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172 Cards in this Set

  • Front
  • Back
headaches are...
UNDERTREATED
primary headache
clinical condition due to a neurologic process (not caused by another disorder)
3 examples of primary HA
migraine, tension-type, clus
% of benign HAs that are primary
Comprise 90% of all benign headaches
secondary HA
have a specific underlying cause
types of secondayr HA
Sinus Headache
post traumatic HA
HA due to organic cause
sinus HA- how to dx
characteristic
tx
◦Dx: based on history & clocklike pattern of symptoms
◦Characteristics: pain located over affected sinuses
◦Treatment: OTC analgesics to blunt pain
Post-Traumatic Headache dx and tx
Dx: based on history
tx is symptomatic- if it's tension headache like they will treat like that, etc.
onset
course of PTHA (when does it worsen, resolve)
start within 24h of head injury
worsen over several weeks
resolve in less than a yea
characteristics of PTHA
features of what type of HA
dull, THROBBING ache
features of tension HA
benign vs. malignant organic HA- as in etiology
◦Benign organic headache – due to cerebrovascular insufficiency or benign tumor
◦Malignant headache – secondary to carcinoma
drug induced HA aka...(2)
Medication-overuse headache, analgesic rebound headache
definition of drug induced HA (2)
like how often of which drug do you have to be taking a drug for it to be associated..
Intake of simple analgesics more than 15 days per month OR

any migraine specific, opioid or combination of medications for at least 10 days per month for 3 months or longer
mechanisms of drug induced/rebound HA (2)
Chronic analgesic exposure causes antinociceptive tolerance & diminished medication effect
◦Medication tolerance & dependence results in repeated “mini-withdrawals” = why they occur more often in the morning
common complaint of drug induced HA
Neck pain is a common complaint
drug induced HA characteristics
Chronic daily headaches despite/because of daily analgesic use (TTH)
incidence of drug induced HA
gender
1%

women more than men
drug induced HA- associated/risk factors (5)
low income, low educational level, smoking, obesity, physical inactivity

poor dumb lazy fat people
pt with hx of what are more susceptible to rebound HA
Patients with histories of migraines are more susceptible to developing rebound headaches
highest risk drugs that cause rebound HA (2)
Opioids and butalbital are highest risk agents
tx of drug induced HA (does it require hospital?)
tx of withdrawal sx- drugs to give (2)

limit what
Stop acute pain meds
◦Detoxification: Sometimes requires hospitalization
Treating Withdrawal sx: NSAIDs -10 days, triptans – 4 days

Limit use of acute migraine therapies to 2-3 days per week to avoid rebound headaches
What is the best way to avoid overuse of abortive medications?
USE PPX meds
pathophys of giant cell/temporal arteritis (2)
Chronic inflammatory process of large blood vessels, particularly arteries of the extracranial carotid tree
◦Causes lymphocytic infiltrate and giant cells to assemble around the lumen
how to dx temporal arteritis (2)
Based on temporal artery biopsy
◦ESR (erythrocyte sedimentation rate) is elevated
temporal arteritis- gender
age
◦Female 2:1 Male
◦10x more common in those over age 80 than those in 5th decade of life
S/Sx of tepmoral arteritis (3)
Severe, continuous throbbing headache, usually over one temporal artery
◦Artery is usually tender, may be thickened or nodular and sometimes pulseless
◦Pain secondary to chewing, talking or swallowing is due to ischemia of the associated muscles when the carotid branches are involved
tx for temporal arteritis
Prednisone 60mg/day for 2-4 weeks even without positive biopsy results to prevent bad consequences (blindness) when waiting for biopsy. will still give even if biopsy comes back neg.
consequences of not treating temporal arteritis
Failure to treat results in blindness and possibly death
temporal arteritis- when can you start to taper steroids

most pt will require tx for how long
◦After normalization of ESR, steroids can be tapered to a level that maintains response
◦Most patients require corticosteroids therapy for 2-3 years
4 types of primary HA
Tension Type Headache
Migraine
Mixed Headache Syndrome
Cluster Headache
3 types of migraines and describe each
◦Classic - migraine with aura
◦Common - migraine without aura
◦Complicated - hemiplegic, ophthalmoplegic, basilar artery (neuro features)
Least studied primary headache disorder
tension type HA- because most ppl self medicate
pathpohys of TTH
Mechanism of pain in chronic TTH originates from myofascial factors & peripheral sensitization of nociceptors
3 initiating stimulus of TTH
Initiating stimulus may include nonphysiologic motor stress, mental stress, local myofascial release of irritants
TTH: infrequent
frequent
chronic
Infrequent episodic TTH 1 or less day/month
frequent episodic TTH = episodes 1-14 days/mo., chronic TTH more than 15 days/mo.
Most common recurrent headache syndrome, mild in nature so 85% of patients self-diagnose & treat
TTH
TTH gender
male 2x more than female in all ages?? ?she said female in class

i think its females...
TTH clinical disease manifestations (4)
premonitory sx? aggravated?
which side of head
pulsatile?

pt complaint

cease or ceaseless
No premonitory symptoms, not aggravated by physical activity, nonpulsatile
Pt complains of gradual progression of dull, nagging pain perceived to be deep
Usually affects both sides of entire head
Tension headache is the ONLY headache that is ceaseless for long periods of time
goal of non pharm therapy for TTH
decrease anxiety and tension in patient
non drug therapy for TTH (3)
Biobehavioral techniques
◦Eliminate caffeine
◦Reaffirmation of patient's self-administered therapy
tx for TTH- start with what?

ppx for chronic
◦Start with simple analgesics: 650mg ASA, l000mg APAP alone or with caffeine- improves ability for analgesic to work??
◦Use tricyclics (amitriptyline) for prophylaxis in patients with chronic headaches
HA emergencies (6)
Headache pain that feels like an explosion or thunderclap
Severe headache that is clearly your “worst-ever”
Persistent headache after head injury
Headache associated with systemic illness
New-onset headache in HIV or cancer patient
onset of hA in pt 50+ yo
associated sx with HA that would institute an emergency (4)
Stiff neck, rash, fever, nausea/vomiting
why are HA in 50+ yo people worrisom (3)
d/t possible etiologies like temp. arteritis, mass lesion, cerebrovascular disease
pathophys of migraine
Migraines are caused by the stimulation of the trigeminal nerve pain pathways - trigeminal fibers in migraineurs develop hypersensitivity/peripheral sensitization which makes them excessively responsive to stimuli that is normally non painful
Migraine attacks involve physiological mechanisms initiated by
migraine specific triggers
won't ask MoA of migraine
--just that for years we thought it was the wrong pathophys
migraine attacks occur when?
what modulates this (2)
Attack occurs when threshold is reduced or triggers are particularly strong or frequent

Internal & environmental factors modulate the point of no return
internal/environmental factors that play a role in migriane attacks (5)
hormonal fluctuations, fatigue, relaxation after stress, meteorological changes, substance abuse
NT/receptors that mediate migraines (2 specific subfamilies)
Serotonin (5-HT) receptor subfamilies (5-HT1 -5-HT7) are mediators of migraines
how to ID migraine triggers
keep migraine diary for 3 months
4 categories of triggers for migraines
diet
environmental
lifestyle
drugs
7 lifestyle factors that can cause migraines
stress or post-stress, depression, fasting, menstruation, excessive sleep, head trauma, fatigue
3 drugs that can cause migraines
HRT, oral contraceptives, nitroglycerin
other triggers
--
Prevalence is highest in men and women between the ages of
30-49 years
HA- genetics
prevalence
gender
avg attacks per month
Genetic
One-year prevalence rate in U.S. is 13%
More women than men
Patients average 1-4 attacks per month
manifestations of symptoms in migraines (3 properties)- duration, clinical course
Attacks last 4-72 hours
Pain increases in severity over time
Aura
what is aura
sensory or physical occurrences that immediately proceed a migraine by minutes or up to an hour
types of aura (5)
Visual (99%) - flashing lights, zigzag lines, blurred or lost vision
Weird ****: Hallucinations, numbness, aphasia (18%), motor
premonitory signs of migraine- definition

average time of onset
signals that occur hours or days prior to an attack (avg. = 10 hrs.)
4 neuro sx of migraine
phonophobia, photophobia, hyperosmia (heightened sense of smell), poor concentration
additional associated sx of migraine (5)
mood changes, excessive yawning, fatigue, rapid mood changes, food cravings
postdrome syndrome (4)
patients feel ‘washed out’, hung over, tired, irritable
COMMON migraine
migraine without aura
dx criteria of common migraine (no A in it) (no aura) (5)

not going to be asked to differentiate
A. At least 5 attacks fulfilling criteria B-D
B. Headache attacks lasting 4-72 hrs
 Untreated or unsuccessfully treated
C. Headache has at least 2 of the following characteristics
Unilateral location, pulsating quality, moderate/severe pain intensity
Aggravation by or causing avoidance of routine physical activity
D. During headache, at least one of the following:
Nausea +/or vomiting, photophobia and phonophobia
E. Not attributed to another disorder
know dx criteria
--
clAssic migraine
migraine with aura
dx criteria of classic migraine (aura)
 Diagnostic Criteria: Similar to above with the addition of one or more transient focal neurological aura symptoms
◦Positive symptoms/negative sx
Gradual development of aura symptom over 4+ min. or several symptoms in succession
Aura symptoms last 4-60 min.
Headache follows aura within 60 min.
positive aura sx (3)
flickering lights, spot or lines in vision, pins & needles
negative aura sx (2)
loss of vision, numbness
migraine alarm sx (5)
May warrant a scan:

aura symptoms always on same body side or with acute onset without spread or either of very brief (less than 5 min.) or unusually long (more than 60 min.)
Sudden change in migraine characteristics
Sudden substantial increase in attack frequency
Onset above the age of 50
Aura without headache, high fever, abnormal neurological exam
estrogen associated migraine MoA
serotonergic tone in women is positively correlated with estrogen levels, so as estrogen levels decline, serotonin concentrations fall, causing a cascade of events
when do estrogen migraines occur

properties in terms of severity and response to tx
Menstrual migraines occur between 2 days before onset of menses and up to 3 days after onset of bleeding

Often more severe than “normal” migraines and more refractory to treatment
most potent and common of all migraine triggers
menstruation
why are period headaaches so annoying
Often more severe than “normal” migraines and more refractory to treatment
What about post-menopausal women?
usually don't have estrogen headaches anymore
what about pregnant women

how to tx
50-80% will experience improvement in HA due to steady high lvls of estrogen

initiate APAP 1000 mg due to CI of triptans and NSAIDS
tx of estrogen migraines
same as for other types of migraines
◦Menstrual migraines respond best to triptans- UTD says triptans..
peds migraines (2) incidences in different kid populations
2.5-4% of prepubescent children experience migraines, slight prevalence in boys
After menarche, migraines become much more prevalent in girls
non pharm therapy of migraines (3)
Patient must change lifestyle, learn to moderate emotions, keep regular schedule of sleep and meals
Rapid treatment is essential**** IMPORTANT. if you want your migraine to go away tx as SOON as you can
Patient should retreat to dark room, avoid disturbances, sleep if possible
◦Abortive treatments of migraines are more effective if given when
early in the course of HA
why is it so important to give abortive tx as early as possible in course of migraine
Lower pretreatment pain severity is strong predictor of treatment response
Due to central sensitization during attack – counteracts triptan and analgesic efficacy if given then (during attack)
large single dose vs. several moderate doses (for migraine abortion)
A large single dose works better than several moderate doses
PO migraine therapies can be compromised by...
PO therapies can be compromised by gastric stasis
2 principles/key points in abortive migraine drug therapy
◦Select non-oral route (lingual, SQ, nasal) for patients who frequently present with nausea/vomiting
◦Use migraine specific agents (triptans, DHE) for those with more severe migraine and/or those who respond poorly to simple analgesics
1st line agents for the treatment of mild to moderate migraine

what is NOT effective?
Simple analgesics & NSAIDS

APAP as monotherapy
effective analgesics for migraine (3 options)
◦Aspirin
◦NSAID
◦Combination acetaminophen +aspirin + caffeine
3 NSAIDS that work for migraines
ibuprofen, naproxen sodium, tolfenamic acid (Other NSAIDS show less benefit)
butalbital MoA
Short to intermediate acting barbiturate
butalbital combo agents- efficacy
disadvantage
Combination agent of limited efficacy with high overuse potential

Combination agents pose greater risk for rebound HA
butalbital agents that are controlled substances
Products containing 50mg butalbital and 325mg ASA are controlled substances
fiorinal
fioricet
fioricet with codeine
--
MoA of ergo alkaloids
Bind to 5HT 1b/d receptors (just like triptans), inhibit trigeminal nerve pathway & nonselective serotonin agonist with activity at several other receptors, which is responsible for extensive side effects
ergot alkaloids line of therapy
NOT FIRST line
idk did she say she wasn't going ot ask anything about ergots?
23:00?
oral forms of ergots- downside
Oral forms have inconsistent effectiveness
4 AE of ergots- most common
N/V most common, peripheral ischemia, coronary vasospasm, severe withdrawal symptoms
Dihydroergotamine (DHE 45) vs. ergotamine
milder adverse effects than ergotamine – no rebound or physical dependence
just be aware that ergotamines are out there- tripants are better
--
drug of choice for nausea (dosing)

other option
DOC: Metoclopramide l0-20mg PO at onset of attack to stimulate gastric motility & decrease nausea
Phenothiazines can be used rectally when PO meds are not possible
triptans were made due to drive to...
Resulted from the drive towards more selectivity 5-HT1B/1D agonist
target receptors for triptans

where they are present (2)
5HT1 receptors are present on cranial arteries and in vasculature of dura mater
moa of triptans (3)
All triptans inhibit release of vasoactive peptides, promote vasoconstriction and block pain pathways in the brainstem
triptans- efficacy across the different types

what to do if one doesn't work
Triptans are all similar in efficacy (relief in 2/3 of patients) and well-tolerated
◦If one doesn’t work….try another
role of triptans in migraine therapy
1st line therapy in those with moderate to severe migraines without risk factors
benefits of taking triptans at onset of symptoms
Taking them at onset of symptoms improves efficacy and side effect profiles
rational polypharm- combo of drugs to use in migraines (3)
combination of triptan + NSAID and/or PO metoclopramide
sumatriptan (2)
◦The only 1st generation agent- most vasoactive issues- want to avoid in cardiac pt
◦Nasal spray and SQ injection are preferred for patients when N/V is significant
imitrex nasal spray- downside
Imitrex nasal spray – horrible
taste
benefits and downsides to SQ injection of imitrex
Subcutaneous provides fastest
onset, greater efficacy, but ↑ adverse
effects
sumatriptan- when to give
2nd dose?
give at onset of HA

2nd dose can be given an hour later but not that helpful/as effective as first dose
zomig (zolmitriptan) preperations (3)
2.5 & 5mg tablets, 5mg nasal spray
zomig vs. sumatriptan- designed to be...(3)
Designed to be more lipophilic and bioavailable than sumatriptan with longer DOA and faster onset of action
zomig initial dose
max dose
Initial dose is 2.5mg then MR in 2 hrs. No more than 10mg/24hrs.

wtf is MR and NMT
zomig-ZMT- what is it
contains what
orally disintegrating tablets, contain phenylalanine
zomig nasal spray dose
5 mg intranasally, may repeat x1 after 2 hours
not going to ask doses
--jk
benefit of zomig
no serious heart issues
4 AE of zomig- and one AE it doesn't have that sumatriptan has
nausea, dizziness, somnolence and paresthesias, no serious coronary effects
pt who fail imitrex- might they respond to zomig?

zomig spray vs. imitrex spray
◦Patients who fail to respond to Imitrex may respond to Zomig
◦Zomig spray is much less obnoxious than Imitrex spray
naratriptan- onset/safety
The “gentle” triptan – slow onset of action and favorable safety profile
naratriptan- issue

advantage/disadvantage compared to imitrex (2)
Problem with patients who have reduced renal fx and/or liver fx

higher bioavailability (70%) & better CNS distribution than Imitrex

disadvantage- less efficacoius
Eletriptan (Relpax) metabolism
exclusively by CYP3A4
6 CIs with triptans
pregnancy, Prinzmetal’s angina, uncontrolled HTN, ischemic heart disease, ischemic stroke, basilar or hemiplegic migraine
3 warnings when using triptans
◦Concurrent or recent (past 2 weeks) use of MAOI
◦Concurrent or recent (past 24 hrs.) use of ergot-type medication
◦Do not administer if headache is atypical- because might be a stroke (ischemic) which will make it worse
triptan rebound HA (3) how many doses can cause

limiting dose
how to prevent
◦As little as 3 doses of a triptan per week caused drug-induced headache  increasing attack frequency may be the first sign of developing a drug-induced headache
◦Most experts recommend using these abortive agents no more than two times per week
◦Use adequate prophylactic therapy to prevent analgesic overuse
Combination Triptans and NSAIDs (3)
Some reports conclude that 1/3 of patients may not respond to triptan monotherapy
◦Resent study found combination of a triptan and NSAID more effective than monotherapy with either drug or placebo and resulted in lower recurrence rate (may be greatest result)

side effects didn't seem to increase
treximet
Imitrex 85mg, Naproxen 500mg
opioids moa
Alter pain sensation in the thalamus – don’t act on underlying headache mechanism
opioids - usage in headaches
Rescue treatments with severe headaches unresponsive to other treatments
other conditions (2) in which opioids are often used for migraines
in pregnancy- safer
Those with contraindications to or adverse effects from other agents
status migrainousis- aka
definition
AKA: Intractable migraine
Exists when headache phase has been present for 72 hours – 1 week
how to tx status migrainosus (3)
Meperidine l25mg IV or IM??
Prednisone 40-60mg PO x 2 days- easy fix
Hospitalization?
when to use migraine ppx (wtf she said she wasn't going to ask about this) (4)
Use when headaches are 4 or more per month, long duration (12 hours or more) or account for significant disability or when vasoconstrictors are contraindicated
goals of migraine PPX (4)
Reduce attack frequency by at least 50%
Reduce severity and duration of headaches
Improve responsiveness to treatment of acute attacks
Improve function and reduce disability
non hormonal PPX options for menstrual migraine (don't have to know dose i guess? she said this earlier) (3)
Naproxen 500mg BID extending to day 3 of menses
Triptans: Dosed over 5 days (2 days before menses and continuing for 3 days into menses)
Frovatriptan 2.5mg BID – prolonged half-life
hormonal PPX options for migraine: goal of using hormones
tx options
◦Goal is to minimize premenstrual decline in estrogen
◦Oral contraceptives +/- supplemental estrogens HS- take at night due to more flux of hormones at night maybe
antihypertensives- migraine ppx options (3)
beta blockers, calcium channel blockers, ACE inhibitors & ARBs
BB options
2 grade A
3 grade B

which ones do NOT work
◦Propranolol, timolol (Grade A) – FDA approved
◦Metoprolol, nadolol, atenolol, (Grade B)
◦BB with ISA do not work for migraines
MoA of BBs in migraines
possibly raise migraine threshold
◦Most evidence & most widely used agents for prophylaxis
beta blockers
Therapeutic trial for BBs
3 months, allow several weeks for onset & titrate dose as necessary
CCBs- which one?
efficacious/recommended?
why is it used sometimes?
trial period
verapamil
modest and inconsistent benefit – not recommended

Used due to low side effect profile, may relieve aura symptoms

4-8 weeks from onest
BBs logical choice when..(2)
htn or anxiety
ACE inhibitors (2) efficacy
CI
◦ Proven efficacy in double blind placebo control study

can't use in preg
Tricyclic antidepressants for migraine ppxFUCK

which one is grade A

MoA

drug of choice for what type of HA
--◦Amitriptyline - Grade A evidence
◦ Other TCA’s have Grade C evidence
probably due to adaptive changes in norepinephrine & 5HT receptors with chronic use

◦Often drug of choice for mixed headache syndrome (common migraine with tension headache)
ANTIEPILEPTIC DRUGS choice for migraine
Divalproex sodium (Grade A evidence) – FDA approved
VPA- preg category
efficacy/onset (2)
use what form to minimize side effects
◦Reduced headache frequency by 50%, onset within 4 weeks
◦Use extended release to minimize side effects
◦Probably as effective as beta blockers
◦FDA pregnancy category D (X if used for migraine ppx)
topamax usage- efficacy
Reduced headache frequency in 1st month at doses of 100-200mg/day
most common AE of topamax (3)
Most common (at therapeutic dose): paresthesia (50%), dysguesia, weight loss(9-12%)
topamax AE at larger target doses (4)
fatigue, xerostomia, impaired memory, language and concentration difficulty
natural meds for HA (1)

safety?
Butterbur (Peasites hybridus) – spasmolytic and analgesic actions

Safety has not been established for use greater than 16 weeks
dangers of butterbur
Other products may contain pyrrolizidine alkaloids – carcinogenic and cause liver & kidney damage
misc agents for migraine ppx (5)
Cyproheptadine PO 4-8 mg TID
Feverfew
Magnesium
B vitamins
Botox
pathophys of cluster headaches

how it presents
Thalamus is “cluster generator”
Attacks victims in rapid fire succession, severe pain
risk factors for cluster HA (5)
Probably some genetic predisposition
Cigarette smoking, caffeine, alcohol use may be factors
Affects 4x male as female
if butterbur- only want to use which brand
petadolex- level A evidence
other brands have **** in it
onset of cluster HA (age)
onset 25-50 yrs. of age
quality of pain in cluster hA
Excruciating, knife-like, single-sided pain that often radiates from orbit to temple, described as explosive, can be throbbing in nature
cluster HA- how long do attacks last

recurrence

most occur when?

pt prefer to remain...
Attacks last 15 min. to 3 hrs. (mean of 50 minutes) and may recur up to 8 times in 24 hours – most occur at night; patients prefer to remain active
5 autonomic sx associated with cluster HA
unilateral and ipsilateral with the pain; ocular tearing and redness, rhinorrhea with simultaneous congestion, sweating, ptosis (drooping eyelid)
Patients with chronic cluster headaches are at risk of (2)
self inflicted trauma
suicide
cluster HA- usually lasts how long
when do attacks usually start
Cluster period lasts 3-16 weeks
◦Attacks often starting during sleep
KNOW THIS
cluster HA can be precipitated by..(3)
vasodilating substances

(alcohol, nitro, histamine)
cluster HA tx- pt often need...
Patients often need BOTH abortive and preventative therapy at the same time
standard abortive therapy for cluster HA
Standard treatment: inhalation of l00% O2 at 7 liters/min for 15 min – works for most patients
triptans in cluster HA
concern is a lot of harm possible esp with sumatriptan
SQ sumatriptan or intranasal
other options for cluster HA (5)
DHE- intranasal
lidocaine- intranasal- numbing...some part of your brain
prednisone- "cluster busting" usually relief within 1-2 days
very hot/cold compresses
vigorous exercise
preventive therapy for cluster HA (5) 2 non pharm, 3 pharm
Avoid triggers (EtOH, NTG etc.)
Trial and error
Lithium carbonate (70% effective) – can be used with verapamil
Verapamil (70% effective) – effect can be seen after 7 days of treatment
Valproic acid
Frovatriptan (Frova) unique property (2)
longest half life (26 hrs.) of all triptans – has a slow onset of action
rizatriptan vs. imitrex
faster and greater relief from headache than Imitrex