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Ana/Phys/Patho I > Unit 5.2: spinal cord - internal structures > Flashcards

Unit 5.2: spinal cord - internal structures Flashcards

1
Q

sensory info _____ the cord
motor info _____ the cord

A
  1. goes up
  2. goes down
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2
Q

there are more ____, ____ pathways than ____, ____ pathways

A

more ascending, sensory than descending, motor

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3
Q

bundle of axons INSIDE the CNS

A

tract

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4
Q

bundle of axons OUTSIDE the CNS

A

nerves

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5
Q

motor/descending pathways AKA

A

efferent pathways

E-fferent; E-xiting the CNS

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6
Q

sensory/ascending pathways AKA:

A

afferent

A-fferent; A-scending to the CNS

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7
Q

what two main tracts make up the efferent/descending pathways?

A
  1. pyramidal
  2. extrapyramidal
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8
Q

what are the pyramidal tracts responsible for?

A

the vast majority of motor function
primarily voluntary movement

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9
Q

what are the extrapyramidal tracts responsible for?

A

lies outside the pyramidal tracts
accessory motor pathways that coordinate complex tasks
involuntary control; helps us “fine-tune” our motor commands

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10
Q

what 3 main tracts make up the afferent/ascending pathways?

A
  1. dorsal column tracts
  2. spinocerebellar tracts
  3. anterolateral system AKA spinothalamic tract
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11
Q

what is the dorsal column medial lemniscal system responsible for?

A

located in the dorsal spinal cord
touch/perception/pressure sensors

passes through the medial lemniscus

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12
Q

what is the anterolateral system responsible for?

A

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

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13
Q

what is Rexed’s laminae?

A

the spinal cord’s gray matter nomenclature system which are labeled from most dorsal to most ventral

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14
Q

Lamina I

A

aka lamina marginalis (on the margin)
sharp pain; “fast” pain
A-delta pain - myelinated neuron fibers

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15
Q

Lamina I, II, III, and V’s horizontal pathway to:

A

anterolateral spinothalamic pathway

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16
Q

Laminae II & III

A

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

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17
Q

Laminae I - VI

A

have mechanoreceptors (pressure sensors)

pain sensory

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18
Q

Lamina VII - IX

A

VII: intermediolateral nucleus
large motor neurons

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19
Q

lamina X

A

cross talk relay section of grey matter

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20
Q

categorize the 5 different spinal tracts

A
  1. spinocerebellar tracts
  2. dorsal-column medial lemniscal system
  3. spinothalamic tracts
  4. corticospinal tracts (AKA pyrdamidal tracts)
  5. extrapyramidal tracts
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21
Q

characterize the DCML pathway

A
  1. very fast signal propogation (all A fibers with all subunits)
  2. fine vibrations
  3. fine pressure
  4. cross over at medulla
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22
Q

what is meant by “cross over” in the DCML pathway?

A

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

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23
Q

the further up the spinal cord you get, the _____ the DCML is

A

wider

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24
Q

where does the doral column gather lower extremity sensory information?

A

Fasiculus gracilis

the gracilis muscle is in the leg

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25
Q

where does the doral column gather upper extremity sensory information?

A

Fasiculus cuneatus

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26
Q

if you have touch sensory information coming in, where does this information split? where does it go?

A
  1. a portion goes to the gray matter (lateral inhibition)
  2. a portion of the sensory info will ascend in the DCML pathway
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27
Q

a feather tickles your right foot; list out the sensory pathway from the foot to the brain

A
  1. tickle information comes from right foot
  2. foot to dorsal root and spinal ganglion (Fasiculus gracilus)
  3. ascends and crosses over at the lower medulla oblongata in the dorsal column nuclei
  4. ascends through the medulla oblongata
  5. medial lemniscus, pons, midbrain
  6. to the ventrobasal complex of thalamus
  7. to the internal capsule
  8. to the left hemisphere parietal lobe
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28
Q

where is the internal capsule located?

A

sits between the thalamus and the parietal lobe of the brain

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29
Q

what is the “Homonculus” depiction?

A

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

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30
Q

list out the primary pathway of the pyramidal tracts

A
  1. signals originate in motor cortex
  2. internal capsule
  3. pyramids of medulla
  4. cross over (pyramidal decussation)
  5. lateral corticospinal tracts
  6. ventral horn
  7. effector organ

80% or 4/5 of our motor function gets routed through this pathway

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31
Q

what is the pyramidal decussation?

A

the crossover point for motor information in the lower ANTERIOR medulla

32
Q

where does cross over occur in the secondary motor pathway?

A

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)

33
Q

where does the motor information descend to in the secondary motor pathway?

A

anterior corticospinal tract
(anterior pyramidal tract)

34
Q

about what percentage of motor function information gets processed through the secondary motor pathway?

A

17%

35
Q

how much perecent of our motor information does not get crossed over in the spinal cord?

A

2-3%

36
Q

describe the “fast pain” pathway of the spinothalamic tract

A

+fast pain
+lateral pathway
+A-delta nociceptors (heavily myelinated)
+NT: glutamate – fast to release, fast to bind, and fast to make changes

37
Q

describe the “slow pain” pathway in the spinothalamic tract

A

+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

38
Q

which laminae does the fast pain pathway have synaptic connections in?

A

lamina I
Lamina marginalis

39
Q

which laminae does the slow pain pathway have synaptic connections in?

A

laminae II & III, then V
Substantia gelatinosa (II & III)

40
Q

“fast pain” spinothalamic tract AKA:

A

Neospinothalamic tract

41
Q

“slow pain” pathway tract AKA

A

Paleospinothalamic tract

42
Q

where does crossover occur with the spinothalamic/anterolateral tracts?

A

at the level of the spinal cord where their effector organ/tissue is

AKA crosses over at the anterior white commisure

43
Q

why are we able to localize fast pain signal origins better than slow pain signal origins?

A

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

44
Q

you burned the tip of your finger on the stove; list out the pathway that this sensory information will travel up to your brain

A
  1. finger tip temperature/pain sensory information
    +this is considered SLOW PAIN (temperature)
  2. dorsal root and spinal ganglion > dorsal horn
  3. lamina II & III (substantia gelatinosa); sometimes V
  4. cross over at AWC
  5. anterior spinothalamic ascending pathway
  6. 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

45
Q

what 3 structures comprise the reticular nuclei?

A
  1. medulla
  2. pons
  3. mesencephalon
46
Q

which type of pain (slow or fast) engages the emotional centers of the brain?

A

slow pain

47
Q

what are the 3 structures that make up the limbic system?

A
  1. amygdala
  2. HYPOthalamus
  3. cingulate gyrus

“amy got mad” > amygdala > emotions

48
Q

list out the fast pain pathway from sensory origin to the parietal lobe

A
  1. origin of fast pain
  2. spinal root ganglion > rootlets > dorsal horn
  3. Lamina I (Lamina marginalis)
  4. crossover at the AWC
  5. lateral spinothalamic pathway
  6. ascends to thalamus
  7. through medulla > ventrobasal complex PARALLEL WITH DCML PATHWAY > posterior nuclear group
  8. parietal lobe
49
Q

categorize the different parts of the extrapyramidal tracts (4)

A
  1. vestibulospinal: helps to keep balance with changes in body position
  2. olivospinal
  3. reticulospinal: maintaining muscular tone (muscles aren’t ever entirely relaxed)
  4. rubrospinal: modulation of voluntary movement similar to what cerebellum does

all are CNS outputs to the spinal cord

50
Q

what is the descending pain suppression system?

A
  1. inhibitory in nature in response to pain/”takes the edge off”
  2. not strongly activated; works in the background
  3. 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)
51
Q

describe the first order descending neuron in the DIC

A

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

52
Q

describe the second order descending neuron in DIC

A

cell body origin: raphe magnus nucleus (RMN)/middle of pons

neuron: serotinergic (releases 5HT when excited) near dorsal horn in SC

NTs: 5-HT

53
Q

describe the third order descending neuron

A

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

54
Q

what are enkephalins?

A

endogenous opiate system in the body

morphine analogs

55
Q

what is the therapy that suppresses pain in the body by activating the DIC?

A

deep brain stimulation

electrodes are placed near the periventricular nuclei or periaqueductal gray to stimulate the DIC to alleviate pain

56
Q

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

A

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

57
Q

how can ECF K+ cause pain?

A

high ECF K+ can typically depolarize cells, and if it’s depolarized enough, it can be considered painful

58
Q

how do SSRIs/antidepressants help manage chronic pain?

A

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)

59
Q

explain what lateral inhibition is

A

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)

60
Q

name 3 IONOTROPIC glutamate receptors

A
  1. AMPA
  2. NMDA
  3. kainate receptors
61
Q

describe AMPA-Rs

A

the main receptor for glutamate
many present

ion channel: Na+

when glutamate binds, Na+ influxes

62
Q

describe NMDA-Rs

A

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

63
Q

why does Mg2+ block the NMDA receptors?

A

the cell wall has a more negative charge drawing in the ++Mg ion

64
Q

name 5 NMDA receptor antagonists

A

NMDA/AMPA-R blockers
1. ethanol
2. lead (poisoning)

selective NMDA-blocking
3. ketamine
4. nitrous gas (N2O)
5. tramadol

65
Q

will you have more NMDA-Rs in early life or later life?

A

later

NMDA-Rs are important in growth and development; NMDA-Rs get implanted over TIME

66
Q

if you have chronic pain, you’ll have _____ receptors at the synapse which will give you _____ APs to ______ sensitivity

A
  1. more
  2. more
  3. increase
67
Q

glutamate is typically an _____ NT

A

excitatory

68
Q

the following metabotropic ion channels open up K+ on pre/post-synaptic neurons in the DIC:

A
  1. enkephalin/opiate-Rs
  2. alpha-2 adrenergic-Rs
69
Q

these type of drugs increase cell membrane permeability to K+/K+ conductance in the first order DIC neuron

A

volatile anesthetics

70
Q

what are (3) alpha-2 receptor agonists that bind to slow down the CNS

A
  1. xylazine (non-specific alpha)
  2. clonidine (alpha 2 > alpha 1)
  3. dexmedetomidine (alpha-2 specific)
71
Q

what are COX-2 & prostaglandin’s roles in the first & second order DIC neurons?

A

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

72
Q

what is iNOS?

A

inducible nitric oxide synthase is an enzyme that increases the synapse sensitivity to pain (much like PGGs but less so)

73
Q

how do Mg2+ supplements aid with chronic pain?

A

Mg2+ can block the NMDA receptors at rest

can cause GI upset if ingested since it is not digested well

74
Q

list 9 chemical signals that will activate nociceptors

A
  1. bradykinin
  2. 5HT
  3. histamine
  4. K+
  5. H+/acidotic conditions
  6. ACh
  7. proteolytic enzymes
  8. ischemia/muscle spasm (a build up of metabolic waste products)
    (9. PGGs - can’t generate AP in nociceptors, but can make receptors more sensistive)
75
Q

list 7 mechanical/thermal signals that will activate nociceptors

A
  1. stretch
  2. crush injury
  3. stabbing
  4. physical tissue damage
  5. proteolytic enzymes
  6. high temps >45 C
  7. low temps <5 C

Ana/Phys/Patho I (16 decks)

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