Nsp Week 1: Somatosensory System Ii (Foreman)

Front 1

Acute pain is relieved in how many weeks?

Back 1

2-4 weeks
(or at most, 6 weeks)

Front 2

What is the difference between paresthesias and dysthesias?

Back 2

Both terms refer to a "pins and needles" sensation
Parasthesia is not unpleasant
Dysthesia is unpleasant

Front 3

What is hyperalgesia?

Back 3

Increase in the pain sensation to a stimulus which is normally painful

Front 4

What is allodynia?

Back 4

Pain sensation resulting from a stimulus that normally does not evoke pain

Front 5

What is analgesia?

Back 5

Absence of pain in response to a stimulus that normally is painful

Front 6

What is anesthesia?

Back 6

Complete loss of sensation, or numbness

Front 7

What is hyperesthesia?

Back 7

Local increase in sensitivity to mild stimuli that accompanies injuries such as burns, bruises, and abrasions

Front 8

Nociceptors generally have receptors that consist of..?

Back 8

Bare nerve endings

Front 9

List 3 classifications of nociceptors

Back 9

1. A-delta (III) mechanosensitive
2. A-delta (III) mechanothermal
3. C-fiber (IV) polymodal

Front 10

Which fibers are responsible for short-latency pricking pain, and second long-latency pain?

Back 10

Short-latency --> A-delta (III) fibers
Long-latency--> C-fibers (IV)

Front 11

What is the structural difference between A-fibers and C-fibers?

Back 11

A-fibers are myelinated, C-fibers are not

Front 12

Where do somatic and visceral A-delta fibers terminate in the spinal cord?

Back 12

Lamina I and V
(Synapse in the dorsal horn with the cells of the spinothalamic tract)

Front 13

Where do somatic and visceral C-fibers terminate?

Back 13

Somatic C-fibers --> Lamina I, II
Visceral C-fibers --> Lamina I, V

Front 14

Which neurotransmitter and receptor are involved in the initial response to a noxious stimulus?

Back 14

Glutamate (released from A-delta and C-fibers)
AMPA receptor (spinothalamic tract cell)

Front 15

Which neurotransmitters and receptors are involved in the "wind up" of spinothalamic tract cells?

Back 15

Glutamate and Substance P
AMPA and NMDA receptors

*More glutamate is released than during initial response, so additional receptors (NMDA) are stimulated

Front 16

Which receptors does glutamate interact with to produce the initial and then the prolonged phase of the EPSPs?

Back 16

Initial phase --> AMPA receptors
Prolonged phase --> NMDA receptors

Front 17

Is "wind up" of spinothalamic cells due to spatial or temporal summation?

Back 17

Temporal summation

Front 18

What is the result of very strong, chronic, noxious stimuli?

Back 18

Large quantities of glutamate and Substance P from primary afferent fibers of nociceptors-->
Activation of SECOND MESSENGER SYSTEMS in spinothalamic tract cells-->
Activation of immediate-early GENES such as fos and jun

*Results in modulation: post-translational processing and central sensitization

Front 19

What is the role of genes such as fos and jun in chronic pain?

Back 19

Fos and jun can alter gene expression, which can change the phenotype of nociceptive neurons and cause a chronic pain state.

*Spinothalamic tract cells become hyperexcitable and respond excessively to both painful and non-painful stimuli, resulting in an increase in the signals they transmit to the brain

Front 20

The anterolateral system involves which spinal tract that localizes painful or thermal stimuli?

Back 20

Spinothalamic tract

Front 21

Describe the path of pain and temperature sensory information through the spinal cord and into the cortex

Back 21

1. Sensory info enters dorsal root ganglion and then dorsal root to reach spinal cord
2. Immediately synapses in dorsal horn with original spinothalamic tract cell
3. This 2nd neuron crosses over immediately and ascends in anterolateral portion of spinal cord
4. Eventually synapses in ventral posterior lateral nucleus of the thalamus
5. 3rd neuron travels to primary somatic sensory cortex

Front 22

How can pain be modulated by first pinching skin and then rubbing the pinched area?

Back 22

Pinching the skin activates C-fibers which increase activity of STT cells
Rubbing the skin activates A-alpha & beta fibers which excite inhibitory interneurons--> decreases the activity of the STT cell receiving the nociceptive input

*Large afferent fibers "close the gate" on pain.

Front 23

Descending fibers from which areas of the CNS excite interneurons in the spinal cord to modulate noxious information?

Which neurotransmitter is released from the interneurons?

Back 23

1. Periaquaductal gray
2. Raphe magnus

*Enkephalin (ENK:1)

Front 24

Describe the two affects that ENK has on neurons in the spinal cord.

Back 24

1. Inhibitory postsynaptic synaptic potential (IPSP) --> Hyperpolarization results from ENK interaction w/ cell bodies that project to the thalamus, medulla, pons, and midbrain.

2. Presynaptic inhibition--> decreased amplitude of EPSP transmitted by A-delta and C-fibers.

*ENK acts on pre- and post-synaptic neurons that participate in the spinothalamic tract.
"pre-synaptic" neurons = A-delta and C-fibers (decreased transmittion)
"post-synaptic" neurons = ascending STT cells (hyperpolarization/ inhibition)

Front 25

Damage to the nerve itself results in what kind of pain?

Back 25

Neuropathic pain

Front 26

What are the classical signs of inflammation?

Back 26

1. Pain
2. Swelling
3. Redness
4. Heat

Front 27

Which neurotransmitters are involved in neurogenic inflammation?

Back 27

1. Substance P --> histamine
2. Calcitonin gene-related peptide (CGRP)

Front 28

Particular nerve fibers responding to ________ are responsible for neurogenic inflammation.

Back 28

Capsaicin

Front 29

What is the pungent active ingredient of hot peppers that results in a burning sensation in tissues?

Back 29

Capsaicin

Front 30

Capsaicin activates which receptors?

Back 30

Vanilloid receptors (VR1)
(aka: transient receptor potential cation channel, subfamily V, member 1, TRPVI receptors)

Front 31

What might be the natural agonist of VR1 (TRPV1) receptors?

Back 31

Heat

VR1 receptors also respond to:
1. pH (might serve to modulate heat responsiveness)
2. Capsaicin

Front 32

Name an agonist that is more powerful at capsaicin receptors, less likely to excite, and more likely to desensitize capsaicin receptors

Back 32

Resinferotoxin

*May be preferable for pain therapy

Front 33

How are capsaicin-ointments useful for pain therapy?

Back 33

After stimulating VR1 receptors, capsaicin can cause desensitization of these receptors, rendering them less responsive

Front 34

Which peptides are responsible for neurogenic edema and redness?

Back 34

Substance P-->
Increases capillary permeability, leading to plasma extravasation and edema.
Also causes vasodilation

CGRP -->
Potent vasodilator, resulting redness, and increased temperature in the damaged area.

Front 35

What causes the "flare" in neurogenic inflammation?

Back 35

This is an effect of axon reflexes
Damage to neurons will send impulses antidromically (backward) along axonal branches --> release peptides near blood vessels --> vasodilation--> flare

Front 36

Which cells release histamine, and which release serotonin after tissue injury?

Back 36

Mast cells --> histamine
RBCs --> serotonin

Front 37

List 4 causes of visceral pain

Back 37

1. Ischemia
2. Chemical stimuli
3. Spasm of hollow viscus
4. Overdistention

Front 38

List some signs associated with visceral pain

Back 38

1. Pain
2. Hyperalgesia, hyperesthesia, or tenderness
3. Autonomic reflexes
4. Somatic reflexes, muscle rigitidy

Front 39

Why is visceral pain felt as somatic pain?

Back 39

Due to convergence of visceral and somatic afferent input onto spinothalamic tract cells
(somatic sensations are more frequent, so brain does not differentiate between the somatic and visceral signals coming from the same STT cell)