Migraine
    • With aura
    • W/o aura
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2
Q

Secondary Headaches

A
  • Head/neck trauma
  • Vascular disorders (CVA)
  • Non-vascular disorders (seizure, tumor)
  • Substance withdrawal
    • Medication overuse headache (MOH)
  • Infection
  • Psychiatric disorder
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3
Q

Depolarization Theory

A

Activation of trigeminal nerve system
* Vasoactive neuropeptide release (calcitonin gene-related peptide (CGRP), neurokinin A, substance P)
* Cortical spreading depression: neuropeptides interact with dural blood vessels–> promotes vasodilation–> neurogenic inflammation–> activation of sensory neurons in trigeminal nerve–> pain

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4
Q

What are some food triggers of migraine?

A
  • Alcohol
  • Caffeine/caffeine withdrawal
  • Chocolate
  • MSG
  • Nitrate-containing foods
  • Tyramine-containing foods
  • Yeast products
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5
Q

What are some environmental triggers of migraine?

A
  • Glare or flickering lights
  • High altitude
  • Loud noises
  • Strong smells/fumes
  • Tobacco smoke
  • Weather changes
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6
Q

What are some behavioral-physiological triggers of migraine?

A
  • Excess or insufficient sleep
  • Fatigue
  • Menstruation, menopause
  • Skipped meals
  • Strenuous physical activity
  • Stress or post-stress
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7
Q

Premonitory phase

A
  • Previously referred to as prodrome and/or warning symptoms
  • Experienced by up to 80% of patients
  • Occurs hours-days before onset of migraine
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8
Q

What are some symptoms of the premonitory phase?

A
  • Allodynia, phonophobia, photophobia, hypersomnia, difficulty concentrating
  • Anxiety, depression, euphoria, drowsiness, fatigue, hyperactivity, restlessness
  • Polyuria, diarrhea, constipation
  • Stiff neck, yawning, thirst, food cravings, anorexia
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9
Q

What are some visual symptoms of an aura?

A

Positive features: scintillating scotomas, fortification spectrum (flashes, diverging lines, zig zagging lines)

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10
Q

What are some sensory and motor symptoms of an aura?

A

Sensory: Paresthesia
Motor: Dysphasia, weakness, aphasia, hemiparesis

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11
Q

Postdrome phase

A
  • Fatigue, irritability, impaired concentration, mood changes
  • Some patients report mild euphoria or feeling unusually refreshed
  • Sudden head movement may precipitate pain
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12
Q

What are the diagnostic criteria of a migraine without aura?

A

≥ 5 attacks meeting all the following criteria:
* Headache 4-72 hours (when untreated or unsuccessfully treated)
* Not better accounted for by another ICHD-3 diagnosis

Headaches with ≥ 2 of the following characteristics:
* Location: unilateral
* Quality: pulsating
* Intensity: moderate or severe
* Aggravation by or causing avoidance of physical activity (e.g., walking or climbing stairs)
AND
Headache with ≥ 1 of the following symptoms
* Nausea and/or vomiting
* Photophobia and phonophobia

SULTANS

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13
Q

What is the diagnostic criteria for migraines with an aura?

A

≥ 2 attacks with the following criteria
* Not better accounted for by another ICHD-3 diagnosis
* ≥ 1 fully reversible aura symptoms:
- Visual
- Sensory
- Speech and/or language
- Motor
- Brain stem
- Retinal
AND
* ≥ 3 characteristics
- ≥ 1 aura symptoms spreads gradually over ≥ 5 minutes
- ≥ 2 aura symptoms occur in succession
- ≥ 1 aura symptoms is unilateral
- ≥ 1 aura symptoms is positive
- Aura is accompanies or followed within 60 minutes by headache

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14
Q

What are some concerning symptoms?

A
  • Systemic s/sx (fever, myalgias, weight loss)
  • Neurologic s/sx (confusion, AMS)
  • Onset (sudden, abrupt, split second)
  • Older patient with new onset (> 40-50 yo)
  • Pattern change (new or different? Frequency? Sx?)
  • Secondary risk factors (HIV, systemic cancer)
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15
Q

What are some migraine symptom assessment tools?

A
  • Migraine Disability Assessment (MIDAS) Test
  • Headache Impact Test (HIT-6)
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16
Q

What is the MOA of analgesics?

A

Prevent neurogenic inflammation in trigeminovascular system by inhibiting prostaglandins

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17
Q

What is the place of therapy of analgesics?

A
  • First line for mild-moderate symptoms
  • Second line: combination products
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18
Q

What are some clinical pearls of analgesics?

A
  • Limit to 3 days/week or 15 days/month to prevent MOH (medication overuse headache)
  • Avoid butalbital-containing products due to abuse potential
  • Acetaminophen/butalbital/caffeine (Fioricet)
  • Aspirin/butalbital/caffeine (Fiorinal)
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19
Q

What are adverse effects of analgesics?

A

NSAIDS:
-Cardiovascular: blood pressure elevation
-Gastrointestinal (GI)
* Short term: dyspepsia
* Long term: GI bleed or ulceration

Renal: Injury with short- or long-term use

APAP: Hepatic injury at elevated doses

Aspirin: Tinnitus, GI bleed or ulceration

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20
Q

What is the MOA of triptans?

A

Selective agonist at 5-HT1B and 5-HT1D (serotonin) receptors
* 5-HT1B mediated vasoconstriction of cerebral blood vessels
* Stimulation of presynaptic 5-HT1D inhibits release of vasoactive neuropeptides (CGRP, substance P) from perivascular trigeminal neurons
* Stimulation of 5-HT1D receptors in brain stem trigeminal nuclei disrupts pain signal transmission

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21
Q

What is the place of therapy of Triptans?

A
  • Severe migraines: first-line
  • Mild-moderate migraines: unresponsive to combination analgesics
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22
Q

Which triptans have the most favorable outcomes?

A
  • Sumatriptan SQ injection
  • Rizatriptan ODT
  • Zolmitriptan ODT
  • Eletriptan tablets
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23
Q

What are some clinical pearls of triptans?

A

Large inter-patient variability:
* If unsuccessful treatment of 3 attacks with one triptan – try a different triptan
* Can consider different med class after 2 failed triptans

Effective, well-tolerated:
* If administered within 4 hours of migraine onset – preferably within the 1st hour
* Increased sustained pain-free response when combined with NSAIDs compared to either drug alone
- Best studied Triptan/NSAID combo: sumatriptan + naproxen (Treximet)

  • Limit use < 3 days/week, < 10 days/month to prevent MOH
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24
Q

What are the contraindications of Triptans?

A
  • Cerebrovascular disease: Stroke, TIA
  • Ischemic Heart Disease
  • Cardiovascular: Uncontrolled HTN, ischemic heart disease
  • Hemiplegic or basilar migraine
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25
Q

What are some drug interactions of triptans?

A
  • SSRI/SNRI: Serotonin syndrome
    (rare; monitor if co-prescribed)
  • Ergot derivative/other triptan within 24 hours (prolonged vasospastic reaction
  • MAOI administration within 2 weeks (everything is contraindicated but use caution with Almotriptan)
  • CYP3A4 inhibitors
  • Propranolol (causes INCREASED concentrations of triptans)
  • Cimetidine (limit zolmitriptan to 2.5 mg or 5 mg/day)
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26
Q

What are some ADE of triptans?

A
  • Dizziness, fatigue, flushing, paresthesias, nausea, vomiting
  • Local injection site inflammation
  • Taste perversion
  • Nasal discomfort (following nasal administration)
  • Angina/coronary ischemia
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27
Q

What is the MOA of Ergot Alkaloid?

A

Nonselective 5-HT1 agonists
* Constrict intracranial blood vessels
* Inhibit neurogenic inflammation in trigeminovascular system

Activate other types of serotonin receptors, alpha-adrenergic, and dopamine receptors

Both venous and arterial constriction occur with therapeutic doses
* Ergotamine tartrate exerts more potent artery vasoconstriction
* Dihydroergotamine exerts more potent venoconstriction

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28
Q

What is the place of therapy of Ergot alkaloids?

A
  • Treat moderate to severe migraines
  • Patients failing triptans
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29
Q

What are the effective routes of administration of ergot alkaloids?

A
  • IV> IM» Inhaled > Sublingual > Oral
  • GI absorption is erratic
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30
Q

What are the contraindications of ergot alkaloids?

A
  • Pregnancy or breastfeeding
  • Cardiovascular: Uncontrolled HTN, peripheral vascular disease, ischemic heart disease, coronary vascular disease
  • Impaired renal/hepatic function
  • Hemiplegic or basilar migraine
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31
Q

What are the drug interactions of ergot alkaloids?

A
  • Concurrent use with CYP3A4 inhibitors (CONTRAINDICATED)
  • Concurrent use with vasoconstrictors, including triptans (CONTRAINDICATIONS)
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32
Q

What are the ADE of triptans?

A

Common:
* Nausea, vomiting, muscle cramps, abdominal pain, numbness/tingling in fingers and toes
Serious:
* Sustained generalized vasoconstriction
* HTN, MI, CVA, gangrene, bowel ischemia, coronary ischemia

33
Q

What is the MOA of CGRP Receptor Antagonists?

A
  • Decreases activity of CGRP
  • Lacks direct vasoconstrictive activity
  • CGRP is a vasoactive peptide that dilates blood vessels, is involved in pain signaling
34
Q

What is the place of therapy of CGRP Receptor Antagonist?

A

Patients with insufficient response or Cl to treatment with triptans

35
Q

What are the contraindications of CGRP receptor antagonists?

A
  • Concomitant use of strong CYP3A4 inhibitors
  • Pregnancy
    • Use not recommended based on animal studies
36
Q

What are the clinical pearls of CGRP Receptor Antagonists?

A
  • Avoid repeat dosing of rimegepant within 24 hours
  • Can repeat ubrogepant x 1 after 2 hours (max daily dose 200 mg)
  • Expensive
37
Q

What are the ADE of CGRP Receptor Antagonists?

A
  • Nausea
  • somnolence
  • dry mouth
38
Q

What is the MOA of Lasmiditan?

A
  • Selective serotonin 5-HT1F receptor subtype agonist
  • Lacks vasoconstrictor activity (i.e., lacks 5-HT1B/1D receptor activity )
39
Q

What are the clinical pearls of Lasmiditan?

A
  • Controlled substance: C-V
  • Do not drive within 8 hours of administration
  • Repeat dosing not indicated
  • Expensive
40
Q

What are the ADE of Lasmiditan?

A

High rate of adverse effects:
* Dizziness (most common), somnolence, paresthesia, fatigue, nausea
Low (<1%) cardiovascular side effects

41
Q

What are some clinical pearls of Frovatriptan?

A
  • Efficacy for menstrual migraine prevention
  • Slowest onset, longest half-life; less frequent side effects
42
Q

What are some clinical pearls of Rizatriptan?

A
  • ODT, tablet
  • Fastest oral onset
  • Dose limited to 5mg for pts on propranolol
43
Q

What are some clinical pearls of Naratriptan?

A
  • Efficacy for menstrual migraine prevention
  • Slow onset; less frequent side effects
44
Q

What are the formulations of Sumatriptan?

A
  • Tablet, nasal spray, injection SQ
45
Q

What are some clinical pearls of Sumatriptan?

A
  • Fast injectable onset, good for severe nausea
46
Q

What are some clinical pearls of zolmitriptan?

A
  • Tablet, ODT, nasal spray
  • Efficacy for menstrual migraine prevention
47
Q

What are some rescue outpatient treatment?

A

SC sumatriptan, DHE injection or intranasal spray, corticosteroids

48
Q

What are some inpatient rescue treatment?

A
  • Parenteral formulations of triptans
  • DHE
  • antiemetics
  • NSAIDs
  • anticonvulsants (valproate sodium and topiramate)
  • corticosteroids or
  • magnesium sulfate
49
Q

What are the parenteral preferred antiemetics?

A
  • Metoclopramide IV, prochlorperazine IM/IV, chlorpromazine IM/IV
  • Administer with diphenhydramine IV (12.5-25 mg) to prevent akathisia and acute dystonic reactions
50
Q

Who are considered candidates for migraine prophylaxis?

A
  • Recurrent attacks producing significant disability
  • Frequent attacks
    • Increased risk for medication overuse headache
  • Ineffective, contraindicated, or intolerant to acute treatment
  • Uncommon migraine variants with risk for severe disruption or neurologic injury
  • Patient preference
51
Q

What is an adequate therapeutic trial of migraine prophylaxis?

A
  • Trial of 2-3 months oral agents or 3-6 months for monoclonal antibodies needed to achieve clinical benefit
  • Maximum effects seen by 6 months of treatment
  • Continued for at least 6-12 months after frequency and severity have diminished
52
Q

What are some FDA approved migraine prophylaxis treatment?

A
  • Propranolol
  • Timolol
  • Divalproex
  • Topiramate
  • Botox
  • CGRP monoclonal antibodies
53
Q

What are some Level A established efficacy for migraine prophylaxis?

A
  • Antiepileptics (Divalproex, Valproate, Topiramate)
  • Beta Blockers (metoprolol, propranolol, timolol)
  • ARB (candesartan)
54
Q

What are some Level B migraine prophylaxis?

A
  • Antidepressants (Amitriptyline, venlafaxine)
  • Beta blockers (atenolol, nadolol)
  • ACE (lisinopril)
55
Q

What is the MOA of CGRP mAbs?

A

A monoclonal antibody that antagonizes CGRP receptor preventing vasodilation during migraine attacks

56
Q

What is the MOA of Botulinum Toxin A?

A

Inhibits acetylcholine release at motor nerve terminals

57
Q

What is the indication for Botulinum Toxin A?

A
  • FDA-approved botulinum toxin for chronic migraines
  • 2016 AAN guidelines = effective for chronic migraine
  • HA ≥ 15 days/mo for ≥ months, with ≥ of 15 HA per month fulfilling criteria for migraine without aura
58
Q

What are the ADR of botulinum toxin A?

A

neck pain, muscle weakness

59
Q

Magnesium Oxide

A

Beneficial for patients with migraine with aura or menstrual migraines

60
Q

Riboflavin (Vitamin B-2)

A
  • “Probably effective” per guidelines
  • ADR: Change in urine color (yellow/orange) otherwise tolerated
61
Q

What is the MOA of Atogepant (Qulipta)?

A

CGRP receptor antagonist

62
Q

What are the indications for Atogepant?

A
  • Patients with < 15 headaches/month
  • High disability from frequent migraines
  • Failure to respond to other preventative therapies
63
Q

What are some considerations of Atogepant?

A
  • Avoid use with recent cardiovascular or cerebrovascular ischemic events
  • ADR: Weight loss, constipation, nausea, fatigue, and drowsiness
64
Q

What are some factors associated with poor outcome of tension headache?

A
  • Coexisting migraine
  • Sleep problems
  • Anxiety/depression
  • Poor stress management
65
Q

What are the clinical presentations of tension headache?

A
  • Mild-moderate intensity pain
  • Dull, non-pulsatile tightness/pressure
  • Bilateral pain (“hatband” pattern)
  • Tender spots/localized nodules in some patient’s cervical or pericranial muscles
  • Episodic or chronic frequency
66
Q

Who are candidates of tension headache prevention?

A
  • Consider in those with > 2 attacks/week, lasting > 3-4 hours, or disability
  • Similar to migraine prevention approach with regards to comorbid conditions and side effect profiles
67
Q

How do you prevent tension headache?

A
  • TCAs most common
  • SSRIs not effective without depression, SNRIs limited evidence
68
Q

Cluster Headache

A
  • The most severe of the primary headache disorders
  • Excruciating, unilateral head pain occurring in series lasting for weeks or months
  • Episodic or chronic
  • Unknown etiology, inflammation of nerves resulting in injury to carotid artery
69
Q

What is the epidemiology of cluster headaches?

A
  • 4:1 female-to-male ratio
  • > 65% tobacco smokers or history of smoking (cessation does NOT improve course)
  • Genetic predisposition
70
Q

What are the clinical presentations of cluster headache?

A
  • A circadian rhythm of painful attacks
  • Occur commonly and suddenly at night in spring/fall
  • Excruciating, penetrating pain with a boring intensity in orbital, supraorbital, and temporal unilateral locations
  • Nasal stuffiness, rhinorrhea, eyelid edema, facial sweating
71
Q

What is the acute treatment of cluster headaches?

A
  • Oxygen: Inhaled oxygen, 100% at 6-12 L/min for 15 minutes
  • Triptans
  • Sumatriptan 6 mg SQ (level A recommendation)
  • Zolmitriptan 5-10 mg inhalation (level A recommendation)
  • Ergotamine derivatives (no controlled trials to support use)
72
Q

How do you prevent cluster headaches?

A
  • Verapamil (1st lines): 360-960 mg/day (level C recommendation)
  • Benefits seen within 2-3 weeks of therapy
  • Lithium carbonate – 600-1200 mg/day (level C recommendation)
  • Levels have not been established, but should be maintained 0.6-1.2 mEq/L
  • Corticosteroids – prednisone 60-100 mg/day for 5 days then taper
  • Suboccipital steroid injection level A recommendation
73
Q

What are the risk factors of medication overuse headache?

A
  • age (less than 50 years old)
  • female
  • smoking
  • physical inactivity
  • high daily caffeine intake (> 540 mg)
74
Q

What are the clinical presentations of MOH?

A
  • Occurs daily or nearly daily, usually present upon awakening
  • Improves transiently with analgesics, returns as the medication wears off
  • Patients often report morning headaches and neck pain due to overnight drug withdrawal or poor sleep
  • Other symptoms: Nausea, anxiety, restlessness, difficulty concentrating, memory problems
  • Headache on > 15 days/month AND pre-existing headache disorder
75
Q

Which drugs can cause MOH?

A
  • Triptan: 10 days/months for > 3 months
  • Ergotamine: 10 days/month > 3 months
  • Opioids: 10 days/month for > 3 months
  • Aspirin: 15 days/month for > 3 months
  • NSAIDs: 15 days/month for > 3 months
  • Acetaminophen: 15 days/month for >3 months
76
Q

How do you prevent MOH?

A
  • ≤ 3 days per month of butalbital-containing analgesics (i.e., Fioricet®, Fiorinal®)
  • ≤ 9 days per month of combination analgesics (caffeine)
  • ≤ 15 days per month of NSAIDs
77
Q

Menstrual-Related Migraine (MRM)

A
  • The most common class of headaches that occur in women
  • Related to a decline in estrogen during menstrual cycle, reducing serotonin production
  • Family history
  • More prevalent in individuals with a history of migraines and those on combined hormonal contraception
78
Q

How do you treat Menstrual-Related Migraine?

A

Triptans:
* Level A: Frovatriptan 2.5 mg daily to BID
* Level B: Naratriptan 1 mg BID or Zolmitriptan 2.5 mg BID-TID
(May start 1-2 days before menses)

NSAIDs
* Naproxen - strongest evidence
* Aspirin - weakest evidence
(May start up to 1 week before menses and continued for no more than 10 days)

Neurology (21 decks)

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