Primary Headaches

Question 1

define a headache

Answer 1

pain in the head and neck

Question 2

types of primary headaches according to the international classification of headache disorders

Answer 2

migraine
tension-type
trigeminal autonomic cephalalgias

Question 3

IHS code for diagnosis

Answer 3

primary (condition itself)
secondary (HA is a symptom)
facial pain

Question 4

areas affected in primary headaches

Answer 4

sensory nerve innervation of the trigeminal nerve outside BBB (opthalamic/maxillary/mandibular)
back of head pain = innervated occipital nerve

Question 5

trigeminal nerve vs occipital nerve pathway

Answer 5

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)

Question 6

peripheral activation

Answer 6

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)

Question 7

nerve fibres innervating cranial circulation

Answer 7

sympathetic fibres - NA/NPY/ATP
parasympathetic fibres - PACAP/AChE/VIP/NOS
sensory fibres - SP/CGRP/NKA/PACAP

Question 8

tension type headaches

Answer 8

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

Question 9

TTH pathophysiology

Answer 9

unknown
no pericranial/cervical muscle tenderness
episodic - pericranial myofascial mechanisms (peripheral sensitization?)
chronic - central nociceptive pathways (central sensitisation?)

Question 10

peripheral vs central sensitisation

Answer 10

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)

Question 11

TTH treatment

Answer 11

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)

Question 12

Botulinum toxin A

Answer 12

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

Question 13

trigeminal autonomic cephalalgias (TACs)

Answer 13

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

Question 14

indomethacine responding headaches

Answer 14

paroxysmal hemicrania
unilateral head pain in 1st distribution of trigeminal nerve
autonomic sympathetic activation (runny nose)
cluster headache is most prevalent

Question 15

indomethacine

Answer 15

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

Question 16

cluster headaches

Answer 16

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)

Question 17

cluster headache diagnosis

Answer 17

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

Question 18

cluster headache chronobiology

Answer 18

most attacks during late day/sleep/early morning - patients try to postpone sleep/bouts
mostly during spring (due to daylight changes)

Question 19

cluster headache pathophysiology

Answer 19

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

Question 20

neuromodulation

Answer 20

deep brain stimulation using electrode (prophylactic treatment for chronic cluster headache)
60-70% effective
limitation: intracranial haemorrhage

Question 21

biomarkers

Answer 21

increase in CGRP/NPY (neuropeptides)
i.v infusion of CGRP triggers attack - remission +CGRP = no attack

Question 22

Genetics in cluster headaches

Answer 22

GWAS
polygenetic risk not familial
loci = regulates CR/inflammation

Question 23

treatment

Answer 23

acute - high flow of oxygen/sumatriptan (SC/nasal)/dihydroergotamine/zolmitriptan (nasal)
transitional - reduces attack frequency (lidocaine block)
prophylactic to transitional

Question 24

vagus nerve stimulation

Answer 24

VG regulates parasympathetic outflow
few found effective

Question 25

cluster headache prevention

Answer 25

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

Question 26

what is the only FDA approved drug for episodic cluster headache prevention

Answer 26

Galcanezumab
anti-CGRP peptide monoclonal antibody
300mg SC-300mg monthly to end cycle
adverse effects: injection site pain/nasopharyngitis/injection site swelling

Question 27

medication overuse headache

Answer 27

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

Question 28

medication overuse headache pathology

Answer 28

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 **