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
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
3
Q
Where does crossover of the DCML pathway occur?
A
Crossover occurs at the Lemniscal Decussation of the Medulla Oblongata
4
Q
Do any of the signals from the DCML interact with the gray matter of the spinal cord?
A
No
need to verify
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
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.
7
Q
Describe the path of a general motor signal through the corticalspinal tracts starting with the cortex.
A
- Cortex
- Internal Capsule
- Medulla Pyramids
- Medulla Decussation
- Antero-Lateral Corticospinal Pathway
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
9
Q
What portion of motor information never crosses over at the pyramidal decussation or further down in the spinal cord?
A
1-2%
10
Q
Where does motor output crossover for the lateral corticospinal tract occur?
A
Medulla Pyramidal Decussation
11
Q
What are the two main paths of the Pyramidal Tracts? Which is the primary?
A
- Lateral Corticospinal Tract (Primary)
- Anterior Corticospinal Tract
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)
13
Q
What are the two Spinocerebellar Tracts?
A
Anterior Spinocerebellar Tract
Posterior Spinocerebellar Tract
14
Q
What information is carried by the spinocerebellar tracts?
A
Feedback on the Coordination of movement.
15
Q
What structure senses information for the Posterior SpinoCerebellar Tract?
A
Spindle Fibers in the Skeletal Muscle
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.
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.
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.
19
Q
Where do the Anterior (Ventral) spinocerebellar tracts end?
A
Superior Cerebellar Peduncle
20
Q
Where do the Posterior (Dorsal) spinocerebellar tracts end?
A
Inferior Cerebellar Peduncle
21
Q
What are the two divisions of the Spinothalamic (Anterolateral) Tracts?
A
Lateral Spinothalamic - Fast pain - A-δ
Anterior Spinothalamic - Slow pain - C
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)
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)
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)
25
Which two neurotransmitters are slower to release, bind, and breakdown? Which neurotransmitter is faster in all aspects?
CGRP & Substance P = Slow
Glutamate = Fast
26
Which lamina are associated with slow pain?
Which tract is utilized with these lamina?
What is another name for this tract?
Lamina II, III, and V
Anterior Spinothalamic Tract
“Paleospinothalamic Tract”
27
Which lamina are associated with fast pain?
What tract is utilized with this lamina?
What is another name for this tract?
Lamina I
Lateral Spinothalamic Tract
Neospinothalamic Tract
28
Where does fast pain processing occur?
What processing occurs alongside it?
Ventrobasal Complex of Hypothalamus
Sensory Information from DCML
29
Where does slow pain cross over at? What tract carries this information?
Anterior White Commissure
Anterior Spinothalamic Tract
30
Why is there poor localization of slow pain?
Only 15% of the signal progresses to the parietal lobe for higher level of processing.
31
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?
* Hypothalamus
* Most slow pain signaling terminates in the pons.
* Fast Pain → Ventrobasal complex of hypothalamus → Parietal Lobe
32
What brain structure determines wakefulness and emotion processing?
Where is this structure located?
Reticular Formation
Interior of Brainstem (spans medulla, pons, and midbrain)
33
What would two byproducts of chronic pain processing be? Why?
Feeling shitty and Sleeping shitty.
Wakefullness and Emotions are processes in Reticular formation of brainstem alongside C-fiber pain.
34
Where does fast pain crossover?
Are these axons carrying this information myelinated all the way through?
Lamina X
Yes, even through Lamina X
35
What are the 4 extrapyramidal tracts?
What are all 4 of these extrapyramidal tracts characterized by?
1. Vestibulospinal
2. Olivospinal
3. Reticulospinal
4. Rubrospinal
All are CNS efferent outputs to spinal cord.
36
What information is pertinent to the Vestibulospinal Tract?
Eye fixation w/ muscle coordination during acceleration
37
What information is pertinent to the Olivospinal Tract?
Cerebellar output to coordinate movement
38
What information is pertinent to the Reticulospinal Tract?
What would occur with injury to this tract?
Maintenance of Muscle Tone
Crazy Movement (flaccidity or jerkiness)
39
What information is pertinent to the Rubrospinal Tract?
Modulation of Voluntary Movement
40
What does DIC stand for in the context of the CNS?
What does the DIC do?
What activates the DIC?
* Descending Inhibitor Complex
* Pain suppression system from CNS output
* Brain or hormones activate DIC
41
Where are two origins for a DIC signal?
1. Periventricular Nuclei
2. Periaqueductal Gray Matter
42
Where does the DIC synapse at?
Which portion of the DIC specifically?
What is released at this synapse?
* The DIC synapses at the synapse of the 1st nociceptor and the 2nd signaling neuron.
* 3rd Order Enkephalin Neurons.
* Enkephalin
43
How do enkephalins decrease pain?
1. Enkephalins bind to receptors on the pre-synaptic neuron and the post-synaptic neuron
2. ↑ pK+
3. ↑ Action Potential Threshold
44
How would physical damage to a free nerve ending cause an action potential?
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.
45
What three factors will indirectly augment a pain response?
1. Histamine
2. Prostaglandins
3. NO
46
How do opiates treat pain?
Opiates bind to receptors on the nociceptor and the synapsing neuron and **↑ pK+ **
47
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?
* α-2
* Dexmedetomidine
48
What 3 organs lack pain receptors?
Lungs - specifically alveoli and small airways
Brain - \*Glial cells\* (need to verify)
Liver - specifically inside the parenchyma
49
What 5 areas in lecture were described as having a lot of pain receptors?
1. Dura Mater/ Meninges
2. Blood Vessels (i.e. coronary arteries)
3. Joints
4. Bones
5. Periosteum
50
What drug class preceded SSRI's?
What usage do these drugs have now?
* Tricyclic Antidepressants
* Used to treat chronic pain and chronic arousal
51
What are the two glutamate receptors?
What ion(s) are influxxed by these two receptors?
1. AMPA - Na+
2. NMDA - Na+ & Ca++
52
What ion blocks NMDA receptors?
What removes this block?
What influxxes once the block is removed?
1. Mg++
2. AMPA depolarization “ejects” Mg++
3. Na+ & Ca++ influx
53
What occurs after after Ca++ influx from NMDA receptors?
1. ↑ PKC
2. ↑ iNOS
3. ↑ NO
4. ↑ COX-2 → ↑PG
54
How do Prostaglandins affect the pain signaling process?
Prostaglandins produced in the 2nd neuron increase release of glutamate by the 1st nociceptor.
55
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?
↑ NO
↑ NO = ↑ NMDA receptors = ↑ pain sensing
56
What two components of the pain cycle increase pain by increasing glutamate release?
Of these two, which increases glutamate sensitivity?
NO and PG's
NO
57
In what two ways do inhalational anesthetics inhibit pain?
1. **Systemic ↑ pK+**
2. Activation of periventricular nuclei and periaqueductal gray matter to **release enkephalins.**
58
How long before the chronic pain potentiation process starts to occur?
1 hour
59
Which two NMDA receptor antagonists were talked about in lecture?
Ketamine
Nitrous Oxide
60
Describe the dissociative nature of ketamine.
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
What toxin is a known NMDA receptor antagonist and is especially unhealthy for children?
Lead
62
Why does lead poisoning affect children more than adults?
Children are still in the process of developing of creating NMDA receptors and forming synapses.
63
Which receptors are strongly associated with memory and learning?
NMDA receptors
64
In which lamina do the 2° neuron of the DIC interface with the 3° neuron of the DIC?
Lamina 1, 2, 3
(dependent on fast pain or slow pain)
65
Where does crossover occur for the DCML?
Lower Medulla
*need to verify*
66
What is the termination point for the posterior spinocerebellar tract?
Inferior Cerebellar Peduncle
67
What is the termination point for the anterior spinocerebellar tract?
Superior Cerebellar Peduncle
68
Which sensors give feedback to the Posterior Spinocerebellar Track?
Muscle Spindle Feedback
69
What sensors give feedback to the Anterior Spinocerebellar Tract?
Golgi Tendon Feedback
70
What type of nerve fiber usually reduces pain in Lateral Inhibition?
A-β
71
Differentiate Parietal and Visceral pain. Which is localizable?
Parietal - pericardium, peritoneum, (essentially fibrous coatings. Parietal is localizable.
Visceral - Deep organ interior. Not localizable.
72
Why is visceral pain usually felt above where the pain is actually occuring?
Pain info is fed into SNS chain and is routed up a couple of levels. So signal is not localized well.
73
Which type of pain works in conjunction with stretch receptors and lines up with dermatomes.
Parietal Pain
74
What 3 examples of referred pain were given in class?
Where is the pain felt for each of these?
* Myocardial Infarction - left shoulder/arm
* Kidney Infection - lower back
* Appendicitis - umbilicus
75
What is the primary characteristic of where referred pain is felt?
Why is this?
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
What are the two generalized causes of pain that were discussed in lecture?
Inflammation and Muscle Spasms.
77
What 5 factors lead to pain felt from inflammation?
* ↑ H+
* Ischemia
* Bradykinin release
* Poor Nutrient delivery
* Proteolytic enzyme release (lysosome necrosis)
78
What causes pain in the case of muscle spasms?
Excessive contraction causing acidosis and ischemia.
79
Of Parietal and Visceral tissues/organs which has the larger pain receptor density?
Parietal
80
At which vertebral level would appendicitis be felt for Parietal pain?
At which vertebral level would appendicitis be felt for Visceral pain?
Parietal = L-1 dermatome
Visceral = T-10 dermatome
81
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?
Thermal probe at 45°C on hand.
High Tolerance ≈ 50° C
Low Tolerance ≈ 40° C
82
What concept is the basis for acupuncture?
Lateral (or Surround) Inhibition
83
What passes through the Tract of Lissauer?
What does NOT pass through the Tract of Lissauer?
All Sensory information
Pain information
84
How is the Tract of Lissaeur best described?
Myelinated Interneurons where multiple levels of the spinal cord are connected.
85
What occurs during a stretch reflex?
In response to a stretch (say the quads):
1. Contraction of Quads occurs to normalize length
2. Antagonistic muscles (hamstrings) are relaxed.
86
What receptor is associated with the stretch reflex?
Muscle Spindle Sensor
87
What reflex keeps us from placing too great of a load on our muscles?
What sensor is used in this reflex?
Tendon Reflex
Golgi Tendon Stretch Sensors
88
Give an example of the Tendon Reflex using the biceps and triceps as an example.
1. A 400lb weight is caught (much too heavy)
2. Biceps relax.
3. Triceps contract (to speed movement away from trigger).
89
What is the primary purpose of the Flexor Reflex?
What should be known about this reflex and the Tract of Lissaeur?
To withdraw from pain.
Pain sensors activated use tract of Lissaeur to activate multiple neurons quickly to contract muscle away from pain. (\*wordy\*)
90
Which reflex involves communication up/down multiple levels of the spinal cord as well as across the cord?
Crossed Extensor Reflex
91
What feeds the radicular arteries of the neck?
How many radicular arteries does the cervical spinal cord have?
Vertebral Arteries
1-3 Radicular Arteries (usually 3)
92
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?
* Aortic Aneurysm repair.
* Prolonged Ischemia of the GRA = Paralysis
* ↑ GRA = Better
93
How is Spinal Cord Perfusion Pressure Calculated?
CordPP = MAP - Cord CSF Pressure (5-10 cmH20)
94
Which 3 arteries perfuse the cervical Posterior Spinal Arteries?
1. Vertebral Arteries
2. Anterior Inferior Cerebellar Artery
3. Posterior Inferior Cerebellar Artery
95
In Brown-Sequard Syndrome which 3 consequences would you expect to see from transection of half of the spinal cord?
1. Loss of Motor ipsilateral of the injury
2. Loss of Sensation ipsilateral of the injury
3. Loss of Pain contralateral the injury
96
How can horrible pain from terminal cancer be treated?
Cordectomy of the spinothalamic tracts to sever pain sensation.
97
What happens to ICP when the aorta is clamped?
Can this be counteracted?
* It increases by 10cmH20
* A prophylactic spinal tap can be done during aneurysm repair to lower pressure. Controversial.
98
Which spinal tracts are inhibitory to motor function?
What can loss of these tracts cause?
Non-pyramidal tracts
Skeletal Muscle Rigidity (Decorticate & Decerebrate)
99
What is a shingles infection?
What virus causes this?
How is the pain in this infection?
* An infection of the Dorsal Root Ganglia
* Herpes Zoster
* Painful (follows dermatomes)
100
What is Tic Douloureux?
Can this be treated?
* 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
Which neurotransmitter is **always** inhibitory in the spinal cord?
Glycine
102
Which neurotransmitter is excitatory and utilized in our pain pathways?
Glutamate
103
Which neurotransmitter is the main inhibitory transmitter of the CNS?
What would happen without this neurotransmitter?
GABA
Seizures, rampant electrical activity, etc.
104
GABA receptors always increase cell wall permeability to _______ and to a lesser degree \_\_\_\_\_\_\_.
Cl-
K+
105
What electrolyte might be utilized for pain control?
What are three theories as to how this might work?
* Mg2+
1. NMDA receptor blocking
2. Ca2+ receptor antagonism
3. Blocking Na+ Channels
106
Which drugs potentiate GABA?
EtOH, Benzo's, and Barbiturates
107
What is the difference between Barbiturates and Benzodiazepines in regards to GABA potentiation?
Which is considered more dangerous?
Barbiturates are direct GABA Agonists.
Benzodiazepines potentiate endogenous GABA.
Barbiturates are far more dangerous, especially when used with another CNS depressant.
108
AcetylCholine, in regards to the CNS, typically makes one more \_\_\_\_\_\_\_.
Thus, AChEsterase Inhibitors would do what?
Aware, Awake, etc.
AChE inhibitors would potentiate CNS awareness.
109
Which type of ACh receptors are found in the CNS?
What other receptor are they similar to?
* muscarinicACh Receptors
* Histamine1 Receptors
110
How does benadryl makes you sleepy?
Why do new antihistamines not have a drowsiness effect?
Benadryl crosses the BBB blocks mACh receptors.
New antihistamines are too large to cross the BBB.
111
Regarding the Pyramidal Tracts, where does crossover occur for:
1. Lateral Corticospinal Pathway?
2. Anterior Corticospinal Pathway?
1. Lateral Corticospinal Crossover: Medulla
2. Anterior Corticospinal Crossover: Spinal Cord
112
Regarding the Pyramidal Tracts, where does crossover occur for:
1. Lateral Corticospinal Pathway?
2. Anterior Corticospinal Pathway?
1. Lateral Corticospinal Crossover: Medulla
2. Anteriro Corticospinal Crossover: Spinal Cord
