Pathway 13-7-7 PROCESSING: THE SECOND STEP IN PAIN PERCEPTION

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Questions and Answers

What primarily encodes the intensity of peripheral stimuli as conveyed to the central nervous system?

Frequency of action potentials (correct)

Type of neuron activated

Onset and duration of depolarization

Time of arrival at the CNS

⭐️Which subnucleus predominantly receives nociceptive input from oral tissues?

Trigeminal spinal tract

Subnucleus interpolaris

Subnucleus oralis

Subnucleus caudalis (correct)

Which of the following best describes the organizational structure of the subnucleus caudalis?

Similar to the dorsal horn of the spinal cord (correct)

Similar to the peripheral nervous system

Similar to the trigeminal ganglion

Similar to the medullary spinal cord

Which statement is true about the location of the trigeminal spinal tract nuclear complex?

It resides in the medulla Signup and view all the answers

What is the primary function of the medullary dorsal horn?

To relay sensory signals to higher brain centers “Processes” Signup and view all the answers

Which of the following components is NOT associated with the functional processing in the medullary dorsal horn?

Motor neuron terminals Signup and view all the answers

What phenomenon describes the misinterpretation of pain signals in the medullary dorsal horn?

Referred pain Signup and view all the answers

Which of the following factors can influence the output from the medullary dorsal horn?

The presence of glial cells and neurotransmitter activity Signup and view all the answers

Which type of sensory nerve fibers primarily convey nociceptive information to the medullary dorsal horn?

Ad and C fiber afferents Signup and view all the answers

What effect do descending neurons from brain structures have on nociceptive transmission in the medullary dorsal horn?

They inhibit nociceptive transmission. Signup and view all the answers

Endogenous opioid peptides are thought to play a role in which phenomenon related to pain control?

The placebo effect. Signup and view all the answers

What type of molecules do glial cells release following nociceptive input that affects pain processing?

Cytokines such as TNF-a and IL-1. Signup and view all the answers

Which amino acid is commonly released by inhibitory interneurons in the medullary dorsal horn?

Glycine. Signup and view all the answers

How do NSAIDs potentially exert their analgesic mechanism in the central nervous system?

By acting on glial modulating agents. Signup and view all the answers

Which type of neuronal input is believed to activate the release of endogenous opioid peptides?

Nociceptive input. Signup and view all the answers

What neurotransmitter is primarily associated with the transmission of signals from primary afferent fibers in the trigeminal ganglion?

Glutamate Signup and view all the answers

⭐️Which receptor class is NOT involved in the signaling of substance P (SP)?

D2 receptor Signup and view all the answers

Where are the cell bodies of the second-order neurons in the trigeminal pain system located?

Medullary dorsal horn Signup and view all the answers

What is the primary role of the trigeminothalamic tract in the pain transmission pathway?

To relay signals to the cerebral cortex Signup and view all the answers

What phenomenon helps explain the misinterpretation of pain originating from one structure being perceived in another?

Referred pain Signup and view all the answers

⭐️Which statement is true regarding the efficacy of NK1 antagonists in pain management?

Their efficacy in humans is generally limited. Signup and view all the answers

Which class of glutamate receptors is specifically implicated in the response to the antihyperalgesic effects in human clinical trials?

AMPA/kainate receptors Signup and view all the answers

What aspect of sensory neuron convergence is most relevant to the clinical observation of tooth pain?

Convergence can lead to dual perception of pain. Signup and view all the answers

What is the primary role of endogenous opioid peptides in pain management?

They inhibit nociceptive transmission. Signup and view all the answers

Which cytokines are released by glial cells in response to nociceptive stimulation?

TNF-a and IL-1 Signup and view all the answers

How can the placebo effect in pain management be influenced?

By administration of naloxone. Signup and view all the answers

What is the primary role of central sensitization in pain perception?

It increases the responsiveness of nociceptive neurons to stimulation Signup and view all the answers

⭐️Which type of nociceptive fibers is implicated in initiating central sensitization?

C fibers Signup and view all the answers

What effect does prolonged input from C nociceptors have on postoperative pain after endodontic procedures?

It serves as a predictor of postoperative pain levels Signup and view all the answers

Which pharmacotherapeutic approach is expected to help reduce central sensitization in the future?

Blocking receptors for proinflammatory mediators Signup and view all the answers

How does central sensitization contribute to the phenomenon of mechanical allodynia in patients with irreversible pulpitis?

It causes adjacent non-injured areas to respond to normally non-painful stimuli Signup and view all the answers

What is the expected pharmacotherapeutic approach to reducing central sensitization in the future?

Decreasing proinflammatory mediators such as PGs and cytokines Signup and view all the answers

How does pretreatment with a glutamate NMDA receptor antagonist affect pain sensitivity related to odontogenic pain?

It reduces the increased receptive field of A beta touch receptors. Signup and view all the answers

Which of the following factors has been implicated in developing tactile hypersensitivity after dental injury?

Activation of proinflammatory prostaglandins Signup and view all the answers

What potential benefit could a reduction in NO synthase levels provide in terms of pain management?

It may decrease central sensitization related to pain. Signup and view all the answers

Study Notes

Peripheral Nociception

Nerve impulses travel to the CNS to convey information about pain.
Information about the intensity, quality, and temporal features of painful stimuli are encoded in the action potential.

Trigeminal Pain System

The trigeminal spinal tract nuclear complex receives action potentials from the trigeminal nerve.
The complex has three distinct subnuclei: oralis, interpolaris, and caudalis.
The majority of nociceptive input is received by the subnucleus caudalis.
Subnucleus caudalis is similar to the dorsal horn of the spinal cord and is often referred to as the medullary dorsal horn.

The Medullary Dorsal Horn

The medullary dorsal horn acts as a relay station, transmitting sensory information from primary afferent nerve fibers to higher brain centers.
It is involved in processing these signals, resulting in various sensory experiences, including hyperalgesia (increased pain), analgesia (reduced pain), and referred pain (misinterpretation of pain origin).
Understanding these processing mechanisms in the medullary dorsal horn offers insights into clinical pain phenomena and allows us to explore potential therapeutic interventions.
Several functional components contribute to this processing:
- Central terminals of primary nociceptors: Ad and C fiber afferents (pain-sensitive fibers) transmit pain signals to the medullary dorsal horn.
- Second-order projecting neurons: These neurons receive information from the primary nociceptors and relay it to higher centers.
- Interneurons: These neurons act as local circuits within the medullary dorsal horn, modulating the flow and processing of pain signals.
- Terminals of descending neurons: Signals from the brain descend to the medullary dorsal horn, influencing pain perception.
- Glial cells: These cells contribute to pain processing by releasing signaling molecules that influence neuronal activity.

Primary Afferent Fibers

These fibers transmit pain signals from the trigeminal ganglion to projection neurons.
Release neurotransmitters glutamate and SP.
Receptors for these neurotransmitters include NMDA, AMPA, and NK1.
Antagonists to these receptors have shown effectiveness in reducing hyperalgesia in animal studies.

Second-Order (Projection) Neurons

Located in the medullary dorsal horn.
Their axons cross the midline and project to the thalamus via the trigeminothalamic tract.
Relay information to the cerebral cortex via the thalamocortical tract.

Referred Pain

Caused by convergence of afferent input from different areas onto the same projection neurons.
Approximately 50% of subnucleus caudalis neurons receive converging input from cutaneous and deep structures.

Local Circuit Interneurons

Found in the medullary dorsal horn.
Can either enhance or diminish the transmission of nociceptive input.
Excitatory interneurons release glutamate or SP, while inhibitory interneurons release glycine or GABA.

Descending Neurons

Terminals from brain structures like the locus coeruleus and nucleus raphe magnus inhibit nociceptive transmission.
Release various neuroeffective agents, including endogenous opioid peptides (EOPs).
EOPs suppress the pain system.
Likely contribute to the placebo effect.

Glial Cells

Play a crucial role in pain processing.
Following nociceptive input, they release cytokines (TNF-a, IL-1) and prostanoids (PGs).
These substances can facilitate the activity of projection neurons.
Glial modulating agents are effective in experimental models of neuropathic pain.

Medullary Dorsal Horn - Nociceptive Transmission

Neurons descending from the locus coeruleus and nucleus raphe magnus inhibit nociceptive transmission in the medullary dorsal horn.
These neurons release endogenous opioid peptides (EOPs) in response to nociceptive input.
EOPs suppress the pain system and are similar in structure to exogenous opiates.
EOPs may contribute to the placebo effect in pain control studies, and this effect can be reversed by naloxone, an opioid antagonist.

Glial Cells in the Medullary Dorsal Horn Complex

Glial cells, previously thought to be solely supportive, are now recognized as important in pain processing.
Following nociceptive input from primary afferents, glia release cytokines (TNF-a, IL-1) and prostaglandins (PGs).
These substances can facilitate the activity of projection neurons.
Glial modulating agents are effective in experimental models of neuropathic pain.
Nonsteroidal anti-inflammatory drugs (NSAIDs) may exert analgesic effects by acting on glial cells.

Central Sensitization

Definition: Increased responsiveness of central nociceptive neurons to peripheral stimulation, beyond peripheral sensitization.
Role in Pain: A major contributor to hyperalgesia and allodynia.
Clinical Significance: Implicated in pain from irreversible pulpitis, with 57% of patients reporting mechanical allodynia.
Spread of Pain: Central sensitization can lead to pain spreading, with both the affected and contralateral teeth experiencing mechanical allodynia.
Triggering Mechanism: Initiated by a barrage of nociceptive impulses from peripheral C fibers, potentially linked to prolonged and intense pain before endodontic intervention.
Minimizing Sensitization: Reducing the nociceptive barrage with techniques like long-acting local anesthetics can help limit the development of central sensitization.
Pharmacological Targets: Reducing inflammation at the medullary dorsal horn and inhibiting the release of proinflammatory agents like prostaglandins, cytokines, and nitric oxide (NO) can reduce sensitization of second-order neurons.
Glutamate NMDA Receptor Antagonists: Blocking these receptors can potentially prevent the expansion of the receptive field of touch receptors in the face after tooth pulp inflammation.
NO Synthesis Inhibition: Reducing nitric oxide synthase levels potentially protects against central sensitization.

### Inflammation and Central Sensitization

Reducing inflammatory mediators in the medullary dorsal horn can lessen the sensitization of second-order neurons.
Drugs that block the receptors of proinflammatory prostaglandins (PGs), cytokines, and nitric oxide (NO) could be used to treat inflammatory pain in the future.
Applying an inflammatory agent to a rat's tooth pulp increases the receptive field of Ab touch receptors on the face, suggesting central sensitization.
Blocking glutamate NMDA receptors can prevent this sensitization, indicating that centrally acting drugs could be effective for treating odontogenic pain.
NO synthesis within the subnucleus caudalis plays a role in developing tactile hypersensitivity after dental injury.
Decreasing NO synthase levels might offer protection from central sensitization.

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