ICL 10.1: Primary Headache Flashcards
what is a primary headache disorder?
headache is the primary feature of the disorder and is not otherwise explained by a significant structural, genetic, or metabolic cause
what are the 3 types of primary headache disorders?
- migraine deadaches
- tension-type headaches
- cluster headaches
there’s also chronic daily headache and medication overuse headaches
24 yo woman w/ pmh anxiety, depression, POTS disease, migraines, presents to ED for new onset R facial paresthesias and severe R frontal headache. She reports current headache similar to migraines, however, has never had tingling followed by numbness of her face before.
Headache features: R frontal initially, now holocephalic, 10/10 pounding
Associated sx: nausea no vomiting, photo/phonophobia, neck stiffness
Exam: VS w/ BP 160s, HR 110 , exam with right facial subjective sensory loss to lt, pp
diagnosis?
migraine!
what populations are effected by migraines?
3:1 females
22-55 years old
what are the ICHD-III diagnostic criteria for a migraine?
at least 5 episodic recurrent headaches lasting 4-72 hours with any 2 of the following pain qualities:
1. unilateral pain
- throbbing pain
- pain worsened by movement
- moderate or severe pain
PLUS 1 of these associated symptoms:
1. nausea
- vomiting
- photophobia and phonophobia
it must also not be better accounted for by another ICHD-3 diagnosis!
what is a migraine aura? what type of aura is the most common?
usually 5-60 minutes, though can be longer –> so these are a lot longer than seizure or TIA auras!
occurs in 25-30% of migraines so not all migraines are preceded by an aura and not all auras are necessarily followed by migraine, they can occur without any headache
visual aura > sensory aura > language aura > motor aura
what is the most common visual migraine aura?
usually the aura people have is a shimmering arc of white or colored lights followed by a blind spot
what is the most common sensory migraine aura?
unilateral paresthesias that progresses to increased numbness
most common in face, tongue, hand
they spread slowly
vs. TIA: sx spread fast
vs. stroke would only have numbness, no tingling
vs. seizure would have tingling with no numbness
what is the most common language migraine aura?
mlild to severe aphasia
occurs when headache is mild vs. pain related difficulty speaking
what is the most common motor migraine aura?
aka hemiplegic migraine
this is the least common type of aura and it usually involves unilateral limb or facial muscles
patients usually have some other type of aura as well
hard to distinguish from stroke….
there is a well described in familial type of hemiplegic migraine
what is the pathophysiology of a migraine?
it’s a disorder of neuronal dysfunction which leads to vascular changes occurring secondarily
then the final common pathway is activation of the trigeminovascular system which then effects the dura and meninges which presents as pain
what is cortical spreading depression?
an electrophysiologically measurable wave of hyperexcitation and increased blood flow, followed by period of reduced neuronal firing, reduced blood flow, that spreads across cortex that happens during a migraine!
this propagation of cortical spreading depression requires activation of NMDA receptors in cortical neurons –> glutamate is the neurotransmitter that’s responsible
the bimodal pattern in cortical spreading depression aka the activation followed by suppression, may explain the migraine aura characterized by positive symptoms like scintillations and tingling which are then followed by negative symptoms like scotoma and numbness
decreased cortical blood flow in humans during migraine aura insufficient to cause injury in normal brain
what causes a migraine?
we don’t really understand it but it’s thought to begin when an episode of diffuse neural dysfunction leads to a cascade of events including vasodilation of cerebral blood vessels and activation of the trigeminovascular system
the dilated cerebral blood vessels cause irritation to the trigeminal nerve endings
this irritation results in the release of vasoactive neuropeptides such as CGRP and substance P from the trigeminal nerve endings which exacerbate vasodilation by producing neurogenic inflammation which is felt as pain
pain impulses from the dilation and inflammation are transmitted from the trigeminal nerve to the trigeminal nucleus caudalis in the brain stem and this is what plays the most important role in processing migraine pain because it relays it to higher-order neurons in the thalamus and cortex resulting in the referred pain that could be perceived anywhere along the trigeminocervical network –> this is why patients may perceive migraine pain in various locations in the head, face and neck
what happens when the trigeminal nucleus caudalis in the brain is activated?
it results in referred pain and cutaneous allodynia (sensitivity to touch)!
this is what happens in a migraine!!
so everything starts in the cortex with diffuse neuronal dysfunction which leads to dilation of the cerebral blood vessels which leads to irritation of the trigeminal nerve endings which results in release of vasoactive NT which causes inflammation and pain which gets transmitted to the TNC which then relays it to the thalamus and cortex which causes referred pain in the dermatomes of the trigeminal nerve
what is central sensitization?
central sensitization is a time-dependent physiologic event which leads to chronic pain
during a migraine attack, neuronal pathways become sensitized in stages!!
- peripheral neurons are activated early in the attack (mild pain phase)
- central neurons are activated later in the attack (full-blown migraine)
if you don’t treat a migraine, these central neurons can become sensitized and continue to fire/cause pain regardless of treatment further into migraine –> but if the pain is stopped early, the cascade of pain responses can be controlled; pain-free results are more easily achieved if pain is treated BEFORE central sensitization occurs
what medication is used to treat migraines?
triptans
how do triptans treat migraines?
during peripheral sensitization of neurons in a migraine, neurons will act on the dura and the second order neurons which can cause pain and throbbing
if you give triptan, it compresses blood vessels and decreases activation of 1st order neurons so that they are no longer acting on the dura and second order neurons and you no longer have pain and throbbing!
however, if you wait until there is central sensitization, both the peripheral first order and central second order neurons are sensitized which leads to full blown migraine with pain, throbbing and allodynia!
if you give triptan now, you stop the peripheral neuron from releasing NTs but the secondary central neuron is also sensitized and the triptan doesn’t work on it – so you decrease pain in the dura and stop the throbbing but there’s still cutaneous allodynia and other symptoms because the central neuron is already sensitized and it’s too late
this is why it’s so important to treat migraines at onset before central sensitization occurs!
what causes bilateral head pain during a migraine attack?
usually migraine have unilateral headache pain but it can sometimes be experienced bilaterally during a migraine
this could be due to referred pain as a result of the activation of bilateral pathways which include the TNC, trigeminal ganglia, and trigeminal nerve
what causes posterior head and neck pain during a migraine?
activation of the TNC can result in referred migraine pain to all regions supplied by the upper cervical nerves (C2, C3, C4, C5)
what information should you elicit during a headache history?
- history
- physical and neurologic exam
- headache characteristics = onset, timing, aura, location, radiation, pain characteristics, duration, frequency, associated signs, exacterbating/relieving factors
- quality of life = ED visits, days or work or school missed, etc.
- headache risk factors = history of head trauma, history or meningoencephalitis, family history
when would you consider doing imagining for a headache?
- change in character
- abnormal neurologic exam
- unresponsive to first line therapy
- PMH suggestive of cancer, MS, stroke, TIA
how do you diagnose a migraine?
clinical!!
you don’t need imaging unless something changes, there’s neuro deficits, or you suspect it’s something else
what is status migrainosus?
migraine attack lasting for more than 72 hours without a headache-free interval of more than 4 hours
what is the emergency treatment for migraine?
- high dose oral NSAIDs
- sumatriptan injection
- IV cocktails = NS bolus + benadryl + anti-nausea + ?
NS bolus is because most patients are dehydrated plus if you’re giving nausea meds and magnesium, both can cause hypotension so give a bolus
NO ROLE OF OPIATES IN MIGRAINE TREATMENT
what are the abortive medications people can use if they’re having a migraine?
abortive means something they can take when they’re having a migraine to break the pain
- NSAIDs
- triptans
use early in highest dose tolerated
- ergots = vasoconstrictors
ergots and triptans contraindicated in cerebral vascular and cardiovascular disease because it constricts blood vessels
what preventative therapies can you give people who are having many headaches/really long lasting headaches?
- life style changes = sleep, exercise, triggers, caffeine, stress, hydration, meditation*****
- antidepressants
- atiepileptics = valproic acid or topiramate
- CGRP monoclonal antibodies
- herbals, vitamines, minerals = riboflavin, magnesium
- antihypertensives = B-blockers like propranolol or timilol
- other = botox, melatonin
what is a tension type headache?
your “regular” headache – it’s the most common type of headache in the general population
it’s fairly uncommon amongst patients seeking medical treatment for headaches – they don’t go to the ER or neurologist for them, they just take NSAIDs or self treat
average age of onset: 20-30 yo
male: female = 4:5
what is the pathophysiology of a tension headache?
unknown
myofacial nociception may be more important in episodic TTH
central sensitization generated by prolonged nociceptive input from the periphery is likely crucial in the pathophysiology of chronic TTH
what is the ICHD-III diagnostic criteria for a tension type headache?
Must experience at least 10 headaches, each lasting 30 minutes to 7 days, with 2+ of these features:
- bilateral headache
- constant* non-throbbing, steady, pressure-like
- mild to moderate intensity
- not worse with physical exertion
MUST have:
1. absence of nausea and vomiting
- absence of photophobia and photophobia together (presence of only 1 doesn’t rule out the diagnosis)
- no aura
chronic TTH = 15 or more days w/ headache / month and is a subtype of chronic daily headache
how do you treat tension type headache?
- NSAIDS > acetaminophen
- combination analgesics like caffeine (but higher risk of rebound headaches)
combos with barbiturates like codeine are NOT recommended because of the risk of dependence
prophylaxis: if frequency more than ~2 days/week and intensity causing disability and there’s no proper response to abortive therapy, then you can try preventatives like tricyclic antidepressant or behavioral therapy
32 yo man presents w/ 6 month history of unilateral headache around L eye. Headaches occur 10 times daily, each headache lasts 20 minutes, though no pain btw/ headaches.
Associated sx: Ipsilateral conjunctival injection, tearing
Exam: Normal
MRI: Normal
cluster headache
what is the most painful type of primary headache?
cluster headache
described as worse than childbirth and renal stones
what is a cluster headache?
- no aura
- peak pain in 10 to 15 minutes
- cluster attack: duration 15 min to 1 hour
- unilateral and localized pain; retroorbital/frontal/temporal; excruciating, boring, burning, not throbbing
- average 1 to 3 attacks a day
- cluster bout: weeks to months, period where person is susceptible to cluster attacks (usually at night)
- 1% of population, men > women, peak incidence btw 20-40 yo
what are some triggers of cluster pain?
- alcohol
- histamine
- nitroglycerine
- hypoxia
what is the clinical presentation of someone having a cluster headache?
Ipsilateral Conjunctival Injection and/or lacrimation
Ipsilateral nasal congestion and rhinorrhea
Ipsilateral eyelid swelling
Ipsilateral forehead sweating
Ipsilateral miosis and/or ptosis (Horner’s syndrome)
Restlessness agitation
Pacing and rocking
Face and head lowered
Hand rubbing the painful area
Violent or self harm
Suicidal
what is the ICHD-III criteria for a cluster headache?
at least 5 attacks with the following criteria:
- severe or very severe unilateral orbital, supraorbital, or temporal pain lasting 15-180 minutes if left untreated
- at least 1 of the following symptoms of signs, ipsilateral to the headache = conjunctival injection or lacrimation, nasal congestion or rhinorrhea, eyelid edema, forehead and facial sweating, forehead and facial flushing, sensation of fullness in the ear, mitosis or ptosis
- sense of restlessness or agitation
- attacks have a frequency between 1 every other day and 8 daily for more than half the time when the disorder is active
how do you treat cluster headaches?
- oxygen: 100%, 8-12 L/min, NRB mask –> this is diagnostic!!
- triptans: fast acting non-oral is best (sumatriptan)
- DHE
- 4% aqueous intranasal lidocaine
- occipital nerve blocks (rare)
what is the prophylactic therapy for cluster headaches?
- verapamil (Ca+2 channel blocker)**
- corticosteroids to shorten length of cycle
start early in headache cycle
daily therapy until 3 weeks headache
free then taper medications and restart with next cycle
what is a chronic daily headache?
general categorical term defined as presence of headache 15 or more days per month for 3 or more months
not a specific type of headache –> it can be chronic tension-type headache, chronic migraine, chronic cluster, etc.
what are rebound headaches?
aka medication overuse headaches
it’s a chronic daily headache and a secondary disorder in which acute medications used excessively causes headache in a headache-prone patient
clinical diagnosis, h/o analgesic use > 2 days/ per week, in a patient with chronic daily headache
most commonly occurs in people with primary headache disorders like migraine, cluster, or tension-type headaches using less effective or nonspecific medications so they’re re-dosing frequently which leads to MOH and it’s a vicious cycle
we don’t really understand the pathophysiology of why this happens…
how do you treat medication overuse headaches?
discontinuation of the medication that is overused and a combination of pharmacological, non-pharmacological, behavioral and physical therapy interventions
- educate
- stop offending medication
- initiate bridge therapy to treat withdrawal symptoms if any
- initiation transitional prophylaxis therapy
- establish acute treatment with limits on usage (limit the NSAID or triptan)
- establish a monthly followup
which medications contribute to medication overuse headaches?
- simple analgesics, especially when used 15 or more days per month
- combination pain relievers when used more than 10 days a month
- triptans and ergotamine when used more than 10 days a month
- opioids when used more than 10 days a month
- caffeine
