headache

most common type of h/a

Tension type H/A aka Stress H/A

risk factors for tension type headache

female sex

fatigue

sleep disturbances/disorders

psychological stress (lower cortisol levels possibly due to chronic stress may contribute)

migraine Hx

depression Hx

alcohol

clinical presentation of TTH

Pain

• mild to moderate (may be severe(

• dull, pressure, head fullness, like a tight cap or a heavy weight on my head or shoulders

Cranial Muscle tenderness (temporal, frontal occipital, causes band pain)

Episodic Tension H/a diagnostic criteria

<15 h/a days per month for atleast 3mo fulfilling all of these criteria:

• headache lasts 30 min-7 days

• minimum of 2 of the following

  • bilateral

  • non pulsating

  • mild-mod

  • not aggravated by routine physical activity like stairs

• no N/V

• no more than one of photophobia or phonophobia

**not better accounted for by another ICHD-3 diagnosis

chronic tension headache diagnostic criteria

h/a on >15 days per month for >3mo, other criteria same as episodic (30mins-7days, bilateral, non pulsating, mild-mod, not aggravated by physical activity, no more than 1 of photophobia/phonia, no N/V)

4 clinical features of migraine

prodrome, aura, h/a, postdrome

migraine prodrome clinical features

appear 24-48hr before h/a onset

light and/or sound sensitivity, fatigue, neck pain, food cravings, yawning

cognitive Sx such as irritability/euphoria and changes to bowel fxn

migraine aura clinical features

focal neurologic sx- usually mix of positive and negative

usually visual - develop over 5min and last <1hr

positive Sx:

• visual (bright lines, shapes, objects)

• auditory (tinnitus, noises, music)

• somatosensory (burning, pain, parasthesia)

• motor (jerking or repetitive rhythmic movements)

negative Sx:

• absence or loss of fxn such as loss of hearing, vision, feeling, or ability to move a part of the body

migraine headache clinical features

unilateral and tends to throb or pulsate, esp as intensity increases

10/10 pain

severity increases over 1- several hours

Nausea, vomiting, photo/phonophobia

routine exercise may exacerbate

in adults if untreated can last 4hr- several days

migraine postdrome clinical features

drained, exhausted, some feel opposite like mild elation or euphoria

light or sound sensitivity or food cravings

lasts hrs-1 day

what is medication overuse h/a

secondary h/a that occurs when overuse of acute medications to treat other h/a disorders results in increased h/a burden

factors related to MOH

association with primary h/a disorders (does not develop if no h/a history)

genetic predisposition

central sensitization (chronic exposure to triptans/analgesics downregulates 5HT rec & changes inhibitory pathways = impairment of antinociceptive acticity and permenant feeling of head pain)

biobehavioral factors (fear of h/a, anticipatory anxiety, drug taking behavior, psychologic drug dependance)

causes of MOH

>9 days per month of triptans/opioids

>14 days per month of NSAIDs/tylenol

>9 days per month of combo of agents

clinical presentation/Sx of MOH

early morning h/a is hallmark- h/a is present or develops upon awakening (due to nocturnal withdrawal of med)

neck pain

pain varies in severity/location- severity increases after period w/o a drug, can rage from mild-severe, likely dictated by baseline h/a disorder

forgetfullness, irritability, fatigue, depression are associated features

acute therapies provide only transient relief

MOH diagnosis

headache occuring on 15+ days per month in a patient with pre existing h/a disorder

regular overuse for >3mo of 1 or more drugs used to Tx acute h/a

med overuse defined as:

10+ days for ergot derivates, triptans, opioids, combo analgesics

15+ days for non opioid analgestics (tylenol, NSAIDs)

things that require ER referal

suspected stroke, TIA, meningitis, head trauma

new h/a w/ cognitive change

any headache that becomes progressively severe, changes in h/a pattern

presents with unilateral eye pain with red eye, fixed and dilated pupil or diminished vision

if h/a came on suddenly

if the h/a is the patients worst h/a

h/a occurs with fever, neck stiffness, or impaired consciousness

h/a is associated with tenderness in the temporal artery (patient is >50yo, presents with new undiagnosed h/a- worry about temporal arteritis)

things requiring Non emergent referral to patients primary cary provider

meds causing h/a: tetracycline, SMX-TMP, ACEi, BB, CCB, OC, steroids, HRT, decongestants, SSRI, PPIs

withdrawal from meds

uncontrolled htn

shingles and post herpetic neuralgia

sinusitis, otitis media, dental abscess- clinical judgement

chronic TTH or frequent migraines

acute h/a goals of therapy

rapid pain relief w/o recurrence (pain free at 2hr, 24hr sustained h/a relief)

restored ability to fxn

minimal need for repeat dosing or rescue meds

reduced subsequent use of resources (ER visits, imaging, HCP, etc)

minimal or no ae from meds

goals of therapy of preventitive Tx

reduce attack freq, duration, severity, disability

improve responsiveness to and avoid escalation in use of acute Tx

reduce resiliance on acute Tx

improve fxn and reduce disability

non pharm for h/a

headache diary- helps identify triggers so can avoid & tracks Sx, pattern, freq, effects of meds etc

rest in quiet dark room

apply cold cloth to head

physio and chiro (if mechanical problems in neck/shoulders)

identify + control triggers

diet headache triggers

missing meals

chocolate

caffeine intake/withdrawal

red wine/alcohol

fruits (citrus, bananas, raisins)

dairy products (cheese)

foods containing MSG, nitrites (processed meats), aspartame/saccharin, sulfites (shrimp), tyramine (cheese, wine), yeast

med triggers h/a

cimetidine

estrogen or OBCs

nifedipine

clomiphene

theophylline

withdrawal of analgesics, decongestants, benzos, ergotamine

enviromental h/a triggers

strong smells, perfumes

loud noises

tobacco smoke

weather

flickering/bright lights

behavioural triggers of h/a

fatigue, stress, anxiety, menopause, prolonged exercise

Options for acute TTH treatment

simple analgesics (acetaminophen/NSAIDs) - preferred

opioids

combos with caffeine (ex: tylenol + caffeiene, ASA + caffeine)

combos with opioids/butalbital (ex: Fiorinol- ASA/caffeine/butabital, Tecnal-ASA/caffeine/butalbital/codeine)

what simple analgesic is most effective for TTH acute Tx

NSAID

how often to use simple analgesics for acute Tx of TTH

no more than 2 days per week

which simple analgesic is least likely to lead to MOH

NSAIDs

what opioid analgesic is not recommended for acute TTH Tx and why

codeine- increased potential for MOH, more ae, limited evidence for efficacy

when to use caffeine combo analgesics (ex: tylenol and caffeine) for TTH acute Tx

when failed simple analgesics

cons of using opioid/bualbital/caffeine combo for TTH acute Tx

increase propensity for MOH

tolerance, dependance, toxicity

what type of drug has no evidence for acute TTH Tx

muscle relaxants (cyclobenzaprine, methocarbamal, baclofen)

when to take acute migraine meds

within 30min of mild pain

how to ensure someone gets an adequate triptan trial for migraine

try selected triptan for 3 attacks, with repeat dosing if needed, and/or increase dose

if still failure, try >/=2 other triptans (20-80% respond) OR add an NSAID (20%)

SC sumatriptan helps 50% of triptan non responders

ensure triptan is taking at earliest onset of migraine pain

how often per month can you use a triptan

max 9 days per month

when to consider ODT triptan

useful if water exacerbates nausea

conveniant and discrete
**doesnt have faster onset

when to consider sc or nasal triptan

if vomiting is preventing absorption, or if faster relief is desired

when are anti emetics useful for migraines

enhance efficacy of other agents and may be useful even in the abscense of N/V

1st line agent for moderate to severe migraine attacks

triptans (5HT1B/1D agonists)

things to consider when picking triptans

1. look at dosage form

   • N/V use ODT (rizatriptan) or nasal sprays (zomitriptan/sumatriptan) or wafers/melts

   • nasal sprays/sc fastest relief

2. look at onset/half life

   • most 30-60min onset and 3hr half life

   • exception: frovatriptan/naratriptan - therefore if rapidly escalating avoid these bc onset of action is 1-3hr for nara, 2 for frova

   • use frova/nara if issues with recurrence of migraines, prolonged migraines or comes back because half life is 25hr frova and 6hr nara

   • nara/frova have decreased incidence of nausea bc of slow onset

triptans SE profile

chest discomfort or tightness (“triptan sensations”- not believed to be cardiac origin)

dizziness, fatigue, drowsiness, nausea, facial flushing, paresthesis

serotonin syndrome (RARE- SSRIs not CI, educate pts)

coronary venospasm potential (females w/ aura greater risk)

drug interactions with triptans

do not use within 24hr of DHE or other triptans (additive vasocontriction/coronary venospasm)

risk of serotonin syndrome (TCA, SSRI, MAOI etc)

• agitation, excitment, tremors, weakness, chills, diarrhea

• MAOI must be d/c for 2wks, caution with others

• DO NOT USE WITH MAOI

inhibitos of CYP3A4 (grapefruit, clarithromycin, cimitidine) may increase bioavailability of almotriptan, eletriptin - CONTRAINDICATED

CYP1A2 interactions with zolmatriptan

frovatriptain- OCPs and propranolol may increase serum conc by 30-60%

contraindications of triptans and ergots

CV/cerebrovascular disease or uncontrolled htn

***if had MI 5 yrs ago not CI, do risk vs benefit

monitoring with triptans/ergots

baseline cardiac evaluation/EKG for females >40 and males >50

when are simple analgesics used for migraine

mild migraines

which simple analgesics have most evidence for migraine

ASA, ibuprofen, naproxen sodium

**AVOID EC or slow release bc want fast absorption/action therefore also need empty stomach

**best choices ibuprofen/naproxen

how often can you take NSAIDs for migraine

<15 days per month

types of dosing used for NSAIDs for migraine

higher doses used for headache and migraine attacks

ergots for migraines place in treatment

2nd line due to increased nausea and decreased efficacy vs triptans

take w/ anti emetic (domperidone, metoclopramide)

can consider for refractory attacks

used for severe and ultra severe

available ergots

dihydroergotamine (DHE)- Migranal

SC, IV, IM, nasal spray

SE profile of ergots

more nausea than triptans

dizziness, fatigue, drowsiness, facial flushing, nausea, parasthesia

chest discomfort or tightness, less than triptans

serotonin syndrome - rare

coronary vasospasm potential (female w/ aura increased risk)

drug interactions with ergots

do not use within 12hr of triptans = additive vasoconstriction/coronary venospasm

risk of serotonin syndrome with other serotonergic agents (TCA, SSRI, MAOI)

• do not use with MAOI or for 2 weeks after d/c

CYP3A4i

examples of po CGRP inhibitors

Rimegepant (Nurtec)

Ubrogepant (Ubrelvy)

pros/cons of po CGRP inhibitors

less effective than triptans?

have a fast onset of action, conveniant dosing and mild-mod SE (nausea, drowsiness)

OK to use in pts with CV disease

decreased risk of MOH

**likely would require failure or intolerance to multiple triptans or CI

CGRP inhibitors drug interactions

metabolized by CYP3a4 therefore CI with strong inhibitors

strong inducers decrease effectiveness

Butorphanol cons

typically a rescue med when other meds have failed

dependancy potential or can cause w/d symptoms in those on long term opioids

what is butorphonal

mixed opioid agonist-antagonist

adjunctive anti emetic therapies for migraine

dopamine antagonists:

• metoclopromide PO, SC, IV (best evidence)

• Domperidone PO

• Prochlorperizine IV/PO

Dimenhydrinate PO/PR/IM/IV

Metoclopramide ae

TD and EPS

Domperidone ae

QT prolongation and heart block

How to deal with acute migraine in pregnancy

Increase emphasis on non pharm

1st line tylenol

ideally optimize prophylactic Tx to avoid having to use acute agents during pregnancy

Sumatriptan may be considered if absolutely necessary (ideally avoid NSAIDs/triptans)

when to consider prophylactic migraine Tx

attacks significantly interfere with patients daily routine despite acute Tx

frequent attacks (4+ a month)

CI to or failure of or over use of acute Tx

adverse rxn to acute Tx

Counselling points for prophylactic Tx

counsel pts as to reasonable expectations

succesful prophylaxis is a decrease in severity/frequency by 50%

how to dose prophylactic migraine Tx

increase dose q 1-2wks until target dose

aim for 8-12 wks at target dose before making a determination on efficacy (benefits often takes 1-2mo to emerge)

**usually dosed daily but can be given episodically prior to triggers (exercise, menstruation)

How to handle ineffectiveness and partial ineffectiveness of prophylactic Txs

partial response: combo

no response: switch

First line prophylactic agents

BB and TCAs *****

Candesartan, topiramate

Which BB have most evidence for prophylactic migraine Tx

propranolol, metoprolol

AE of BB

fatigue, decreased HR/BP, vivid dreams (propranolol), mask hypoglycemia in T2DM

Important drug Int with propranolol

inhibits metabolism of rizaptriptan (use lower riza dose or switch triptans)

**or just use metoprolol

TCAs used for migraine prophylaxis

amitriptyline, nortriptyline (less ev and more expensive but better tolerated)

AE TCAs

anticholinergic, dizzy, drowsy, fatigue, weight gain

topiramate SE

sedation, renal stones, weight loss

topiramate considerations with females

teratogenic, CI In preg, if women with child bearing age must ensure adequate contraception (preferably avoid)

topiramte drug int

Many CYP450

Candesartan SE and monitoring

decreased BP, increased K (monitor SCr, electrolytes, BP), cough, rash

2nd line migraine prophylactic agents

Herbals: Mg, Riboflavin

CGRP antagonists (Fremanezumab (Ajovy), Erenumab (Aimovig), Galcanezumab (Emgality))

SNRI: Venlafaxine, Duloxetine

CCB: Verapamil, Flunarizine

Divalproex

When are CGRP antagonists used as prophylactic

usually fail 2 oral agents

AE CGRP antagonists SC

injection site rxns, hypersensitivity, htn

SNRI ae

increased HR, BP, tremor, agitation, insomnia (take qAM), sweating, decreased appetite, anticholinergic

CCB side effects

decreased HR, BP, constipation

DI with verapamil

Why is topirimate first line prophylaxis but DVP is second

as effective but more costly and less well tolerated

DVP SE

sedation, nausea, hair loss, weight gain, rash

if someone is a smoker what med may you use for prophylaxis

notriptyline

3rd line prophylactic agents

Pizotigen (5HT2 antagonist)

CCBs: lisinopril, telmisartan

gabapentin

other herbals: butterbur, feverfew, coenzyme Q10, melatonin

Botox (only effective if >/=15 h/a days per month)

if someone has insomnia what prophylaxis med may you use

amitriptyline

if someone has htn what prophylaxis med may you use

BB, candesartan, lisinopril, or possibly verapamil

if someone has chronic pain what prophylaxis med may you use

amitriptyline, venlafaxine, duloxetine, topiramate, gabapentin

if someone has depression/anxiety what prophylaxis med may you use

venlafaxine, duloxetine or amitriptlyine

optimize non pharm (CBT, lifestyle changes)

what is considered resolution of MOH

return to episodic h/a (<15 days per mo); allow 3mo to establish new baseline

options to Tx MOH

1. stop overused med abruptly

2. stop or taper the overused med while starting prophylactic med

3. start prophylactic med only (as h/a decreases, overused meds can be decreased)

also bridging stratgey?

pros/cons of stopping overused med abruptly in MOH

Pro:

• avoids additional long term meds, cost, ae

• may start prophylaxis meds later after w/d

Con:

• increase potential for worsening w/d sx in the short term

• pt may be unable to tolerate w/d Sx

• if unsuccesful may need to initiate prophylaxis

pros/cons of stopping/tapering overused med while starting prophylactic med in MOH

Pro:

• may give best chance of success

• addition of prophylaxis helps prevent MOH in future

• prophylaxis may decrease pts fear of w/d

Con:

• increased cost and inconveniance (starting prophylaxis daily)

• increased potential of ae

• prophylaxis can take 8-12wks to see full benefit, if unsuccessful with starting prophylaxis may need to initiate w/d later

• increased potential for worsening sx in short term

pros/cons of starting prophylactic med only in MOH

Pro:

• decrease potential for severe and sudden w/d sx

• may give best chance of success

• prophylaxis may decrease pts fear of w/d

• addition of prophylaxis help prevent MOH in future

Con:

• increased cost and inconveniance

• increased potential for ae

• prophylaxis can take 8-12wks to see full benefit therefore if unsuccesful may need to initiate w/d later

withdrawal symptoms MOH

headaches increase in severity and freq before they improve

anxiety, nausea, vomiting, problems with sleep can occur

Sx usually last 2-10 days but can be 2-4 weeks

which meds must be tapered off vs abruptly d/c

simple analgesics, triptans, ergotamine can d/c abruptly

opioids and butalbital can be d/c abruptly if only periodic use; if chronic use/high dose must taper (over 2-4wks guided by pt response)

what is bridging strategy for MOH

consider temporary meds if w/d sx are not manageable (have smth prn or regular for first 1-2wks)

may need something daily for a few weeks while waiting for prophylaxis to kick in (or even if not using prophylaxis)

meds used: NSAIDs, prednisone, metoclopramide, avoid opioids and barbituates

non pharm strategies for moh

to prevent relapse, non-drug alternatives should be emphasized

20min relaxation period daily (eyes closed, muscles relax)

avoid pressure on head and neck muscles (ex: holding chin down while reading, reading in poor light, phone on shoulder)

recognize warning sx (jaw clench, tight neck, pressure behind eyes)

cold compress/ice packs on back of neck (20 on 10 off)

moist or hot pack may help

finger pressure in area of h/a, massage

avoid alcohol