Headache Flashcards
Primary headache
migraine (episodic, chronic)
tension type
trigeminal autonomic cephalgia (TACs) - e.g. cluster headaches
Secondary headache
headache and neck trauma extra-cranial vascular disease tumour infection abnormal CSF pressure: hyper/hypotension drugs
Episodic migraine headache characteristics
2 of: unilateral location throbbing quality worse with exertion moderate to severe intensity
Episodic migraine associated symptoms
1 of:
- nausea/vomiting
- stimulus sensitivity (light, sound, normally pleasant smells)
Episodic migraine headache diagnosis
2 characteristics + 1 associated symptom
5 attacks with 1 year history + normal exam
–> migraine without aura
Migraine with aura - visual symptoms
scintillations peripheral field loss photopsia central scotoma zigzag areas surrounding an area of gradual visual loss highly specific, short-lived symptoms ~20% of patients
Migraine with aura - nonvisual symptoms
common: sensory, cognitive
rare: motor, basilar, retinal (blind in 1 eye)
Migraine with aura - clinical findings
Gradual onset of one or more reversible symptoms
Symptoms develop over > 4 minutes, or in succession
Duration
Triggers of migraines
menstrual periods alcohol/foods weather change oversleeping exposure to odours let down period of stress
Chronic migraine diagnosis
Headache >15 days/month
Average headache > 4 hours
Headaches meet criteria for migraine > 8 days/month
With/without medication overuse (> 10 days/month for over 3 months)
primary disorder of the brain
often occurs after repeated attacks of episodic migraine
disorder of cortical hyperexcitability and dysfunctional brainstem pain modulating centres
Migraine progression
often gradual, months-years
neither inexorable/irreversible
happens in ~3% of episodic migraine sufferers
Prevalence of chronic migraine
2% of population 5x higher in women 80% of cases seen in a headache specialty clinic are CM 2.5% of EM will progress to CM in a year 50% are overusing medications
Episodic tension-type headache
"mild migraine"/entry point to migraine Generalized, nonpulsating pressure mild-moderate intensity No aggrevation with activity No nausea/vomiting Photophobia/sonophobia absent (or only 1 present)
sinus headache
recurrent frontal headache
nasal stuffiness/obstruction
meets criteria for migraine (>95% of “sinus headache” are migraine)
Trigeminal autonomic cephalgias (TACs)
cluster headache ice-pick cough coital benign exertional chronic paroxysmal hemicrania
Cluster headache characteristics
Severe unilateral orbital pain
short duration, 2 weeks without an attack
Cluster headache associated autonomic symptoms
Unilateral Conjunctival injection tearing rhinorrhea/nasal congestion ptosis/miosis: rare
Migraine pathophysiology
brainstem/occipital cortex
Cortical spreading depression
- wave of intense cortical neuron activity followed by neuronal suppression
- velocity 2-3 mm/min
- probably underlines visual aura
- possibly occurs in clinically silent areas of cortex (migraines without aura)
Primary cause of migraine headache
Hyperexcitable cortex
Dysmodulated brain - activation in dorsal pons
Non-pharmacologic acute therapy of migraines
cold (decrease v/d)
pressure
rest - dark/quiet atmosphere
Migraine symptomatic acute therapy
simple analgesics NSAIDs combination analgesics Opioids Acetaminophen not really too effective
Specific agents for migraine symptoms
Ergotamine: first drug released, therapeutic gain is awful
Dihydroergotamine: much less vasoactive, important use in iv line in hospitals
Triptans
Triptans
Sumatriptan: highly effective and relatively safe; multiple modes of administration naratriptan zomitriptan rizatriptan almotriptan electriptan frovotriptan
Triptan MOA
Decreased transmission through trigeminovascular system
Vasoconstriction
Modulation at trigeminal nucleus caudalis
Triptan clinical considerations
No triptan is shown to be clinically superior to another
choose based on patient preference
safe to use with SSRIs
assess efficacy/side effects regularly
Switch triptans to achieve optimal results
Consider adjunctive therapy with NSAIDs (naproxen), anti-emetic (metoclopramide)
Rapid onset attack therapy (early peak)
almotriptan eletriptan rizatriptan sumatriptan zolmitriptan
Slow onset/recurrence: late peak therapy
naratriptan
frovatriptan
Nocturnal onset migraine therapy
zolmitriptan/rizatriptan wafers
Nausea/vomiting migraine therapy
sumatriptan/zomitriptan nasal spray
sumatriptan injectible
Side effect-sensitive patient migraine therapy
almotriptan/naratriptan/frovatriptan
Acute treatment of migraine steps
Mild: ASA/caffeine, 10 mg metoclopramide
30-45 min: 100 mg sumtriptan (moderate headache)
2 hours: 30 mg codeine/caffeine/acetaminophen
Migraine prophylaxis
Individualized assess overall impact failure to control with acute agents sequential use of available agents use adequate dose and duration of therapy
Non-pharmacologic migraine prophylaxis
relaxation training
biofeedback
CBT
not covered!!
Pharmacologic migraine prophylaxis
B-blockers: propranolol, nadolol
TCA: amitriptyline
Ca channel blockers: flunarizine (makes you fat/depressed)
serotonergic agents: pizotifen
Anti-convulsants:
Neurotoxin - studied for chronic migraines (botox)
Cluster headache treatment
aggressive approach
start preventative drug +/- steroids
acute agents for breakthrough headaches
treat until 2 weeks headache-free, or usual duration of patient’s cluster
Cluster headache acute therapy
Gold standard: Sumatriptan intra-nasal/subcutaneous
ergotamine tartrate DHE intra-nasal/subcut Oxygen inhalation (10-12L/minute)
Cluster headache preventative therapy
Verapamil Prednisone (transitional) topiramate lithium divalproex
Chronic migraine treatment
avoidance of aggravators
triptans
biobehavioural
Prophylaxis (topiramate, botox)
Botox MOA in CM
when used for prophylaxis of headache in adults with chronic migraine, acts as inhibitor of NTs associated with genesis of pain
Presumed mechanism: blocking peripheral signals to CNS –> inhibits central sensitization
