(Transcribed from Dr. Glasser’s lecture, 16 June 2000 by Brian Buschman)
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In the spine 1A fibers go to supply the:
1) Myotactic reflex
2) Direct input to the fasciculus cuneatus and gracillius (conscious proprioception and unconscious proprioception via the fibers that synapse in the accessory cuneate nucleus).
3) Dorsal nucleus of Clark (unconscious proprioception, LL).
The 1A fibers of the trigeminal nucleus are pretty much the same as in the spinal cord yet they have their cell bodies in the mesencephalic nucleus and project to:
1) Motor nucleus for the jaw drop reflex.
2) Chief sensory for conscious proprioception (when they ascend in the VTTT to the VPM and to areas 3, 1, 2).
3) Unconscious proprioception is carried via an unknown pathway.
Trigeminal 1B fibers come into the spinal nucleus and enter the cerebellum via the ICP for unconscious proprioception.
These two sets of fibers summarize all of the unconscious proprioception from V except for that which relays in the ION (via climbing fibers) and through the reticular formation (he said is clinically insignificant).
There are methods that many neuronal systems use to focus the sensory relay that do so by inhibiting adjacent fibers. Three types of inhibition is used in these types of systems:
1) Lateral feedback inhibition is when a neuron will stimulate interneurons that will inhibit adjacent neurons that carry signals parallel to the activated neuron.
2) Local feedback inhibition involves the second order neuron giving branches that shut off neighboring neurons so it’s signal is noticed more clearly.
3) Coricofugal feedback inhibition uses higher centers to feedback onto lower sensory neurons to shut them off selectively. This is a method for the cortex to regulate it’s sensory input. This is what you use when you tune out the crying of a baby at the next table at a restaurant.
The reason that areas 3, 1, 2 are labeled as such and not as 1, 2, 3 is because after they were numbered it was discovered that VPL and VPM project to area 3 which projects to 1 and 2.
We have discussed how slow pain is carried by a bilateral, diffuse relay. It follows Lissauer’s tract from the DRG and makes a stop in the substancia gelatinousa using substance P at it’s NT. It then ascends using diffuse tracts to the VPL and to areas 3, 1, 2. Slow pain has large receptive fields such as the pain associated with an MI.
It has been found that stimulation of the dorsal column fibers will cause a block in pain for a period of time. The strange thing is that pain does not travel in the dorsal fibers, but in the anteriolateral spinal thalamic tract (fast pain) and diffuse tracts (slow pain), yet dorsal column stimulation blocks the pain. When this was investigated it was proposed that large diameter fibers (epicritic fibers) and small diameter fibers (c-fiber and A-delta fibers) carry sensations through relays to the thalamus. The relay in the nucleus proprius is stimulated by the 1st order fibers. The theory states that large fibers stimulate an interneuron on the substancia gelatinousa which causes presynaptic inhibition of both sizes of 1o fibers before they synapse in the nucleus proprius.
It is now known that the large diameter fibers do not stimulate the 2o fibers in the nucleus propitious but they do act to inhibit small fibers in an interneuron relay. The small fibers stimulate pain via the nucleus proprius and synapse on the regulatory interneuron in the substancia gelatinousa. They act to inhibit the regulatory interneuron thereby shutting off the inhibition.
It is known that morphine blocks pain at the level of the periaqueductal gray. It is strange that we have receptors for morphine but it turns out that morphine has a functional unit similar to b-endorphin. Either morphine or b-endorphin suppress pain by the following sequence:
1) Stimulation of neurons in the periaqueductal gray which stimulate fibers in the midbrain raphe.
2) That fiber is a 5-HT fiber that stimulates an interneuron in the substancia gelatinousa.
3) The interneuron presynapticly inhibits the DRG fiber’s passage of pain by using an unknown enkaphaline.
Analgesia can also be stimulated by:
1) Higher centers but we are not sure how.
2) Conscious suppression as needed. Like if you are having tea from fancy china and still a little you don’t just drop the cup.
3) Stress induced analgesia. Such as when a football player is able to keep playing when he has a broken bone.
Stress induced analgesia is a result of the mechanisms of release of ACTH. Stress stimulates the formation of ACTH from it’s prohormone. When it is cleaved to give ACTH the other cleavage product is b-endorphin which has the obvious effect.
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