Ch 15 part II: Pain Perception

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Last updated 8:07 PM on 10/17/26
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33 Terms

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Three types of pain

Inflammatory, neuropathetic, nociceptive

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Inflammatory pain

Caused by damage to tissues and joints or by tumour cells

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Neuropathic pain

Caused by damage to the nervous system

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Nociceptive pain

Signals impending damage to the skin

Respond to heat, chemicals, severe pressure, and cold

Threshold of eliciting receptor response must be balanced to warn of damage but not be affected by normal activity

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Classifying nociceptors

Axons terminate in unspecialized “free endings”

Categorize according to properties of axons associated with them (fibre type, conduction speed, stimuli they respond to)

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Main types of nociceptors fibres

A delta nociceptors (thinly myelinated and respond to sharp, fast pain)

C nocicpetors (unmyelinated and responsible for slow)

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Mechanical nociceptors

Delta and C fibres

Respond to mechanical forces that can damage tissue/ activate high threshold mechanoreceptors (pinching, pressure, stretching)

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Thermal nociceptors

Delta and C fibres

Extreme temperatures: noxious heat (hot) and noxious cold (cold)

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Chemical nociceptors

More C fibres than delta fibres (C fibres are primarily chemical detectors)

Respond to chemical irritants and inflammatory mediators (bradykinin, prostaglandins, histamine, serotonin, substance P, low pH)

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Polymodal nociceptors

Mainly C fibres

Respond to multiple types of stimuli

Respond to combination of mechanical, thermal, and chemical stimuli

Ex: inflammatory pain, tissue damage, chronic pain conditions

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Nociceptor summary

Free nerve endings that detect potentially harmful stimuli

Classified as mechanical, thermal, chemical, or polymodal based on the types of stimuli that activate them

Primarily carried by A delta (fast, sharp pain) and C (slower, dull pain) fibres

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Signals from nociceptors in the skin are transmitted to

The spinal cord and then up the spinal cord in a pathway that lead to the brain

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Spinothalamic Pathwa


Carries pain and temperature information from body to thalamus (then cortex)

  1. Nociceptors/ thermoreceptors

  2. First order neuron (DRG)

  3. Synapse in dorsal horn

  4. Decussation (in spinal cord)

  5. Ascent (through brainstem to thalamus)

  6. Thalamus (VPL)

  7. Somatosensory cortex


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  1. Nociceptors/ Thermoreceptors


Free nerve endings in skin (and other tissues) detect harmful stimuli (pain) or temperature change

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First order neuron

Afferent fiber (A delta or C) carries signal to the dorsal horn of the spinal cord

Cell body in the dorsal root ganglion

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Synapse in dorsal horn

Afferent fibre synapses (mainly in lamina I, II, V) with a second order neuron

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Decussation

Second order neuron crosses to the opposite side in the anterior white commissure (within 1-2 spinal segments)

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Ascent

The crossed fibres travel in the anterolateral (spinothalamic) tract through the brainstem to the thalamus

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Thalamus

Synapses in the ventral posterolateral (VPL) nucleus of the thalamus

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Cortex

Third-order neuron projects to the somatosensory cortex for conscious perception and localization

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Key features of spinothalamic pathway

Carries pain (nociception) and temperature (thermoreception)

Uses A delta (fast, sharp pain) and C (slower, dull pain) fibres

Crosses to the opposite side within 1-2 spinal segments

Travels in the anterolateral system (spinothalamic tract)

Synapses in the VPL nucleus of the thalamus

Projects to the S1 and other areas

<p>Carries pain (nociception) and temperature (thermoreception)</p><p>Uses A delta (fast, sharp pain) and C (slower, dull pain) fibres</p><p>Crosses to the opposite side within 1-2 spinal segments </p><p>Travels in the anterolateral system (spinothalamic tract)</p><p>Synapses in the VPL nucleus of the thalamus</p><p>Projects to the S1 and other areas </p>
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Direct pathway model

Early model of pain perception stated that nociceptors are stimulated and send signals to the brain

But we know pain to be multimodal phenomenon containing a sensory/ affective component

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Problems with direct pathway model

Pain can occur when there is no stimulation of skin (phantom limbs)

Extensive wounds but no reported severe pain

Pain can be affected by expectation, mental state/ emotions, attention

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Gate control theory of pain

Asserts that non painful input closes the “gates” to painful input, prevents pain sensation from traveling to CNS

Stimulation by non-noxious input can suppress pain

Additional pathways that influence the signals from spinal cord to brain can open or close a gate in the spinal cord

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Cells in the dorsal horn of the spinal cord receive input from

Nociceptors, mechanoreceptors, descending pathways

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What regulates pain perception

Descending pathways

(Brain can send signals down to the spinal cord that either decrease or increase the transmission of pain signals)

Help to regulate how much pain we perceive

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Descending pathway inhibits pain

Descending signal releases serotonin, norepinephrine or endorphins

Less pain signal reaches the brain

Decreased pain perception

(Eg during stress, positive expectation or effective analgesia)

To dorsal columns

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Descending pathway enhances pain

Releases substance P and increases excitability

More pain signal reaches the brain

Increased pain perception

(Stress, anxiety, negative expectation)

To anterolateral system

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Top-down processes in pain perception

Expectation, shifting attention, emotion

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Placebo effect

Positive expectations can produce beneficial effects

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Nocebo effects

Negative expectations can produce unpleasant/ harmful effects

(Thinks drug discontinued, pain comes back)

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What did MRI show about expectation of pain

Brain’s pain networks responded to different extents according to the volunteers expectations at each stage and matched their reports of pain

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Brain areas involved in pain perception

Insula, thalamus, somatosensory cortex, anterior cingulate cotex, prefrontal cortex, cerebellum, brainstem