Orofacial Pain Flashcards
Structures in the oral cavity and maxillofacial region (11)
- Teeth
- Gingiva
- Mucosa
- Salivary glands
- Muscles
- Bone
- Ligaments
- Tendons
- Blood and lymphatic vessels
- Taste buds (special sensory)
- Nerves (motor and sensory)
— is the most prevalent pain in the facial region.
Toothache (odontalgia)
–% reported a history of toothache in the previous 6-month period.
12 to 14
Not all pains are the —.
Not all toothaches are the —.
And not all toothaches are in fact toothaches (i.e., odontalgia).
sam same
Odontogenic (2)
- Pulpal
* Periodontal
Non-Odontogenic (7)
- Sinus/nasal
- Myofascial
- Neurovascular
- Neuropathic
- Cardiogenic (rare)
- Systemic (rare)
- Idiopathic
Other forms of orofacial pain (5)
- Mucosal Pain
- Temporomandibular Disorders
- Orofacial Neuropathic Pain
- Neurovascular Pain (Headaches)
- Sleep Disorders* (not really pain)
TMJ
• Prevalence
General population – F:M /
Patient population – F:M /
6: 4
7. 5:1
TMJ
• Bimodal distribution
More prevalent in
younger adults & older adults
• TMD involving joint sounds
35% have — TM joint sounds
3.6-7.0% — TM joint sound
asymptomatic
symptomatic
TMJ
• Fluctuating, remitting, self-limiting
— uncommon
progression
“Unpleasant sensory and emotional experience
associated with actual or potential tissue damage
or described in terms of such damage”
pain
Why do we feel pain?
Instills protective behavior
but if unabated, pain can be harmful
Principles of pain (3)
• It is always subjective.
• It may or may not be tied to a stimulus.
• It is always a consequence of an emotional
experience and psychological state
How do we experience pain (usually)? (5)
• Environmental stimulus (thermal, mechanical, chemical, polymodal)
• Receptor activation
• Generation of action potential
• Transmission through primary afferent to dorsal horn (trigeminal spinal track nucleus)
• Projection from dorsal horn/TSTN to brain for perception and interpretation
Pain location, intensity, reflexes, and meaning (supraspinal structures)
“--- is not pain until it reaches and is processed by higher centers (supraspinal structures)"
Nociception
Descending Pathway (2)
Spinal
Supraspinal
Spinal (2)
- Endogenous opioid signaling.
* Non-opioid inhibitory neurotransmitters.
• Non-opioid inhibitory neurotransmitters. (4)
Serotonin
Noradrenaline
GABA
Glycine
Supraspinal
- Influenced by psychological factors.
- Neurons from the cortex and amygdala.
- Periaqueductal gray & rostroventral medulla
Pain Modulation
Dynamic process – can occur at multiple levels
of the ascending and descending pathways.
modulation (3)
supraspinal
spinal
peripheral
Neuronal Sensitization
• Arises when
neurotransmitters are left to linger in the synapse.
- Due to failure(s) in diffusion, enzymatic destruction, reuptake.
Neuronal Sensitization
• Prolonging the effect on the
post-synaptic neuron
Neuronal Sensitization
• Allows subthreshold input to
recruit a response
Neuronal Sensitization
• — discharge.
Spontaneous
Neuronal Sensitization
• Increased size of
receptive field
Normal input
Increased responsiveness of
nociceptive neurons
Subthreshold input
Recruitment of a
response
Peripheral sensitization
Nociceptive neurons at — of receptive field
periphery
peripheral sensitization
• Increased responsiveness of
nociceptive neurons
peripheral sensitization
• Reduced threshold to
stimulation
• Reduced threshold to stimulation.
Primary hyperalgesia
Hyperalgesia
An increased pain experience in
response to a painful stimulus
Central sensitization
Nociceptive neurons in the
central nervous system
central sensitization
Increased responsiveness to
normal/subthreshold afferent input
• Increased responsiveness to normal/subthreshold afferent input. (2)
Primary and secondary hyperalgesia
Allodynia
central sensitization
• May also result from dysfunctional
endogenous pain control
Allodynia
Pain resulting from a stimulus
that does not normally
provoke pain.
Revised Gate Control Theory
• Myelinated (fast) non-nociceptive afferent fiber can activate
inhibitory interneurons modulating nociceptive transmission.
• Reason you instinctively wave, hold, clench your fingers when they
burn.
• Reason why T.E.N.S. helps relieve pain .
Diffuse noxious inhibitor control
• The threshold for nociception can be raised when another noxious
stimulus is provoked in another area.
Placebo effect
- Psychological
* Leads to release of endogenous analgesic substances.
Different ways to categorize different pains (3)
- Neurophysiology
- Structures involved
- Timing
Nociceptive pain (2)
• Pain resulting from damage or threatened
damage to non-neural tissue
• Activation of nociceptors.
Neuropathic pain (1)
• Pain resulting from the presence of a lesion or
disease of the somatosensory nervous system.
Nociplastic pain (4)
• New concept.
• Pain that arises from altered nociception.
• Does not satisfy the definitions of nociceptive
or neuropathic pain.
• It is possible for a patient to present with
nociceptive and nociplastic pain at the same
time.
types of pain (2)
acute
chronic
Acute Pain
• Pain with close temporal relationship to a (3)
• Tends to respond to treatment in a — dose-dependent fashion
stimulus, injury, or disease
linear
Chronic Pain
• Pain that has lasted
• Does not typically respond to treatment in a — dose-dependent fashion.
• Presence of other/multiple ongoing pains is a predictor for transition from
• More influence of — factors.
• More – to treat.
>3 months linear acute to chronic psychosocial difficult
Most Common Disorders (4)
- Anxiety
- Major depression
- Personality disorders
- Pain distress
Coping Mechanisms (5)
- Internal locus of control
- Perceived control
- Catastrophic thinking
- Hypervigilance
- Fear avoidance
Assessment (3)
• Pain intensity • Pain distress • Pain-related interference Functional limitation, disability • Oral Habits
Homotopic Pain
• Site = Source
Treat site of pain, effective
Heterotopic pain
• Site ≠ Source
Treat site of pain, ineffective
- Central Pain
- Source is central but perceived peripherally
* Example: Brain tumor (brain does not have nociceptors)
- Projected pain
- Pain follows same nerve distribution as primary source
- Dermatome or motor distribution
- Hyperalgesia may be present
- Example: Post-herpetic neuralgia
- Referred Pain
• Pain in different nerve than primary source and is spontaneous (non-provoked)
• Sensitization of interneurons – central sensitization
• Not aggravated by palpation
• Does not respond to anesthesia at site of pain –must block source of pain
• Does not typically cross midline (only if generated at midline)
• Can refers upward: cervical to trigeminal, mandibular to maxillary
• Example: Mandibular molar affected, but perceived at maxillary molar
Same nerve root
Evaluation of Pain (6)
- What kind of pain are they experiencing and describing?
- Why are they in pain? What is the cause/source?
- Where is the site of pain? How does it relate to the cause/source?
- Is the pain acute or chronic?
- Are there any other contributing factors? Inflammation/Psychosocial?
- How can we modulate their pain?
Pain Management
Understand why the patient is in pain (MOST IMPORTANT)
• Treat source(s) and cause(s) of the pain
Determine what type of treatment goal is appropriate and achievable
• Curative intent
• Palliative intent
Limit tissue damage
Get patient through adaptive phase
Manage chronic pain
More aggressive care if palliative care is ineffective to control symptoms
or of there is significantly decreased quality of life.
Multidisciplinary approach may be necessary
