Orofacial Pain Flashcards
What is pain?
An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
What are the different pain assessments that can be used when a patient presents with facial pain?
- 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
What are the steps that lead to us feeling pain?
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
What is unusual in terms of anatomy about facial pain?
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)
What is the artery, CN, muscles and skeletal features that come from 1st pharyngeal arch?
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
What is the artery, CN, muscles and skeletal features that come from 2nd pharyngeal arch?
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
What is the artery, CN, muscles and skeletal features that come from 3rd pharyngeal arch?
Artery- Internal carotid
CN- Glossopharyngeal
Muscles- Stylopharnygeus
Skeletal features- greater horn/body of hyoid
What is the artery, CN, muscles and skeletal features that come from 4th pharyngeal arch?
Artery- subclavian
CN- vagus
Muscles- pharyngeal/laryngeal musculature
Skeletal features- Laryngeal cartilages
What are the extra functions of the facial nerve?
- Sensory root- supplying ear
- Motor- stapedius
- Chorda tympani fibres carried with it- taste
- Stimulatory supply to salivary glands (greater petrosal nerve)
Why is it difficult for patients to distinguish whether pain coming from trigeminal root and upper cervical root?
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
How is cardiac pain felt?
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)
How does the somatic reflex arc work?
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
How does the autonomic reflex arc work?
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
What is the mechanism of peripheral nociception?
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
What is the gate control of pain theory?
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
What occurs as a result of descending facilitation?
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
What is ascending inhibition?
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)
How can neuroplasticity stop gate control of pain?
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
What factors can cause increased pain sensitisation?
- Inflammatory molecules can cause changes
- Sensory receptors become more adapted to pain
- Myelin sheaths can become altered allowing pain to pass more easily
How can learned pain be prevented?
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
What are the features of chronic regional pain syndrome?
- 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
Why is autonomic pain particularly disabling?
autonomic nerves trigger thalamic response (primitive part of brain)
- Makes us think there is a significant risk to existence
- Distraction is difficult
Why is looking for autonomic attributes in patient’s condition helpful for diagnosis?
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
