Sinus/nasal Myofascial Neurovascular Neuropathic Cardiogenic (rare) Systemic (rare) Idiopathic

Endogenous opioid signaling. Non-opioid inhibitory neurotransmitters.

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

Orofacial Pain Flashcards by sophie rosen

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)

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— is the most prevalent pain in the facial region.

Toothache (odontalgia)

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

12 to 14

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

sam same

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Odontogenic (2)

Pulpal

* Periodontal

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Non-Odontogenic (7)

Sinus/nasal
Myofascial
Neurovascular
Neuropathic
Cardiogenic (rare)
Systemic (rare)
Idiopathic

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Other forms of orofacial pain (5)

Mucosal Pain
Temporomandibular Disorders
Orofacial Neuropathic Pain
Neurovascular Pain (Headaches)
Sleep Disorders* (not really pain)

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

6: 4

7. 5:1

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TMJ
• Bimodal distribution
 More prevalent in

younger adults & older adults

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

asymptomatic

symptomatic

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

progression

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

pain

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Why do we feel pain?

Instills protective behavior

but if unabated, pain can be harmful

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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

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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)

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

Nociception

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Descending Pathway (2)

Spinal

Supraspinal

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Spinal (2)

Endogenous opioid signaling.

* Non-opioid inhibitory neurotransmitters.

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• Non-opioid inhibitory neurotransmitters. (4)

 Serotonin
 Noradrenaline
 GABA
 Glycine

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Supraspinal

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

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Pain Modulation

Dynamic process – can occur at multiple levels

of the ascending and descending pathways.

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modulation (3)

supraspinal
spinal
peripheral

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Neuronal Sensitization

• Arises when

neurotransmitters are left to linger in the synapse.

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

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Neuronal Sensitization

• Prolonging the effect on the

Study These Flashcards

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

1. Central Pain

* Source is central but perceived peripherally | * Example: Brain tumor (brain does not have nociceptors)

2. Projected pain

* Pain follows same nerve distribution as primary source * Dermatome or motor distribution * Hyperalgesia may be present * Example: Post-herpetic neuralgia

3. 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)

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?

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

Orofacial Pain Flashcards

(59 cards)