Lecture 2 Test 3 Flashcards
2 types of pain anterolateral system (ascending) tracts
Lateral spinothalamic tract
Anterior spinothalamic tract
Extrapyramidal tracts (descending motor) ex.
Vestibulospinal tract; eye fixation, balance
Olivospinal tract; movement coordination
Reticulospinal tract; muscle tone
Rubrospinal tract; monitoring, adjusting voluntary movements
Main motor output pathway
Pyramidal tracts
What is the body’s Inhibitory pain system; helps the body deal with pain
Descending pain suppression system
Where do incoming sensory information go into?
Dorsal roots, dorsal horn
Name for ascending pain pathway
Anterolateral spinothalamic pathway
Does pain sensory get crossed over at the spinal cord right away?
Yes, before it ascends to the brain
What info travels through the DCML pathway?
Pressure sensor information (what we’re holding, what surface we’re in contact with)
Explain the descending primary pathway sequence
Cortex > internal capsule > Ventrobasal complex > X-over Medulla decussation > lateral corticospinal tracts > anterior horn > Anterior roots > spine nerve > motor response
How many % of our somatic motor sensations/functions go through the primary pathway?
80% and x-over is at the medulla
How many % of our somatic motor sensations/functions go through the anterior corticospinal tract??
17% and x-over is at the level of the cord
How many % of sensory that doesn’t cross over any?
3% of motor function
Fast pain is transmitted through what type of fibers?
Myelinated A(d) neuron fibers (nociceptors / free nerve ending)
Fast pain gets transmitted through the …..
Lateral neospinothalamic tract
What neurotransmitter is used for fast pain?
Glutamate (binds quick, released quick)
What part of the brain gets the fast pain?
Parietal lobe
What is DCML?
(Dorsal column medial lemniscus ) pathway
what part of the parietal lobe (post central gyrus) takes care of the lower extremity
Top
what part of the parietal lobe (post central gyrus) takes care of the face
bottom
what part of the parietal lobe (post central gyrus) takes care of the upper extremity
Mid bottom
what part of the parietal lobe (post central gyrus) takes care of the trunk
Mid top
Is fast pain easy to localize?
Yes
Is slow pain easy to localize?
No
Where does the cross over occur for the pain pathway?
AWC (anterior white commissure) same level where the information comes in
Other name for fast pain pathway
Neospinothalamic tract (Neo= new)
Name for Slow pain pathway
Paleospinothalamic pathway (paleo = old)
Which lamina takes care of fast pain?
Lamina I
Which lamina takes care of slow pain?
Lamine II & III and V
What type of fibers transmit slow pain?
non myelinated C fibers
Neurotransmitter for slow pain?
Substance P, Glutamate, CGRP (calcitonin gene related peptide)
Where in the brain does slow pain travel to?
Top of the brainstem no more higher than the thalamus.
What other sensors do slow pain get associated with?
Temperature sensors, vibration sensors
Where does slow pain crossover?
AWC at the level of the cord
What tract/pathway does slow pain use?
Anterior paleospinothalamic tract
What does the somatosensory area do for fast pain signal?
Helps localize where the pain originated.
What else do slow pain affect?
Emotional centers
Where do most slow pain signals terminate?
RETICULAR FORMATION (brain stem)
1st order descending neuron for Descending Inhibitory Complex (DIC)
Pariaqueductal gray or Periventricular nucleus (anterior 3rd ventricle)
1st order descending neuron releases what in the middle of the pons?
Enkephalins (excitatory)
Where is the 2nd order descending neuron for DIC located?
middle of the pons (Raphe Magnus Nucleus) Serotonergic neuron (5-HT)
Where is serotonin released by the 5-HT?
in the spinal cord, dorsal horn. Enkephalin (inhibitory) neuron (3rd order DIC)
Enkephalin receptor aka
opiate receptor
What is enkephalin?
Inhibitory neurotransmitter in the cord; Morphine analog (shut down pain transmission signals)
slow pain pathway process
Slow Pain sensor > Nociceptor (C fiber) > spinal nerve > dorsal root ganglion > dorsal roots > dorsal rootlets > synapse lamina II, III, V > x-over AWC > ascend anterior paleospinothalamic tract > terminate at brainstem
Fast pain pathway process
Fast Pain > Nociceptor (A(d) fibers)> spinal nerve > dorsal root > dorsal rootlets > dorsal horn > synapse > lamina I > x-over AWC > ascend lateral neospinothalamic tract > brain stem > ventrobasal complex > internal capsule > parietal lobe
Descending pain suppression system (DIC) process
Periventricular nuclei > (1st order descending neuron) excitatory Enkephalin neuron 1 released in the Pons > Raphe Magnus Nucleus (RMN) > (2nd order descending neuron) Serotonergic neuron > release serotonin > (3rd order descending neuron) release Enkephalin Inhibitory neuron 2 > Pain is either shut down in (presynaptic neuron) or shuts down the post synaptic neuron of the ascending pathway.
Examples of Pain origins
lactic acid build up, excess k+, Histamine, serotonin in the periphery, Ach, PGs augment pain, bradykinin
How does SSRI (Paxil, Prozac, Tricyclic) help with pain?
Helps manage chronic pain by stopping the Reuptake of serotonin and augment the 3rd order inhibitory effect.
Some side effects from older drugs like tricyclic (TCA) can be useful.
Drowsiness for sleep, people with chronic pain has a hard time sleeping.
What happens when neurons for pain and pressure are next to each other at the dorsal horn?
One shuts off the other (lateral inhibition)
acupuncture works through…..
lateral inhibition
Is glutamate inhibitory or excitatory?
Excitatory
What can block NDMA-R (pain receptor)
ETOH, Lead, Ketamine (dissociative), NO, tramadol
AMPA-R (glutamate pain receptor) process
(1st order pain sensor neuron) > glutamate in vesicle next to membrane > AP causes Ca++ influx > release glutamate into synapse > bind to AMPA-R of 2nd neuron > Na+ influx > Action potential > send info up the brain.
NDMA-R (glutamate pain receptor) process
(1st order pain sensor neuron) > glutamate in vesicle next to membrane > AP causes Ca++ influx > release glutamate into synapse > bind to glutamate NMDA-R (2nd receptor; slower; occurs AFTER AMPA-R) > Ca++ influx > Mg+ efflux after depolarization caused by AMPA-R
Chronic pain has more of what type of pain receptors?
AMPA- R and NMDA-R
What are the Ionotropic glutamate pain receptors
AMPA-R
NMDA-R
Kanate-R (mediates GABA activity in the brain)
Categories of glutamate pain receptors
Ionotropic and metabotropic (GCPR)
Neurotransmitter for Fast pain
Glutamate
Neurotransmitter for Slow pain
Glutamate as well but mainly Substance P and CGRP
Is fast pain myelinated or non-myelinated?
Myelinated
Is slow pain myelinated or non-myelinated?
Non-myelinated but may or may not
What is lateral inhibition?
When pain sensors are inhibited in the cord or the periphery
Are ionotropic and metabotropic glutamate receptors inhibitory or excitatory?
Excitatory
Where are metabotropic glutamate receptors located?
In the brain
What is the body’s endogenous opiate system?
Enkephalins; Endorphins
Enkephalin receptors (opiate receptors) are what type of receptors?
GCPR
Enkephalin receptors and A2 receptors are linked to?
Potassium channels
What happens to the cell when enkephalin receptors are activated?
Potassium channels open and release K+ into the ECF to inhibit the cell (make negative)
What happens when A2 agonist is activated at the pre or post synaptic neurons?
Potassium channels open and release K+ to inhibit the cell (make negative)
Examples of A2 receptor agonist
(slows down CNS)
Xylazine (also for A1)
Clonidine (more specific A2)
Precedex (most specific A2)
Which A2 agonist is used by drug users and what is the other name for it?
Xylazine aka Horse tranq
How does volatile anesthetics work in the synapse?
Open potassium channels (conductance) to suppress the CNS
For our class which way does potassium go?
Out of the cell!!!
Cox 2 (increase pain sensitivity) and produces PGs due to?
Induced by pain
Prostaglandins (PGs) produces more of what in the presynaptic and post synaptic neurons?
More action potentials
What else amps up pain signals in the synapse other than PGs?
iNOS
Which electrolyte helps with chronic pain?
Magnesium but risk for toxicity and cause diarrhea
Does increase calcium levels in ECF impact pain?
No