Lecture 11: Pain and Temperature Sensations - Engineering Course Study Material

Free nerve endings

Used by temperature and pain receptors

Modified/covered nerve endings

Used by touch and pressure receptors

Trp receptors

Cation channel family that mediates thermoreception and nociception

Types of Trp receptors

Warm receptors

Cold receptors

Pain receptors

What do pain receptors detect?

Extreme heat

Extreme cold

Extreme pressure

Trp agonists

Menthol/mint

Capsaican

Menthol/mint

Trp agonist that makes your tongue feel cold

Capsaican

Trp agonist that makes your tongue feel like it's burning

Types of thermoreceptors

Warm and cold receptors

Nociceptive thermoreceptors

Warm and cold receptors

Low threshold thermoreceptor

Responds to mild stimuli

Nociceptive thermoreceptor

High threshold thermoreceptor

Responds to strong stimuli

Types of nociceptors

Nociceptive thermoreceptors

Mechanoreceptors

Chemoreceptors

Polymodal nociceptors

Silent/sleep nociceptors

Where are nociceptors found?

Anywhere but the CNS

Chemoreceptors

React to pro-inflammation chemicals such as histamines and prostaglandins

Silent/sleep nociceptors

Respond to pressure only after activation by pro-inflammation chemicals

Example of silent/sleep nociceptors

Inactive in healthy joint

Ankle sprain leads to inflammation

Activation by pro-inflammation chemicals

How will increased receptor potential affect Trp sensory transduction?

It will lead to increased AP firing frequency

Types of pain

Superficial pain

Deep pain

First pain

Second pain

Superficial pain

Pain from surface of skin or mucous membrane

Deep pain

Pain from structures in deeper layers of skin

First pain

Felt less than 1s after stimulation

Sharp

Localized

Transmitted by myelinated A delta fibers

Second pain

Felt after first pain ends

Diffused

Long-lasting

Throbbing

Transmitted by unmyelinated C fibers

List the receptor types from highest transmission speed to lowest transmission speed

Proprioceptors (largest axon diameter) (A alpha)

Touch receptors (A beta)

First pain receptors and thermoreceptors (A delta)

Second pain receptors (lowest axon diameter) (C)

2 types of pain transmission pathways

Anterolateral pathway

Trigeminothalamic pathway

Anterolateral pathway

A delta neuron enters spinal cord (1st order)

Interneuron at dorsal horn crosses over spinal cord (2nd order)

Interneuron synapses at thalamus with contralateral somatosensory cortical neuron (3rd order)

Where are the cell bodies of nociceptors and thermoreceptors?

Dorsal root ganglia

Trigeminothalamic pathway

Cranial sensory neuron enters brainstem at medulla (1st order)

Medullar interneuron crosses over (2nd order)

Medullar interneuron synapses at thalamus with contralateral SC neurons (3rd order)

Pain matrix

Brain areas consistently involved in perception of pain

Processing of first pain

Interprets location, intensity, and quality

Uses thalamus, S1, and S2

Processing of second pain

Interprets feeling and memory of pain

Uses many brain regions

Why do people perceive pain differently?

Pain regulatory pathways can be inhibited or facilitated to increase or decrease pain

3 methods of pain regulation

Periaqueductal gray

Spinal cord gating

Placebo effect

Periaqueductal gray (PAG)

Pain signal ascends anterolateral pathway

PAG in brain recognizes ascension

Endorphins are released and descend

Inhibition of 2nd order neuron by increasing K+ conductance

Inhibition of 1st order neuron by decreasing NT release

Endorphins

Peptides that decrease pain signal transmission

Gate control theory

Suggests pain signals can be regulated at the spinal cord before they reach the brain

Unmodulated (open) spinal cord gating

C (pain) fibers activated by pain

Inhibitory interneurons inactive

Full pain signal to brain

Modulated (closed) spinal cord gating

Rubbing of painful area

C (pain) fibers and A beta (touch) fibers activated simultaneously

A beta fibers activate inhibitory interneurons

C fiber signal is blocked/reduced

Decreased pain signal to brain

Placebo effect

Beneficial physiological response following administration of inert "remedy"

Pain is real

Relief is real

Brain's reward system activated

Endorphins released

Brown-Sequard syndrome

Caused by hemisection

Decreased ipsilateral touch/pressure

Decreased contralateral pain/temperature

No perturbations above lesion

Hemisection

Lesion at one side of spinal cord

What causes the dissociation of pain/temperature and touch/pressure senses in Brown-Sequard syndrome?

Pain and temperature is transmitted via the anterolateral pathway which crosses as soon as it enters the spinal cord

Touch and pressure is transmitted via the dorsal column pathway which crosses over at the medulla past the spinal cord

Referred pain

Perception of visceral pain from another superficial part of the body

Visceral pain

Internal organ pain

Convergence theory

Explanation for referred pain

Suggests sensory neuron from diseased/injured internal organ and a cutaneous nociceptor activates the same 2nd order neuron and the brain reads pain coming from both sites

Phantom limb pain

Perception of pain coming from a body part that is no longer there

Experienced by amputees

Feeling can be continuous or discontinuous

Often felt as clenched sensation

3 hypotheses of phantom limb pain

Central hypothesis

Spinal hypothesis

Peripheral hypothesis

Central hypothesis

Rewiring of brain

Neurons from other body parts take over brain areas from missing body part

Spinal hypothesis

Severing of peripheral nerves during amputation activates spinal pain pathways

Peripheral hypothesis

Severed nerves in amputated regions form balls that continue sending nerve impulses perceived as pain

Mirror therapy

Uses visual feedback to trick brain into thinking there is feedback from phantom limb

Example of mirror therapy

Patient places limb in clenched position felt by clenched phantom limb

Unclench good limb and mirror compartment shows phantom limb unclenching

Pain is relieved