Somatosensory Pain + Temp

What body pathway carries sharp cutting pain and cool/cold temperature information?

The neospinothalamic pathway.

What body pathway carries dull burning pain and warm and hot temperature information?

The paleospinothalamic pathway.

What body pathway carries deep aching pain?

The archispinothalamic pathway.

What face pathway carries pain information?

The spinal trigeminal pathway.

What body pathway carries itch, tickle, and crude touch?

The paleospinothalamic pathway.

Which pain and temperature body pathways are part of the spinothalamic/anterolateral system according to the overview?

Neospinothalamic, paleospinothalamic, and archispinothalamic pathways.

According to the pain definition, is pain only a sensory experience?

No. It is both a sensory and an emotional experience.

Can pain be associated with potential tissue damage even if actual damage has not occurred?

Yes.

What is nociception?

The neural encoding and processing of noxious stimuli.

What are noxious stimuli?

Stimuli that can elicit tissue damage and activate nociceptors.

What are nociceptors?

Sensory receptors that detect signals from damaged tissue or the threat of damage and also respond to chemicals released from damaged tissue.

What physical form do nociceptor endings have?

They are free (bare) nerve endings.

Where are nociceptors found?

Skin, muscle, joints, bone, and viscera.

Is pain processing simply an increase in normal cutaneous sensory processing?

No. Pain processing is independent of normal cutaneous processing.

How do peripheral axons responsible for normal stimulation respond when a stimulus becomes painful?

They do not increase their firing frequency simply because the stimulus becomes painful.

When do nociceptive afferents begin to fire strongly?

When stimuli reach high intensities.

Does direct stimulation of large Ia, II, or Aβ fibers produce pain?

No.

What does the thermoreceptor-versus-nociceptor graph show as temperature rises?

Thermoreceptor firing rises at lower non-noxious temperatures and levels off, whereas nociceptor firing begins at higher, noxious temperatures and then increases.

Around what temperature does the slide's graph mark the transition into clearly noxious heat?

Around 45°C.

On what fiber types are nociceptors found?

Small A-delta (Aδ) and C fibers.

What kinds of stimuli do Aδ nociceptors respond to overall?

Intense mechanical and thermal stimuli, with Type I and Type II Aδ nociceptors differing in preference.

What does it mean that C fibers are polymodal?

They respond to thermal, mechanical, and chemical noxious stimuli.

Which fiber type carries the most nociceptors according to the handwritten annotation?

C fibers.

What stimuli activate Type I Aδ fibers?

Dangerous mechanical and chemical stimulation.

How well do Type I Aδ fibers respond to heat?

They do not respond well to heat.

What stimulus preferentially activates Type II Aδ fibers?

Thermal stimulation, especially heat.

How well do Type II Aδ fibers respond to mechanical and chemical stimulation?

They do not respond well to mechanical and chemical stimulation.

How do C fibers respond across types of noxious stimuli?

They are polymodal and respond about equally to all types of noxious stimuli.

What is the professor's shorthand distinction among the three nociceptor types?

Type I Aδ = mechanical/chemical; Type II Aδ = heat; C = all/polymodal.

What receptor type is associated with pain and temperature Aδ afferents in the table?

Free nerve endings.

What receptor type is associated with pain, temperature, and itch C afferents in the table?

Free nerve endings.

Which afferent types are shown for proprioception in the comparison table?

Ia and II fibers.

How do Aδ and C fibers compare with Ia/II and Aβ fibers in size and conduction speed?

Aδ and especially C fibers are smaller and slower; Ia/II and Aβ fibers are larger and faster.

Which fibers produce first pain?

Aδ fibers.

Which fibers produce second pain?

C fibers.

What is first pain like?

Sharp and fast; the slide also calls it epicritic pain.

What is second pain like?

Dull, aching, longer-lasting; the slide also calls it protopathic pain.

What is the conduction velocity listed for C fibers in the first/second pain slide?

Less than 1 m/s.

Why does Aδ-mediated pain arrive before C-fiber-mediated pain according to the handwritten note?

Aδ fibers are myelinated and therefore conduct faster than unmyelinated C fibers.

Are Aδ fibers myelinated or unmyelinated?

Myelinated.

Are C fibers myelinated or unmyelinated?

Unmyelinated.

What typical pain sequence occurs after being hit by an object or scraping the skin?

A sharp first pain followed by a dull, aching, longer-lasting second pain.

What happens to the pain profile if Aδ fibers are selectively lesioned, according to the figure/annotation?

The sharp first pain disappears, while the slower second pain remains.

What happens to the pain profile if C-fiber signaling is absent in the figure?

The longer-lasting second pain is lost while the sharp first pain remains.

What key concept is demonstrated by first versus second pain?

The two phases of pain are carried by different fiber types.

Into how many functional categories does the slide divide skin nociceptors?

Four.

What are the four functional categories of skin nociceptors?

High-threshold mechano-nociceptors, thermal nociceptors, chemical nociceptors, and polymodal nociceptors.

What activates high-threshold mechano-nociceptors?

Only intense mechanical stimulation.

What examples of intense mechanical stimulation are given for high-threshold mechano-nociceptors?

Pinching, cutting, or stretching.

What activates thermal nociceptors according to this slide?

Intense mechanical stimulation as well as thermal stimuli.

What activates chemical nociceptors?

Chemical substances only.

What activates polymodal nociceptors?

All high-intensity stimulus types represented by the previous three categories.

What nociceptor/receptor types are found in joint capsules and ligaments?

High-threshold mechanoreceptors, polymodal nociceptors, and silent nociceptors.

When do silent joint nociceptors respond?

At the onset of inflammation.

What nociceptor types are listed for visceral organs?

Mechanical pressure, temperature, chemical, and silent nociceptors.

What channels are present in Aδ and C-fiber nerve endings for nociceptive transduction?

Transient receptor potential (TRP) channels.

What kinds of stimuli can TRP channels in Aδ and C-fiber endings respond to?

Temperature, pressure, and inflammatory agents.

What does TRPV1 stand for?

Transient receptor potential vanilloid type-1.

What temperature activates TRPV1?

Heat above about 43°C.

Why is >43°C important for TRPV1?

It is the threshold at which heat is perceived as noxious.

What endocannabinoid activates TRPV1?

Anandamide.

What food compound activates TRPV1?

Capsaicin, the pungent compound in hot chili peppers.

Why can spicy food produce a burning/hot sensation according to the annotation?

Capsaicin activates TRPV1, a channel involved in sensing noxious heat.

What handwritten distinction is made between normal warmth and intense heat?

Normal warmth can activate thermoreceptors, whereas intense heat activates nociceptors.

What are two other names for TRPV1?

Capsaicin receptor and vanilloid receptor 1.

What endogenous ligands are TRPV1 channels suggested to have developed to detect?

Endovanilloids and/or endocannabinoids.

What are endovanilloids compared with structurally/functionally on the slide?

They resemble capsaicin.

When and where are endovanilloids produced?

Peripherally in response to injury.

What other TRP family members are listed besides TRPV1?

TRPV2 and TRPA1.

What functions are attributed to TRPV2, TRPA1, and ASIC on the slide?

They act as mechanoreceptors or detect chemical irritants.

Is TRPV1 selective for only one cation?

No. It is a nonselective cation channel.

Which ions can pass through TRPV1?

Na+ and Ca2+.

What sequence does the handwritten annotation give for TRPV1 activation by intense heat/capsaicin?

TRPV1 is closed → capsaicin or enough intense heat opens TRPV1 → Na+ and Ca2+ enter the sensory ending → the membrane depolarizes → sufficient depolarization leads to an action potential.

What is hyperalgesia?

Increased sensitivity to painful stimuli.

What example of hyperalgesia is given?

Increased temperature sensitivity after sunburn.

Is the hyperalgesia mechanism emphasized here peripheral or central?

Peripheral, at the level of the nociceptors.

What causes peripheral nociceptor sensitization after tissue damage/inflammation?

Release of inflammatory mediators.

Which inflammatory mediators are specifically emphasized as sensitizing nociceptors?

Prostaglandins, histamine, and Substance P.

What do prostaglandins, histamine, and Substance P do to nociceptors?

Increase their sensitivity to noxious stimuli.

How can tissue injury affect nociceptors near, but not directly at, the injury?

Inflammatory mediators spread and increase the sensitivity of nearby nociceptors.

What everyday sunburn example is used in the handwritten notes to illustrate sensitization?

A shirt touching normal skin does not hurt, but light contact with sunburned skin can hurt.

What sensory pathway is labeled carrying injury-related signals centrally in the sensitization figure?

The anterolateral system.

Where is the nociceptor cell body labeled in the sensitization figure?

The dorsal root ganglion.

What is allodynia?

Pain sensation in response to non-painful stimuli.

What example is given to distinguish normal sensation from allodynia after sunburn?

A shirt touching normal skin causes no pain, but a shirt touching sunburned skin can cause pain.

What neural change underlies the central sensitization described on the slide?

Increased excitability of dorsal horn neurons.

During central sensitization, what can innocuous stimuli such as touching the skin activate?

Second-order dorsal horn neurons that receive nociceptive inputs.

What is "wind-up"?

Persistent increases in excitability and synaptic transmission.

How are hyperalgesia and allodynia different in the lecture?

Hyperalgesia is increased sensitivity to painful stimuli; allodynia is pain caused by normally non-painful stimuli.

Which receptors are labeled postsynaptically during the transient Aδ-fiber response in the central sensitization figure?

AMPA and NMDA receptors.

What postsynaptic effect is labeled for the Aδ-fiber response?

Fast membrane depolarization that is transient.

Which transmitters are labeled in the C-fiber terminal in the wind-up figure?

Glutamate and Substance P.

Which postsynaptic receptors are labeled during C-fiber stimulation?

AMPA, NMDA, and NK1 receptors, along with ion channels.

What postsynaptic effect is labeled for repeated/C-fiber stimulation?

Long-lasting, cumulative depolarization.

What ion is prominently shown entering during enhanced excitability/wind-up?

Ca2+.

What happens to TRPV1 activity after prolonged exposure to capsaicin?

TRPV1 activity decreases, producing desensitization.

What intracellular factor is implicated in TRPV1 desensitization?

Signaling pathways that regulate intracellular calcium concentrations.

What clinical/pharmacologic effect is thought to result from TRPV1 desensitization?

The paradoxical analgesic and anti-inflammatory effects of capsaicin.

Where does the anterolateral pain pathway cross the midline?

At the level of the spinal cord, not the medulla.

Where are the cell bodies of first-order somatosensory afferents shown in the pain pathway diagram?

In the dorsal root ganglia.