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MSII Pharmacology > Unit 3 - Pharmacotherapy of Primary Headache Syndromes > Flashcards

Unit 3 - Pharmacotherapy of Primary Headache Syndromes Flashcards

1
Q

what are primary headaches?

A

headache itself is the disease

  1. migraine (w/ or w/o aura, or other types)
  2. tension-type (episodic, chronic, other)
  3. cluster (episodic, chronic, paroxysmal hemicrania, other)
  4. miscellaneous (idiopathic, external compression, cold stimulus, benign exertion or cough (associated with sex)
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2
Q

what are secondary headaches?

A

headaches are caused by or associated with something else

  • head trauma
  • vascular disorder (or non-vascular disorder)
  • substances
  • non-cephalagic infection
  • metabolic disorder
  • disorder of facial or cranial structures
  • -cranial neuralgias: trigeminal, occipital, glossopharyngeal
  • not classifiable
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3
Q

what must one look for in history of headaches? what happens if there are red flags?

A
  • attack onset, duration, timing, and frequency
  • pain location, severity, and quality
  • associated features
  • aggravating, ameliorating, and precipitating factors
  • impact, PMH, SH, FH
  • caveats: patient may have more than one headache disorder (each receives own diagnosis), but not necessary to Dx each individual headache attack

if there are red flags, it’s probably a secondary headache disorder –> run diagnostic tests

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4
Q

what is the prevalence of episodic tension-type, migraines, and chronic daily headaches?

A

ETT: most common (>40% prevalence in men and women)
migraines: 17% prevalent in females, 6% in men
chronic daily: 5% prevalent in females, 3% in men

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5
Q

what age group is prevalence of migraines highest?

A

25-55 age group

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6
Q

what are the phases of migraines?

A
  1. prodrome
  2. aura
  3. headache
  4. resolution
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7
Q

what is migraine prodrome?

A

first phase of migraines, in 20% of patients

  • occurs hours to days before onset
  • change in mental status: drowsy, depressed, irritable, hyperactive, euphoric, talkative
  • neurological changes: phono/photophobia, yawning, difficulty concentrating, dysphasia
  • general changes: anorexia, food craving, thirst, urination, fluid retention, diarrhea/constipation, stiff neck
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8
Q

what is migraine aura?

A

second phase of migraines (15%) that is defining factor (w/ or w/o aura)

  • complex of focal neurologic symptoms (positive or negative) that precedes, accompanies, or follows headache
  • duration is anywhere from 4 to 60 minutes
  • aura may occur alone, and patients may have more than one type of aura
  • -visual area is most common, then paresthesias (Jacksonian march typical)
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9
Q

what is the headache phase of migraine?

A

third phase of migraine

  • usually unilateral, throbbing, moderate-severe, and aggravated by activity but relieved at rest
  • -may evolve from unilateral to bilateral and vice versa
  • most often starts between 5 AM to noon, and lasts 4-72 hours
  • -gradual onset (peak 2-12 hours) and resolution
  • pain associated with anorexia, nausea, vomiting, osmo/photo/phonophobia (seeks dark quiet room)
  • -other: blurry vision, nasal stuffiness, diarrhea, pallor, abdominal cramps, diaphoresis, scalp/neck tenderness, lightheadedness, fatigue, irritability
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10
Q

what is the resolution phase of migraines?

A

fourth and last phase

  • headache wanes and person may feel tired, washed out, or irritable
  • scalp tenderness, impaired concentration, depression
  • rarely feel refreshed or euphoric
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11
Q

baseline pathophysiology of migraine?

A
  1. strong familial association and early onset of disorder –> genetic component
    - familial hemiplegic migraine is the only type of migraine with identified genetic locus (Xm 19p13; Ca channel mutations)
  2. “sensitive brain” hyperexcitability leads to susceptibility to migraine
    - migraine patients have exaggerated responses to normal stimuli
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12
Q

prodrome pathophysiology of migraine

A

symptoms suggest hypothalamic role, but little else known

-potentially suprachiasmatic nucleus

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13
Q

aura phase pathophysiology of migraine?

A

associated with reduction in cerebral blood flow that moves across cortex at 3 mm/min

  • usually begins in occipital lobe
  • oligemia not due to vasoconstriction and doesn’t respect cerebral vascular territories
  • -likely result of neuronal dysfunction (cortical spreading depression)
  • -rates of progression of spreading oligemia, migrainous scotoma, and spreading depression are equal (but unknown how common these changes are)
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14
Q

what is cortical spreading depression?

A

neuronal dysfunction during aura

-precedes vascular changes

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15
Q

pathophysiology of headache phase

A

activation of trigeminovascular system

  • dura and meningeal blood vessels are innervated by V1
  • during attack, nerve fibers release vasodilating and permeability-promoting peptides from perivascular nerve endings
  • -promotes “sterile” inflammation that causes increased intracranial mechanosensitivity and hyperalgesia to previously innocuous stimuli (coughing, head movement)
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16
Q

what is released by trigeminal nucleus and sensory nerve fibers during migraines? what blocks release?

A

vasodilating and permeability-promoting peptides

  • substance P
  • calcitonin gene-related peptide
  • neurokine A

release blocked by Triptans (mediate prejunctional 5-HT1b/d receptors)

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17
Q

what are the steps to activating the trigeminovascular system?

A
  1. vasodilation
  2. neuropeptide release
    - causes vasodilation and neurogenic inflammation
  3. pain signal transmission
  4. central pain transmission

but what exactly activates the system is unknown

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18
Q

what are the three types of headache treatment?

A
  1. preventive (prophylactic)
  2. behavioral (begin with this)
  3. acute (abortive or symptomatic)

can combine all 3

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19
Q

what are nonpharmacologic treatments of headache?

A
  • healthy habits: adequate sleep, regular balanced meals, regular exercise, stop smoking, etc.
  • psychological factors should be addressed
  • psychophysiological Rx: reassurance, stress management, relaxation Rx, biofeedback
  • trigger identification and avoidance (but cannot avoid weather-related migraines)
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20
Q

what are acute/abortive/symptomatic pharmacological therapies?

A

used after attack has begun to reverse or stop progression

  • treatment is tailored to be specific to patient and characteristics of migraine syndrome (headache severity)
  • -be aware of PMH, allergies, Rx (current and previous)
  • -mode of administration depends on headache characteristics and associated N/V (can’t give oral)
  • -statified care preferred over step care
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21
Q

what should one give if headaches are mild to moderate?

A

NSAIDs –> triptans, DHE

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22
Q

what should one give if headaches are severe?

A

oral triptans/DHE –> parenteral triptan/DHE, steroids, Depakote, neuroleptics/opiods

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23
Q

what is the difference between nonspecific and specific migraine medications? examples?

A

nonspecific: effective for migraine and non-headache pain disorders
- NSAIDs, COX2 inhibitors, combo analgesics, neuroleptics, antiemetics, corticosteroids, opioids
- mild/moderate headache intensities, pregnant, children, CV risk, etc.
- overuse of barbiturate-containing can cause drug-induced headaches

specific: effective for migraine, but not non-headache pain disorders
- ergotamines/DHE
- triptans

24
Q

explain “rebound headaches” from medication overdose?

A

most symptomatic medications, when taken daily, cause “rebound” phenomenon

  • caffeine and barbiturate-containing medications and narcotics are leading culprits
  • specific migraine medications may also cause regound
  • medication overuse is most common cause of chronic daily headaches
25
Q

describe analgesics for migraine

A

acute, non-specific treatment

  • inhibit COX (esp. COX2i)
  • aspirin, acetaminophen, naproxen, indomethacin, piroxicam, diclofenac, ibuprofen
  • -combo of acetaminophen, aspirin, and caffeine (Excedrin) effective in moderate migraine
  • -acetaminophen preferred in kids b/c danger of Reye’s with other NSAIDs
26
Q

describe barbiturates for migraine

A

acute, non-specific treatment

  • never been shown to be effective in RCT
  • -used only when specific migraine Rx not available or contraindicated
  • frequent side-effects are drowsiness and dizziness
  • -risk of overuse and withdrawal
  • -limit use to 2-3 treatment days per week
27
Q

describe opiods for migraine

A

acute, non-specific treatment

  • various forms (codeine, merperidine, oxycodone, hydromorphone, morphine, methadone, butorphanol) in oral, parenteral, or transnasal formulations
  • high risk for overuse and development of chonic daily headaches (limit to 2 days a week)
  • used if pregnant women, or if other treatments not tolerated
28
Q

describe steroids for migraine

A

acute, non-specific

  • various oral and parenteral forms available
  • unknown mechanisms
  • usually only for brief periods of time in prolonged headache states (only for a couple days)
29
Q

describe ergotamine and dihydroergotamine (DHE) for migraine

  • mechanism
  • forms
  • side effects
  • contra-indications
A

acute, specific treatment

  • alpha adrenergic and serotonergic agonist
  • -DHE is weaker arterial vasoconstrictor, less emetic, and has less effect on uterus
  • reduce cell activity in trigeminal pathway (second order neurons in caudal brainstem)
  • ergotamine can be combo with caffeine, oral tablet, or suppository
  • DHE can be nasal spray, IM, or IV formulation
  • maximum 2 days/week usage
  • side effects: N/V, chest pain, abdominal pain, dizziness
  • avoided in pregnant women, uncontrolled HTN, sepsis, renal/hepatic failure, cerebral/coronary/peripheral vascular disease
30
Q

what is DHE IV mainly used for?

A

status migrainosus (severe and intractable constant headache state that lasts >72 hours)

31
Q

describe triptans for migraines

  • types and mechanism
  • what else are they effective for?
  • side effects?
A

acute, specific treatment

  • premier migraine abortive medications
  • 7 possible triptans, differing in onset and duration of action, side effect profile, and formulation
  • -all penetrate CNS to some extent, thus constricting extracerebral intracranial vessels and inhibiting trigeminovascular system
  • -5-HT1B/D agonists
  • can take more than once without worry of overdose
  • reduce photo/phonophobia, N/V, but no evidence that supports use during aura
  • avoid in vascular disease, uncontrolled HTN, complicated migraine
  • side effects: flushing, tingling, dizziness, chest discomfort (non-cardiac; from esophageal blood vessel spasm; in 4% of patients)
32
Q

how good is the pain relief with triptans in different forms?

A

80% patients have relief with subcutaneous doses
60% efficacy if oral
-headache recurs in 1/3 of patients

33
Q

what is the only triptan that can be injected?

A

Sumatriptan

34
Q

what are the triptans that can be a nasal spray?

A

Sumatriptan, zolmitriptan

35
Q

what are the triptans that are orally disintegrating?

A

Rizatriptan, zolmitriptan

36
Q

what are the triptans that are oral tablets?

A

all 7 of them

37
Q

adjunctive treatment for migraines

A

acute treatment that involves antiemetics and neuroleptics

38
Q

describe preventive treatment of migraines?

  • types?
  • dosage?
A

to reduce frequency, duration, and severity of migraine

  • long-term, preemptive, and short-term
  • most are used at relatively low doses
  • -increased slowly until therapeutic effects develop, side effects occur, or therapeutic ceiling is reached
  • improve response to acute therapies
39
Q

what are requirements for drugs for chronic prevention of migraines?

A
  • recurrent severe migraines > 3/mo
  • recurrent mild-moderate migraines >2/wk
  • inability to use effective symptomatic Rx
  • overuse of acute medications
  • patient preference
  • special migraine syndromes (hemiplegic, etc.)
40
Q

can preventive treatment for migraines be used during pregnancy?

A

should be avoided unless severe pain or disability create benefits from medication that overshadow risk

41
Q

what are the major preventive migraine medications?

A
  • antidepressants
  • antihypertensives
  • antiepileptics
  • vitamins/minerals
  • NSAIDs and COX2i also included
42
Q

describe antidepressant treatment for migraines?

  • types
  • names?
  • ASE?
A

preventive treatment (tricyclic antidepressants and SSRIs)

TCA:

  • amitriptyline, nortriptyline, protriptyline
  • -ami: fairly consistent supportive data for efficacy
  • ASE: dry mouth, constipation, weight gain, cardiac toxicity, orthostatic hypotension

SSRI:

  • fluoxetine, paroxetine, sertraline
  • sometimes used to treat coexistent depression and chronic daily headache
  • ASE: weight gain, sexual dysfunction
43
Q

antihypertensives for migraine treatment?

  • types
  • names
  • ASE
  • contraindications
A

preventive (beta-blockers and Ca-channel blockers)

BB:

  • propranolol (most used), timolol, nadolol, atenolol
  • -N/A have longer half-life and tolerability, but P/T are FDA-approved
  • ASE: drowsiness, depression, decreased libido, hypotension, memory disturbance
  • CI: asthma, diabetes, CHF, Raynaud’s

CCB:

  • Verapamil
  • most useful if prolonged or disabling aura (hemiplegic migraine)
  • ASE: constipation, dizziness
44
Q

antiepileptics for migraine treatment?

  • names?
  • ASE
A

valproic acid: ER divalproex Na is more common and approved

  • ASE: sedation, hair loss, weight gain, tremor, cognitive changes
  • -serious: hepatotoxicity, blood dyscrasias, pancreatitis
  • -must obtain CBC and LFT (liver function test) at baseline

topiramate: most frequently used AED, FDA approved
- ASE: cognitive changes, paresthesias (commonly fingertips, lips), weight loss
- -3% of patients in clinical trials got kidney stones (as metabolized through kidneys)
- -acute angle-closure glaucoma rare but potential adverse reaction
- -decreases serum bicarbonate levels

45
Q

onabotulinum toxin A (Botox) for migraine treatment?

  • administration?
  • mech?
  • ASE?
A

FDA approved for chronic migraine (>15x/m for >3mo)

  • 155 units every 12 weeks in 31 fixed-site, fixed-dose injections with additional max 40 units at physician’s discretion
  • unknown mechanism (possibly decreases afferent stimulation of trigeminovascular system, downregulation of sensory and parasympathetic receptors, etc.
  • ASE: injection site pain, headache post-injection, neck weakness, ptosis (like Horner’s) possible
  • -serious distant spread of toxin effect, dysphagia, dysarthria, or dyspnea not expected
46
Q

what are tension-type headaches?

  • definition?
  • type of pain?
A

most common primary headache syndrome

  • divided into episodic and chronic (but can evolve from E to C)
  • TTH varies widely in frequency, duration, severity
  • no prodrome or aura
  • dull, achy, non-pulsatile, pressure-like pain (band-like)
  • -bilateral, mild-moderate in severity (if severe, must be migraine)
  • -may have neck discomfort or tenderness
  • -photo/phonophobia and nausea are mild if present at all
  • -poor sleep is known trigger
47
Q

pathophysiology of TTH?

A

poorly understood

  • initially believed to be (but disproven) due to sustained muscle contraction of pericranial muscles as consequence of stress
  • no clear association with depression or anxiety
48
Q

treatment types for TTH?

A

behavioral, acute, and preventive

  • acute: simple analgesics (naproxen, ketorolac, indomethacin) that may be in combo (with opioids, barbiturates, caffeine)
  • -no role for muscle relaxants for ETTH
  • preventive: considered if frequency (>2/wk), duration (>4hr), and severity of ETTH may lead to significant disability or medication overuse
  • -mainstay for CTTH treatment
  • -includes TCA (amitriptyline), SSRIs, muscle relaxants (tizanidine), and Botox (into pericranial muscles)
49
Q

what are cluster headaches?

A

episodic and chronic

  • clockwork daily and annual rhythm
  • more often in men (4:1), onset 27-31 yo
  • -14-39-fold increase in risk of cluster in 1st-degree relative
  • some patients have heavy facial features (leonine men, masculine women) which may be due to smoking
50
Q

difference between episodic and chronic cluster headaches?

A

episodic: occurs in periods lasting 7d to 1yr, separated by pain-free periods lasting 1 mo
chronic: attacks occur for >1yr w/o remission or with remissions lasting <1mo

51
Q

what are cluster headache symptoms?

A
  1. severe unilateral orbital, supraorbital, temporal pain lasting 15 min to 3 hr
  2. frequency: one every second day to 8 per day
  3. associated with: lacrimation, nasal congestion, rhinorrhea, forehead/facial swelling, Horner’s, eyelid edema, conjunctivial injection, sense of restlessness or agitation during headache
52
Q

how do cluster headaches differ from migraines?

A

CH patients are restless when they experience a headache, to the point that they may kill themselves
-peaks very quickly (from when it starts to when it gets worse)

53
Q

cluster headache pathophysiology?

A

overlaps with migraines

  • location of pain implies involvement of opthalmic division of trigeminal nerve
  • sympathetic dysfunction and parasympathetic overreaction
  • annual rhythm and daily occurence suggest hypothalamic source
54
Q

what are treatments for cluster headaches?

A

can be acute/abortive or preventive

-patients should not nap during the day, or drink alcohol if experiencing a cluster

55
Q

what are acute therapies for cluster headaches?

A

since attacks peak quickly, acute treatments must be fast-acting

  • O2: high-flow delivered via non-breathing mask effective in 15 minutes
  • -safe, cost-effective, and portable –> top choice
  • triptans: sumatriptan SC also 70% effective in 15 minutes (first-line)
  • -nasal spray not as effective, as is zolmitriptan nasal spray
  • DHE: IM and nasal spray are effective
  • anesthetics: local intranasal agents (lidocaine) are limited in effectiveness
56
Q

what are preventive treatments for cluster headaches?

A

indicated when attacks are too frequent, severe, rapid onset/short-lived, or symptomatic Rx not effective

  • for short-term and long-term prevention
  • -short (21-28-day courses when already experiencing cluster): oral corticosteroids (prednisone, methylprednisone), daily DHE
  • -long: verapamil, topiramate, divalproex sodium, lithium
57
Q

information on lithium as headache treatment?

  • mech
  • ASE
  • toxicities
  • drug reactions
A

preventive treatment for cluster headaches

  • alters circadian rhythms, but its mode of action is unknown
  • 78% of CCH, 63% of ECH respond
  • blood levels necessary to monitor efficacy
  • ASE: weakness, nausea, thirst, tremor, lethargy, blurred vision, slurred speech
  • toxicity: vomiting, anorexia, diarrhea, confusion, nystagmus, extrapyramidal signs, seizures
  • don’t use indomethacin or Na-depleting diuretics (increase lithium levels)

MSII Pharmacology (43 decks)

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