Chapter 12 Flashcards
neuropathic in nature
the actual trigger for the actual pain was compression of the axon and not of the free nerve endings (perceived pain as originating from his butt, but on examination there was no injury of any kind (cause of injury) nociceptors of butt and thigh were not being depolarized but axons were depolarizing along their
coarse (along the axon itself)
The nerve is sick which created the pain, not started with the free nerve ending nociceptors.
Non-nociceptive pain includes:
Neuropathic pain-nerve injured somehow proximal to the nociceptors
Central sensitivity syndromes- effect of top down pathways on signals of pain or perception of pain
Pain syndromes- don’t cover
Nociceptive pain
continuing pain stimulus
Pain neurons functioning normally
Central axon that synapses in the dorsal horn with another neuron that goes up to the brain.
Is a continuing pain stimulus but the pain neurons are functioning normally. Sending action potentials that sends a synapse to continue on.
Symptoms of neuropathic pain
Paresthesia- sensory message that arises in the absence of any sensory receptor stimulation- a nonpainful sensory feeling that arises without the stimulation of sensory receptors
Dysesthesia- A sensory symptom that is unpleasant or painful. Abnormal unpleasant sensation either spontaneous or evoked
Allodynia- Unpleasant feeling in response to a stimulation that would not normally produce an unpleasant feeling (sunburn example)
Secondary hyperalgesia- higher than normal pain- a pain that is out of proportion to the stimulus creating it, stimulus would normally be somewhat painful but it now sensitive and would send pain that is out of proportion to what is causing the sensation
Mechanisms of neuropathic pain: ectopic foci
(in another place pain starts)- distal end to pain neuron has been damaged/cut off (could be demyelinated, could be the peripheral axon has been killed and is degenerating). Will try to put modality gated channels and ligand gated channels up into the injured membrane (no longer has a normal sensory receptor) at injured spot will insert modality and ligand gated channels to try and sensation.
Carpal tunnel syndrome the median nerve is damaged at the transverse carpal ligament. Patient reports tingling in thumb and first two fingers. Feeling sensation in peripheral sensation when you tap not on the receptors but on the axon itself. Because the axon puts some modality gated channels in its membrane and will then give the sensation of peripheral sensation. Shows that there is damage at the location of tapping and we have stimulated the neuron inappropriately.
*NEUROPATHIC SENSATION
Mechanisms of neuropathic pain: ephaptic transmission
Short circuit, people with gione barre (peripheral demyelinated disease) when multiple neurons get demyelinated (touch and pain neurons) at point where they have been demylinated there can be a short circuit and an action potential on touch neuron can jump over and activate the pain neuron. Simple touch produces pain because of the short circuit. a neuropathic possibility.
Mechanisms of neuropathic pain: central sensitization
When there is a strong, or long lasting pain signal your NS may say oh that is strong and long lasting, you must want that, I will remodel and make it easier to send that signal. NS decides the impulse is important and remodels synapse and it learns pain (long term potentiation) this is maladaptation. the initial long and strong stimulus can now make you sensitive to things that are of a mild stimulus because the synapse is way better at passing messages through.
Hyperalgesia- potential for what is mentioned above. It is mal adaptive because patients feel pain inappropriately.
Mechanisms of neuropathic pain: structural reorganization
For some reason, after a long and strong pain stimulus the central axon of the pain neuron backs up from the synapse, a touch neuron will send a collateral branch over to reconnect with the synapse of the pain axon.
Second order pain neuron has lost input and calls for input, a nearby touch neuron collaterally sprouts and innervates/reestablishes a synapse with the pain neuron. possible mechanism for Allodynia.
Sites that generate neuropathic pain
Peripheral neurons
- ectopic foci
- ephaptic transmission
Central neurons
-Phantom limb sensation (if knee is taken away and no longer connected to its second order neuron. They synapse will call for sensory input and it is possible for the thigh to have collateral sprouting and supply some of the neurons that use to feel the knee. If you touch the thigh, the touch of the thigh could be perceived as coming from a missing knee, Because the thigh neuron sprouts and innervates the neuron of the knee.
If neurons are in touch system they can lead to phantom touch and if in pain system they can lead to phantom pain.
Denervation hypersensitivity- sticks receptors in post-synaptic membrane to try and get signals back and can suddenly become active because of neurotransmitter floating by. can become active without touch.
Central sensitivity syndromes
Antinociception is reduced and/or pronociception is increased.
Brain does not shut off pain signals on their way in and also creates an easier path for pain signals to come in.
Motivational-affective and Cognitive-evaluative centers- possible for the brain to influence from the top down.
Real injury to the system- injured and feels nociceptive pain that comes with the tissue injury. After initial injury the patient feels uncertainty (will I get better or not, will I have to quit my job or not). This is a threat and I need to know about any future pain or injuries like this because it is a threat to my species so I will turn down the antinociception (wont presynaptically inhibit the pain signals anymore) I am also going to increase the pronociception (increase presynaptic facilitation) so I know when the next signal like that gets here. With repetitive activation/stimulation causes LTP to occur.
What we need to do is to unlearn the pain response, turn down the pronociception and turn up the antinocicieption. We can do that through medications for the top down piece, and may work at the synapse piece.
