Orofacial Pain

Question 1

What is pain?

Answer 1

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

Question 2

What are the different pain assessments that can be used when a patient presents with facial pain?

Answer 2

• McGill pain questionnaire- gives choice of words that they patient may relate to pain
• Emotional symptoms- Hospital anxiety and depression scale (can see how chronic pain impacts patients’ life)
• Oral health impact profile (QoL)- looks at activities that are stopped by pain

Question 3

What are the steps that lead to us feeling pain?

Answer 3

Nociception- pain is generated (can be inappropriate or interfered with)

Peripheral nerve transmission (transmits pain from nociceptive receptors to CNS)
 Can interfere with this by medicine
 Damage to peripheral nerves can lead to sensation of chronic pain

Spinal modulation

Central appreciation

Question 4

What is unusual in terms of anatomy about facial pain?

Answer 4

It sometimes doesn’t follow distribution/anatomical boundaries of the nerve (consider other nerves supply that could be causing pain not as you would expect)

Question 5

What is the artery, CN, muscles and skeletal features that come from 1st pharyngeal arch?

Answer 5

Artery- maxillary

CN- Trigeminal

Muscles- MoM, tensor tympani, mylohyoid, tensor veli palatani, anterior belly of digastric

Skeletal features- incas, malleus, tympanic ring, meckel’s cartilage, sphenomandibular ligament

Question 6

What is the artery, CN, muscles and skeletal features that come from 2nd pharyngeal arch?

Answer 6

Artery- hyoid artery, stapedial artery

CN- Facial

Muscles- muscles of facial expression, stapedius, stylohyoid, posterior belly of digastric

Skeletal features- Stapes, styloid process, lesser horn/body of hyoid, stylohyoid ligament

Question 7

What is the artery, CN, muscles and skeletal features that come from 3rd pharyngeal arch?

Answer 7

Artery- Internal carotid

CN- Glossopharyngeal

Muscles- Stylopharnygeus

Skeletal features- greater horn/body of hyoid

Question 8

What is the artery, CN, muscles and skeletal features that come from 4th pharyngeal arch?

Answer 8

Artery- subclavian

CN- vagus

Muscles- pharyngeal/laryngeal musculature

Skeletal features- Laryngeal cartilages

Question 9

What are the extra functions of the facial nerve?

Answer 9

• Sensory root- supplying ear
• Motor- stapedius
• Chorda tympani fibres carried with it- taste
• Stimulatory supply to salivary glands (greater petrosal nerve)

Question 10

Why is it difficult for patients to distinguish whether pain coming from trigeminal root and upper cervical root?

Answer 10

Nerves coming into CNS through trigeminal root- Synapse somewhere between mesencephalon and spinal tissues
- Many overlapping connections can occur up and down trigeminal nucleus
- Upper cervical nerves often share connections from sensation going into CNS with synapses from Trigeminal nerve
- Sensory nerve supply of head and neck can be through any of branches of higher number cranial nerves or upper cervical nerves

Question 11

How is cardiac pain felt?

Answer 11

Pain felt as if it was somatic pain (but heart has no somatic supply)
-> Autonomic nerves carry this pain in an indistinguishable way from somatic to brain
-> Pain can be referred to areas that the autonomic nerve co-innervates (left arm, sternum, neck, jaw)

Question 12

How does the somatic reflex arc work?

Answer 12

Damage to area of somatic nerve supply
-> Signal passes up somatic nerve, through inter-neuron then into CNS
-> In addition at that level within spinal cord, produces synapse which causes efferent response causing muscle contraction to pull part of body away from

Question 13

How does the autonomic reflex arc work?

Answer 13

Sensory supply sends info into spinal cord- produces signal to brain AND reflex through sympathetic trunk ganglion
-> Results in effector change in sweat glands, nasal congestion (mucosal oedema), lacrimation or vasomotor changes in vessels (swelling/redness)
-> Symptoms are consequence of autonomic pain- important in history

Question 14

What is the mechanism of peripheral nociception?

Answer 14

Tissue damage results in release of 5HT and bradykinin (chemical mediators- Substance P/Prostaglandins)
-> These act on chemoreceptor (noci) within tissues producing action potential which is transmitted through peripheral nerve to brain via spinal cord

Question 15

What is the gate control of pain theory?

Answer 15

Painful stimulus applied causing pain response in nociceptor via peripheral nerve into spinal column (stimulates ascending pain c fibre which goes to brain)
-> At same time standard touch sensation is sent to brain which is sent via AB fibres
-> Crossing between these fibres- touch fibre stimulation can inhibit pain signals from passing into CNS
-> Rubbing painful area can block some of pain sensation

Question 16

What occurs as a result of descending facilitation?

Answer 16

Respond to lower threshold of pain signals (if you are anticipating pain)
-> True pain- brain experiences low level pain signal in same way as severe due to activation of inter-neuron which carries signal the same way as minor pain signal facilitated from CNS

Question 17

What is ascending inhibition?

Answer 17

Interneuron is prevented from sending pain signals to brain
->ain signals are still occurring, but brain is not aware as interneuron has been rendered less sensitive (can function normally)

Question 18

How can neuroplasticity stop gate control of pain?

Answer 18

Sprouting of spinal sensory nerves can stimulate interneuron (that may usually be blocked by Ab sensory fibres) if pain is continuously coming from a particular area (sensation then makes it easier for sensation to trigger pain)
- CNS adapts to pain- making it easier for pain to continue to pass
- Pain can remain even when source is removed due to creation of positive connection between normal sensation and pain interneurons

Question 19

What factors can cause increased pain sensitisation?

Answer 19

• Inflammatory molecules can cause changes
• Sensory receptors become more adapted to pain
• Myelin sheaths can become altered allowing pain to pass more easily

Question 20

How can learned pain be prevented?

Answer 20

LA/NSAIDs- control peripheral sensitisation

LA on primary afferent nerve can reduce sensations causing adaptions
- Inhibit dorsal root ganglion from processing
- Apply medications which change neurotransmitters to make adaption less likely

Opioids, TCAs, SSRI, B agonists are used to act on synapses to reduce pain perception and reduce adaptive change

Once in CNS- ketamine and gabapentin can be useful

Question 21

What are the features of chronic regional pain syndrome?

Answer 21

• Not necessarily a pain problem- has pain features
• Pain is delocalised- doesn’t fit anatomical boundaries (due to referred pain or anatomical confusion in CNS)
• Gripping, tight, burning
• Can be bilateral
• Colour changes, swelling and heat- due to autonomic reflexes in spinal cord via efferent response

Question 22

Why is autonomic pain particularly disabling?

Answer 22

autonomic nerves trigger thalamic response (primitive part of brain)
- Makes us think there is a significant risk to existence
- Distraction is difficult

Question 23

Why is looking for autonomic attributes in patient’s condition helpful for diagnosis?

Answer 23

Can be helpful for diagnosing pain coming from many different areas which do not seemingly match up
-> Areas that have same autonomic supply are linked