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A&P > CNS Focused Study (Exam II) > Flashcards

CNS Focused Study (Exam II) Flashcards

1
Q

What are two portions of the Dorsal Column Medial Lemniscus Pathway? What information do the two portions transmit?

A

Fasciculus Cuneatus - Upper Body Sensation

Fasciculus Grascilis - Lower Body Sensation

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2
Q

What sensory information does the DCML pathway transmit? How fast is the signal propogation?

A
  • High Fidelity Sensory

(pinpoint touch, pressure, vibration, think hands)

  • Very Fast
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3
Q

Where does crossover of the DCML pathway occur?

A

Crossover occurs at the Lemniscal Decussation of the Medulla Oblongata

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4
Q

Do any of the signals from the DCML interact with the gray matter of the spinal cord?

A

No

need to verify

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5
Q

What structure organizes sensory information from the DCML and directs it to the appropriate processing region of the cerebrum?

A

Ventrobasal Complex of the Thalamus

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6
Q

Where does sensory pain information crossover in the CNS?

How does this compare to regular sensory information?

A

Pain crosses over at spinal cord.

Sensory information crosses over at Medulla/Pons.

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7
Q

Describe the path of a general motor signal through the corticalspinal tracts starting with the cortex.

A
  1. Cortex
  2. Internal Capsule
  3. Medulla Pyramids
  4. Medulla Decussation
  5. Antero-Lateral Corticospinal Pathway
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8
Q

How much information is transmitted through the Lateral Corticospinal Pathway?

How does this compare to the Anterior Corticospinal Pathway?

A
  • Lateral Corticospinal = 90% of motor output
  • Anterior Corticospinal = 8-9% of motor output
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9
Q

What portion of motor information never crosses over at the pyramidal decussation or further down in the spinal cord?

A

1-2%

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10
Q

Where does motor output crossover for the lateral corticospinal tract occur?

A

Medulla Pyramidal Decussation

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11
Q

What are the two main paths of the Pyramidal Tracts? Which is the primary?

A
  • Lateral Corticospinal Tract (Primary)
  • Anterior Corticospinal Tract
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12
Q

Where does crossover occur for the Anterior Corticospinal Tract?

A

The level of activity initiation

(Ex. Signal going to calf muscle, crossover occurs at spinal nerve controlling calf)

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13
Q

What are the two Spinocerebellar Tracts?

A

Anterior Spinocerebellar Tract

Posterior Spinocerebellar Tract

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14
Q

What information is carried by the spinocerebellar tracts?

A

Feedback on the Coordination of movement.

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15
Q

What structure senses information for the Posterior SpinoCerebellar Tract?

A

Spindle Fibers in the Skeletal Muscle

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16
Q

What is the structure of spindle fibers and how does this relate to the information they transmit?

Where is this information sent primarily?

A
  • Spring-like structure that “senses” contraction/stretch of muscle.
  • Information is sent primarily to the Posterior Spinocerebellar tract.
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17
Q

Are muscle spindle fibers myelinated or unmyelinated? What does this mean in terms of pathophysiology?

A
  • Spindle fibers are myelinated.
  • Spindle fibers can be affected by demyelinating pathologies such as MS or Guillan Barre.
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18
Q

What sensors located in tendons send information to the spinocerebellar tract on muscle contraction?

Which spinocerebellar tract is this information primarily sent to?

A
  • Golgi Tendon Stretch Sensors
  • Anterior spinocerebellar tract.
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19
Q

Where do the Anterior (Ventral) spinocerebellar tracts end?

A

Superior Cerebellar Peduncle

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20
Q

Where do the Posterior (Dorsal) spinocerebellar tracts end?

A

Inferior Cerebellar Peduncle

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21
Q

What are the two divisions of the Spinothalamic (Anterolateral) Tracts?

A

Lateral Spinothalamic - Fast pain - A-δ

Anterior Spinothalamic - Slow pain - C

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22
Q

Where are A-δ fibers found in the spinothalamic tract?

What neurotransmitter(s) is used by this pathway?

How precise is the information delivered by this pathway?

A
  • Lateral Pathway
  • Glutamate
  • Very precise (detailed pinpoint info)
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23
Q

Where are C-fibers found in the spinothalamic tract?

What neurotransmitter(s) is used by this pathway?

How precise is the information delivered by this pathway?

A
  • Anterior Pathway
  • Glutamate, Substance P, CGRP
  • Imprecise (think stomach pain)
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24
Q

What two sensory receptor types run alongside C-fibers?

What is the consequence of this?

A

Thermoreceptors and Vibration receptors

*When slow pain is “activated” you can feeling heat, cold, tickles, and itching* (needs verification)

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25
Q

Which two neurotransmitters are slower to release, bind, and breakdown? Which neurotransmitter is faster in all aspects?

A

CGRP & Substance P = Slow

Glutamate = Fast

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26
Q

Which lamina are associated with slow pain?

Which tract is utilized with these lamina?

What is another name for this tract?

A

Lamina II, III, and V

Anterior Spinothalamic Tract

“Paleospinothalamic Tract”

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27
Q

Which lamina are associated with fast pain?

What tract is utilized with this lamina?

What is another name for this tract?

A

Lamina I

Lateral Spinothalamic Tract

Neospinothalamic Tract

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28
Q

Where does fast pain processing occur?

What processing occurs alongside it?

A

Ventrobasal Complex of Hypothalamus

Sensory Information from DCML

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29
Q

Where does slow pain cross over at? What tract carries this information?

A

Anterior White Commissure

Anterior Spinothalamic Tract

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30
Q

Why is there poor localization of slow pain?

A

Only 15% of the signal progresses to the parietal lobe for higher level of processing.

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31
Q

Where are both fast pain and slow pain processed?

Where does most of slow pain signalling terminate?

How does this compare to fast pain signaling?

A
  • Hypothalamus
  • Most slow pain signaling terminates in the pons.
  • Fast Pain → Ventrobasal complex of hypothalamus → Parietal Lobe
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32
Q

What brain structure determines wakefulness and emotion processing?

Where is this structure located?

A

Reticular Formation

Interior of Brainstem (spans medulla, pons, and midbrain)

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33
Q

What would two byproducts of chronic pain processing be? Why?

A

Feeling shitty and Sleeping shitty.

Wakefullness and Emotions are processes in Reticular formation of brainstem alongside C-fiber pain.

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34
Q

Where does fast pain crossover?

Are these axons carrying this information myelinated all the way through?

A

Lamina X

Yes, even through Lamina X

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35
Q

What are the 4 extrapyramidal tracts?

What are all 4 of these extrapyramidal tracts characterized by?

A
  1. Vestibulospinal
  2. Olivospinal
  3. Reticulospinal
  4. Rubrospinal

All are CNS efferent outputs to spinal cord.

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36
Q

What information is pertinent to the Vestibulospinal Tract?

A

Eye fixation w/ muscle coordination during acceleration

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37
Q

What information is pertinent to the Olivospinal Tract?

A

Cerebellar output to coordinate movement

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38
Q

What information is pertinent to the Reticulospinal Tract?

What would occur with injury to this tract?

A

Maintenance of Muscle Tone

Crazy Movement (flaccidity or jerkiness)

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39
Q

What information is pertinent to the Rubrospinal Tract?

A

Modulation of Voluntary Movement

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40
Q

What does DIC stand for in the context of the CNS?

What does the DIC do?

What activates the DIC?

A
  • Descending Inhibitor Complex
  • Pain suppression system from CNS output
  • Brain or hormones activate DIC
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41
Q

Where are two origins for a DIC signal?

A
  1. Periventricular Nuclei
  2. Periaqueductal Gray Matter
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42
Q

Where does the DIC synapse at?

Which portion of the DIC specifically?

What is released at this synapse?

A
  • The DIC synapses at the synapse of the 1st nociceptor and the 2nd signaling neuron.
  • 3rd Order Enkephalin Neurons.
  • Enkephalin
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43
Q

How do enkephalins decrease pain?

A
  1. Enkephalins bind to receptors on the pre-synaptic neuron and the post-synaptic neuron
  2. ↑ pK+
  3. ↑ Action Potential Threshold
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44
Q

How would physical damage to a free nerve ending cause an action potential?

A
  1. ↑ K+
  2. ↑ H+
  3. Physical damage to cell (crushing, burning, etc.) would cause an increase of both of the above, thus causing a Na+ influx.
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45
Q

What three factors will indirectly augment a pain response?

A
  1. Histamine
  2. Prostaglandins
  3. NO
46
Q

How do opiates treat pain?

A

Opiates bind to receptors on the nociceptor and the synapsing neuron and ↑ pK+

47
Q

What other receptor is relevant (besides µ, δ and κ) in decreasing pain on the presynaptic nociceptor?

What drug would be relevant in utilizing this receptor?

A
  • α-2
  • Dexmedetomidine
48
Q

What 3 organs lack pain receptors?

A

Lungs - specifically alveoli and small airways

Brain - *Glial cells* (need to verify)

Liver - specifically inside the parenchyma

49
Q

What 5 areas in lecture were described as having a lot of pain receptors?

A
  1. Dura Mater/ Meninges
  2. Blood Vessels (i.e. coronary arteries)
  3. Joints
  4. Bones
  5. Periosteum
50
Q

What drug class preceded SSRI’s?

What usage do these drugs have now?

A
  • Tricyclic Antidepressants
  • Used to treat chronic pain and chronic arousal
51
Q

What are the two glutamate receptors?

What ion(s) are influxxed by these two receptors?

A
  1. AMPA - Na+
  2. NMDA - Na+ & Ca++
52
Q

What ion blocks NMDA receptors?

What removes this block?

What influxxes once the block is removed?

A
  1. Mg++
  2. AMPA depolarization “ejects” Mg++
  3. Na+ & Ca++ influx
53
Q

What occurs after after Ca++ influx from NMDA receptors?

A
  1. ↑ PKC
  2. ↑ iNOS
  3. ↑ NO
  4. ↑ COX-2 → ↑PG
54
Q

How do Prostaglandins affect the pain signaling process?

A

Prostaglandins produced in the 2nd neuron increase release of glutamate by the 1st nociceptor.

55
Q

What compound in the pain signaling process potentiates pain, causing it to become worse, and also influences chronic pain development?

How does this compound do this?

A

↑ NO

↑ NO = ↑ NMDA receptors = ↑ pain sensing

56
Q

What two components of the pain cycle increase pain by increasing glutamate release?

Of these two, which increases glutamate sensitivity?

A

NO and PG’s

NO

57
Q

In what two ways do inhalational anesthetics inhibit pain?

A
  1. Systemic ↑ pK+
  2. Activation of periventricular nuclei and periaqueductal gray matter to release enkephalins.
58
Q

How long before the chronic pain potentiation process starts to occur?

A

1 hour

59
Q

Which two NMDA receptor antagonists were talked about in lecture?

A

Ketamine

Nitrous Oxide

60
Q

Describe the dissociative nature of ketamine.

A

Ketamine is dissociative because it is a non-competitive NMDA receptor antagonist. This means it blocks signaling between neurons in the pain signaling system.

61
Q

What toxin is a known NMDA receptor antagonist and is especially unhealthy for children?

A

Lead

62
Q

Why does lead poisoning affect children more than adults?

A

Children are still in the process of developing of creating NMDA receptors and forming synapses.

63
Q

Which receptors are strongly associated with memory and learning?

A

NMDA receptors

64
Q

In which lamina do the 2° neuron of the DIC interface with the 3° neuron of the DIC?

A

Lamina 1, 2, 3

(dependent on fast pain or slow pain)

65
Q

Where does crossover occur for the DCML?

A

Lower Medulla

need to verify

66
Q

What is the termination point for the posterior spinocerebellar tract?

A

Inferior Cerebellar Peduncle

67
Q

What is the termination point for the anterior spinocerebellar tract?

A

Superior Cerebellar Peduncle

68
Q

Which sensors give feedback to the Posterior Spinocerebellar Track?

A

Muscle Spindle Feedback

69
Q

What sensors give feedback to the Anterior Spinocerebellar Tract?

A

Golgi Tendon Feedback

70
Q

What type of nerve fiber usually reduces pain in Lateral Inhibition?

A

A-β

71
Q

Differentiate Parietal and Visceral pain. Which is localizable?

A

Parietal - pericardium, peritoneum, (essentially fibrous coatings. Parietal is localizable.

Visceral - Deep organ interior. Not localizable.

72
Q

Why is visceral pain usually felt above where the pain is actually occuring?

A

Pain info is fed into SNS chain and is routed up a couple of levels. So signal is not localized well.

73
Q

Which type of pain works in conjunction with stretch receptors and lines up with dermatomes.

A

Parietal Pain

74
Q

What 3 examples of referred pain were given in class?

Where is the pain felt for each of these?

A
  • Myocardial Infarction - left shoulder/arm
  • Kidney Infection - lower back
  • Appendicitis - umbilicus
75
Q

What is the primary characteristic of where referred pain is felt?

Why is this?

A

Referred pain is felt above the site of injury/inflammation.

This is due to the signal traversing the SNS up a couple of interneurons. *better phrasing needed*

76
Q

What are the two generalized causes of pain that were discussed in lecture?

A

Inflammation and Muscle Spasms.

77
Q

What 5 factors lead to pain felt from inflammation?

A
  • ↑ H+
  • Ischemia
  • Bradykinin release
  • Poor Nutrient delivery
  • Proteolytic enzyme release (lysosome necrosis)
78
Q

What causes pain in the case of muscle spasms?

A

Excessive contraction causing acidosis and ischemia.

79
Q

Of Parietal and Visceral tissues/organs which has the larger pain receptor density?

A

Parietal

80
Q

At which vertebral level would appendicitis be felt for Parietal pain?

At which vertebral level would appendicitis be felt for Visceral pain?

A

Parietal = L-1 dermatome

Visceral = T-10 dermatome

81
Q

How is an individual’s pain threshold determined in a pain study?

What would categorize as a low pain tolerance?

What would categorize as a high pain tolerance?

A

Thermal probe at 45°C on hand.

High Tolerance ≈ 50° C

Low Tolerance ≈ 40° C

82
Q

What concept is the basis for acupuncture?

A

Lateral (or Surround) Inhibition

83
Q

What passes through the Tract of Lissauer?

What does NOT pass through the Tract of Lissauer?

A

All Sensory information

Pain information

84
Q

How is the Tract of Lissaeur best described?

A

Myelinated Interneurons where multiple levels of the spinal cord are connected.

85
Q

What occurs during a stretch reflex?

A

In response to a stretch (say the quads):

  1. Contraction of Quads occurs to normalize length
  2. Antagonistic muscles (hamstrings) are relaxed.
86
Q

What receptor is associated with the stretch reflex?

A

Muscle Spindle Sensor

87
Q

What reflex keeps us from placing too great of a load on our muscles?

What sensor is used in this reflex?

A

Tendon Reflex

Golgi Tendon Stretch Sensors

88
Q

Give an example of the Tendon Reflex using the biceps and triceps as an example.

A
  1. A 400lb weight is caught (much too heavy)
  2. Biceps relax.
  3. Triceps contract (to speed movement away from trigger).
89
Q

What is the primary purpose of the Flexor Reflex?

What should be known about this reflex and the Tract of Lissaeur?

A

To withdraw from pain.

Pain sensors activated use tract of Lissaeur to activate multiple neurons quickly to contract muscle away from pain. (*wordy*)

90
Q

Which reflex involves communication up/down multiple levels of the spinal cord as well as across the cord?

A

Crossed Extensor Reflex

91
Q

What feeds the radicular arteries of the neck?

How many radicular arteries does the cervical spinal cord have?

A

Vertebral Arteries

1-3 Radicular Arteries (usually 3)

92
Q

In what surgery is the Great Radicular Artery relevant?

What consequences could occur from blocking of the Great Radicular Artery?

Is it better to have a GRA thats higher or lower?

A
  • Aortic Aneurysm repair.
  • Prolonged Ischemia of the GRA = Paralysis
  • ↑ GRA = Better
93
Q

How is Spinal Cord Perfusion Pressure Calculated?

A

CordPP = MAP - Cord CSF Pressure (5-10 cmH20)

94
Q

Which 3 arteries perfuse the cervical Posterior Spinal Arteries?

A
  1. Vertebral Arteries
  2. Anterior Inferior Cerebellar Artery
  3. Posterior Inferior Cerebellar Artery
95
Q

In Brown-Sequard Syndrome which 3 consequences would you expect to see from transection of half of the spinal cord?

A
  1. Loss of Motor ipsilateral of the injury
  2. Loss of Sensation ipsilateral of the injury
  3. Loss of Pain contralateral the injury
96
Q

How can horrible pain from terminal cancer be treated?

A

Cordectomy of the spinothalamic tracts to sever pain sensation.

97
Q

What happens to ICP when the aorta is clamped?

Can this be counteracted?

A
  • It increases by 10cmH20
  • A prophylactic spinal tap can be done during aneurysm repair to lower pressure. Controversial.
98
Q

Which spinal tracts are inhibitory to motor function?

What can loss of these tracts cause?

A

Non-pyramidal tracts

Skeletal Muscle Rigidity (Decorticate & Decerebrate)

99
Q

What is a shingles infection?

What virus causes this?

How is the pain in this infection?

A
  • An infection of the Dorsal Root Ganglia
  • Herpes Zoster
  • Painful (follows dermatomes)
100
Q

What is Tic Douloureux?

Can this be treated?

A
  • Overactive and painful Cranial Nerve 5 (Trigeminal) and Cranial Nerve 9 (Glossopharyngeal).
  • CN 5 can be cut but CN 9 is too hard to access.
101
Q

Which neurotransmitter is always inhibitory in the spinal cord?

A

Glycine

102
Q

Which neurotransmitter is excitatory and utilized in our pain pathways?

A

Glutamate

103
Q

Which neurotransmitter is the main inhibitory transmitter of the CNS?

What would happen without this neurotransmitter?

A

GABA

Seizures, rampant electrical activity, etc.

104
Q

GABA receptors always increase cell wall permeability to _______ and to a lesser degree _______.

A

Cl-

K+

105
Q

What electrolyte might be utilized for pain control?

What are three theories as to how this might work?

A
  • Mg2+
  1. NMDA receptor blocking
  2. Ca2+ receptor antagonism
  3. Blocking Na+ Channels
106
Q

Which drugs potentiate GABA?

A

EtOH, Benzo’s, and Barbiturates

107
Q

What is the difference between Barbiturates and Benzodiazepines in regards to GABA potentiation?

Which is considered more dangerous?

A

Barbiturates are direct GABA Agonists.

Benzodiazepines potentiate endogenous GABA.

Barbiturates are far more dangerous, especially when used with another CNS depressant.

108
Q

AcetylCholine, in regards to the CNS, typically makes one more _______.

Thus, AChEsterase Inhibitors would do what?

A

Aware, Awake, etc.

AChE inhibitors would potentiate CNS awareness.

109
Q

Which type of ACh receptors are found in the CNS?

What other receptor are they similar to?

A
  • muscarinicACh Receptors
  • Histamine1 Receptors
110
Q

How does benadryl makes you sleepy?

Why do new antihistamines not have a drowsiness effect?

A

Benadryl crosses the BBB blocks mACh receptors.

New antihistamines are too large to cross the BBB.

111
Q

Regarding the Pyramidal Tracts, where does crossover occur for:

  1. Lateral Corticospinal Pathway?
  2. Anterior Corticospinal Pathway?
A
  1. Lateral Corticospinal Crossover: Medulla
  2. Anterior Corticospinal Crossover: Spinal Cord
112
Q

Regarding the Pyramidal Tracts, where does crossover occur for:

  1. Lateral Corticospinal Pathway?
  2. Anterior Corticospinal Pathway?
A
  1. Lateral Corticospinal Crossover: Medulla
  2. Anteriro Corticospinal Crossover: Spinal Cord

A&P (17 decks)

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