key points chronic orofacial pain Flashcards
neuralgia
intense stabbing pain brief severe along course of affected nerve usually irritation/damage to nerve
typical epidemiology of TN pt
elderly >60s
F
causes of TN
idiopathic *classical - vascular compression CN5 secondary - MS - intracranial tumours - others: skull-base bone deformity, CT disease, AV malformation
TN red flags
younger pt (<40yrs)
sensory deficit in facial region
- hearing loss - acoustic neuroma
other CN lesions
TN investigations
test CNs
MRI - all pts get one
TN presentation
unilateral stabbing - 5-10s - attack: cluster of stabs (few mins) triggers - cutaneous, wind/cold, touch, chewing/jaw movements paroxysmal (no pain between attacks) or concomitant continuous pain (superimposed stabbing attacks) remissions and relapses can be on continuum with other CN nerve pain disorders mask like face excruciating pain no obv ppt pathology
TN drug therapy
1st line - carbamazepine - oxcarbazepine - lamotrigine (slow onset) 2nd line - gabapentin - pregabalin - phenytoin - baclofen
carbamazepine SEs - clinical
blood dyscrasias - thrombocytopenia, neutropenia, pancytopenia electrolyte imbalances (hyponatraemia) - caution with PPIs/diuretics neurological deficits - paraesthesia - vestibular problems - dizziness liver toxicity skin reactions (potentially life-threatening)
carbamazepine blood monitoring
weekly for 1st month then monthly
FBC, urea, LFT, electrolytes
TN surgery indications
significant SEs
approaching max tolerable medical management even if pain controlled
‘younger’ pts with significant drug use
TN surgical options
*MVD - need vessel impinging on CN5 nerve root destructive central procedures - radiofrequency thermocoagulation - retrogasserian glycerol injection - balloon compression stereotactic radiosurgery - y-knife destructive peripheral neurectomies
TN surgical complications
local effects - peripheral txs (cryotherapy) sensory loss - corneal reflex - general sensation - hearing loss motor deficits reversible/irreversible
PTN causes
HSV
trauma (<6m)
idiopathic
PTN presentation
pain localised to distribution of CN5
burning/squeezing/pins and needles
primary pain continuous/near continuous
- superimposed brief pain paroxysms may occur, but not
the predominant pain type
often cutaneous allodynia (much larger than punctuate trigger zones in TN) and/or sensory deficits
TACs
unilateral head pain - predominantly V1 v severe/excruciating usually prominent cranial p/s autonomic features (ipsilateral) - conjunctival injection/lacrimation - nasal congestion/rhinorrhoea - eyelid oedema - ear fullness - miosis and ptosis (Horner's syndrome) orbital and temporal pain
cluster headache - attack
rapid onset and cessation duration: 15mins-3hrs pt restless and agitated during attack migrainous symptoms often present - premonitory symptoms: tiredness, yawning - associated symptoms: nausea, vomiting, photophobia, phonophobia - aura in 14%
cluster headache - bout
episodic 80-90%
chronic cluster 10-20%
cluster headache - bout - episodic
cluster of attacks into bouts - 1-3m with remission at least 1m
attack freq: one every other day to 8 per day
may be continuous background pain/symptom free between attacks
alcohol triggers attack during bout but not in remission
cluster headache circadian periodicity
striking
attacks same time each day
bouts same time each year
cluster headache - bout - chronic cluster
bouts >1yr without remission or remissions last less than 1m
cluster headache drug therapy groups
abortive (attack)
abortive (bout)
preventative
CGRP monoclonal ABs
cluster headache drug therapy - abortive (attack)
SC sumitriptan/nasal zolmatriptan
100% O2
cluster headache drug therapy - abortive (bout)
occipital depomedrone/lidocaine injection
tapering course prednisolone
cluster headache drug therapy - preventative
verapamil (not if cardiac conduction problems)
lithium (renal toxicity and diabetes insipidus)
methysergide
topiramate
cluster headache drug therapy - when would CGRP monoclonal ABs be indicated?
failed normal drug tx
paroxysmal hemicrania
rapid onset and cessation
duration 2-30mins
2-40 attacks per day (no circadian rhythm)
50% restless and agitated
may have migrainous symptoms
10% attacks may be ppt by bending/rotating head
background continuous pain can be present
80% chronic PH, 20% episodic PH
absolute response to indomethacin
- one of diagnostic criteria
paroxysmal hemicrania tx
no abortive tx
prophylaxis with indomethacin
alternatives if can’t take NSAIDs not great - COX2 inhibitors, topiramate
where are nuclei located?
within CNS
where are ganglia located?
outside CNS
how do we feel pain?
nociception
peripheral nerve transmission
spinal modulation
central appreciation
assessment of the pain pt
numerical scale 1-10 - 1D - no effect/emotional impact physical symptoms - pain scores (mcGill) emotional symptoms - psychological scores - HAD QOL scores: Oral Health Impact Profile - disability score
sensory nerve supply
somatic - voluntary control of body movements via skeletal muscles
autonomic
- sym, p/s
somatic reflex arc
automatic response
always involve CNS
autonomic reflex arc
motor output: 2MNs, one in spinal cord, one in PNS in autonomic ganglion
effector - smooth muscle/sweat gland/adrenal medulla
reflex vascular vasodilation - fills with blood - swelling and hot - indicates autonomic pain transmission
in CNS may/may not be interconnector neuron involved
long reflex arc
involves spinal cord - somatic and autonomic
short reflex
autonomic
completely peripheral
synapse in peripheral ganglion
peripheral sensitisation
increased responsiveness and reduced threshold of nociceptive neurons in periphery to the stimulation of their receptive fields
neuronal plasticity
sprouting of spinal segment nerves
- sensory fibre becomes stimulatory so if you touch it it
feels sore
a way body manages pain unhelpfully
pain modulating receptors - biochemical
adrenergic
opiate
NMDA
Melzak and Wall Gate Control of Chronic Pain
squeeze/rub area - cause sensory info to go up own nerve into brain, then synapse with pain nerve fibres
- make pain signal less easy to transmit - less pain
also descending nerves from brain can switch pain fibres on/off more
e.g. if you expect pain it makes nerve easier to fire
pain is not absolute
nociceptive pain
caused by activity in neural pathways in response to potentially tissue damaging stimuli
examples of nociceptive pain
post-op pain mechanical low back pain sports/exercise injuries sickle cell crisis arthritis
mixed pain type
caused by combination of both primary injury and secondary effects
complex/chronic regional pain syndrome - aetiology
often triggered by an injury
complex/chronic regional pain syndrome - presentation
delocalised pain
- bilateral
- often autonomic nerve damage - don’t follow boundary
of somatic nerve
gripping, tight, burning
feeling of swelling and heat (increased blood flow)
colour change in overlying skin
autonomic changes
significantly disabling
analgesics e.g. ibuprofen won’t help but centrally acting e.g. morphine will as they interfere with pain process
- swelling and erythema may persist due to reflex arc, happens lower down
autonomic nerve version of neuropathic pain
neuropathic pain definition
initiated or caused by primary lesion or dysfunction in rhe somatosensory nervous system
types of neuropathic pain
1 - diabetic neuropathy 2 - post-herpetic neuralgia spinal cord injury neuropathic low back pain distal polyneuropathy (e.g. diabetic, HIV) central post-stroke pain TN CRPS MS
neuropathic pain symptoms
constant burning/aching pain
fixed location
often fixed intensity
- nerve damage there all time
can be difficult as the pt perceives the pain in the end tissue not where the nerve is damaged
usually history of ‘injury’
- facial trauma, ext, ‘routine’ tx without complications
- can follow HZ episode
- destructive tx for pain
can get non-specific neuropathic pain
if autonomic nerve may get associated heat/swelling
neuropathic pain genetic predisposition?
nerve ion channels that heal badly after injury - persistent info gives persistent info reporting
inherited neurodegeneration
metabolic/endocrine abnormalities
neuropathic pain disease process
infection/inflammation
neurotoxicity
tumour infiltration
metabolic abnormality
neuropathic pain therapeutic intervention
surgery
chemo
irradiation
neuropathic pain management
systemic medication
- pregabalin, gabapentin - nerve conduction
- tricyclic - works centrally, reduces pain transmission in
CNS
- valproate
- mirtazepine
- opioids
topical medication
- capsaicin, EMLA, benzdamine, ketamine
physical: TENS, acupuncture
psychological: distraction, positive outlook, correct abnormal illness behaviour
atypical odontalgia
dental pain without dental pathology
distinct pattern of pain
- pain free or mild between episodes
- intense unbearable pain
- 2-3wks duration, settles spontaneouslyatypical odontalgia sequelae
acute pulpitis pain endo relieves/reduces pain pain returns after short time extraction relieves pain pain returns in adjacent tooth after short time pt referred
features of atypical odontalgia
acute pulpitis symptoms
‘irrational’ behaviour - high motivational drive
‘beg’ for extractions
go elsewhere with modified story if extraction refused
suspect in pt with unusual ext distribution
atypical odontalgia management
primary care - refer oral med chronic strategy - reduce chronic pain exposure - reduce freq of acute episodes oral med acute strategy - have a plan to control pain - opioid analgesics? high intensity, short duration - be prepared to ext tooth if needed
persistent idiopathic facial pain definition
pain which poorly fits into standard chronic pain syndromes - neuropathic - CRPS - TMD - TN - migrainous pain - atypical odontalgia =often diagnosis of exclusion
persistent idiopathic facial pain presentation
often high disability level - autonomic component
similar symptoms to neuropathic pain in character
often anatomically challenging
often associated symptoms - heat, pressure, swelling
- usually nothing seen by observer
management of persistent idiopathic facial pain
believe pt - don't blame any associated depression for symptoms don't increase damage - surgery not helpful holistic strategy - QOL issues - pain control a bonus - realistic outcomes - pt and clinician - use QOL/pain scores as tx monitor often respond poorly to tx
oral dysaesthesia/BMS
abnormal sensory perception in absence of abnormal stimulus all modes of oral sensation involved - burning/nipping - dysgeusia - paraesthesic feeling - dry mouth feeling
oral dysaesthesia/BMS - predisposing factors to eliminate
deficiency states - haematinics, zinc, vit B1, B6
fungal and viral infections
anxiety and stress
oral dysaesthesia/BMS aetiology
F, usually >50yrs dissociated anxiety disorder often associated symptoms - poor sleep pattern - early waking - swallowing problems 'globus' sensation - IBS, dyspepsia, back pain - body pain conditions - fibromyalgia
oral dysaesthesia/BMS site
lips and tongue tip/margin - parafct
multiple other sites - dysaesthesia
dysgeusia
bad taste/smell/halitosis
nothing detected
remember ENT, perio/dental infection, GORD
dry mouth dysaesthesia
worst when waking at night
eating ok
anxiety
touch dysaesthesia
pins and needles/tingling normal sensation to objective testing - pin/needle elicit pain CN test essential - exclude organic neurological disease - infection/tumour/MS MRI
management of dysaesthesia
tricyclics (for anxiety) 'neuropathic' meds - gabapentin, pregabalin slow tx 3-6m - get reduction in freq of symptoms explain to pt about condition assess degree of anxiety tx empower pt - control neuropathic topical meds - clonazepam? reassurance correct deficiencies
carbamazepine SEs - pt term
skin rash dizzy/tired nausea headaches dry mouth weight gain
