L15: Nociception Flashcards
What kind of receptors are activated when there are harmful stimuli being applied to skin or subcutaneous tissues? Where are these cell bodies located?
Nociceptors -cell bodies (like the somatosensory recepotrs) are located in the dorsal root and trigeminal ganglia
Which receptors are considered the least differentiated sensory receptors in the skin?
Nociceptors exist as free nerve endings that do not have peripheral structures that transduce & filter peripheral stimuli
Pain in humans is mediated by different classes of nociceptive afferent fibers? List & describe them
1) thermal or mechanical nociceptors contributes to “first pain”
- small-diameter
- thinly myelinated Aδ fibers
- conduct at 5-30 m/s
- activation is associated with sharp, pricking pain
2) Polymodal nociceptors lead to “second pain”
- small-diameter
- unmyelinated C fibers
- conduct slow at 0.5-2 m/s
- activation is associated with a variety of high-intensity mechanical, chemical, and hot or cold stimuli
T/F: Nociceptors begin to discharge when there’s a stimulus.
False -nociceptors begin to discharge only when the stimulus is intense enough to cause damage
In general, when the stimulus is intense enough to activate Aδ fibers (“first pain”) in a peripheral nerve, a tingling sensation is reported. When will you feel sharp pain?
If the stimulation is intense enough, you can feel sharp pain.
First, a stimulus intense enough to activate Aδ fibers will cause a tingling sensation. If the stimulus is intense enough, it can result in sharp pain. When the stimulus intensity is increased further, what other receptors can be activated and what kind of feeling results?
If the stimulus intensity is increased further, the C fibers are activated resulting in a duller, longer-lasting sensation of pain. This duller, longer-lasting sensation of pain is referred to as “second pain.”
Is it possible to selectively anesthetize C fibers and Aδ fibers?
Yes.
What is vanilloid receptor TrpV1? What activates this receptor?
It is a receptor that is found in both C and Aδ fibers and is a Na+ voltage gated channel. It is activated by capsaicin, heat, acids and anandamide.
What is endovanilloids?
It mimics the vanilloid receptor TrpV1 (found in both C and Aδ fibers)
What is hyperalgesia?
Enhanced sensitivity and responsitivity to stimulation of the area in and around the damaged tissue.
When peripheral tissues are damaged, is the sensation of pain in response to following stimuli enhanced or depressed?
Enhanced leading to hyperalgesia
What is happening on the molecular level that peripheral damage leads to hyperalgesia?
When tissue is damaged, it releases various substances, such as bradykinin, histamine, prostaglandins that will enhance the responsiveness of nociceptive endings.
When nociceptors are electrically stimulated, it causes a local release of substances (e.g. substance P) that results in
vasodilation, swelling and the release of histamine from mast cells. Histamine will enhance the responsiveness of nociceptive endings, which partially accounts for the phenomenon of hyperalgesia in areas post-injury.
Can local pain be sensed when nociceptive pathways are damaged?
Yes, pain can arise spontaneously in the absence of activity in nociceptors.
Brachial Plexus avulsion is an example of loss of afferent input from the periphery to the spinal cord, but pain is still felt. Explain the pain found in these patients.
These patients feel a burning pain in the dermatomes corresponding to the denervated area. The pain is due to hyperactivity of dorsal horn neurons in the deafferented region of the cord.
Both C & Aδ nociceptive fibers enter spinal cord via the dorsal roots. They split upon entering the spinal cord. Branches of these axons ascend and descend for a few segments as part of which tract?
dorsolateral tract aka lissaur’s tract
In the gray matter of the spinal cord, there are layers (I - IX). Nociceptive fibers terminate primarily in which layers?
Lamina I & II in the superficial dorsal horn
**some Aδ fibers fibers project more deeply into lamina V
Why are lamina I neurons (in gray matter of spinal cord) termed nociceptive specific (NS) neurons?
b/c they contain a high density of projection neurons that process pain information, and are excited solely by C and Aδ fibers.
Lamina V neurons (in gray matter of spinal cord) are known as wide dynamic range (WDR) neurons. Why are they called WDR neurons?
b/c these neurons contain input from both mechanoreceptors & nociceptors, responding to both somatosensory and noxious stimuli. WDR neurons have much bigger receptive fields than do nociceptive specific neurons.
What is referred pain?
displacement of pain from a visceral structure to a somatic area of the body b/c of convergence of visceral & cutaneous nociceptors onto the same dorsal horn projection neurons.
Explain “phantom limb” and “phantom pain”
the limb is no longer there (e.g. amputated), but the person still senses it b/c cortical input still exists for that limb. Thus, if one believes it’s there, then one can feel “phantom pain,” which is hard to treat.
Briefly summarize how nociceptive info from body & face is conveyed to the primary somatosensory cortex (post-central gyrus).
- pain info from the body ascends to the primary somatosensory cortex by first entering dorsal root and crossing over at the level of the spinal cord. It will ascend to the thalamus as the anterolateral tract and synapse at the VPL of the thalamus, before being projected to post-central gyrus
- pain info from the face will pass trigeminal ganglion and descends to synapse at the spinal nucleus of V before ascending to the thalamus as the spinal tract of V and synapsing at the VPM before going to post-central gyrus.
If large areas of the somatosensory cortex is damaged, will it result in impaired responses to noxious stimuli or loss of pain?
No, clinical studies have shown that damage to large areas of the somatosensory cortex does not result in impaired responses to noxious stimuli or loss of pain.
Explain the condition of dissociated sensory loss following a spinal cord injury.
- since epicritic info (mechanosensation: touch, pressure, vibration, position sense) ascends ipsilaterally before descussating in the medulla; spinal cord injury will cause ipsilateral loss of sensation
- anterolateral pathway carrying protopathic (nociceptive info) decussates in the spinal cord; spinal cord injury will cause contralateral loss of pain sensation.
hence, dissociated sensory loss involves a loss of epicritic info on the same side of the spinal cord lesion and a contralateral loss of pain info. There will also be a zone of complete loss above the epicritis loss due to bth nociceptive and epicritic fibers enter spinal cord.
