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Oral medicine > Chronic orofacial pain > Flashcards

Chronic orofacial pain Flashcards

1
Q

what is a neuralgia?

A

an intense stabbing pain

pain usually brief but may be severe

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2
Q

where does neuralgic pain appear?

A

it extends along the course of the affected nerve

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3
Q

what is neuralgia usually caused by?

A

irritation of or damage to a nerve (but not exclusively)

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4
Q

which nerves that mediate sensation in the head can be involved in neuralgia?

A

trigeminal (most common form)
glossopharyngeal and vagus
nervus intermedius (geniculate neuralgia) - branch of facial nerve
occipital

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5
Q

incidence of trigeminal neuralgia

A

4.3:100 000 pop (USA)

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6
Q

gender distribution of trigeminal neuralgia

A

higher in females

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7
Q

age group usually affected by trigeminal neuralgia

A

elderly - predominantly in 60s and above

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8
Q

causes of trigeminal neuralgia

A

idiopathic
classical - vascular compression of the trigeminal nerve (most common known cause)
secondary
- multiple sclerosis
- space-occupying lesion (intra-cranial tumours - benign/malignant)
- others: skull-base bone deformity, CT disease, arteriovenous malformation

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9
Q

classical Trigeminal Neuralgia - why doesn’t a vessel near CN5 necessarily mean it is this?

A

need vascular trigeminal conflict - compression

often need high resolution MRI with contrast

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10
Q

trigeminal neuralgia - where does the pain appear?

A

unilateral maxillary or mandibular division pain > ophthalmic division

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11
Q

trigeminal neuralgia type of pain

A

stabbing pain

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12
Q

trigeminal neuralgia duration

A

5-10s
single stabs
each attack is a cluster/group of stabs (up to a few mins)
if >few mins likely not trigeminal neuralgia

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13
Q

trigeminal neuralgia triggers

A

cutaneous
wind/cold
touch
chewing/jaw movements

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14
Q

paroxysmal trigeminal neuralgia

A

no pain at all between the stabbing attacks

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15
Q

concomitant continuous pain in trigeminal neuralgia

A

superimposed stabbing attacks

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16
Q

is trigeminal neuralgia continuous?

A

no - get remissions and relapses

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17
Q

why can trigeminal neuralgia present as a hybrid?

A

because it is on continuum with other cranial nerve pain disorders

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18
Q

other presentations of trigeminal neuralgia

A

acute spasms of ‘sharp shooting pain’

  • may be more than one division
  • may be bilateral
  • may have burning component
  • may have vasomotor component
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19
Q

why do trigeminal neuralgia patients often have a ‘mask-like’ face?

A

inexpressive as fear of making a facial movement that may set off an attack

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20
Q

trigeminal neuralgia - how does the excruciating pain appear?

A

disabling

patient will freeze

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21
Q

what is the crucial aspect when considering trigeminal neuralgia?

A

no obvious precipitating pathology

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22
Q

trigeminal neuralgia red flags

A

younger patient (<40yrs)
sensory deficit in facial region
- hearing loss - acoustic neuroma
other cranial nerve lesions

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23
Q

what are two crucial investigations in trigeminal neuralgia?

A

test cranial nerves (identify sensory deficit)

MRI

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24
Q

what drug group is predominantly used to treat trigeminal neuralgia?

A

anti epileptic drugs

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25
Q

first line drugs for trigeminal neuralgia

A

carbamazepine
oxcarbazepine
lamotrigine

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26
Q

what is the modified release carbamazepine called and why is it good in trigeminal neuralgia?

A

Tegretol

good to decrease SEs as prevents fluctuations in serum concentration

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27
Q

lamotrigine onset of action

A

slow

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28
Q

second line drugs for trigeminal neuralgia

A

gabapentin
pregabalin
phenytoin
baclofen

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29
Q

trigeminal neuralgia - which drug should patients be responsive to?

A

carbamazepine if tolerated

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30
Q

trigeminal neuralgia - what should drug therapy aim for?

A

maximise efficacy and minimise SEs

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31
Q

trigeminal neuralgia - when is it often difficult to control pain?

A

first thing in the morning

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32
Q

trigeminal neuralgia - what can a pain diary be used for?

A

identify modifications necessary to therapy

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33
Q

can trigeminal neuralgia be responsive to LA?

A

yes

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34
Q

carbamazepine side effects

A 
blood dyscrasias
electrolyte imbalances (hyponatraemia)
neurological deficits
liver toxicity
skin reactions
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35
Q

carbamazepine blood dyscrasias

A

thrombocytopenia
neutropenia
pancytopenia

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36
Q

carbamazepine electrolyte imbalances

A

hyponatraemia

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37
Q

what should you be careful combining carbamazepine with?

A

diuretics or PPIs that can cause hyponatraemia

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38
Q

carbamazepine neurological deficits

A

paraesthesia
vestibular problems
dizziness

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39
Q

carbamazepine - how severe can skin reactions be?

A

potentially life-threatening

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40
Q

blood monitoring on carbamazepine

A

weekly basis for first month then monthly

FBC, urea, LFT, electrolytes

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41
Q

should you prescribe carbamazepine in GDP?

A

BNF dental preparations
SDCEP guidelines
expertise
facilities for monitoring toxicity

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42
Q

trigeminal neuralgia -when would surgery not usually be recommended?

A

if patient managing on medical therapy with moderate drug use and no significant SEs

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43
Q

trigeminal neuralgia - when to consider surgery

A

when approaching maximum tolerable medical management even if pain controlled
‘younger’ patients with significant drug use - will have many years of drug use

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44
Q

trigeminal neuralgia surgical options

A 
microvascular decompression (MVD)
destructive central procedures
stereotactic radiosurgery
destructive peripheral neurectomies
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45
Q

trigeminal neuralgia - what is the preferred surgical treatment where possible?

A

MVD

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46
Q

trigeminal neuralgia - what does MVD require?

A

a vessel impinging on the trigeminal nerve root

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47
Q

trigeminal neuralgia MVD 12month mortality and morbidity

A

1% mortality

10% morbidity

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48
Q

trigeminal neuralgia - destructive central procedures

A

radio frequency thermocoagulation
retrogasserian glycerol injection
balloon compression

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49
Q

trigeminal neuralgia - balloon compression mortality at 9months

A

2%

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50
Q

trigeminal neuralgia - stereotactic radiosurgery

A

gamma knife - targeted radiation at the trigeminal ganglion to kill trigeminal nerve cells
good safety profile but only available in Sheffield

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51
Q

trigeminal neuralgia - destructive peripheral neurectomies

A

only performed as a last resort after trial LA

6 months pain free without medication - can result in allodynia as well as TN

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52
Q

trigeminal neuralgia - complications after surgery

A 
local effects - peripheral treatments (cryotherapy)
sensory loss
 - corneal reflex
 - general sensation
 - hearing loss
motor deficits
may be reversible or irreversible
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53
Q

causes of painful trigeminal neuropathy

A

herpes zoster virus (related to active VZV infection, post-herpetic ‘neuralgia’)
trauma (pain develops <6m of traumatic event)
idiopathic

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54
Q

painful trigeminal neuropathy - where is the pain usually localised to?

A

the distribution(s) of the trigeminal nerve

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55
Q

painful trigeminal neuropathy - how is the pain commonly described?

A

burning or squeezing

likened to pins and needles

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56
Q

painful trigeminal neuropathy - duration and presentation of pain

A

primary pain is usually continuous or near-continuous

superimposed brief pain paroxysms may occur, but not the predominant pain type

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57
Q

what symptoms more commonly present in painful trigeminal neuropathy than in Trigeminal Neuralgia?

A

clinically evident cutaneous allodynia - much larger than the punctate trigger zones present in TN
and/or
sensory deficits

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58
Q

what is allodynia?

A

pain elicited on innocuous stimuli e.g. touch

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59
Q

how are TN and PTN linked?

A

thought to be on continuum of the same spectrum

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60
Q

trigeminal autonomic cephalgias - symptoms

A 
unilateral head pain - predominantly V1
v severe/excruciating
usually prominent cranial parasympathetic autonomic features (ipsilateral to the headache)
 - conjunctival injection/lacrimation
 - nasal congestion/rhinorrhoea
 - eyelid oedema
 - ear fullness
 - mitosis and ptosis (Horner's syndrome)
attack frequency and severity differs
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61
Q

cluster headache attack frequency (daily)

A

1 every other day - 8 per day

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62
Q

paroxysmal hemicrania attack frequency (daily)

A

1 to 2 - 40

no circadian rhythm

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63
Q

SUNCT attack frequency (daily)

A

3-200

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64
Q

what does SUNCT stand for?

A 
Short-lasting
Unilateral
Neuralgiform with
Conjunctival injection and 
Tearing
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65
Q

cluster headache duration of attack

A

15-180mins (majority 45-90mins)

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66
Q

paroxysmal hemicrania duration of attack

A

2-30mins

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67
Q

SUNCT duration of attack

A

5-240 secs

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68
Q

cluster headache pain quality

A

sharp, throbbing

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69
Q

paroxysmal hemicrania pain quality

A

sharp, throbbing

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70
Q

SUNCT pain quality

A

stabbing, burning

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71
Q

cluster headache pain intensity

A

v severe “suicide headache”

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72
Q

paroxysmal hemicrania pain intensity

A

v severe

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73
Q

SUNCT pain intensity

A

v severe

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74
Q

cluster headache circadian periodicity

A

70%

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75
Q

paroxysmal hemicrania circadian periodicity

A

45%

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76
Q

SUNCT circadian periodicity

A

absent

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77
Q

cluster headache - the attack: pain location

A

mainly orbital and temporal - affects first division of CN5

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78
Q

cluster headache - the attack: unilateral or bilateral?

A

strictly unilateral

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79
Q

cluster headache - the attack: onset

A

rapid

max within 9mins in 86%

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80
Q

cluster headache - the attack: resolution

A

rapid cessation of pain

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81
Q

how do patients appear during a cluster headache attack (compared to migraines)?

A

restless and agitated

vs migraines - motion sensitivity (want to stay still)

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82
Q

cluster headache attack other symptoms

A

prominent ipsilateral autonomic symptoms

migrainous symptoms often present

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83
Q

migrainous symptoms

A

premonitory symptoms - tiredness, yawning
associated symptoms - nausea, vomiting, photophobia, phonophobia
aura in 14%

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84
Q

what % of cluster headache bouts are episodic?

A

80-90%

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85
Q

what % of cluster headache bouts are chronic?

A

10-20%

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86
Q

episodic cluster bouts defintion

A

attacks ‘cluster’ into bouts typically 1-3months with remission lasting at least one month

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87
Q

episodic cluster headaches pain between attacks?

A

may be continuous background pain between attacks or symptom free between attacks

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88
Q

episodic cluster headaches and alcohol

A

triggers attacks during a bout but not in remission

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89
Q

cluster headaches circadian periodicity

A

attacks occur at same time each day

bouts occur at the same time each year

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90
Q

chronic cluster headaches definition

A

bouts last >1 year without remission
or
remissions last <1 month

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91
Q

location of pain in paroxysmal hemicrania

A

mainly orbital and temporal

strictly unilateral

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92
Q

paroxysmal hemicrania - onset

A

rapid

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93
Q

paroxysmal hemicrania - resolution

A

rapid cessation of pain

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94
Q

paroxysmal hemicrania - what % are restless and agitated during an attack?

A

50%

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95
Q

paroxysmal hemicrania other symptoms

A

prominent ipsilateral autonomic symptoms

migrainous symptoms may be present

96
Q

what can 10% of paroxysmal hemicrania attacks be precipitated by?

A

rotating or bending the head

97
Q

paroxysmal hemicrania - any background continuous pain?

98
Q

what % have chronic paroxysmal hemicrania?

99
Q

what % have episodic paroxysmal hemicrania?

100
Q

paroxysmal hemicrania - which drug do patients have an absolute response to (and is one of the diagnostic criteria)?

A

indomethacin (NSAID)

101
Q

drug therapy for cluster headache - abortive for attack

A

subcutaneous sumatriptan 6mg or nasal zolmatriptan 5mg
100% O2 7-12l/min via a non-rebreathing mask (effective and safe)
- no smokers in household for home oxygen therapy

102
Q

drug therapy for cluster headache - abortive for bout

A

occipital depomedrone/lidocaine injection (inject great occipital nerve)
or tapering course of oral prednisolone

103
Q

drug therapy for cluster headache - preventative

A

verapamil
lithium
methysergide
topiramate

104
Q

drug therapy for cluster headache - preventative verapamil

A

(high doses may be required) - contraindicated in patients with cardiac conduction problems, otherwise safety profile good

105
Q

drug therapy for cluster headache - preventative lithium

A

can cause renal toxicity and diabetes insipidus, safety profile not great

106
Q

drug therapy for cluster headache - preventative methysergide

A

inpatient setting

retroperitoneal fibrosis

107
Q

when would patients usually only qualify for CGRP monoclonal antibodies to treat cluster headaches preventatively?

A

if they have failed normal drug treatment

108
Q

abortive treatment for paroxysmal hemicrania

109
Q

prophylactic treatment for paroxysmal hemicrania

A

indomethacin

alternatives if can’t take NSAIDs not great - COX2 inhibitors, topiramate

110
Q

definition of pain

A

an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage

111
Q

what can cloud a patients description of pain?

A

experience - what patient tells us is based on their experience and language skills

112
Q

which group of patients find it difficult to describe pain?

113
Q

4 ways of assessing a pain patient

A

numerical scale 1-10
physical symptoms
emotional symptoms
QOL scores

114
Q

assessment of the pain patient - numerical scale

A

1-10
1D - can’t show effect or emotional impact
can use a 100mm line without numbers and ask patient to point to severity of pain then measure - can be more accurate than when patient sees numbers

115
Q

assessment of the pain patient - physical symptoms

A

pain scores McGill - choose a word from each box to describe quality of pain

116
Q

assessment of the pain patient - emotional symptoms

A

psychological scores - HAD - Hospital Anxiety and Depression Scale - look at emotional impact of pain

117
Q

assessment of the pain patient - QOL scores

A

Oral Health Impact Profile

disability score: what you can’t do because of pain

118
Q

how do we feel pain?

A

nociception
peripheral nerve transmission
spinal modulation
central appreciation
pain is a decision your brain makes - understood in brain
- acute
- chronic - pain can be a decision your brain makes even when no tissue damage

119
Q

motor supply to the face

A

facial nerve

120
Q

motor branches of the facial nerve

A 
temporal
zygomatic
buccal
mandibular
cervical
121
Q

facial nerve - temporal branch

A

frontalis and procerus

122
Q

facial nerve - zygomatic branch

A

eye and around orbit, mid face and smile

123
Q

facial nerve - buccal branch

A

buccinator and upper lip

124
Q

facial nerve - mandibular branch

A

L lip and orbicularis oris

125
Q

facial nerve - cervical branch

126
Q

sensory supply to the face

A

trigeminal nerve

127
Q

ophthalmic nerve sensory branches to face

A 
supratrochlear
supraorbital
lacrimal
infratrochlear
external nasal
128
Q

mandibular nerve sensory branches to face

A

auriculotemporal
mental
buccal

129
Q

maxillary nerve sensory branches to face

A

zygomaticotemporal
zygomaticofacial
infraorbital

130
Q

which nerve other than trigeminal provides sensory innervation to the face?

A

great auricular C2, C3

131
Q

which nerves provide sensory innervation to the back of the head?

A

spinal nerves

  • greater occipital C3
  • third occipital C3
  • lesser occipital C2, C3
  • great auricular C2, C3
132
Q

which cranial nerve is associated with the first pharyngeal arch?

A

trigeminal nerve

133
Q

which cranial nerve is associated with the second pharyngeal arch?

A

facial nerve

134
Q

which cranial nerve is associated with the third pharyngeal arch?

A

glossopharyngeal nerve

135
Q

which cranial nerve is associated with the fourth pharyngeal arch?

A

vagus (superior laryngeal branch)

136
Q

what does the maxillary prominence (dorsal portion) become?

A

future maxilla, zygomatic bone and part of the temporal bone

associated with the maxillary cartilage - gives rise to the incus

137
Q

what does the mandibular prominence (ventral portion) become?

A

the future mandible

associated with Meckel’s cartilage - gives rise to the malleus and sphenomandibular ligament

138
Q

motor branch of facial nerve

A

muscles of facial expression

139
Q

sensory branch of facial nerve

A

small area around concha of external ear

140
Q

special sensory branch of facial nerve

A

taste to anterior 2/3 of tongue via chorda tympani

141
Q

p/s branch of the facial nerve

A

glands - submandibular, sublingual, lacrimal

142
Q

2 roots of facial nerve

A

motor root and sensory root

143
Q

nerves branching off facial nerve before the stylomastoid foramen

A

greater petrosal nerve
nerve to stapedius
chorda tympani

144
Q

nerves branching off facial nerve after the stylomastoid foramen

A

posterior auricular nerve
nerve to digastric
nerve to stylohyoid
terminal motor branches

145
Q

sensory innervation of the external ear

A 
lesser occipital C2, C3
facial
great auricular C2, V3
auricular branch of vagus
auriculotemporal
146
Q

what nerve supplies the internal surface of the tympanic membrane?

147
Q

where are the cells in the trigeminal ganglion derived from?

A

neural crest

148
Q

what are the 3 trigeminal nuclei and where are they located?

A

mesencephalic nucleus - midbrain
principle sensory nucleus (pontine trigeminal nucleus) - pons
spinal nucleus - medulla

149
Q

nuclei vs ganglia

A

nuclei situated within CNS

ganglia outside CNS

150
Q

what does the trigeminal ganglion bring in?

A

peripheral nerves

151
Q

why do all the nerves synapse in the trigeminal ganglion?

A

join up in same place as all came from same place embryologically

152
Q

referred pain

A

where pain is felt is not where it is generated

nerves all in close proximity so sometimes misperception - because of way nerves connect into the trigeminal nucleus

153
Q

what condition is referred pain common in?

A

TMD - pain over midface

154
Q

what can sensory nerve supply be split into?

A

somatic (part of CNS associated with voluntary control of body movements via skeletal muscles)
autonomic
- sympathetic
- parasympathetic

155
Q

give an example of autonomic referred pain?

A

jaw pain when climbing stairs - may be angina

156
Q

somatic reflex arc

A

sensory neuron - relay neuron - motor neuron
always involve CNS
info to brain but also local connection to motor nerve
automatic response - for protection

157
Q

how does the autonomic reflex arc vary from the somatic?

A

motor output side
in CNS may or may not be an interconnector neuron involved
motor output involves 2 motor neurons

158
Q

motor output in autonomic reflex arc

A

2 motor neurons
first located in CNS (spinal cord)
second in PNS in an autonomic ganglion

159
Q

what is the effector in an autonomic reflex arc?

A

not skeletal muscle
may be smooth muscle e.g. gut wall, or sweat gland or adrenal medulla
peristalsis, nausea, sweating etc

160
Q

what symptoms indicate autonomic pain transmission - reflex arc?

A

reflex vascular vasodilatation - sore area fills with blood - swelling and hot

161
Q

long reflex

A

involves spinal cord - somatic and autonomic

sensory receptor cell synapse with motor in CNS - if autonomic also peripheral ganglion

162
Q

short reflex

A

autonomic only
completely peripheral, only involves the local integration of sensory input with motor output
sensory receptor cell synapses only in peripheral ganglion

163
Q

peripheral sensitisation

A

“increased responsiveness and reduced threshold of nociceptive neurons in the periphery to the stimulation of their receptive fields”

164
Q

Gate control of chronic pain (Melzak and Wall)

A

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

can also get descending facilitation/inhibition - descending nerves from brain
- e.g. if you expect pain it makes nerve easier to fire

165
Q

neuronal plasticity

A

sprouting of spinal segment nerves - sensory fibre becomes stimulatory - so if you touch it it feels sore

a way body manages pain unhelpfully - normal feeling being felt as pain
can have real pain without a findable cause

166
Q

pain modulating receptors - biochemical

A

adrenergic - effect on pain
opiate - effect on mood

NMDA - causes misery and pain (ketamine binds to this)

167
Q

pain sensitisation

A

inflammation - sensitisation
peripheral or central
chemical balance within pain is complicated

168
Q

learned pain

A

brain can learn to expect pain from an area - even when you remove cause they might still feel it

169
Q

drugs which target nerve endings

A

LAs

NSAIDs

170
Q

drugs which target the primary afferent nerve

171
Q

drugs which target the dorsal root ganglion

A

LAs, a2 agonists

172
Q

drugs which target the dorsal horn

A

opioids
ketamine
gabapentinoids

173
Q

drugs which target the descending noradrenergic and serotoninergic inhibitory fibres

A

opioids
a2 agonists
TCAs
SSRIs

174
Q

location of CRPS

A

delocalised pain
spreads around ‘anatomical’ boundaries
bilateral
often autonomic nerve damage - don’t follow boundary of somatic nerves

175
Q

symptoms of CRPS

A

gripping, tight, burning
feeling of swelling and heat (increased blood flow)
colour change in overlying skin
significantly disabling
autonomic changes - autonomic nerve version of neuropathic pain

176
Q

management of CRPS

A

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)

177
Q

nociceptive pain

A

caused by activity in neural pathways in response to potentially tissue damaging stimuli

178
Q

examples of nociceptive pain

A 
post-op pain
mechanical low back pain
sports/exercise injuries
sickle cell crisis
arthritis
179
Q

mixed type pain

A

caused by a combination of both primary injury or secondary effects

180
Q

what is neuropathic pain initiated/caused by?

A

primary lesion or dysfunction in the somatosensory nervous system
usually a history of ‘injury’ - can follow facial trauma, extractions, ‘routine’ treatment without complications
can get non-specific neuropathic pain

181
Q

types of neuropathic pain

A

spinal cord injury
diabetic neuropathy
post-herpetic neuralgia (virus damages nerves)
neuropathic low back pain
distal polyneuropathy (e.g. diabetic, HIV)
central post-stroke pain (damage parts of brain processing pain)
trigeminal neuralgia
CRPS
MS

182
Q

most common type of neuropathic pain

A

diabetic neuropathy

183
Q

symptoms of neuropathic pain

A

constant burning/aching pain
fixed location
often a fixed intensity
- nerve damage there all the time and in the same place all of the time

184
Q

neuropathic pain - genetic predisposition?

A

nerve ion channels that heal badly after injury
persistent inflow gives persistent information reporting
- inherit a particular type of channel that heals less well - more likely to get neuropathic pain

185
Q

why can patient management with neuropathic pain be difficult?

A

patient perceives the pain in the end tissue not where the nerve is damaged

186
Q

when can you see neuropathic pain dentally?

A

after a tooth extraction if tear nerve endings - analgesics not working
can present similarly to toothache - don’t extract as won’t get rid of pain

187
Q

potential causes of neuropathic pain - 4 broad categories

A

disease process
trauma
genetic predisposition
therapeutic intervention

188
Q

potential causes of neuropathic pain - disease process

A

infection/inflammation
neurotoxicity
tumour infiltration
metabolic abnormality

189
Q

potential causes of neuropathic pain - trauma

A

external injury
nerve compression
inflammation

190
Q

potential causes of neuropathic pain - genetic predisposition

A

inherited neurodegeneration

metabolic/endocrine abnormalities

191
Q

potential causes of neuropathic pain - therapeutic intervention

A

surgery
chemotherapy
irradiation

192
Q

neuropathic pain - if autonomic nerve associated what other symptoms may you get?

A

associated heat/swelling

193
Q

options for management of neuropathic pain

A

systemic medication
topical medication
physical
psychological

194
Q

systemic medication for neuropathic pain

A

pregabalin
gabapentin
>they work on nerve conduction to turn down the vol

tricyclics - works centrally, reduces transmission in CNS

valproate
mirtazepine
opioid analgesics

195
Q

topical medication for neuropathic pain

A

capsaicin
EMLA
benzdamine
ketamine

196
Q

how does capsaicin work for neuropathic pain?

A

like gate theory - switches off nerve to pain

but hard to use in mouth - chilli peppers - can give burning sensation

197
Q

physical management of neuropathic pain

A

TENS - occ helpful (low frequency)

acupuncture - good results

198
Q

psychological management of neuropathic pain

A

distraction- train patient not to pay attention to pain
correct abnormal illness behaviour - people don’t do things because of pain - make QOL better
improve self-esteem/positive outlook

199
Q

understanding pain - barbie

A

your brain has a map of you “barbie”, then projects pain to the actual bit of you - you have learned to ‘feel’ it in arras. brain projects it into a reconstruction of yourself

200
Q

understanding pain - if you change balance of neurotransmitters what happens?

A

brain percepts things differently as env of perception has changed

201
Q

phantom limbs

A

pts can still tell you exactly what it feels like as they feel it the same as we feel our arm
brain continues perception of arm even though physical inflammation gone
body perceives phantom as it perceives limb
often brain barbie persists as it was initially

202
Q

phantom limbs- how do you re-educate the brain to behave differently with a phantom?

A

mirrored box

203
Q

neglect as consequence of stroke

A

limbs don’t match up with barbie

204
Q

body dysmorphia

A

perception of how you see your body is wrong

due to change in biochemistry and perception

205
Q

cognitive deduction

A

make wrong decision about what is real

206
Q

atypical odontalgia

A

dental pain without dental pathology (toothache without any disease)
treating the tooth won’t make barbie’s tooth better
v difficult to diagnose

207
Q

gender distribution of atypical odontalgia

208
Q

atypical odontalgia - distinct pattern of pain

A

pain free or mild between episodes
intense unbearable pain
- 2-3 weeks duration
- settles spontaneously

209
Q

sequelae of atypical odontalgia

A 
acute pulpitis pain
endo relieves or reduces pain
- pain returns after a short time
extraction relieves pain
 - pain returns in adjacent tooth after a short time
endo relieves/reduces pain
 - pain returns after a short time
extraction relieves pain
 - pain returns in adjacent tooth after a short time
pt referred
210
Q

features of atypical odontalgia

A

typical acute pulpitis symptoms
‘irrational behaviour’ - high motivational drive
‘beg’ for dental extractions
go elsewhere with modified story if extraction refused
suspect in patient with unusual extraction distribution

211
Q

management of atypical odontalgia - primary care

212
Q

management of atypical odontalgia - oral medicine

A

chronic strategy
- 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

213
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 a diagnosis of exclusion - exclude all the other categories
214
Q

symptoms of persistent idiopathic facial pain

A

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

215
Q

management of persistent idiopathic facial pain

A 
believe pt - do not blame any associated depression for symptoms
do not increase damage - surgery is not helpful
adopt holistic strategy
 - QOL issues
 - pain control a bonus
 - realistic outcomes - pt and clinician
use QOL/pain scores as tx monitor
often respond poorly to treatment
216
Q

oral dysaesthesia

A

abnormal sensory perception in absence of abnormal stimulus
somatoform or neuropathic?
- where is the problem?
anxiety makes barbie confused - usually anxious but not depressed
ALL modes of oral sensation involved
- burning or ‘nipping’ feeling. thermal
- dysgeusia. taste
- paraesthesic feeling. touch
- dry mouth feeling. moistness

217
Q

oral dysaesthesia - predisposing factors

A

deficiency states?
- haematinics, zinc, vit B1, B6
fungal and viral infections?
anxiety and stress? - tend to be chronic worriers

218
Q

aetiology of oral dysaesthesia

A

F sex predominance
dissociated anxiety disorder
often associated symptoms
- poor sleep pattern - early morning waking
- swallowing problems - ‘globus sensation’ - catching in throat when eating, GORD
- IBS, dyspepsia, back pain
- body pain conditions, fibromyalgia

219
Q

burning mouth syndrome

A

dysaesthesia most likely to be associated with haematinic deficiency
site important
- lips and tongue tip/margin = parafct. - clenching and rubbing tongue on back of teeth - provide splint
- multiple other sites - dysaesthesia

220
Q

dysgeusia

A 
bad taste/ bad smell/ halitosis
nothing detected by practitioner (barbie has it)
nothing found on examination
remember
 - ENT causes - chronic sinusitis
 - perio/dental infection
 - GORD
nothing detected by patients partner?
leads to patient being isolated
221
Q

touch dysaesthesia

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
MRI essential - demyelination/tumour - MS can cause it

222
Q

dry mouth dysaesthesia

A

very common
C/O debilitating dry mouth/Sjogrens
eating ok, worse when waken at night
usually the most obviously associated with anxiety disorders
feel they have a dry mouth even if they don’t - it is a perceptual change

223
Q

management of dysaesthesia - medication

A

tricyclic antidepressants (for anxiety) e.g. nortriptyline
- SE is dry mouth - they feel it differently to their other “dry mouth”
“neuropathic” medication - gabapentin, pregabalin (slso anxiolytic)
slow tx - takes 3-6m, work gradually - get decrease in frequency of symptoms

neuropathic topical medication

  • clonazepam - topical?
  • works as some patients may have neuropathic problem whereas some may have perceptual problem
224
Q

management of dysaesthesia - other than medication

A

explain the condition to the pt

  • ‘pins and needles’ in the taste etc
  • ‘feeling’ problem rather than physical problem - we need to treat the feeling rather than the presenting problem
assess degree of anxiety
 - anxiolytic medication - nortriptyline, mirtazepine
 - clinical psychology
tx empower the patient
 - control is important
225
Q

classifying TMD patients

A

joint degeneration (doesn’t mean pain)
- pain on use plus crepitus, +/- rest pain
internal derangement - disc issues, meniscus
- locking open or closed
no joint pathology

226
Q

what is the cause of TMD?

A

occlusion - not cause of TMD in vast majority of patients
grinding
clenching
stress

227
Q

patients seeking treatment for TMD

A

F higher - more likely to present
want rid of pain
- occasionally noise or locking is the problem
don’t want to take meds or change lifestyle
don’t see any activity which aggravates the condition

228
Q

TMD disorders

A 
multi-axis problem
usually systemic disorder
 - 'pain vulnerable people'
 - many systemic symptoms
high anxiety and low depression
 - no psychiatric diagnosis in most cases
parafct a strong feature 
 - scalloping of tongue, ridging on buccal mucosa
229
Q

TMD disorders - what is barbie doing?

A

anxiety making barbie confused?
barbie reporting on body pathology?
is pain peripheral - sore muscles - making barbie sore?
is barbie sore - central pain - causing muscle contraction?
- barbie’s pain can make you clench your teeth

230
Q

physical signs in TMD

A 
clicking joint
locking with reduction
limitation of opening mouth
tenderness of MofM
tenderness of cervico-cranial muscles
231
Q

TMD with no pathology

A

can have a motor output even if nothing happening

232
Q

TMD history

A 
acute pain in face and neck
ANY chronic face, head and neck pain
symptoms show periodicity
 - morning/evening exacerbation
parafct clenching
history is the key to successful management
233
Q

TMD examination findings

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
234
Q

TMD investigations

A

usually none indicated for ‘functional’ disorders
indications for imaging
- US 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

235
Q

management of TMD

A 
eliminate organic cause
'empower' pt
 - cognitive therapy
 - chronic disease - self-help
physical therapy
 - CBT education+/- exercises
      - soft diet and analgesics
 - bite splint
biochemical manipulation
 - tricyclic (not SSRI)
 - other anxiolytic meds
physiotherapy
acupuncture
clinical psychology
236
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 disharmony, physical abuse

Oral medicine (14 decks)

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