Flashcards in Thalamus - Integration of Sensation and Pain (20) Deck (38):
What is the pathway responsible for transmitting all ascending nociceptive pathways and collaterals?
Anterolateral spinothalamic tract
What are the two main divisions of the anterolateral spinothalamic pathway?
1. Neo-spinothalamic tract
2. Paleospinothalamic tract
What is the other name for the neo-spinothalamic tract and what general information about pain does it transmit?
Lateral sensory-discriminative component --> location, intensity, and quality of pain; responsible for "fast" pain
*theres a sharp pain in my left arm!
What is the other name for the paleo-spinothalamic tract and what function does it have?
Medial affective-motivational pathway --> influences emotional and visceral responses to pain as well the descending modulation of pain; dull, throbbing, poorly localized pain
* it hurts and I don't like it!
What types of afferent fibers are the main input to the neo-spinothalamic tract (lateral sensory-discriminatory component)?
A delta fibers --> synapse in laminae I, IV, V in dorsal horn
What thalamic nuclei receive info from the neo-spinothalamic tract?
VPL (body) and VPM (limb)
Where in the brain do fibers in neo-spinothalamic tract ultimately send its fibers?
To the primary somatosensory cortex
To which 3 thalamic nuclei does the paleo-thalamic tract(medial affective-motivational pathway) send fibers?
1. Intralaminar centromedian (CM) nucleus
2. Parafascicular (PF) nucleus
3. Dorsal medial (DM) nucleus
* these are part of the white matter that divides the medial and lateral portions of the thalamus
To what four more medial cortical areas do fibers of the paleo-spinothalamic ultimately go to?
1. Anterior cingulate cortex
Initiates direct behavioral responses to pain and also is active during actual pain, perceived pain, and also when watching someone else in pain
Anterior cingulate cortex
This structure in the medial system relays pain info to the limbic system, where pain-related learning and memory are processed
Projections to this structure initiate the visceral response to pain
Projections to the superior colliculus via the spinomesencephalic tract have what function?
Influence eye movements to direct gaze to the site of injury
Which free nerve ending receptor senses hot temperature and capsaicin?
* ~109 degrees (43 C)
What free nerve ending receptor senses cold temperature?
*77F (25 C)
Which type of afferent nerve fibers transmit temperature and mechanical stimulus that is hard enough to potentially cause injury?
A delta fibers
Which fibers transmit noxious chemical information?
* these, like the A delta, also transmit info from mechanoreceptors that have a high threshold and therefore only fire when the stimulus is intense enough to potentially cause damage
Where do cell bodies form both A delta and C fibers reside?
In dorsal root ganglia
What three NTs do A delta and C fibers release?
2. Substance P
3. Calcitonin-gene related peptide (CGRP)
* are released both to the 2nd order neuron in the spinal cord and also to the periphery
What two receptors does glutamate activate on secondary neurons in the ventral horn?
1. AMPA receptor
2. NMDA receptor
What receptor does Substance P activate?
What receptor does CGRP activate?
What 5 products are released by nociceptive receptors by tissue injury? * collectively, what do these do to initiate a pain response?
1. Serotonin (5-HT)
* these activate free nerve endings to fire an AP
Subsequent release of substance P and CGRP from free nerve endings in the periphery causes release of what 2 things at the site of injury?
Histamine --> vasodilation
What does the combination of inflammation and release of substance P and CGRP do?
Sensitizes the peripheral nerves so the threshold for activation is lowered
What other thing happens that serves to amplify the pain response?
The inflammatory chemical milieu activates previously silent nociceptive receptors on free nerve endings
*activated by inflammatory molecules, not by noxious stimuli
What are the neurons in laminae I and II that respond only to A delta or C fibers and encode only pain?
nociceptive specific neurons (SPN); (NS in the book)
Which neurons in the dorsal horn respond to all fibers but respond specifically to the input from C fibers to encode the intensity of the pain stimulus?
Wide dynamic range neurons (WDRNs)
* also responsively or Wind Up
Glutamate activation of WDRN _____ receptors and CGRP activation of WDRN CGRP receptors leads to WDRN depolarization... How does this activate the NMDA channel?
AMPA; relieves the Mg2+ block of the NMDA channel
How does activation of the WDRN NMDA channel via relief of the Mg++ block help begin the process of Wind Up (signal amplification)?
There is enhanced Ca2+ influx through the NMDA channel causes insertion of more Na+ channels and blockade of K+ channels---> increased responsiveness
How does substance p work to contribute to Wind Up?
Activates NK1 receptors, which prolongs the WDRN depolarization
* all the changes lead to reduced threshold and prolonged depolarization --> sensitization
What are the functional consequences of the Wind Up process in terms of chronic pain?
Relatively brief C-fiber stimulation can lead to long-lasting changes in the pain pathways that keep them overly sensitive--> leads to hyperalgesia
Why does rubbing a painful spot help relieve some of the pain? (gate-control theory of pain)
Shift the balance towards touch (via A beta activation) which detracts some of the input being sent through the pain pathway via C fibers
Cortex, amygdala, and hypothalamus all send fibers through what two structures to modulate lamina II neurons in the dorsal horn? Function of these descending pathways?
Through the Periaqueductal gray area and reticular formation--> serve to modulate NS and WDRN neurons and coma either facilitate or inhibit pain signals. Is useful to tell you to ignore the pain if there are more pressing issues or to take care of the pain if not (salience filter)
How do opioid receptors work to blunt the effects of pain?
Block presynaptic Ca2+ channels and/ or opening of postsynaptic K+ channels --> hyperpolarize the postsynaptic neuron and reduce APs
What is likely responsible for the phenomenon of referred pain?
Sharing of visceral nociceptive activity within the dermatomal systematic and the viscera are sparsely populated by nociceptive receptors
What is different about where the 1st order neurons involved in the visceral pain pathway compared to those involved in other nociceptive signaling (anterolateral/ spinothalamic)?
They bypass the dorsal horn nuclei and synapse instead on intermediate gray zone neurons lying near the central canal---> so travel with the dorsal column pathway instead