Unit 5.2: spinal cord - internal structures Flashcards
sensory info _____ the cord
motor info _____ the cord
- goes up
- goes down
there are more ____, ____ pathways than ____, ____ pathways
more ascending, sensory than descending, motor
bundle of axons INSIDE the CNS
tract
bundle of axons OUTSIDE the CNS
nerves
motor/descending pathways AKA
efferent pathways
E-fferent; E-xiting the CNS
sensory/ascending pathways AKA:
afferent
A-fferent; A-scending to the CNS
what two main tracts make up the efferent/descending pathways?
- pyramidal
- extrapyramidal
what are the pyramidal tracts responsible for?
the vast majority of motor function
primarily voluntary movement
what are the extrapyramidal tracts responsible for?
lies outside the pyramidal tracts
accessory motor pathways that coordinate complex tasks
involuntary control; helps us “fine-tune” our motor commands
what 3 main tracts make up the afferent/ascending pathways?
- dorsal column tracts
- spinocerebellar tracts
- anterolateral system AKA spinothalamic tract
what is the dorsal column medial lemniscal system responsible for?
located in the dorsal spinal cord
touch/perception/pressure sensors
passes through the medial lemniscus
what is the anterolateral system responsible for?
has 2 parts: 1. anterior and 2. lateral; hence anterolateral
AKA spinothalamic tract because it transmits info from spinal cord to the thalamus; hence, spinothalamic
transmits pain information
what is Rexed’s laminae?
the spinal cord’s gray matter nomenclature system which are labeled from most dorsal to most ventral
Lamina I
aka lamina marginalis (on the margin)
sharp pain; “fast” pain
A-delta pain - myelinated neuron fibers
Lamina I, II, III, and V’s horizontal pathway to:
anterolateral spinothalamic pathway
Laminae II & III
AKA substantia gelatinosa
slow pain
C-fibers (nociceptors are unmyelinated) – this is why this is termed “slow pain” pathway
has a synaptic connection with Lamina V
Laminae I - VI
have mechanoreceptors (pressure sensors)
pain sensory
Lamina VII - IX
VII: intermediolateral nucleus
large motor neurons
lamina X
cross talk relay section of grey matter
categorize the 5 different spinal tracts
- spinocerebellar tracts
- dorsal-column medial lemniscal system
- spinothalamic tracts
- corticospinal tracts (AKA pyrdamidal tracts)
- extrapyramidal tracts
characterize the DCML pathway
- very fast signal propogation (all A fibers with all subunits)
- fine vibrations
- fine pressure
- cross over at medulla
what is meant by “cross over” in the DCML pathway?
typically the sensory information sent from the left hemisphere of the brain will cross over in the medulla to take care of the right side of the body’s motor function & vice versa
the further up the spinal cord you get, the _____ the DCML is
wider
where does the doral column gather lower extremity sensory information?
Fasiculus gracilis
the gracilis muscle is in the leg
where does the doral column gather upper extremity sensory information?
Fasiculus cuneatus
if you have touch sensory information coming in, where does this information split? where does it go?
- a portion goes to the gray matter (lateral inhibition)
- a portion of the sensory info will ascend in the DCML pathway
a feather tickles your right foot; list out the sensory pathway from the foot to the brain
- tickle information comes from right foot
- foot to dorsal root and spinal ganglion (Fasiculus gracilus)
- ascends and crosses over at the lower medulla oblongata in the dorsal column nuclei
- ascends through the medulla oblongata
- medial lemniscus, pons, midbrain
- to the ventrobasal complex of thalamus
- to the internal capsule
- to the left hemisphere parietal lobe
where is the internal capsule located?
sits between the thalamus and the parietal lobe of the brain
what is the “Homonculus” depiction?
two types:
1. sensory homonoculus (post-central gyrus)
2. motor homonculus (pre-central gyrus)
this drawing maps out what areas of the body are affected by sensation (in postcentral gyrus)
ex) the hand has more real-estate on the postcentral gyrus than the trunk does; the drawing illiustrates the proportion of sensory receptors to each body part on the post-central gyrus – so our hands have more sensory receptors than our trunk does
list out the primary pathway of the pyramidal tracts
- signals originate in motor cortex
- internal capsule
- pyramids of medulla
- cross over (pyramidal decussation)
- lateral corticospinal tracts
- ventral horn
- effector organ
80% or 4/5 of our motor function gets routed through this pathway
what is the pyramidal decussation?
the crossover point for motor information in the lower ANTERIOR medulla
where does cross over occur in the secondary motor pathway?
cross over occurs in the spinal cord; this cross over point is much lower in the spinal cord than the primary motor pathway (which happens in the pyramidal decussation in the lower, anterior medulla)
cross over in the secondary motor pathway occurs where the level where the neurons can communicate with the motor neuron in the anterior horn (at the level of the SC)
where does the motor information descend to in the secondary motor pathway?
anterior corticospinal tract
(anterior pyramidal tract)
about what percentage of motor function information gets processed through the secondary motor pathway?
17%
how much perecent of our motor information does not get crossed over in the spinal cord?
2-3%
describe the “fast pain” pathway of the spinothalamic tract
+fast pain
+lateral pathway
+A-delta nociceptors (heavily myelinated)
+NT: glutamate – fast to release, fast to bind, and fast to make changes
describe the “slow pain” pathway in the spinothalamic tract
+slow pain
+anterior pathway
+C-fibers (non-myelinated)
+NTs: glutamate (slow in this pathway), substance P, CGRP (calcitonin gene-related peptide)
+NTs are slow to release, slow to bind, and slow to make changes
+themoreceptors/heat/vibration
substance P is the main NT
which laminae does the fast pain pathway have synaptic connections in?
lamina I
Lamina marginalis
which laminae does the slow pain pathway have synaptic connections in?
laminae II & III, then V
Substantia gelatinosa (II & III)
“fast pain” spinothalamic tract AKA:
Neospinothalamic tract
“slow pain” pathway tract AKA
Paleospinothalamic tract
where does crossover occur with the spinothalamic/anterolateral tracts?
at the level of the spinal cord where their effector organ/tissue is
AKA crosses over at the anterior white commisure
why are we able to localize fast pain signal origins better than slow pain signal origins?
fast pain: detailed localization; gets routed parallel with DCML pathway to parietal lobe – so you’re able to tell where you got injured
slow pain: poor localization (not all sensory info will make it to the parietal lobe, most will terminate in the reticular formation of the brainstem) – can generalize pain area but cannot pinpoint
you burned the tip of your finger on the stove; list out the pathway that this sensory information will travel up to your brain
- finger tip temperature/pain sensory information
+this is considered SLOW PAIN (temperature) - dorsal root and spinal ganglion > dorsal horn
- lamina II & III (substantia gelatinosa); sometimes V
- cross over at AWC
- anterior spinothalamic ascending pathway
- up the spinal cord > lower medulla > medulla oblongata > mesencephalon > terminates in the RETICULAR FORMATION of the brainstem
most of the time will not reach the part of the brain where we can localize pain
ENGAGES THE LIMBIC SYSTEM
what 3 structures comprise the reticular nuclei?
- medulla
- pons
- mesencephalon
which type of pain (slow or fast) engages the emotional centers of the brain?
slow pain
what are the 3 structures that make up the limbic system?
- amygdala
- HYPOthalamus
- cingulate gyrus
“amy got mad” > amygdala > emotions
list out the fast pain pathway from sensory origin to the parietal lobe
- origin of fast pain
- spinal root ganglion > rootlets > dorsal horn
- Lamina I (Lamina marginalis)
- crossover at the AWC
- lateral spinothalamic pathway
- ascends to thalamus
- through medulla > ventrobasal complex PARALLEL WITH DCML PATHWAY > posterior nuclear group
- parietal lobe
categorize the different parts of the extrapyramidal tracts (4)
- vestibulospinal: helps to keep balance with changes in body position
- olivospinal
- reticulospinal: maintaining muscular tone (muscles aren’t ever entirely relaxed)
- rubrospinal: modulation of voluntary movement similar to what cerebellum does
all are CNS outputs to the spinal cord
what is the descending pain suppression system?
- inhibitory in nature in response to pain/”takes the edge off”
- not strongly activated; works in the background
- comprised of 3 neurons known as the descending inhibitory complex (DIC)
+periventricular & periaqueductal grey (enkephalins)
+raphe nucleus (serotonin)
+dorsla spinal cord complex: tract of lissauer, lamina marginalis, substantia gelatinosa (5HT and enkephalin)
describe the first order descending neuron in the DIC
cell body origin: **periventricular nucleus OR periaqueductal gray
**
“peri-ventricular”: around the ventricles
“peri-aqueductal”: near the cerebral aqueduct
neuron: fires AP to the middle of the pons via enkephalin neurons
NTs: enkephalins released in brain stem are EXCITATORY
describe the second order descending neuron in DIC
cell body origin: raphe magnus nucleus (RMN)/middle of pons
neuron: serotinergic (releases 5HT when excited) near dorsal horn in SC
NTs: 5-HT
describe the third order descending neuron
cell body origin: dorsal horn
neuron: enkephalin secreting neuron
NT: enkephalin released to nociceptors; enkephalins released in the spinal cord are INHIBITORY, so when enkephalin is released to bind to nociceptors, pain is “inhibited”
NT release:
1. nociceptors
2. second neuron in the anterolateral system projecting to the thalamus
what are enkephalins?
endogenous opiate system in the body
morphine analogs
what is the therapy that suppresses pain in the body by activating the DIC?
deep brain stimulation
electrodes are placed near the periventricular nuclei or periaqueductal gray to stimulate the DIC to alleviate pain
how does enkephalin shut down pain signals in the pre-synaptic side of the synapse as well as the post-synaptic side of the synapse
because
1. the nociceptors have enkephalin receptors
2. & the secondary neuron in the anterolateral pathway also has enkephalin receptors
so when enkephalin binds in the SPINAL CORD, the NT is inhibitory and shuts down the neurons
how can ECF K+ cause pain?
high ECF K+ can typically depolarize cells, and if it’s depolarized enough, it can be considered painful
how do SSRIs/antidepressants help manage chronic pain?
these drugs inhibit reuptake of serotonin, so 5HT will increase in the synapse and can get recycled to bind to the 3rd order descending pathaway of the DIC ( to help release more enkephalins)
explain what lateral inhibition is
neighboring neurons can shut down their parallel neuron
ex) the DCML and nociceptors parallel each other; pressure signal can shut down a pain signal
ex) you grab your finger that just got smashed – this can help blunt the pain
(probably also how accupuncture works)
name 3 IONOTROPIC glutamate receptors
- AMPA
- NMDA
- kainate receptors
describe AMPA-Rs
the main receptor for glutamate
many present
ion channel: Na+
when glutamate binds, Na+ influxes
describe NMDA-Rs
slower than AMPA-R
ion channel: VG Ca2+ (sometimes Na+ as well)
once glutamate is bound and prior depolarization has occured, Ca2+ can influx into the cell
this receptor needs PRIOR depolarization d/t being BLOCKED by ICF Mg2+ at REST
why does Mg2+ block the NMDA receptors?
the cell wall has a more negative charge drawing in the ++Mg ion
name 5 NMDA receptor antagonists
NMDA/AMPA-R blockers
1. ethanol
2. lead (poisoning)
selective NMDA-blocking
3. ketamine
4. nitrous gas (N2O)
5. tramadol
will you have more NMDA-Rs in early life or later life?
later
NMDA-Rs are important in growth and development; NMDA-Rs get implanted over TIME
if you have chronic pain, you’ll have _____ receptors at the synapse which will give you _____ APs to ______ sensitivity
- more
- more
- increase
glutamate is typically an _____ NT
excitatory
the following metabotropic ion channels open up K+ on pre/post-synaptic neurons in the DIC:
- enkephalin/opiate-Rs
- alpha-2 adrenergic-Rs
these type of drugs increase cell membrane permeability to K+/K+ conductance in the first order DIC neuron
volatile anesthetics
what are (3) alpha-2 receptor agonists that bind to slow down the CNS
- xylazine (non-specific alpha)
- clonidine (alpha 2 > alpha 1)
- dexmedetomidine (alpha-2 specific)
what are COX-2 & prostaglandin’s roles in the first & second order DIC neurons?
COX-2 is induced in response to pain
COX-2 produces PGGs that can increase sensitivity to pain stimuli
COX-2/PGGs will increase the likelihood of AP firing, but will not actually conduct APs
what is iNOS?
inducible nitric oxide synthase is an enzyme that increases the synapse sensitivity to pain (much like PGGs but less so)
how do Mg2+ supplements aid with chronic pain?
Mg2+ can block the NMDA receptors at rest
can cause GI upset if ingested since it is not digested well
list 9 chemical signals that will activate nociceptors
- bradykinin
- 5HT
- histamine
- K+
- H+/acidotic conditions
- ACh
- proteolytic enzymes
- ischemia/muscle spasm (a build up of metabolic waste products)
(9. PGGs - can’t generate AP in nociceptors, but can make receptors more sensistive)
list 7 mechanical/thermal signals that will activate nociceptors
- stretch
- crush injury
- stabbing
- physical tissue damage
- proteolytic enzymes
- high temps >45 C
- low temps <5 C
