Primary Headaches Flashcards
define a headache
pain in the head and neck
types of primary headaches according to the international classification of headache disorders
migraine
tension-type
trigeminal autonomic cephalalgias
IHS code for diagnosis
primary (condition itself)
secondary (HA is a symptom)
facial pain
areas affected in primary headaches
sensory nerve innervation of the trigeminal nerve outside BBB (opthalamic/maxillary/mandibular)
back of head pain = innervated occipital nerve
trigeminal nerve vs occipital nerve pathway
trigeminal nerve ganglion projects to upper SC (TCC) - thalamus (3rd order neuron) - cortex (info painful)
occipital nerve projects to ascending trigeminal pain pathway (modulated by MB/cortical structures)
peripheral activation
innervation of dura matter by trigeminal sensory fibres
trigeminal fibres contain receptors (transducer channels) - activated by noxious stimulus - AP - NaV activation- release glutamate
decreasing diameter of fibres: Aa+B Adelta C fibres (pain)
nerve fibres innervating cranial circulation
sympathetic fibres - NA/NPY/ATP
parasympathetic fibres - PACAP/AChE/VIP/NOS
sensory fibres - SP/CGRP/NKA/PACAP
tension type headaches
very common (60-80%) prevalence 3:1 w:m
features: tightness/not severe/not aggregated by movement/lasts 30mins to days/ with w/o pericranial tenderness
no: nausea/photo/phonophobia (unlike migraine)
3% population has chronic TTH (>15 days) chronic>15 days/6 months episodic <15 days
TTH pathophysiology
unknown
no pericranial/cervical muscle tenderness
episodic - pericranial myofascial mechanisms (peripheral sensitization?)
chronic - central nociceptive pathways (central sensitisation?)
peripheral vs central sensitisation
peripheral (muscle sensitivity): trigeminal ganglion innervates pericranial muscle. trigeminal nerve releases glutamate and other neuropeptides to activate ascending trigeminal pathway
central: peripheral 1st order neurons sensitised & 2nd order neuron sensitised (via lower threshold and more APs) even 3rd order neurons in thalamus sensitised (sensitivity in brain areas which process pain)
TTH treatment
lack of studies
simple analgesics: paracetamol/NSAIDS (no more than 10 days per month)
non pharmacological: sleep/stress relief/massage (due to muscle tenderness)/hydration
botulinum toxin A (block muscle activity/paralytic)
Botulinum toxin A
cleaves SNAP25 on sensory fibres (trigeminal) - no SNARE complex - blocks NT release
in double blind placebo = no sig difference between placebo and treatment in freq/duration of headaches
trigeminal autonomic cephalalgias (TACs)
episodic and chronic classified separately (different treatment/encourages more research)
short to long duration: SUNCT-paroxysmal hemicrania - cluster headache
short to long frequency of attack: cluster - paroxysmal hemicrania - SUNCT
indomethacine responding headaches
paroxysmal hemicrania
unilateral head pain in 1st distribution of trigeminal nerve
autonomic sympathetic activation (runny nose)
cluster headache is most prevalent
indomethacine
NSAID
non selective COX inhibitor - blocks prostaglandin synthesis (by COX)
PG role: mediate inflammation/fever/pain
unknown pharmacology
used with PP1/H2 blockers to offer gastroprotection (causes GI problems) cannot continue
cluster headaches
m:f 3:1 5years for diagnosis
excruciating pain behind the eyes/stabbling like/unilateral/restless
lasts: 15 mins to 3 hours
triggers: alcohol/smell
bout then remission (no cluster here)
cluster headache diagnosis
severe unilateral/supraorbital/temporal pain
episodic cluster: remission of 3 months/years chronic - no remission < 3 months/year
**cluster attack ** episode of cluster headache during REM sleep
cluster cycle/bout - attack then remission/seasonal variation/10% no remission 90% remission<2 months
cluster headache chronobiology
most attacks during late day/sleep/early morning - patients try to postpone sleep/bouts
mostly during spring (due to daylight changes)
cluster headache pathophysiology
hypothalamus contains many nuclei (signals by trigeminocervical complex TCC) (SCN - sleep/wake cycle)
increased blood flow in posterior hypothalamus (due to region involved in migraine)
patients are restless - difficult to place in the scanner
SPG-facial nerve - activates PNS symptoms
neuromodulation
deep brain stimulation using electrode (prophylactic treatment for chronic cluster headache)
60-70% effective
limitation: intracranial haemorrhage
biomarkers
increase in CGRP/NPY (neuropeptides)
i.v infusion of CGRP triggers attack - remission +CGRP = no attack
Genetics in cluster headaches
GWAS
polygenetic risk not familial
loci = regulates CR/inflammation
treatment
acute - high flow of oxygen/sumatriptan (SC/nasal)/dihydroergotamine/zolmitriptan (nasal)
transitional - reduces attack frequency (lidocaine block)
prophylactic to transitional
vagus nerve stimulation
VG regulates parasympathetic outflow
few found effective
cluster headache prevention
verapamil (CCB/vasodilator increases O2)
lithium (therapeutic levels for bipolar disorder)
valproate (anticonvulsant/therapeutic levels for seizures)
consideration for: topiramate/gabapentin/cyproheptadine
unknown mechanism of action of pathology
what is the only FDA approved drug for episodic cluster headache prevention
Galcanezumab
anti-CGRP peptide monoclonal antibody
300mg SC-300mg monthly to end cycle
adverse effects: injection site pain/nasopharyngitis/injection site swelling
medication overuse headache
due to excessive: triptans/opiates/NSAIDS/paracetamol - not caused by aspirin
reduced intake = less headache (up to 50%)
no more than 14 days a month for simple analgesics
treatment: propranolol/botox/withdraw analgesics
medication overuse headache pathology
unknown pathophysiology
associated with: amygdala/addiction
genetic predisposition has been hypothesised
animal models: changes in 5HT system/upregulation of vasoactive and pro-inflammatory mediators, increased susceptibility to cortical spreading depression, central sensitisation, increased in nociceptive field **—need for understanding in humans **
