Facial Pain Flashcards
1
Q
Which areas can pain be felt along the pain transmission pathway
A
- nociception
- peripheral nerve
- spinal modulation
- central appreciation
2
Q
What fibres mediate nociceptive pain
A
a delta
c
3
Q
Describe the nociception pathway
A
- Nociceptors detect noxious stimuli, they are peripheral cell nerve endings
- Noxious stimuli stimulates a action potential
- Afferent nerves (peripheral nerves) carry the action potential and relay the message to the central nerveous system (A-delta and C fibres)
- CNS relay cells carry the message through the spinal dorsal horn/spinal trigeminal nucleus - relay nerves can produce reflex for protection, bypassing the brain
- The message is carried via the CNS pathway - spinothalamic tract or anterior-tigeminothalamic tract
- It is then recieved by the forebain (thalamus)
4
Q
How can peripheral nerves cause pain
A
- These are the nerves that carry the stimuli from the nociceptors to the central nervous system
- Damage to peripheral nerves can cause chronic pain
5
Q
What is spinal modulation
A
This is the process of alterations in the pain signals along the transmission pathway of pain
It explains why individuals respond to the same stimuli differently
6
Q
What forms from the first pharyngeal arch
A
Trigeminal nerve, muscles of mastication, malleus, incus, meckel’s cartilage
7
Q
What forms from the second pharyngeal arch
A
Facial nerve, muscles of facial expression, hyoid
8
Q
What forms from the third pharyngeal arch
A
Glossopharyngeal nerve, stylopharyngeus, common carotid artery, hyoid
9
Q
What forms from the fourth and sixth pharyngeal arch
A
Vagus nerve, muscles of pharynx and larynx, aortic arch, laryngeal cartilages
10
Q
What are the somatic nerves that supply the H&N
A
CN 5, 7, 9, 10 as well as C1, C2, C3
11
Q
Can pain be transmitted through autonomic nerves
A
yes
12
Q
What is referred pain
A
- Pain is felt in one part of the body but it originates from somewhere else
13
Q
Why does referred pain happen
A
- Tends to be referred to areas of common embryological origin
- Referral is due to convergence of inputs into the CNS
- Both somatic and autonomic nerves can produce referred pa
14
Q
Describe the peripheral nociception pathway
A
- Tissue damage causes production of substance P prostaglandins, 5-HT bradykinin which act on the nociceptor to produce an action potential that is transmitted through peripheral nerves and ends up as a signal in the spinal cord
15
Q
What is the gatecontrol theory of pain
A
- Rubbing the skin where the pain is can disrupt the sensation of pain in a phenomenon referred to as gate control theory
- Rubbing the skin causes the A-beta fibres to transmit mechanical stimuli impulses and these fibres projection into the spinal cord, one of the branches activates an inhibitory interneuron
- The inhibitory interneuron causes the inhibition of secondary order pain projecting neuron and by inhibiting this, it stops the conduction of pain via the pain pathway
16
Q
What is descending inhibition
A
Descending inhibition is where you allow function to continue despite pain input, the interneuron has been rendered less sensitive
17
Q
What is descending facilitation
A
results in pain being felt more than normal - linked to pain expectation
18
Q
What is neuronal plasticity
A
- Defined as the ability of neural networks in the brain to change through growth and reorganization
- It is when the brain is rewired to function in some way that differs to how it previously functioned
19
Q
Describe how chronic pain results in neuronal plasticity
A
These patients will feel prolonged pain at sights which may have previously had injury but are now currently health
During the period of tissue damage, noxious stimuli and inflammation caused an elevation of nociceptive input from the periphery to the CNS
Prolonged nociception from the periphery then elicits a neuroplastic response at the cortical level to change its somatotopic organisation for the painful site, inducing pain sensitisation
Pain/central sensitisation is defined as an increased responsiveness of nociceptors in the CNS to either normal or sub-threshold afferent input
20
Q
What type of pain does neuronal plasticity result in
A
This type of pain is called nociplastic pain, and is one of 3 pain mechanisms, the other 2 being known as neuropathic pain & nociceptive pain (i.e normal pain)
21
Q
How do we manage these chronic pain px who are at risk of experiencing neuronal plasticity
A
- We want to try and prevent these changes by use of early pain management e.g LA or NSAID will reduce the likelihood of adaptations occuring
22
Q
What are different ways of carrying out a pain assessment
A
- Physical symptoms can be assessed using PAIN scores (McGill)
- Emotional symptoms can be assessed using psychological scores (HAD)
- QoL scores can be useful too (OHIP)
23
Q
What is chronic regional pain
A
- This is a problem that arises from the neuronal plasticity which produces nociplastic pain
24
Q
How does chronic regional pain present
A
- Pain becomes delocalised, pain may be felt elsewhere
- Px may feel pain bilaterally
- May describe the pain as gripping, tight or a burning sensation
- They may also have a feeling of swelling and heat - likely linked to the vasomotor component. Vasodilation resulting from the pain signals, increasing blood flow to the tissues
- Colour changes may be seen in the skin
- Significantly disabling
25
What makes neuropathic pain different from nociceptive pain
Stimulus is generated beyond the nociceptor which remains unactivated
Somewhere between the brain & the nociceptor, there is damage and signals are being sent to the brain
26
What are examples of neuropathic pain
* post-herpetic neuralgia
* trigeminal neuralgia
* neuropathic lower back pain
27
How does zoster virus cause post-herpetic neuralgia
The virus inhabits the nerve and causes damage and the damage remains after the virus & its other symptoms e.g herpetic lesions are gone, resulting in this post-herpetic neuropathic pain
28
What is the presentation of neuropathic pain
Usually constant as nerve damage is there consistently
Usually at a fixed level as the nerve damage remains the same
Fixed location as the nerve supplies a location
Some evidence that some people have a genetic predisposition - their nerve ion channels do not heal properly after injury
29
What is the common injury with neuropathic pain
Usually accompanies a history of 'injury'
‣ Facial trauma
‣ Extractions
‣ 'Routine' tx without complication
‣ Herpes zoster episode (shingles) - known as post-herpetic neuralgia
30
What can the treatments for neuropathic pain be divided into
* systemic medication
* topical medication
* physical
* psychological
31
What are examples of systemic medication that can be used to treat neuropathic pain
* pregabalin
* gabapentin
* tricyclic
32
What are examples topical medication for neuropathic pain
* capasaicin
* EMLA
* benzydamine
33
What are examples of physical tx for neuropathic pain
* TENS - low frequency electrical stimulation
* acupuncture
34
What are psychological treatments for neuropathic pain
* distraction
* correct abnormal illness behaviour
* improve self esteem and increase positive outlook
35
What is atypical odontalgia
* Dental pain without dental pathology
36
What is the presentation of atypical odontalgia
◦ Distinct pattern of pain
◦ Equal sex distribution
◦ Pain free or mild between
◦ Intense unbearable pain for 2-3 week duration and then settles spontaneously
37
What may atypical odontalgia be confused with
acute pulpitis, resulting in unneccessary treatment that only helps the pain in the short term but it returns after a short period of time
38
Before referring an atypical odontalgia px to secondary care, what should you do
* Exclude all possible causes of odontogenic pain
◦ Pulpal pathology
◦ Periapical pathology
◦ Tooth fracture
39
If an atypical odontalgia px does not have any possible dental causes to explain their pain, what should you do next
do an anaesthetic test - does the pain respond to LA, if it does then indicates peripheral nerve damage and appropriate tx should be prescribed: topical anaesthesia, anticonvulsants, tricyclic antidepressants
40
If an atypical odontalgia px comes back with negatiev for anaesthetic test, what should you do
If anaesthetic test is negative, consider MRI
If you see this as a GDP, refer in to secondary care
41
What is the chronic strategy for atypical odontalgia in secondary care
‣ Reduce chronic pain experience
‣ Reduce frequency of acute episodes
42
What is the acute strategy for atypical odontalgia in secondary care
‣ Have a plan to control pain - opioid analgesia as required
‣ High intensity/short duration
‣ Extraction of teeth if needed
43
What is persistent idiopathic facial pain
* Used to be called atypical facial pain - this is an old term and shouldn't be used
* It is a pain that fits poorly into the standard chronic pain syndromes
44
What chronic pain syndromes does persistent idiopathic facial pain not fit into
◦ Neuropathic
◦ CRPS
◦ TMD
◦ Trigeminal Neuralgia
◦ Migrainous Pain
◦ Atypical Odontalgia
45
How does persistent idiopathic facial pain usually present
* Often high disability level - autonomic component
46
What is the best tx for persistent idiopathic facial pain
Clinical psychology is the most successful tx for them, rather than medication
47
What is the management of persistent idiopathic facial pain
Believe patient
Do not increase damage - surgery is not helpful and can worsen the pain
Adopt holistic strategy
‣ Address any QoL issues
‣ Pain control is a bonus
‣ Realistic outcomes - px and clinician
Use QoL and pain scores as tx monitor
48
What is oral dysaesthesia
* Abnormal sensory perception in absence of abnormal stimulus
* Could be neuropathic or somatoform
49
What is neuropathic pain
the nerves carrying the information to the brain are functioning incorrectly
50
What is somatoform pain
the understanding of the incoming information is misunderstood
51
What condition are somatoform conditions usually linked with
often linked to anxiety as anxiety can change the way the perception of the brain works and with oral dysaesthesia, anxiety is the most commonly linked condition
52
How can oral dysaesthesia present
* all modes of oral sensation involved
* burning mouth syndrome
* dysgeusia
* touch dysaesthesia
* dry mouth dysaesthesia
53
What is burning mouth syndrome most likely to be linked to
‣ Dysaesthesia most likely to be associated with haematinic deficiency resulting in changes to the mucosa of the mouth
54
Why is the site of burning mouth syndrome significant
‣ The site of the symptoms is important - if it is felt in the lips, tongue tip and margins it is likely due to parafunction
‣ If they experience pain in other areas e.g palate, most likely dysaesthesia
55
What is dysgeusia
‣ Complain of bad taste/bad smell/halitosis
‣ No findings on examination
56
How should you manage dysgeusia
‣ Ask the px if these bad smells have been noticed by any one around them
‣ Rule out any other causes
* ENT causes e.g chronic sinusitis
* Periodontal/dental infection
* GORD
57
What is touch dysaesthesia
‣ Px feel a tingling and pins and needles like sensation
‣ They will show a normal sensation to objective testing
58
What should be carried out in a px with touch dysaesthesia
‣ It is important to do a cranial nerve test and MRI to exclude organic neurological disease such as demyeliniation of nerves or any tumours
‣ Exclude local causes e.g infection and tumour
59
What is dry mouth dysaesthesia
‣ Very common
‣ Complain of debilitating dry mouth
‣ Worse when waken at night
60
How should you manage dry mouth dysaesthesia
‣ Usually the most obviously associated with anxiety disorders
‣ Do the usual salivary tests
61
What are predisposing factors for oral dysaesthesia
* deficiency states
* fungal and viral infections
* anxiety and stress
* gender
62
What deficiency states can predispose to oral dysaesthesia
‣ Haematinics
‣ Zinc
‣ Vitamin B1 and B6
63
What gender is most likely to have oral dysaesthesia
women
64
What is the management of oral dysaesthesia
* explain condition to px
* assess degree of anxiety
* consider anxiolytic medication
* clinical psychology
* neuropathic medication
* give px control over tx
65
What conditions can TMD be classified into
* joint degeneration
* internal derangement
66
What should we be looking out for when thinking of joint degeneration
‣ Pain?
‣ Crepitus?
‣ Pain at rest?
‣ Pain localised
‣ Often have other arthritic diseases
67
What is internal derangement
‣ Locking on opening and closing
68
What are signs to look out for with TMD
◦ Clicking joint
◦ Locking with reduction
◦ Limitation of opening mouth
◦ Tenderness of masticatory muscles
◦ Tenderness of cervico-cranial muscles
69
What do we look for in the history for TMD
◦ Acute pain in face and neck
◦ Any chronic face, head and neck pain
◦ Symptoms show periodicity - morning and evening exacerbation
◦ Parafunctional clenching
◦ History is clear for successful management
70
What are important examination findings for TMD
◦ Focal muscle tenderness
◦ Tenderness over TMJ
◦ Limited mouth opening
◦ Joint noise
◦ Deviation on opening
‣ Common finding with muscle dysfunction
71
What investigations do we do for TMD
* usually none
* imaging if indicates
72
When is ultrasound indicated for TMD
* If functional visualisation of disc movement needed
73
When is CBCT indicated for TMD
* If bony problem suspected
74
When is MRI indicated for TMD
* Gold standard
* Only for those with severe locking etc
75
When is arthroscopy indicated for TMD
to directly visualise the disc
76
What can management of TMD be split into
* information
* physical therapy
* biochemical manipulation
* acupuncture
* clinical psychology
77
What does phsyical therapy for TMD consist of
‣ CBT
‣ Physiotherapy
‣ Bite splint
‣ Soft diet
‣ Analgesia
78
What does biochemical manipulation for TMD consist of
‣ Tricyclic antidepressants - not SSRI, SSRI linked to increased symptoms
‣ Other anxiolytic medication e.g diazepam but only for short periods
79
What should we be aware of with children presenting with TMD
◦ Tendency to anxiety neurosis
◦ Maladaptive response to normal change
◦ May experience abuse at school or at home
