facial pain Flashcards

1
Q

pain definition

A

“an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage”
International Association for the Study of Pain

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2
Q

assessment of pain

A

Physical symptoms
* PAIN scores (McGill) – questionnaire, gives clinician some idea of what pt experiencing

Emotional symptoms
* Psychological scores (Hospital Anxiety and Depression scale (HAD) – useful to see how the pt perceives life with chronic pain)

QOL scores (Oral Health Impact Profile (OHIP) – what can you not to due to the pain e.g. chew, bite, yawn)

takes time, complex

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2
Q

assessment of pain

A

Physical symptoms
* PAIN scores (McGill) – questionnaire, gives clinician some idea of what pt experiencing

Emotional symptoms
* Psychological scores (Hospital Anxiety and Depression scale (HAD) – useful to see how the pt perceives life with chronic pain)

QOL scores (Oral Health Impact Profile (OHIP) – what can you not to due to the pain e.g. chew, bite, yawn)

takes time, complex

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3
Q

assessment of pain

A

Physical symptoms
* PAIN scores (McGill) – questionnaire, gives clinician some idea of what pt experiencing

Emotional symptoms
* Psychological scores (Hospital Anxiety and Depression scale (HAD) – useful to see how the pt perceives life with chronic pain)

QOL scores (Oral Health Impact Profile (OHIP) – what can you not to due to the pain e.g. chew, bite, yawn)

takes time, complex

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4
Q

how do we feel pain?

4

A
  • Nociception – generation of pain
  • Peripheral Nerve Transmission – nociception signal into CNS, damage to peripheral nerve can lead to chronic pain
  • Spinal Modulation – in spinal cord where nerves synapse – can adapt and control them to defer or induce meaning of pain
  • Central Appreciation
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5
Q

sensory nerve supply to the face by

A

trigeminal nerve (CNV)

somatic

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6
Q

how is referred pain generated

A

complicated
from embryonic nerve supply development

Pharyngeal arches and clefts – important as form head and neck systems
* Structure of nerve migrate – carry nerve and blood supply with them – can make head and neck appear v complex

pain location can be misinterpreted as source is elsewhere – co-synapse to same area of trigeminal nucleus

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7
Q

sensory (somatic) nerve supply of head and neck can be from

A

V, VII, IX, X & Cervical 1-3

Autonomic
* sympathetic
* parasympathetic
afferent info coming into CNS, relayed and then carried into brain and perceived as arisen in facial tissue (e.g. issues in any main salivary glands)
- pain transmitted through autonomic nerves
* e.g. cardiac pain – no somatic nerve supply, so autonomic nerves carry to brain

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8
Q

1st pharyngeal arch related to

nerve, artery

A

trigeminal nerve and maxillary artery – midface generally

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9
Q

2nd pharyngeal arch related to

nerve, artery

A

facial nerve and hyoid and stapedial artery

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10
Q

3rd pharyngeal arch related to

nerve, artery

A

glossopharyngeal nerve and internal carotid artery

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11
Q

4th pharyngeal arch related to

nerve, and vessels

A

vagus nerve and right subclavian artery and aorta

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12
Q

branches of facial nerve

A

temporal

zygomatic (1 and 2)

buccal

mandibular

cervical

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13
Q

autonomic referred pain of cardiac felt in

A

left arm
sternum
jaw

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14
Q

somatic reflex arc

A

pain produces a change
pass up to CNS via spinal cord – efferent would be sent when spinal cord receives it to cause muscle constriction to pull part of body away from sight of damage

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15
Q

autonomic reflex arc

A

when signal goes to brain – a efferent signal is sent out at same time (sweat glands, blood vessel dilation)
* have somatic reflex arc, but autonomic mediated pain will also have autonomic mediated changes
* e.g. changes in blood flow – swelling and red; lacrimation; nasal congestion (mucosal oedema)

consequence of autonomic pain
* symptoms we get are good guide for source of pain and what nerves pain going through (autonomic or somatic)

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16
Q

peripheral nociception

A

tissue damage causes chemical mediators to be released, act on nociceptor (chemoceptor) in the tissue to produce an action potential, which is transmitted through the peripheral nerve into spinal cord

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17
Q

perpheral sensitisation

A

spinal cord sends the information into the brain

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18
Q

gate control of chronic pain

A

pain response into peripheral nerve and into spinal nerve, stimulate ascending pain fibre to the brain

same information transmitted through standard touch – different pathway to the brain

there is some crossing between these fibres
* touch fibres stimulated inhibit the pain ascending pathway to CNS
* rubbing painful area makes pain less obvious – block pain sensation by normal touch sensation

descending facilitation and inhibition
* respond at lower threshold to pain or higher (e..g. want to keep functioning despite high levels of pain signals)
* inc or red sensitivity of interneuron

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19
Q

change in gate control of chronic pain

A

Neuronal Plasticity

Sprouting of Spinal Segment Nerves
* Easier for pain signals to be passed to the brain
* Even if cause of pain is removed but due to the positive connection existing normal sensation and pain interneurons

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20
Q

pain sensitisation

A

Complex process – happens peripheral and central

Chronic pain causes change in peripheral and central nervous system so pain felt even after intervention

(Change in gate control of pain)

21
Q

how to prevent learned pain (chronic pain)

A

Prevent changes by early management of pain

Reduce pain reception so chance of adaptive change

22
Q

consequences of adaptive pain response

5

A

CRPS - chronic regional pain

Delocalised pain
* Spreads around ‘anatomical’ boundaries
* bilateral
* ‘gripping’, tight, burning

Feeling of swelling & heat

Colour change in overlying skin – due to efferent reflexes

Autonomic changes

Significantly disabling

23
Q

pain history

A

S - Site
O - Onset
C - Character
R - Radiation
A - Associations
T – Time Course
E – Exacerbating/Relieving
S - Severity

24
Q

what is neuropathic pain

A

pain stimulated beyond nociceptor
* no nociception taking place, but pain perception happening, damage happened to pathway sending pain signal to brain – feel pain caused by tissue but the there is no pathological cause in that tissue to cause the pain

Constant burning/aching pain
Fixed location
Often a fixed intensity
Genetic predisposition?
* Nerve ion channels that heal badly after injury
* Persisting inflow gives persisting information reporting

Post herpetic neuralgia type of neuropathic pain – limit damage at time ptpresents, consequence neuropathic pain reduced

25
Q

characteristics of neuropathic pain

A

usuallly a history of ‘injury’
* Can follow facial trauma
* Can follow extractions (nerve avulsed and healed in a way so constant CNS signal after XLA = constant neuropathic pain)
* Can follow ‘routine’ treatment without complications
* Can follow Herpes Zoster (Shingles) episode - POST HERPETIC NEURALGIA
* Can follow destructive treatment for pain

Constant, fixed pain as same nerve damage is there 24/7

can have a genetic predisposition - inherited neurodegeneration, metabolic/endo abnormalities (persisitent inflow)

26
Q

neuropathic pain management

systemic medication

3 main

A
  • **Pregabalin
  • Gabapentin
  • Tricyclic**
  • Valproate
  • Mirtazepine
  • Opioid analgesics

Don’t stop afferent information going into CNS but reduce pain transmission within CNS (effect of signal being passed to central appreciation by slowing pain within the brain)

27
Q

neurpathic pain management

topical medication

4

A
  • Capsaicin
  • EMLA
  • Benzdamine
  • Ketamine

Reduce the pain transmission within CNS using peripheral nerve sensory activation over the area of pain (Gate theory

28
Q

neurpathic pain management

topical medication

4

A
  • Capsaicin
  • EMLA
  • Benzdamine
  • Ketamine

Reduce the pain transmission within CNS using peripheral nerve sensory activation over the area of pain (Gate theory

29
Q

alternative managements for neuopathic pain

2 categories

A

Physical (short duration)
* TENS – occasionally helpful (Gate theory), Low frequency TENS
* Acupuncture – good results

Psychological
* Distraction
* Correct abnormal illness behaviour
* Improve self esteem/positive outlook

30
Q

what is atypical odontalgia

A

Dental pain without dental pathology

Distinct pattern of pain
* Equal sex distribution
* Pain free or mild between episodes
* Intense unbearable pain
* 2-3 weeks duration
* Settles spontaneously

31
Q

what should a GDP in case of atypical odontalgia

A

PRIMARY CARE – REFER!

Oral Medicine Management

Chronic strategy – medication (gabapentin)
* Reduce chronic pain experience
* Reduce frequency of acute episodes

Acute strategy
* Have a plan to control pain
* opioid analgesics as required
* high intensity/short duration

Be prepared to extract tooth if needed – keep on offer as pt may not try other tx methods

32
Q

persistent idiopathic facial pain

A

Pain which poorly fits into standard chronic pain syndromes
* Neuropathic
* CRPS
* TMD
* Trigeminal Neuralgia
* Migrainous Pain
* Atypical odontalgia

Often high disability level – suggest a high autonomic component, but not clear from symptoms

Challenge to tx – clinical psychology sometimes more successful

used to be called atypical facial pain

32
Q

persistent idiopathic facial pain

A

Pain which poorly fits into standard chronic pain syndromes
* Neuropathic
* CRPS
* TMD
* Trigeminal Neuralgia
* Migrainous Pain
* Atypical odontalgia

Often high disability level – suggest a high autonomic component, but not clear from symptoms

Challenge to tx – clinical psychology sometimes more successful

used to be called atypical facial pain

33
Q

management of persistent idiopathic facial pain

A

Believe patient
* Do not blame any associated depression for symptoms (they are suffering chronic pain – depression is likely consequence)

Do not increase damage
* likely a degree neuropathic pain involved so surgery is not helpful (can cause more nerve damage)

Adopt holistic strategy
* Quality of life issues and disability should be addressed
* Pain control a bonus
* Realistic outcomes – Patient & Clinician

Use QOL/pain scores as treatment monitor

34
Q

phantom pain and congnitive deduction

A

Phantom Pain
* Brain learns how the body is – understanding persists throughout life even if source of pain removed will still feel pain

Cognitive deduction
* Phantom pain – incorrect cognitive deduction – feel the pain that is still there even through limb is not, hard to tx as not typical neurological pain to tx, need to override the peripheral nerve sensation that the pt has that the phantom limb is in pain – trick with mirrors?
* What the pt perceives and what is physically happening may not be the same

35
Q

what is oral dysesthesia

A

Abnormal sensory PERCEPTION in ABSENCE OF ABNORMAL STIMULUS

Somatoform (perception) or Neuropathic (abnormal sensory stimulus)

ALL modes of oral sensation involved
* Burning or ‘nipping’ feeling
* Dysgeusia (bad taste)
* Paraesthesic feeling
* Dry mouth feeling

Issue can be neuropathic but is frequently somatoform – decision about condition wrong rather than there being any disease inside the mouth

36
Q

4 predisposing factors to oral dysesthesia

A

Deficiency states?
* haematinics
* zinc
* vit B1, B6

Fungal and Viral infections?

Anxiety and stress?

Gender – more women present to OM than men

Ensure there is no tx medical problems

37
Q

burning mouth syndrome

A

Dysaesthesia most likely to be associated with haematinic deficiency
* Correct deficiency – should go away

SITE important!
* Lips & tongue tip/margin = parafunction (tongue thrust) *tx this – lower acrylic Essix types splint to prevent damage to mucosa *
* Multiple other sites – dysaesthesia (dorsom of tongue, vault of palate)

38
Q

dysgeusia

A

‘bad taste’ - ‘bad smell’ - ‘Halitosis’
* nothing detected by practitioner
* nothing found on examination
* pt still perceives they have it – so will become isolated as anxious others able to detect the bad smell – start overthinking things

REMEMBER – eliminate other causes
* ENT causes - chronic sinusitis
* perio/dental infection
* pouches
* GORD

39
Q

touch dyseaseshesia

A

‘pins and needles’ - ‘tingling’

Normal sensation to objective testing
* Pin/needle elicit pain!

CRANIAL NERVES test essential
* MUST exclude organic neurological disease

MUST exclude local causes
* infection
* Tumour (true numbness of tissue)

MRI Essential – demyelination/tumour

40
Q

dry mouth dysesthesia

A

VERY common

c/o debilitating dry mouth/‘sjogrens’
* but Eating OK – then not salivary gland issue
* worse when waken at night

usually the most obviously associated with anxiety disorders

investigate - same as sjogrens
* all negative, but likely reduced salivary flow issue due to anxiety

tx – need to explain that medication can cause a dry mouth to tx dry mouth (get 2 dry mouths – the annoying dysesthesia and the medication related dry mouth, as tx continues dysesthesia will go away and be left with tolerable medication dry mouth)

41
Q

management of dysesthesia

3 steps

A

Explain the condition to the patient
* ‘pins and needles’ in the taste (feels funny but looks normal; mouth is normal but feels abnormal) etc

Assess degree of anxiety
* Anxiolytic medication
* Clinical psychology

Treatment empower the patient
Control is important

42
Q

medication for dysesthesia

2 classes

A

depending on pt problem

Anxiolytic based medication (preference)
* Nortriptyline
* Mirtazepine
* Vortioxetine

Neuropathic Medication
* Gabapentin/Pregabalin
* Clonazepam – topical?

43
Q

TMD
3 basic categories to put pts in

A

Joint Degeneration
* pain on use & crepitus, +/- rest pain

Internal derangement
* LOCKING open or closed

No joint pathology

44
Q

possible causes of TMD when no joint pathology

4

A

occlusion
grinding
clenching
stress

45
Q

what to look for when assessing pt who has TM pain

7

A
  • clicking joint
  • locking with reduction
  • limitation of opening mouth
  • tenderness of masticatory muscles
  • tenderness of cervico-cranial muscles
  • signs of parafunction - scalloped tongue, erythema tongue tip, buccal linea alba, cracked teeth
  • see if systemic problems – need systemic management (CBT or medication)
46
Q

history for TMD

A

Acute pain in face & neck

ANY chronic face, head and neck pain

symptoms show periodicity
morning/evening exacerbation

parafunctional clenching

History is the KEY to successful management

47
Q

signs of TMD on examination

7

A

Focal muscle tenderness
* masticatory
* sternomastoid
* Trapezius

tenderness over TMJ itself

limitation of opening
* progressive

Joint noise
* incidental - degenerative OA changes
* related to muscle dysfunction – click

Deviation on opening
* common finding with muscle dysfunction

Dental occlusion upset

signs of parafuntion - scalloped tongue, erythema tongue tip, buccal linea alba, cracked teeth

48
Q

investigation options for TMD

3 routes

A

usually none indicated for ‘functional’ disorders

Indications for Imaging
* Ultrasound Scan - if functional visualisation of disc movement is needed
* DPT or CBCT - if bony problem suspected
* MRI - best image of the disc

Arthroscopy to directly visualise the disc

49
Q

managemenet of TMD
8 steps

A

Information – how to self help – give pt information booklet #

CBT education (stress management) +/- exercises

Soft diet and analgesia

Bite splint (essix first as easiest)

Biochemical manipulation
* Tricyclic (not SSRIs)
* other anxiolytic medication

Physiotherapy

Acupuncture

Clinical Psychology

50
Q

children and TMD

A

tendency to anxiety neurosis
* ‘anxious parents have anxious children’
* maladaptive response to ‘normal’ change

reaction to abuse
* school - bullying, fear of failure
* home - parental dysharmony, physical abuse