ic5 - headaches and migraines Flashcards
what do you use to classify headaches and how would you classify them
classify into primary, secondary and neuropathies, facial pain and others
[primary] migraine, tension type headaches, trigeminal autonomic cephalagias, other primary HA disorders
[secondary] trauma/ injury to head and/or neck, cranial or cervical vascular disorder, non vascular intracranial disorder, infection, homeostasis disorder, HA or facial pain attributed to disorder of any facial feature, psychiatric disorder
[neuropathies, facial pain and others] painful lesions of the cranial nerves and other facial pain, other HA disorders
what do the red flags s/sx point towards to
they point towards secondary headache
what are the red flags of headaches
use SNNOOP10 guide
systemic sx like fever
neoplasm (hx of)
neurologic deficit or dysfunction
onset of HA sudden or abrupt
older age (>50yo)
pattern change or recent onset of HA
positional headache
precipitated by sneezing, coughing or exercise
papilledema
progressive HA with atypical presentation
pregnancy or puerperium
painful eye with autonomic features
post traumatic onset of headache
pathology of immune system (HIV/ immunocompromised)
painkiller overuse or new drug at onset of HA
what are the types of tension headaches
episodic (frequent or infrequent) and chronic
[episodic infrequent] >10 HA <1d/m on average, <12 HA a year
[episodic frequent] >10 HA occurring on 1-14d/m on avg for >3m
[chronic] HA on more than 15d/m for >3m and assoc with vit deficiencies
what are the risk factors of tension headache
females (3:2), depression and anxiety disorders, insomnia, temporomandibular joint disorder, vitamin deficiencies (B12, D)
what are the clinical features of tension headaches
gradual or constant onset
mild to moderate intensity
characteristics: non pulsating, tightening/ pressing, band/ visor like, fullness
location: bilateral, frontal, nuchal occipital
better in the morning, worse in the evening
may not worsen with activity but improve with rest
others: difficulty concentrating, muscle stiffness and tightness, decr in appetite, some sensitivity to light and sound
no prodrome, N/V or aura sx
what is the diagnostic criteria of tension headache
more than two of the following: bilateral, non pulsating, pressing/ tightening pain, mild to moderate, not worse with exertion
no N/V, not both photo and phonophobia
at least 10 of such headache episodes that occur for at least 30mins within 7 days
exclude other possible causes through imaging or redflags s/sx
what are the triggers for tension headaches
dehydration hunger, sleep deprivation, anxiety or stress, poor posture (excessive neck flexion), alcohol, caffeine, cold or flu or sinus infection, noise exposure
why might episodic tension headaches become chronic in nature
it can become chronic if there is central sensitisation (incr responsiveness of nociceptors in CNS)
what is the goals of tx for tension headaches
pain relief and prevent progression to chronic TTH
what is the tx for tension headaches
identify and avoid triggers (usage of headache diary) and pt education
self limiting, rest
pharmacological acute tx: [for episodic] paracetamol (alone or w caffeine), aspirin, NSAIDs [for chronic] tricyclic antidepressants and cognitive behavioral therapy
pharmacological for prophylactic tx: amitriptyline (first line), mirtazapine, venlafaxine
non pharm tx: CBT, biofeedback, relaxation, physical and/or occupational therapy, lifestyle modification incl sleep hygiene
what drugs is assoc with tension headaches resulting from medication overuse
paracetamol, NSAIDs, opioids, triptans, barbiturates
how might tension headaches arise from medication overuse
typically headache -> medication -> pain relief
but in this case, headache -> medication -> short term pain relief -> rebound headache -> higher medication doses -> short term pain relief (viscious cycle)
how would you classify migraines
episodic (migraine without aura migraine with aura) and chronic migraines
[episodic migraine] at least 5 migraine attacks lasting 4-72h during lifetime
-> then look at w/wo aura
[episodic migraine wo aura] at least 5 attacks fulfilling (i) to (iii)
(i) headache attacks lasting 4-72h
(ii) headache has at least 2 of the following: unilateral, pulsating, moderate to severe, aggravation or causing avoidance of routine physical activity
(iii) phono/photophobia, N/V during headache experience
[episodic migraine w aura] at least 2 attacks fulfilling (i) and (ii)
(i) at least 1 of the following fully reversible aura sx: visual, sensory, speech and/or language, motor, brainstem, retinal
(ii) at least 3 of the following: at least 1 aura sx spread gradually over 5mins or longer, aura sx occur in succession, each individual aura sx last 5-60min, at least one aura sx is unilateral, at least one aura sx is positive, aura is accompanied or followed within 60mins by headache
[chronic migraine] at least 15 MHDs and at least 8 MMDs for >3m
what does MHD and MMD refer to
MHD is monthly headache day which refers to a day with migraine type or tension type headache
MMD is monthly migraine day which refers to at least 2 migraine characteristics
what are the phases of a migraine attack
phase 1: premonitory - lasts few hrs to days (fatigue, cognitive difficulties, mood changes, food cravings, yawning, neck pain)
phase 2: aura - 5-60mins (visual, retinal, motor, brainstem, speech and/or language, sensory)
phase 3: HA - 4-72h (N/V, photo/phonophobia)
phase 4: postdrome - <12-24h (feeling tired or weary, difficulty concentrating, neck stiffness)
what is the tx for migraines (acute and adjuntive)
[acute tx] NSAIDs, triptans, ergotamine, MAb that blocks CGRP receptor or CGRP
[adjunctive tx] antiemetics
what is the moa of NSAIDs
anti inflamm, analgesic and antipyretic properties mediated by blockade of COX enzymes and subsequent inhibition of PG synthesis
what is the moa of triptans (vs sumatriptan)
triptans are 5HT1B and D receptor agonists that results in a decrease in trigeminal neuronal activity and causes vasoconstriction of cerebral blood vessels, inhibition of vasoactive peptide release by trigeminal neurons and inhibition of nociception
sumatriptan is a selective 5HT1D receptor agonist and thus causes vasoconstriction in carotid artery circulation but does not alter cerebral blood flow
what are the indications for triptans
for acute tx of migraine if analgesics do not adequately relieve pain
largely replaced ergot alkaloids as triptans have better s/e profile bc ergotamine has greater vasoconstrictive effects
what are the c/i for triptans
HTN, coronary heart disease, raynaud’s disease, pregnancy and lactation, hx of ischemic stroke
due to its vasconstrictive effects
what is the significance of CGRP (structure, function, role in migraine attack)
calcitonin gene related peptide (CGRP) is present in trigeminal nerve fiber and vessels which triggers the whole cascade of pain to spread
CGRP is a 37AA peptide found throughout body that functions as a vasodilator
levels of CGRP found to increase during a migraine attacks
list the drugs that are CGRP receptor blocker and CGRP blocker
CGRP receptor blockers are erenumab and -gepants (atogepant, rimegepant, ubrogepant)’
CGRP blockers are -zumab (eptinezumab, fremanezumab, galcanezumab)
what is the moa of -gepants
CGRP receptor antagonists which binds to CGRP receptors and prevent signalling
compare the difference between antiCGRP Ab and antiCGRP receptor Ab
anti-CGRP Ab binds to CGRP
anti-CGRP receptor Ab binds to CGRP receptor
what is the potential indication for anti-CGRP Ab
for use of prevention of migraines (certain -gepants)
what are the limitations of anti-CGRP therapies
CGRP hypothesised to act as a ‘vasodilator safeguard’ during ischemia thus mild and transient ischemic events might be worsened if receive long term CGRP blockade tx
and long term safety data required
list an example of antiemetics and why might it be used
metoclopramide to address N sx
how to assess efficacy of tx
headache diary, disability assessment (eg. MIDAS score), s/e from medications
what is the criteria for migraine prophylaxis
there are two criterias for migraine prophylaxis: AHS and EHF
AHS is based on number of HA days per month and degree of disability caused by attacks
EHF states to offer if not well controlled with acute tx alone
[AHS] prevention offered if (i) at least 6 MHDs with no disability (ii) at least 4 MHDs with some disability (iii) at least 3 MHDs with severe disability; prevention considered if (i) 4-5 MHDs with no disability (ii) 3 MHDs with some disability (iii) 2 MHDs with moderate disability
[EHF] migraine prophylaxis indicated if (i) migraine impairs QoL AND (ii) (a) attacks cause disability on 2 or more days per month and optimised acute tx does not prevent above OR (b) risk of overfrequent use of acute tx and pt willing to take daily meds
what are the drugs used for migraine prophylaxis
BB, antiepileptics
what are some migraine triggers
nutritional deficiencies
dairy products
processed food
sugar
alcohol
not eating
chocolate
weather
lights
neck pain
exercise
sleep disturbances
sleeping late
heat
muscle ache
excessive sexual activity
perfume or odor
allergies
hormone disruption
sinuses
smoke
stress
environmental stress
caffeine
MSG
artificial sweeteners
gluten
