IC5 Flashcards
what is the SNOOP10 guide? list the guide
red flags for secondary headaches:
SN2O2P10
systemic symptoms eg fever
neoplasm (abnormal mass)
neurologic deficit/dysfunction
onset sudden or abrupt
old age >50y/o
pattern change
positional headache
precipitated by sneezing, coughing, exercise
papilledema
progressive w/ atypical presentation
pregnancy/puerperium
painful eye w/ autonomic features
post traumatic onset
pathology of immune system (HIV/immunocompromised)
painkiller overuse/new drug.
history taking for headache
LOTAARRRP
location
onset
type
associated = any weakness, dizziness, FEVER?
recurring = frequency? quality
precipitating = exercise, sneezing, coughing? recent injury? painkiller use?
get history of painkiller use.
distinguishing features of primary headache (tension-type)
include pain location ,type, intensity, QOL, other symptoms, duration
bilateral pain
tightening
mild-moderate
does not affect/affected by daily activities
no other symptoms
30min to 7 days
distinguishing features of primary headache (migraine)
include pain location ,type, intensity, QOL, other symptoms, duration
unilateral pain
throbbing
moderate-severe
affects/affected by daily activities
nausea/vomiting, sensitivity to light, sight, aura
4-72hours
distinguishing features of primary headache (cluster headache)
include pain location ,type, intensity, QOL, other symptoms, duration
unilateral pain
variable
severe-VERY severe
restless/agitation
cranial autonomic symptoms on the side of the headache (runny nose, congestion, watery/swollen/red eye)
15-180min
what is the clinical presentation of TTH?
NO premonitory symptoms and aura
bilateral
non-pulsatile tightness or pressure
mild-moderate
pericranial/cervical muscle tenderness
ICHD3 classification for infreq ETTH?
frequency of atleast 10 headache episodes occuring on avg <1 day/month (<12days/year)
duration 30min-7 days
and any of the following:
1) two of the following:
- bilateral
- pressing/tightening non pulsatile
- mild-moderate
- not aggravated by routine phy activity
2) both of the following
- no N/V
- no more than one of photophobia/phonophobia
3) not better accounted for by another ICHD3 diagnosis
ICHD3 classification for frequent ETTH?
frequency of atleast 10 headache episodes occuring on avg 1-14 days/month (12-180days/year)
duration 30min-7 days
and any of the following:
1) two of the following:
- bilateral
- pressing/tightening non pulsatile
- mild-moderate
- not aggravated by routine phy activity
2) both of the following
- no N/V
- no more than one of photophobia/phonophobia
3) not better accounted for by another ICHD3 diagnosis
ICHD3 classification for CTTH?
frequency of ≥15 days/month on avg >3 months (≥180days/year)
duration hours to days, or unremitting
and any of the following:
1) two of the following:
- bilateral
- pressing/tightening non pulsatile
- mild-moderate
- not aggravated by routine phy activity
2) both of the following
- neither moderate or severe N/V
- no more than one of photophobia/phonophobia/mild nausea
3) not better accounted for by another ICHD3 diagnosis
triggers for TTH?
physical emotional stress
activities where head is held in one position for a long time
alcohol
caffeine
cold/flu or sinus infections
dehydration
hunger
TTH pathophysiology?
myofascial mechanisms? = due to head being in the same position for long?
vascular mechanisms? = increased or abnormal blood flow in the cerebral arteries
= both peripheral sensitisation
genetic disposition/polymorphism?
central mechanisms? = altered pain perception and dysfunction in descending pain modulation?
goals of therapy for TTH?
pain relieve
prevent progression to chronic TTH
consider patient education to identify triggers, eg. a headache diary
acute phx management for TTH?
paracetamol (alone or with caffeine)
aspirin
NSAIDs: ibuprofen, naproxen, diclofenac, ketoprofen
prophylactic phx management for TTH
amitriptyline (1st line) (TCA)
mirtazapine, venlafaxine
non phx management for TTH?
cognitive behavioural therapy, biofeedback, relaxation
physical and/or occupational therapy
lifestyle modification (include sleep hygiene)
proposed phases (and duration) of migraine attack?
prodrome
- hours to days
aura
- 5-60min
headache
- 4-72 hours
postdrome
- <12-24h
what are some prodrome symptoms in migraine
fatigue
cognitive difficulties
mood changes
food cravings
neck pain
yawning
aura symptoms in migraine
related to cortex and cortical spreading
- visual aura
- sensory and speech disturbance
- motor symptoms.
headache symptoms in migraine
nausea with or without vomitting
photophobia
phonophobia
post-drome symptoms in migraine
tired or weary
difficulty concentrating
neck stiffness
ICHD3 criteria for migraine without aura
A. At least 5 attacks fulfilling criteria B-D
B. Headache attacks lasting 4–72 hours (when untreated or unsuccessfully treated)
C. Headache has at least 2 of the following 4 characteristics:
1. Unilateral location
2. Pulsating quality
3. Moderate or severe pain intensity
4. Aggravation by or causing avoidance of routine physical activity (e.g., walking or climbing stairs)
D. During headache at least 1 of the following:
1. Nausea and/or vomiting
2. Photophobia and phonophobia
E. Not better accounted for by another ICHD-3 diagnosis
ICHD3 criteria for migraine with aura
A. At least 2 attacks fulfilling criteria B-C
B. At least 1 of the following fully reversible aura symptoms:
1. Visual
2. Sensory
3. Speech and/or language
4. Motor
5. Brainstem
6. Retinal
C. At least 3 of the following 6 characteristics:
1. At least 1 aura symptom spreads gradually over ≥5 minutes
2. 2 or more aura symptoms occur in succession
3. Each individual aura symptom lasts 5–60 minutes
4. At least 1 aura symptom is unilateral
5. At least 1 aura symptom is positive
6. The aura is accompanied, or followed within 60 minutes, by headache
D. Not better accounted for by another ICHD-3 diagnosis
ICHD3 classification for chronic migraine
≥15 monthly headache days (MHD)
≥8 monthly migraine days (MMD)
for >3 months
criteria for MMD
≥2 migraine characterics: unilateral, pulsating, mod/severe, aggravated by QOL
AND if no aura, ≥1 of following
- photophobia/phonophobia, N/V
nonphx management of migraine
patient education and empowerment
- identify triggers
- headache diary
- adopt a healthy lifestyle (regular eating, sleep, exercise habits).
acute treatment goals for headache
rapid, consistent freedom from pain and associated symptoms, without recurrence
restored ability to function
minimal need for repeat dosing/resuce meds
optimal self care and reduced subsequent use of resources
minimal or no adr
cost-effective tx
what are the drugs with established efficacy for migraine
triptans
ergotamine derivatives
gepants
lasmiditan
nonspecific: NSAIDs (eg diclofenac, ibuprofen, naproxen), paracetamol+caffeine
principles for acute treatment of migraine
what to consider for tx of acute migraine, eg treatment plan?
acute treatment should be taken as early as possible. =should have significant beneficial response in 2h, 24h pain free sustained response, and reduced disabiltiy during attacks
stratified approach by starting with simple analgesics. (parecetamol > nsaids > triptans)
consider anti emetics with N/V symptoms
choose appropriate dosage forms and formulation
eg nausea exacerbated with water= choose orally disintegrating tablets
eg severe n/v or full-blown symptoms = parenteral formulation
MOA of NSAIDs for migraine
inhibit prostaglandin synthesis
= prevent subsequent neurogenically mediated inflammation in the trigeminovascular system.
indication for NSAIDs in migraine (and ones with established efficacy)
aspirin
diclofenac
ibuprofen
naproxen
celecoxib
adr of NSAIDs in migraine
hypersx, GI (dyspepsia, N/V/D), CNS (drowsy/dizzy)
c/i or caution for nsaid in migraine
previous PUD, renal disease, severe CVD, hypersx
triptans MOA
5ht1b and 5ht1d selective receptor agonist
- vasoconstriction of intracranial extracerebral blood vessels
- inhibit vasoactive peptide released by trigeminal neurons
- inhibit nociception transmission within trigeminocervical complex.
C/I for triptans
stroke/TIA
ischemic CAD
coronary artery vasospasm
uncontrolled HTN
PVD
GI ischemia
history of hemiplegic/basilar migraine
how to use triptans for migraine
take early in course of attack
pain intensity is mild
if there is lack of response, switch to another triptan
some patients experience recurrence within 48h = take an additional dose
ADR triptans
pressure on chest
nausea
fatigue
distal paraesthesia
DDI for triptans
concurrnet ergotamine/ergot type medication within 24h
concurrent MAOi or within 2 weeks of discontinuation of MAOi therapy (sumatriptan broken down by MAOi)
ergotamine MOA and locally available drug
local: ergotamine1mg/caffeine100mg
ergotamine:
1) 5ht1b/1d on intracranial vessel vasoconstriction
2) inhibit NE uptake at alpha-adrenoreceptor = prolonged vasoconstriction (more concern with ischemic ADR)
caffeine: adenosine A1, A2A, A2B receptor antagonist = vasoconstriction cerebral vasculature
may also enhance GI absorption of ergotamine by increase solubility of ergotamine and decrease GI pH.
ADR of ergotamine
N/V
cramps
insomnia,
transient lower limb muscle pain
Contraindications of ergotamine
stroke/TIA
ischemic CAD
coronary artery vasospasm
uncontrolled HTN
PVD
GI ischemia
history of hemiplegic/basilar migraine
DDI or ergotamine (and outcome)
concurrent triptans 24h
potent cyp3a4 inhiibtors
increases the risk for vasospasm = cerebral ischemia AND/OR schema of extremities
opiod use in migraine?
not recommended due to lack of evidence, risk of dependence/abuse/withdrawal syndrome
criteria for initiating gepants and ditans for migraine?
prescription from licensed clinician
patients atleast 18 y/o
diagnosis by ICHD3 migraine with aura, migraine without aura, chronic migraine.
either of the following: contraindicated to/unable to tolerate triptans, inadequate response to ≥2 triptans.
criteria for medication overuse headache
occuring ≥15days/month in patients with pre-existing headacheh and developing as consequence of regular overuse of acute or symptomatic hradahce medication
paracetamol or ≥1 nsaid on ≥15 days/month for >3 months
triptan or ≥1 opioid on ≥10 days/month for >3months
criteria for preventive treatment
AHS guideline
prevention should be offered if
≥6 MHD, no degree of disability
≥4 MHD, some degree of disability
≥3 MHD, severe degree of disability
EHF guideline
prevention offered if
1) migraine impairs quality of life
AND either
2a) attack cause disability on ≥2 days per month and optimised acute therapy does not prevent the above
2b) risk of over frequent use of acute therapy and patient willing to take daily medication.
what is CGRP involvement in migraine?
CGRP neuropeptide rises during migraine episodes = contribute to inflammatory processes, neurogenic inflammation, blood flow in the cerebral (smooth muscle) blood vessels, and pain transmission
what are the antiCGRP therapies
gepants
anti-CGRP antibodies
anti-CGRP receptor antibodies
medications with evidence of efficacy for preventive migraine treatment
parenteral: eptinezumab, erenumab, fremanezumab, galcanezumab
oral:
heart drugs:
candesartan,
metoprolol, timolol, propanolol
anti seizure:
valproate sodium, divalproex sodium
antimigraine:
frovitriptan
what is the mechanism of action of gepants
CGRP receptor antagonists, which bind to CGRP receptor and prevent signalling
what is the mechanism of action of antiCGRP antibodies and examples?
prevent CGRP from interacting with the receptor
includes monoclonal antibodies like eptinezumab and other -nezumab drugs.
what is the MOA of antiCGRP receptor antibodies and any examples?
bind to CGRP receptor and prevent signalling
monoclonal antibody = erenumab
what are some ADRs of CGRP blockade (including clinically reported and animal studies)
clinically reported:
GASTRO: constipation, nausea
BLOOD: raynaud (decreased blood flow to finger), hypertension
BONE: joint pain
THROAT: nasopharyngitis.
animal studies
- delayed wound healing
- block cardiopulmonary protective effect
- decreased survival in sepsis model
- bone loss
- reproductive toxicity
studies on long term use of CGRP receptors?
unknown. may not want to use long term because effects are unknown?
role of CGRP in the body
endogenous CGRP has multiple protective roles in CNS, immune, skin, GI, bone, pregnancy, endocrine, cardiovascular.
criteria for initiating CGRP mABs
meet 1 and 2 + either 3-5
1) prescribed by licensed clinician
2) ≥18 y/o
3) diagnosis of ICHD3 migraine with or without aura + inability to tolerate/inadequate RESPONSE to 8 WEEK trial dose to the other meds/treatment (4-7MMDs)
4) - ICHD3 migraine with or without aura …. (MIDAS or HIT)
5) ICHD3 chronic migraine and…
contraindication or inability to tolerate 2 or more oral triptans
what is the criteria for continuing CGRP mABs
either
1) reduction in mean MHDs or headaches of at least moderate severity of ≥50% relative to the pretreatment baseline
2) clinically meaningful improvement in any specific outcome measureMENTS
eg MIDAS decrease ≥5pts if 11-20
by 30% if >20
principles for preventive treatment of migraine
4S 1O
1) start low and titrate
- if there is partial but suboptimal response or dose limiting ADR= consider combining preventive drugs from diff classes.
2) reaching therapeutic dose
- set initial target dose and stop titration once maximal dose reached, efficacy optimal, AE become intolerable.
3) set adequate trial
- minimum 8 wks at target therapeutic dose before effectiveness can be determined = switch if no response after the 8 weeks.
- min 3 months for monthly injectable cgrp dosing and 6 months for quarterly dosing.
4) set realistic expectations
- define treatment success for the patient: 50% reduction in freq, significant decrease in attack duration? severity? improved response to acute treatment? reduction in disability and improve in QOL? psychological distress?
5) optimise drug selection and maximise adherence
- tolerability, headache subtype, concomitant meds, weight, ease of use, contra VS patient preferences… comorbis, preg, response, cost, insurance coverage.
how to assess treatment efficacy
headache diary
disability assessment eg MIDAS
grade: 0-5, 6-10, 11-20, 21+
ADR
migraine pathophysiology in depth (relate to prodromal symptoms):
prodrome
- neuropeptides, hypothalamus activation
- hypothalamus affects homeostatic functions resulting in changes in appetite, fatigue..
aura
- cortical spreading depression.
- due to hyperexcitation (depolarisaiton wave that inhibits cortical actvity = reduced blood flow) followed by depression in brain activity.
headache
- CGRP invovlement = sensitisation of peripheral/central trigeminovascular system= pain
prodrome
- similar to prodrome.
