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845 > Headache Background > Flashcards

Headache Background Flashcards

1
Q

Secondary Headache

A
  • Underlying pathological causes

- Head/neck trauma, cranial vascular disorder, psychiatric disorders, lumbar puncture, inflammation, hematoma

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2
Q

Tension Headache

A
  • Most common kind of headache
  • Sustained contractions ofscalp and neck muscles secondary to anxiety or stress
  • Dull, aching pain
  • Across forehead or on sides and back of head
  • Rarely seek treatment unless is occurs daily
  • Treatment: NSAIDs, muscle relaxant, SSRIs, TCA
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3
Q

Cluster Headache

A
  • Severe unilateral pain, sudden onset/offset and short duration
  • Dilation of blood vessels in the pained area (redness in eye, congestion, sweating)
  • Restricted: unilateral areas of nose, temple, and eye socket
  • Triggers from alcohol and strong odors
  • Associated with trigeminal-sacularactivation and neuroendocrine disturbances
  • Acute treatment: sumatriptan and high-flow oxygen
  • Multiple prophylaxis drugs
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4
Q

Migraine Headache

A
  • Most common headache diagnoses which patients get treatment for
  • Diagnose based on recollection of systems and exclusion of secondary causes
  • Associated with brain hypersensitivity and lowered threshold for trigeminal-vascular activation
  • Can have neck stiffness (like tension HA) and nasal stuffiness/discharge (like sinus HA) as well
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5
Q

3 Predictive Migraine Symptoms

A
  1. Moderate to severe disability
  2. Photophobia
  3. Nausea

Others: unilateral throbbing, vomiting, phonophobia, increased pain with physical exertion

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6
Q

Auras

A
  • Migraine with aura: most common visually, 10-15 minutes before CSD
  • No auras are more common with migraines
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7
Q

Migraine Triggers

A
  • Menses, stress, changes to schedules, loud noises, odors, flickering lights
  • Foods: tyramine (wine/cheese), chocolate (phenylethylamines), nitrites
  • Drug withdrawal: alcohol, caggeine
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8
Q

Sinus Headaches

A
  • Nasal stuffiness or discharge
  • Can be treated with nasal costicosteroids or antibiotics if caused by infection
  • May need surgery
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9
Q

CSD

A
  • Cortical spreading depression
  • Possible migraine initiation mechanism
  • Depression of neuronal activity spreads across the cortex
  • Most likely responsible for aura
  • Begins in occipital region and spreads towards the frontal cortex in a propagating wave
  • Wave is hyperactivity followed by prolonged suppression in neuronal activity
  • Associated with decreased cerebral blood flow (vasoconstriction)
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10
Q

Trigeminovascular System

A
  • Trigeminal nerve fibers around basal cerebral and meningeal vessels triggers
  • Starts viscous cycle when nerve terminals release CGRP (vasodilation), substance P (extravasation), VIP, and other mediators
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11
Q

Mediators create…

A
  • Local neurogenic inflammation
  • Trigger vasodilation
  • Orthodromic stimulation of the trigeminal nerve terminals back into the brain
  • Painful messages then transmitted to thalamus and cortex via trigeminal nucleus which makes pain arise as well as N/V and autonomic activation
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12
Q

Abortive Therapies

A
  • Complete pain relief, return to normal function within 2 hours of taking medication
  • Decreased pain relief efficacy if central sensitization is developed

Options

  • NSAIDs
  • Triptans
  • Lasmiditan
  • Ubrogepant
  • Ergot Alkaloids
  • Butalbital containing analgesics
  • Opioids
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13
Q

NSAIDs

A
  • Abortive therapy and intermittent preventative
  • First-line treatment for all migraine attacks
  • Inhibits prostaglandin synthesis which prevents neurogenic inflammation mechanisms
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14
Q

Triptans

A
  • First-line therapy for abortive therapy and acute treatment
  • 5HT1B/1D agonists
  • Oral, SQ, and nasal spray options available
  • SQ good for patients with severe N/V
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15
Q

Triptan Options

A
  • Sumatriptan (Imitrex) - SQ, nasal
  • Zomitriptan (Zomig) - intranasal
  • Almotryptan (Axert)
  • Eletriptan (Relpax)
  • Rizatriptan (Maxalt)
  • Naratriptan (Amerge)
  • Frovatriptan (Froval)

half life increases going down list

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16
Q

Triptan MoA

A
  • agonists of 5HT1B/1D
  • 1B receptors mediate vasoconstriction
  • 1D receptors inhibit the release of neuropeptides from trigeminal neurons, preventing neurogenic inflammation
  • 1B/1D/1F receptors interrupt pain signals in trigeminal nucleus
17
Q

Lasmiditan

A
  • Rayvow
  • Class: Ditan
  • Selective 5HT1F agonist
  • No vasoconstiction activity
  • Ditans penetrate CNS better
  • Risk for 5HT syndrome, discourage use with triptans
  • CV, may cause euphoria and hallucinations
18
Q

Triptan/Ditan CI

A
  • Don’t combine triptans or use with vasoconstrictor due to risk of CV and hypertensive side efefcts
  • 5HT syndrome, especially when combined with SSRIs and SNRIs
19
Q

Triptan Metabolism/Excretion

A
  • Rizatriptan, sumatriptan, zomitriptan, and almotryptin are metabolized MAO (don’t give MAOI for at least 2 weeks)
  • Frovatriptan and Naratriptan are partially renally excreted (caution with renal problems)
20
Q

Ubrogepant/Rimegepant

A
  • Ubrelvy/Nurtec
  • Latter has longer half life
  • CGRP receptor antagonists
  • Prevents CGRP vasodilation and pain sensitization
  • Rimegepant should be avoided in the renal/hepatic impaired
21
Q

Ergot Alkaloids

A
  • Abortive or acute treatment
  • DON’T use prophylactically
  • Produce vasoconstiction and decrease neurogenic inflammation
  • Interrupts pain signals in trigeminal nucleus
  • Black box: peripheral ischemia when given with CYP3A4 inhibitors
  • EX: Ergotamine tartrate, Dihydroergotamine mesylate
22
Q

Ergotamine Tartrate

A
  • Oral, SL, IM, IV, suppository
  • Also combined with caffeine
  • SE: intense vasoconstriction, stimulates CTZ (N/V), Ergotism (vascular, sensorimotor disturbances), thrombotic occlusion of smaller arteries and gangrenous extremities, psychic aberrations/hallucinations
23
Q

Dihydroergotamine Mesylate

A
  • IV, SC, IM favored to intractable migraine

- Intranasal is monotherapy for acute migraine attacks

24
Q

Butalbital-Containing Analgesics

A
  • Fioicet (APAP, caffeine) and Fiorinal (aspirin, caffeine)
  • Usually used for tension headcahce
  • Potential for overuse which could lead to overuse and rebound headaches
25
Q

Opioids

A
  • Can cause overuse/rebound headaches
  • No proof to superiority to triptans for migraine treatment
  • NOT first line therapy
  • Only use when other standard treatments failed
  • Butorphanol nasal spray has good evidence for effectiveness
26
Q

Overuse Headache

A
  • Results from frequent use of acute medication
  • Pattern of increasing headache frequency leading to daily headaches
  • Limit abortive use to 2-3x a week to avoid
  • Avoid butalbital and opioids due to increased incidence of overuse HA
  • Consider preventative migraine therapy instead
27
Q

Prophylaxis/Preventative Therapy

A
  • Daily administration for 3-12 months
  • Prophylaxis usually takes 4-6 weeks to work
  • Consider if using abortive meds >2x/week, attacks last >48 hours, or CI/failure to abortive therapy
28
Q

Botox

A
  • Approved for chronic migraines
  • Chronic migraines: >14 days/month, doesn’t work for less frequency (inhibits ACh release)
  • Given every 12 weeks
  • Warning: toxin could spread to other areas of body and cause botulism symptoms, difficulty breathing/swallowing could be life threatening
29
Q

Beta Blockers

A
  • Level A Preventative Therapy
  • MoA: blocking beta adrenergic mediated cerebral vasodilation
  • Selective and non-selective work but agents with intrinsic activity have less efficacy
  • SE: well tolerated, sedation, fatigue, dizzy
  • CI: asthma, heart problems, hypotension, depression
  • ACE-I, ARBs, and Ca++ channel blockers have also been used (2nd or 3rd line)
30
Q

Antiepileptic Drugs

A
  • Prevents trigeminal nerve activity

- Affects the spreading of cortical depression

31
Q

Topiramate

A
  • Topamax
  • Level A Preventative Therapy
  • Prolongs inactivation of Na+ channels
  • Also a AMPA/kainate antagonist
  • Good choice for those with epilepsy, bipolar disorder, anxiety, and obesity
  • Keep doses low to avoid kidney stones, sedation, cognitive changes, and glaucoma
32
Q

Gabapentin

A
  • Neurontin
  • Third Line Preventative Therapy
  • SE: sedation
33
Q

Valproic Acid

A
  • Divalproex
  • Level A Preventative Therapy
  • Prolongs inactivation of Na+ channels and reduces Ca++ T currents
  • AE: CNS (sedation, tremor, weight GAIN)
  • Monitoring: blood dyscrasias, pancreatitis, and liver problems
  • Black Box: hepatotoxicity, pancreatitis, teratogenicity
  • Category X for females in child bearing years
34
Q

TCAs

A
  • Second Line Preventative Therapy

- Inhibits central cortical depression and sympathetic activity

35
Q

Amitriptyline

A
  • Elavil
  • 50-70% reduction in number and intensity of migraine attacks
  • Lower doses than used for depression
  • SE: anticholinergic, weight gain, sedation, tachycardia
36
Q

SNRI

A
  • Venlafaxine (Effexor)
  • 2nd Line Preventative Therapy
  • Black Box: suicidal thinking and ideation in children, adolescents, and young adults
37
Q

CGRP Monoclonal Antibody Examples

A
  • Erenumab (Aimovig)
  • Fremanezumab (Ajovy)
  • Galacanezumab (Emgality)
  • Eptinezumab (Vyepti)
38
Q

CGRP Monoclonal Antibody MoA

A
  • Aimovig is a CGRP Receptor Ab Target
  • All others bind to CGRP in synapse to prevent neurotransmitter from activating the receptor
  • Substance P is coreleased with CGRP which leads to pain signals and leakage of materials to further promote neurogenic inflammation
  • All have ~1 month half life
39
Q

Midrin

A
  • Additional abortive therapy
  • Isometheptene mucate, Dichloralphenazone, APAP
  • Isomethe: sympathomimetic amine, acts by constricting dilated cranial/cerebral arterioles
  • Dichoral: mild sedative
  • APAP: analgesic

845 (24 decks)

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