Headache Background Flashcards
1
Q
Secondary Headache
A
- Underlying pathological causes
- Head/neck trauma, cranial vascular disorder, psychiatric disorders, lumbar puncture, inflammation, hematoma
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
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
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
5
Q
3 Predictive Migraine Symptoms
A
- Moderate to severe disability
- Photophobia
- Nausea
Others: unilateral throbbing, vomiting, phonophobia, increased pain with physical exertion
6
Q
Auras
A
- Migraine with aura: most common visually, 10-15 minutes before CSD
- No auras are more common with migraines
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
8
Q
Sinus Headaches
A
- Nasal stuffiness or discharge
- Can be treated with nasal costicosteroids or antibiotics if caused by infection
- May need surgery
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)
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
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
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
13
Q
NSAIDs
A
- Abortive therapy and intermittent preventative
- First-line treatment for all migraine attacks
- Inhibits prostaglandin synthesis which prevents neurogenic inflammation mechanisms
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
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
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
