Facial Pain Flashcards

1
Q

What is pain?

A

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

Patient will usually describe their pain in relation to something they have already experiences- “worse than child birth”.

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2
Q

What modes of assessment could you use during the history process for a pain patient?

A

QOL scores- determines how the pain is affecting the patient’s every day life

McGill’s pain score- the patient ticks one in each box which most describes the patient’s pain.

Psychological scores- how does the pain make you feel?
- State- Trait anxiety inventory.
- Back depression inventory II.

Quality of sleep
- Pittsburgh sleep quality index
- Epwirth Sleepiness scale

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3
Q

How do we feel pain?

A

Peripheral nociceptors will detect a painful stimulus.
This is transmitted through the peripheral nerve to the spinal cord.
Then from the spinal cord, via the ascending pain C fibres.

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4
Q

What forms the head and neck?

A

Pharyngeal arches and pharyngeal clefts

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5
Q

What does the first pharyngeal arch give rise to?

A

Trigeminal nerve, structures supplied by this nerve- MOM, digastric, mylohyoid, etc.

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6
Q

What does the second pharyngeal arch give rise to?

A

Facial nerve, muscles of facial expression, stapedius, Digastric, stylohyoid muscle, styloid process.

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7
Q

Why is it important to know what arises from each pharyngeal arch, with regards to pain?

A

The pain the patient is describing might not make sense initially but think about the embryological origin and it might start to make sense.

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8
Q

Describe the branches of the facial nerve.

A

Sensory root- supplies the ear
Motor root- muscles of facial expression

Greater petrosal nerve- secretomotor to the lacrimal gland

Nerve to Stapedius- motor innervation to the stapedius muscle

Chorda Tympani- taste to anterior 2/3 of the tongue and secretomotor fibres to sublingual and submandibular.

Posterior auricular nerve- mastoid process and skin overlying the auricle.

Nerve to digastric- digastric muscle

Nerve to stylohyoid- stylohyoid.

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9
Q

Why is it important to understand the different branches of the facial nerve?

A

Patient symptoms can tell you which part of the facial nerve is damaged.

i.e. if they are very sensitive to loud noises, this would suggest the nerve to stapedius is damaged.

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10
Q

What nerves are involved in somatic nerve control?

A

CN V, VII, IX, X and Cervical 1-3.

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11
Q

What is referred pain?

A

Pain location is misinterpreted

Patient’s source of pain and the patient’s perceived location of the pain is different.

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12
Q

What is the anatomical basis of sensory referred pain?

A

Different nerves from different areas of the head and neck can synapse in the same place- i.e. trigeminal nucleus.

So this can cause pain to be felt at other locations.

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13
Q

What are autonomic nerves?

A

Sympathetic and parasympathetic nerves- cannot control autonomic nerves but they control you.

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14
Q

Why can pain transmitted to the brain via autonomic nerves be misinterpreted?

A

The nerve supply of a lot of different structures in the head and neck co-ales to one cervical ganglion in the spinal cord, which is then sent to the brain.

So the source of the pain and the feeling of pain can be coming from two different places.

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15
Q

Describe the somatic reflex arc?

A

Pain produces a change which causes damage to an ear of somatic nerve supply.

Signal will pass up the somatic nerve (afferent), through the interneuron and then to the CNS.

But also, at the level of the spinal cord, there is another neuron (motor), which is producing a synapse with the interneuron (efferent), which will pull the affected limb away from the sight of damage and cause muscle contraction.

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16
Q

Describe the autonomic reflex arc?

A

Sensory nerves supply information in through the autonomic nerve supply, into the spinal cord and then signals can either stay in the spinal cord and/or go up to the brain.

The reflex arc then comes from the spinal cord, via the sympathetic ganglion, to produce an autonomic reflex.

This might result in sweating, oedema, erythema, eyes water.

When patients say they have pain, they may also say they get really sweaty and red- this is the autonomic vasomotor reflex.

This would suggest they have autonomic changes in their pain.

17
Q

Describe the process of peripheral nociception?

A

Tissue damage causes release of 5-HT and Bradykinin.

These will act on the nociceptor, produce an action potential and this is transmitted via the peripheral nerve to the spinal cord.

18
Q

What is Peripheral sensitisation and does it occur in nociception?

A

Substance P and Prostaglandins are also released following tissue damage and act as neurotransmitters to trigger the nociceptor.

They also act to peripherally sensitise the tissues by increasing pro-inflammatory mediators.

19
Q

Describe the gate control theory of pain?

A

Pain is felt in the periphery, send a pain signal to the nociceptor via the peripheral nerve and into the spinal column.
- The ascending pain nerve, C fibre is then stimulated and signals to the brain that there is a painful stimuli.

Standard touch felt in the periphery is transmitted via the sensory fibre and it stops the nociceptor from firing to the brain- inhibitory effect.
- you also have the Abeta fibres which transmit sensory stimuli to the brain- not painful.

Cross over between the pain fibres and sensory fibres has an inhibitory effect.
- When the touch signal is transmitted, it helps prevent any pain signal coming in from the periphery form passing that info to the CNS.
- So when you have a painful sensation and you rub it, the painful sensation is blocked via the inhibitory fibres caused by the touch sensation.

Also have descending facilitation and descending inhibition.

20
Q

In terms of chronic pain, describe descending facilitation and descending inhibition?

A

Pain signal has already been sent to the brain from the spinal cord, via the ascending nerve fibres.

Once this signal reaches the brain, pain is felt but the brain then sends descending nerve fibres, which can facilitate further pain (chronic pain) or inhibit (stop the pain).

The descending facilitation pathway primes the nociceptor to respond to a less painful stimuli that you usually wouldn’t perceive as painful and it gets you geared up for a potential future stimuli.

21
Q

What is neuronal plasticity?

A

Neuronal plasticity occurs in chronic pain.

If you have chronic pain, you can get sprouting from the spinal sensory nerves which connect to the interneuron within the spinal cord and can stimulate this pathway- so the adaptations within the CNS, make it easier for pain to be passed to the brain from simple touch.
Sensation makes it easier for pain signals to be passed to the brain.

Even if the pain cause is removed, the patient may still feel pain because they have the connection between normal sensation and pain interneurons.

22
Q

What is Chronic Regional Pain Syndrome?

A

A stimulus triggers the reflex arc, usually caused by a previous injury to the limb or organ, which causes a reaction.

Delocalised pain- spreads around anatomical boundaries.
Bilateral
“gripping”, tight, burning.

Feeling of swelling and heat, colour change in overlying skin, autonomic changes.

Significantly disabling.

23
Q

What is the difference between nociceptive pain and neuropathic pain?

A

Nociceptive pain- caused by activity in neural pathways in response to potential tissue-damaging stimuli.

Neuropathic pain- Initiated or caused by primary lesions or dysfunction in the nervous system.

24
Q

How would you assess someone who was in pain?

A

SOCRATES

Could use PAIN scores by McGill for physical symptoms.
Psychological score to assess emotional symptoms (HAD).
QoL scores to determine the impact that the pain has on the patient’s day to day life.

25
Q

Give examples of disorders that are classed as neuropathic pain?

A

Trigeminal neuralgia
CRPS
Postherpetic neuralgia
Diabetic neuropathy
Multiple Sclerosis

26
Q

What are the signs and symptoms of neuropathic pain?

A

Constant burning/aching pain
Fixed level of pain
Fixed location- the nerve damage equates to a particular tissue in the body

Genetic presdisposition- susceptibility of nerve damage relating to the type of injury.

Usually a history of injury- any damage to the tissues.
In susceptible person, even innocuous triggers will cause them pain.

27
Q

What typical “injuries” may cause neuropathic pain?

A

Facial trauma
Extractions
Surgery
Chemotherapy/radiotherapy
Routine treatment without complications
Herpes zoster virus- shingles episode.
Nerve compression
Inflammation
Genetic predisposition

28
Q

What topical medication may be used for neuropathic pain?

A

Capsaicin
EMLA
Benzdamine
Ketamine

They irritate the surface of the skin, around the area that of where the pain is coming from and this helps to gait the patient off to their pain perception.

29
Q

What systemic drugs may be used for neuropathic pain?

A

Pregabalin
Gabapentin
Tricyclic
Duloxetine

30
Q

What alternative neuropathic pain management methods could be utilised?

A

Physical
- TENS- irritates the surface of nerves and gaits off the pain signals.
- Acupuncture

Psychological
- Distraction
- Correct illness behaviours
- Improve self esteem

31
Q

What is Atypical Odontalgia?

A

Dental pain without dental pathology.

32
Q

What are the signs and symptoms of Atypical Odontalgia?

A

Distinct pattern of pain- patient will have pain free episodes but when they get the pain, it is unbearable.
Pain will last for a few weeks and then spontaneously settle but then return weeks later.

Equal sex distribution.

33
Q

What should a dentist do about Atypical Odontalgia?

A

History
I/O and E/O
Vitality test- if negative provide endo treatment, if positive then further tests.
Take PA radiograph- look for PA radiolucency.
Check for cracked tooth- if positive- provide endo or XLA. If negative- perform anaesthetic test.
If the pain goes away when the tooth is anaesthetised- need to determine whether it is a dental issue or peripheral issue.
If pain persists, then refer to specialist.
Check for hyperocclusion- adjust if required.

34
Q

As a GDP, what would you do to manage a patient who you suspects has Atypical Odontalgia?

A

If no dental pain indicated and pain persists- refer to oral medicine.

Opioid analgesics are require- Dihydrocodeine.

35
Q

What cohorts of patients cannot take dihydrocodeine?

A

Hypotension
Asthma
Pregnancy/breast feeding
Renal/hepatic disease
Elderly/children

36
Q

What are the side effects of Dihydrocodeine?

A

Nausea/vomiting
Constipation
Drowsiness

37
Q

What is the dosage of dihydrocodeine that dentists can prescribe?

A

30mg every 4-6 hours as necessary.
Take during acute pain episodes.

38
Q

What is Persistent Idiopathic Facial Pain?

A

Pain which poorly fits into standard chronic pain syndromes.

Patients usually have a high disability level from their pain.

39
Q

As a GDP, what is your role if a patient has Persistent Idiopathic Facial Pain?

A

Believe the patient when they say they are experiencing pain.

Do not increase damage- surgery is not helpful.

Adopt holistic strategy- quality of life issues, pain control, realistic outcomes.