Somatosensory Circuitry/phys Pain, Temp

Front 1

T/F sensation of pain arises from excessive stimulation of same receptors generating other sensations

Back 1

False. nociception depends on specifically dedicated receptors and pathways

Front 2

Where do nociceptor cell bodies lie?

Back 2

Dorsal root ganglion (BODY) or trigeminal ganglion (HEAD)

Front 3

How do peripheral nociceptors terminate?

Back 3

Free nerve endings

Front 4

nociceptor axons are relatively (fast, slow)

Back 4

SLOW. usually they're unmyelinated

Front 5

What groups of axons do nociceptors fall into?

Back 5

Aδ (myelinated) or C fibers (unmyelinated)

Front 6

major ascending pathway for info about pain and temp

Back 6

spinothalamic tract

Front 7

another name for spinothalamic tract

Back 7

anterolateral (in contrast to mechnosensory pathway being the dorsal column-medial lemniscus system)

Front 8

what is dissociated sensory loss?

Back 8

A spinal cord lesion will result in diminished pain/temp sensation contralaterally, and diminished mechanosensory info ipsilaterally.

Front 9

Lissauer’s Tract

Back 9

Where the neurons from dorsal horn of spinal ascend several levels and spread out.

Front 10

absence of Lissauer’s tract is associated with

Back 10

Congenital lack of pain sensation in humans

Front 11

Where does the 2nd order neuron of pain pathway cross?

Back 11

Ventral white commissure of spinal cord

Front 12

After crossing the ventral white commissure, the axons ______

Back 12

axon ascends in the lateral funiculus or white matter

Front 13

Where are the cells of origin of the lateral spinothalamic tract?

Back 13

cells of origin of this tract are located in the contralateral dorsal horn of the spinal cord.

Front 14

Where does the 2ndary neuron synapse?

Back 14

VPL of thalamus

Front 15

Because many of the primary afferent axons ascend several segments before synapsing, the majority of the loss due to a lesion, will affect the dermatomes beginning __ segments below.

Back 15

2

Front 16

lesion at T2 in the lateral funiculus of the spinal cord will show what?

Back 16

T4 (and below) since that is where the axons originally entered the spinal cord.

Front 17

T/F It is Called the Lateral Spinothalamic Tract AFTER crossing in the spinal cord.

Back 17

T

Front 18

Where are the cell bodies of origin of lateral spinothalamic tract? (not first order cell bodies)

Back 18

Contralateral Dorsal Horn of the Spinal Cord

Front 19

Where does it project or terminate? Means where do those axons SYNAPSE?

Back 19

Ipsilateral VPL of thalamus.

Front 20

Head area is represented more (medial, lateral) in thalamus but (medial, lateral) in cortex.

Back 20

medial (VPM); lateral

Front 21

How does the affective/motivational component of pain arise?

Back 21

As axon ascends it gives off collaterals to lots of regions (reticular formation, etc) making their way to ACC and insular cortex. Implications are that it can be difficult to eliminate chronic pain because of all the collaterals.

Front 22

Pattern of dissociated sensory loss (contralteral pain & temp with ipsilateral touch) is a signature of _______

Back 22

spinal cord lesions

Front 23

What is the <b>dorsal column </b> pain pathway?

Back 23

It's for visceral pain.

Pelvic and abdominal viscera
send afferents to gracile and cuneate nuclei which travels thru medial lemniscus, crossing at level of medulla

Front 24

Drugs that block nociceptive synaptic transmission into the intermediate gray of the sacral spinal cord blocks what?

Back 24

the responses of neurons in the nucleus gracilius to noxious visceral stimuli

Front 25

What is midline myelotomy ?

Back 25

neuroablative operation with the intent of interrupting the midline of the dorsal column, has demonstrated efficacy in the treatment of otherwise intractable abdominal and pelvic cancer pain.

Front 26

What does the Spinal Trigeminal Nucleus do?

Back 26

extends from the pons to C3 of the spinal cord and carries pain, temperature and some touch.

Front 27

Where do the afferents to the spinal trigeminal nucleus come from?

Back 27

All three branches of Trigeminal N.

Front 28

When neurons reach the Spinal Trigeminal Nucleus, what order are they?

Back 28

Second order, because there has already been one synapse in the trigeminal ganglion.

Front 29

From where does the Spinal Trigeminal Nucleus extend (what levels)?

Back 29

Pons to C3

Front 30

What is the spinal trigeminal tract?

Back 30

tract that leads to nucleus in the medulla that receives information about deep/crude touch, pain, and temperature from the ipsilateral face. The facial, glossopharyngeal, and vagus nerves also convey pain information from their areas to the spinal trigeminal nucleus.

Front 31

What other nerves (other than V) are associated with the spinal tract and spinal nucleus?

Back 31

CN VII (facial); CN IX (glossopharyngeal); and CN X (vagus) which makes sense because they all innervate some skin on the head region

Front 32

Where are the cell bodies of origin of the spinal trigeminal tract?

Back 32

Ipsilateral Cranial Nerve Ganglia of V, VII, IX, and X

Front 33

Where does the spinal trigeminal tract end/terminate?

Back 33

Ipsilateral Spinal Trigeminal Nucleus

Front 34

Where are the cell bodies of origin of the Ventral Trigeminothalamic Tract?

Back 34

Contralateral Trigeminal Nucleus

Front 35

Where does the Ventral Trigeminothalamic Tract end/terminate?

Back 35

VPM of thalamus

Front 36

What is Syringomyelia?

Back 36

damage to the spinal cord due to the formation of a fluid-filled area within the cord.

gliosis and cavitation of the cervical segments of spinal cord and brainstem (occasionally occurs at other levels of the spinal cord. Interrupts the lateral and anterior spinothalamic tracts as they cross the spinal cord in anterior gray and white commissures.

Front 37

What are symptoms of Syringomyelia?

Back 37

Bilateral loss of pain and temperature at the level of the lesion (segments involved).

Front 38

Wallenburg / Lateral Medullary Syndrome

Back 38

lesion of the dorsolateral medulla (occlusion of posterior inferior cerebellar artery)

Front 39

Symptoms of Wallenburg/Lateral Medullary Syndrome?

Back 39

produces ipsilateral loss of pain and temperature in the head/face (spinal tract & nucleus of V) and contralateral loss of pain and temperature in the body due to interruption of spinal lemniscus.

Also ataxia

Front 40

Damage to what can cause Wallenburg syndrome?

Back 40

Posterior inferior cerebellar artery

Front 41

NOCICEPTION

Back 41

response to noxious stimuli and tissue damage (burn, cut, pin prick, crush).

Front 42

T/F/ stimulation of nociceptors does always results in the sensation of pain.

Back 42

F. Pain is the psychological construct; nociception is the physical

Front 43

What fiber type are Mechanosensitive nociceptors?

Back 43

A&delta;

Front 44

What are Mechanosensitive nociceptors stimulated by?

Back 44

Squeezing, pressure.

Front 45

What are Mechanothermal nociceptors stimulated by?

Back 45

Excessive heat or cold

Front 46

What fiber type are Mechanothermal nociceptors?

Back 46

A&delta; / Group III

Front 47

What are Polymodal nociceptors stimulated by?

Back 47

Wide range of thermal, mechanical, or chemical stimuli. Thought be an evolutionarily older system.

Front 48

What fiber type are polymodal nociceptors?

Back 48

C (slowest) / Group IV

Front 49

Why are the receptive fields of all pain-sensitive neurons relatively large, especially in thalamus and cortex?

Back 49

Presumably because the detection of pain is more important than its precise localization

Front 50

T/F nociceptive axons begin to discharge only when the strength of the stimulas reaches high levels

Back 50

T. This is in contrast to other receptors (eg., regular thermal receptors that do not fire any harder at extremely high levels)

Front 51

T/F Nociception requires special neurons, not simply greater discharge of neurons that respond to normal stimulus intensities

Back 51

T

Front 52

What are the two categories of pain perception?

Back 52

First pain (A&delta;) and second pain (C)

Front 53

EPICRITIC vs PROTOPATHIC pain

Back 53

Epicritic - first pain
Protopathic - second pain

Front 54

Causes first pain

Back 54

A&delta; fibers / Group III

Front 55

Causes second pain

Back 55

C fibers / Group IV

Front 56

Description of first pain

Back 56

Sharp, well-localized, acute, rapid onset

Front 57

Description of second pain

Back 57

Duller, more diffuse, takes longer to happen, described as throbbing and burning. Occurs in chronic pain

Front 58

What are the layers of Lissauer's tract relating to pain?

Back 58

Layer I, II, and V

Front 59

What does Layer I (Nociceptor specific (NS) receive input from?

Back 59

Both A and C fibers

Front 60

What does Layer II (Substantia Gelatinosa (SG)) receive input from? What is in it?

Back 60

Mostly C fibers. but some A&delta; fibers too.

It's special because this is where the inhibitory interneurons are located. They can inhibit the neuron in the NS layer AND WDR layer

Front 61

What does Layer V (Wide Dynamic Range (WDR)) receive input from? What is in it?

Back 61

primarily receive info from A deltas (also get input from inhibitory cells). Has dendites that go into other layers. Called WDR or polymodal. Can detect touch, pressure, and pain. Larger diameter fibers

Front 62

Which layer are the following found in?
A) WDR
B) NS
C) Inhibitory interneurons

Back 62

A) Layer V
B) I
C) II (Substantia gelatinosa)

Front 63

painful stimulus causes firing of this cell. C fiber activity synapses onto it.

Back 63

Layer I - NS neurons

Front 64

This layer can modulate or stop painful activity. Anything that stimulates this slows down pain.

Back 64

Layer II - Substantia Gelatinosa layer - inhibitory interneurons

Front 65

These neurons interpret higher frequency/more stimulation as pain. At low frequencies they give sensation of course touch.

Back 65

Layer V - WDR

Front 66

What is the vanilloid receptor? (VR-1 or TRPV1)

Back 66

A specific receptor associated with nociceptive afferent endings. Found in both C and A&delta; fibers and is activated by moderate heat.(~45C)

ALSO activated by capsaicin

Front 67

What is the vanilloid-like receptor? (VRL-1 or TRPV2)

Back 67

Receptor with a higher threshold response to heat, NOT sensitive to capsaicin, and is found in A&delta; fibers.

Front 68

Which receptor - TRPV1 (vanilloid) or TRPV2 (vanilloid-like) is

A) sensitive to capsaicin
B) Found in A&delta; fibers ONLY
C) Found in both C and A&delta; fibers

Back 68

A) TRPV1 / VR-1
B) TRPV2 / VRL - 1
C) TRPV1

Front 69

Which receptor- TRPV1 (vanilloid) or TRPV2 (vanilloid-like) is activated by a HIGHER temperature (>50C as opposed to ~45C)

Back 69

Vanilloid-like receptor

Front 70

What are the TRP channels?

Back 70

Transient-receptor potential channels. Known to comprise a large number of receptors sensitive to different ranges of heat and cold.

Front 71

Why did the nervous system evolve receptors that are sensitive to chili peppers (capsaicin?)

Back 71

They detect endogenous substances whose chemical structure resembles that of capsaicin.

Front 72

Other Modalities (other than pain) Mediated by the Anterolateral System

Back 72

Non-discriminative touch (crude touch)
Warmth (warm fibers), TRPV3 and TRPV4
Cold (cool fibers), TRPM8
Itch (histamine)
Slow mechanical touch (sensual touch)
Burn sensation, related to metabolites (lactic acid)

Front 73

Itch is usually associated with ______ activating the free nerve endings.

Back 73

histamine

Front 74

What do cold and warm fibers respond best to?

Back 74

CHANGES in temperature - not absolute values.

For example, COLD FIBERS - respond best to decreasing skin temperatures (approx. 20 - 40 degrees C )

Front 75

What is difference in responding between cold fibers, warm fibers, and nociceptive fibers?

Back 75

COLD FIBERS - respond best to decreasing skin temperatures (approx. 20 - 40 degrees C )

WARM FIBERS - respond best to increasing skin temperatures (approx. 30 - 40 degrees C )

NOCICIEPTOR FIBERS – respond at extreme temperatures (>42 degrees C, less than 17 degrees C) where tissue damage can occur.

Front 76

What is referred pain?

Back 76

There are few/no neurons specialized for visceral pain. Instead they're conveyed centrally via dorsal horn neurons that are also concerned with cutaneous pain.

Referred pain is the disorder of an internal organ perceived as cutaneous pain.

Front 77

What is hyperalgesia?

Back 77

Following an injury, sensations that would normally be described as minor pain are described as more intense pain

Front 78

What causes hyperalgesia peripherally (at site of injury)?

Back 78

Following injury damaged cells release substances that make nociceptive fibers in that area more sensitive to pain - an "inflammatory soup" including arachidonic acid, prostaglandins, nerve growth factor, histamine, etc.

Front 79

T/F Substances released by damaged tissue AND nociceptors contribute to inflammatory response

Back 79

T

Front 80

What is Substance P's and CGPR (calcitonin gene-related product)'s role in inflammatory response?

Back 80

Causes vasodilation, swelling, and histamine release from mast cells

Front 81

Damaged cells release cyclooxygenase (COX), which accelerates the synthesis of what?

Back 81

prostaglandins

Front 82

__________ sensitize the nerve fibers causing increased pain.

Back 82

Prostoglandins

Front 83

What are the central hyperalgesia/sensitization mechanisms?

Back 83

Immediate onset, activity dependent increase in the excitability of neurons in the dorsal horn of the spinal cord following high levels of activity in nociceptive afferents.

Activity levels that were subthreshold prior to sensitizing event now become sufficient to generate APs.

Front 84

Allodynia : defn

Back 84

Induction of pain by what is normally an innocuous stimulus. Typically occurs immediately after the painful event, can outlast stimulus by several hours.

Front 85

Windup : defn

Back 85

Repeated low-frequency stimulation of pain fibers leads to increase sensitivity of neurons in the dorsal horn.

The same stimulus over time becomes more painful (“winds up”)

Front 86

Neuropathic pain: defn

Back 86

Occurs where afferent fibers or central pathways themselves are damaged; a frequent complication in pathological conditions that include diabetes, etc.

It's chronic, intensely painful, and difficult to treat.

Front 87

A sensation of pain from a body part that is not present (e.g. amputated limbs)

Back 87

Phantom pain

Front 88

What does stimulation of the <b>periaqueductal gray matter </b> induce?

Back 88

Analgesia; also inhibits activity of nociceptive projection neurons in dorsal horn

Front 89

T/F Descending projections have an overall inhibitory influence on nociceptive projection neurons in the dorsal horn (reduce pain).

Back 89

T. Release various NTs that modulate activity in the spinal cord projection neurons. A release of these sbustances is generally inhibitory.

Front 90

What is the Gate Theory of pain?

Back 90

Activation of mechanoreceptors (non-nociceptors) modulates the transmission of nociception to higher centers.

This happens because A&beta; fiber (mechanoreceptor) synapses on an inhibitory local circuit neuron (layer II in substantia gelatinosa) that inhibits the nociceptor.

Explains why rubbing an area after an injury reduces pain

Front 91

How do C fibers play in the Gate Theory of pain?

Back 91

C fibers INHIBIT the inhibitory interneurons (resulting in sensation of pain) while A&beta; fibers ACTIVATE them, resulting in decreased sensation

Front 92

What's the significance of Endogenous Opioids?

Back 92

Involved in modulation/attenuation of nociceptive afferents. Present in periaqueductal gray area.

They provide a mechanism by which higher centers decrease activity relayed by nociceptive afferents.

Front 93

enkephalins, endorphins, and dynorphins

Back 93

endogenous opioids

Front 94

_________ are found in synaptic terminals of local circuit neurons in the dorsal horn.

Back 94

Enkephalins

Front 95

What does Release of enkephalins into the prepsynaptic terminals of nociceptor fibers do?

Back 95

inhibits the activation of the pain projection neurons.