Orofacial Pain Flashcards

1
Q

Structures in the oral cavity and maxillofacial region (11)

A
  • Teeth
  • Gingiva
  • Mucosa
  • Salivary glands
  • Muscles
  • Bone
  • Ligaments
  • Tendons
  • Blood and lymphatic vessels
  • Taste buds (special sensory)
  • Nerves (motor and sensory)
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2
Q

— is the most prevalent pain in the facial region.

A

Toothache (odontalgia)

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3
Q

–% reported a history of toothache in the previous 6-month period.

A

12 to 14

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4
Q

Not all pains are the —.
Not all toothaches are the —.
And not all toothaches are in fact toothaches (i.e., odontalgia).

A

sam same

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5
Q

Odontogenic (2)

A
  • Pulpal

* Periodontal

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6
Q

Non-Odontogenic (7)

A
  • Sinus/nasal
  • Myofascial
  • Neurovascular
  • Neuropathic
  • Cardiogenic (rare)
  • Systemic (rare)
  • Idiopathic
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7
Q

Other forms of orofacial pain (5)

A
  • Mucosal Pain
  • Temporomandibular Disorders
  • Orofacial Neuropathic Pain
  • Neurovascular Pain (Headaches)
  • Sleep Disorders* (not really pain)
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8
Q

TMJ
• Prevalence
 General population – F:M /
 Patient population – F:M /

A

6: 4

7. 5:1

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9
Q

TMJ
• Bimodal distribution
 More prevalent in

A

younger adults & older adults

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10
Q

• TMD involving joint sounds
 35% have — TM joint sounds
 3.6-7.0% — TM joint sound

A

asymptomatic

symptomatic

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11
Q

TMJ
• Fluctuating, remitting, self-limiting
 — uncommon

A

progression

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12
Q

“Unpleasant sensory and emotional experience
associated with actual or potential tissue damage
or described in terms of such damage”

A

pain

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13
Q

Why do we feel pain?

A

Instills protective behavior

but if unabated, pain can be harmful

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14
Q

Principles of pain (3)

A

• 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

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15
Q

How do we experience pain (usually)? (5)

A

• 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)

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16
Q
“--- is not pain until it reaches and is processed by
higher centers (supraspinal structures)"
A

Nociception

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17
Q

Descending Pathway (2)

A

Spinal

Supraspinal

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18
Q

Spinal (2)

A
  • Endogenous opioid signaling.

* Non-opioid inhibitory neurotransmitters.

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19
Q

• Non-opioid inhibitory neurotransmitters. (4)

A

 Serotonin
 Noradrenaline
 GABA
 Glycine

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20
Q

Supraspinal

A
  • Influenced by psychological factors.
  • Neurons from the cortex and amygdala.
  • Periaqueductal gray & rostroventral medulla
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21
Q

Pain Modulation

A

Dynamic process – can occur at multiple levels

of the ascending and descending pathways.

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22
Q

modulation (3)

A

supraspinal
spinal
peripheral

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23
Q

Neuronal Sensitization

• Arises when

A

neurotransmitters are left to linger in the synapse.

- Due to failure(s) in diffusion, enzymatic destruction, reuptake.

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24
Q

Neuronal Sensitization

• Prolonging the effect on the

A

post-synaptic neuron

25
Q

Neuronal Sensitization

• Allows subthreshold input to

A

recruit a response

26
Q

Neuronal Sensitization

• — discharge.

A

Spontaneous

27
Q

Neuronal Sensitization

• Increased size of

A

receptive field

28
Q

Normal input

 Increased responsiveness of

A

nociceptive neurons

29
Q

Subthreshold input

Recruitment of a

A

response

30
Q

Peripheral sensitization

Nociceptive neurons at — of receptive field

A

periphery

31
Q

peripheral sensitization

• Increased responsiveness of

A

nociceptive neurons

32
Q

peripheral sensitization

• Reduced threshold to

A

stimulation

33
Q

• Reduced threshold to stimulation.

A

Primary hyperalgesia

34
Q

Hyperalgesia

A

An increased pain experience in

response to a painful stimulus

35
Q

Central sensitization

Nociceptive neurons in the

A

central nervous system

36
Q

central sensitization

Increased responsiveness to

A

normal/subthreshold afferent input

37
Q

• Increased responsiveness to normal/subthreshold afferent input. (2)

A

 Primary and secondary hyperalgesia

 Allodynia

38
Q

central sensitization

• May also result from dysfunctional

A

endogenous pain control

39
Q

Allodynia

A

Pain resulting from a stimulus
that does not normally
provoke pain.

40
Q

Revised Gate Control Theory

A

• 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 .

41
Q

Diffuse noxious inhibitor control

A

• The threshold for nociception can be raised when another noxious
stimulus is provoked in another area.

42
Q

Placebo effect

A
  • Psychological

* Leads to release of endogenous analgesic substances.

43
Q

Different ways to categorize different pains (3)

A
  • Neurophysiology
  • Structures involved
  • Timing
44
Q

Nociceptive pain (2)

A

• Pain resulting from damage or threatened
damage to non-neural tissue
• Activation of nociceptors.

45
Q

Neuropathic pain (1)

A

• Pain resulting from the presence of a lesion or

disease of the somatosensory nervous system.

46
Q

Nociplastic pain (4)

A

• 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.

47
Q

types of pain (2)

A

acute

chronic

48
Q

Acute Pain
• Pain with close temporal relationship to a (3)
• Tends to respond to treatment in a — dose-dependent fashion

A

stimulus, injury, or disease

linear

49
Q

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.

A
>3 months
linear
acute to chronic
psychosocial
difficult
50
Q

Most Common Disorders (4)

A
  • Anxiety
  • Major depression
  • Personality disorders
  • Pain distress
51
Q

Coping Mechanisms (5)

A
  • Internal locus of control
  • Perceived control
  • Catastrophic thinking
  • Hypervigilance
  • Fear avoidance
52
Q

Assessment (3)

A
• Pain intensity
• Pain distress
• Pain-related interference
 Functional limitation, disability
• Oral Habits
53
Q

Homotopic Pain

A

• Site = Source

Treat site of pain, effective

54
Q

Heterotopic pain

A

• Site ≠ Source

Treat site of pain, ineffective

55
Q
  1. Central Pain
A
  • Source is central but perceived peripherally

* Example: Brain tumor (brain does not have nociceptors)

56
Q
  1. Projected pain
A
  • Pain follows same nerve distribution as primary source
  • Dermatome or motor distribution
  • Hyperalgesia may be present
  • Example: Post-herpetic neuralgia
57
Q
  1. Referred Pain
A

• 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

58
Q

Evaluation of Pain (6)

A
  1. What kind of pain are they experiencing and describing?
  2. Why are they in pain? What is the cause/source?
  3. Where is the site of pain? How does it relate to the cause/source?
  4. Is the pain acute or chronic?
  5. Are there any other contributing factors? Inflammation/Psychosocial?
  6. How can we modulate their pain?
59
Q

Pain Management

A

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