Nociception and Pain

Question 1

What occurs in primary hyperalgesia?

Answer 1

Local tissue damage heightens sensation of pain to subsequent stimulus.

-Occurs at site of tissue damage

Question 2

WHich receptors become more sensitive in primary hyperalgesia?

Answer 2

Nociceptors

Question 3

What are some examples of chemical mediators that are released by damaged tissue that can result in increased sensitivity?

Answer 3

1) K+
2) 5-HT, serotonin
3) Histamine
4) Bradykinin (most potent nociceptor known)
5) Prostaglandins

Question 4

What can substance P cause?

Answer 4

1) Histamine release from mast cells

2) Vasodilation (flare) around area leading to release of proteins and other factors

Question 5

What occurs in secondary hyperalgesia?

Answer 5

It is centraql sensitization in which C fibers are persistently active and the EPSPs on the dorsal horn neurons progressively increase.

Question 6

What type of hyperalgesia is associated with “wind-up” and what is it caused by?

Answer 6

Secondary hyperalgesia

Casued by glutamate released from C fiber endings acting on NMDA receptors on the dorsal horn cells. It is very similar to Long-term potentiation (LTP). NMDA receptor activation also induces supersensitivity and hyperexcitability in the dorsal horn neurons

Question 7

What is Allodynia?

Answer 7

A pain in response to a stimulus which does not normally produce pain. It results from mechanoreceptors projecting to neurons in the nociceptive pathway.

1 ). normally mechanoreceptor input too small to activate
nociceptive neuron
2). after injury, central nociceptive neurons become sensitized (central sensitization) and now mechanoreceptor input excites second order nociceptive neurons

Question 8

What fibers innervate the pulp and the rest of the oral cavity and face?

Answer 8

A-delta and C fibers whose cell bodies lie in the trigeminal ganglion

Question 9

Nociceptive fibers synapse on cells in the __________________________ nucleus which is arranged much like the dorsal horn of the spinal cord.

Answer 9

Spinal trigeminal nucleus

Question 10

The axons of the spinal trigeminal cells cross over and project to the contralateral _______________.

Answer 10

Thalamus

Question 11

Nociceptive fibers enter the spinal cord through the _____________ part of the dorsal root.

Answer 11

Lateral

Question 12

__________ produces fast EPSP on dorsal horn neurons in spinal cord.

Answer 12

Glutamate

Question 13

What fibers release substance P?

Answer 13

C fibers

Question 14

__________________ produces slow EPSP on dorsal horn neurons in spinal cord.

Answer 14

Substance P

Question 15

What tract of neurons is the most prominent and best studied tract?

Answer 15

Spinothalamic

Question 16

_____________________________ is the cutting of the spinothalamic tract for relief of intractable pain. This provides initial relief but often the pain returns indicating other pathways are involved

Answer 16

Anterolateral cordotomy

Question 17

Where do the axons of the spinothalamic tract project to in the brain?

Answer 17

Thalamus (reticular formation)

Question 18

Where do third order thalamic neurons project to?

Answer 18

Cortex

Question 19

Does extensive damage to somatosensory cortex result in loss of pain?

Answer 19

NO - bc there’s no orderly arrangment of nociceptive inputs to the somatosensory cortex.

Question 20

What is the most common and usual type of pain?

Answer 20

Nociceptive pain - caused from activation of nociceptors

Question 21

What is causalgia?

Answer 21

Peripheral nerve injury - also known as reflex sympathetic dystrophy syndrome

Question 22

Causalgia is described clinically as “sympathetically mediated pain” and can be reduced or abolished by blocking sympathetic activity or depleting ______________________.

Answer 22

Catecholamines

Question 23

What is the most painful disease in all of medicine and is also referred to as suicide disease?

Answer 23

Trigeminal Neuralgia

Question 24

What is another name for trigeminal neuralgia?

Answer 24

Tic douloureux

Question 25

What is trigeminal neuralgia described as by patients?

Answer 25

A stabbing or electric shock-like pain usually felt only on one side of the face that maybe triggered by brushing teeth, talking, touching the face, and chewing.

Question 26

What are the causes of tic douloureux?

Answer 26

1) Most common - enlarged looping artery or vein pressing on the trigeminal nerve root at the brain stem. The repeated pulsations of the vessel eventually produce irritation and abnormal signals 2) Multiple sclerosis 3) Tumor

Question 27

Often trigeminal neuralgia can be mistaken for what?

Answer 27

Tooth pathology - often results in loss of one or more of the patients natural teeth before a correct diagnosis is made

Question 28

What is a referred pain associated with tic douloureux?

Answer 28

Classic referred pain is visceral pain that is felt as pain in some distant somatic structure for ex: cardiac pain that is felt as pain in the left arm

Question 29

What is the mechanism for the referred visceral pain in trigeminal neuralgia?

Answer 29

Pain fibers from the visceral structure and the somatic structure to which the pain is referred, enter the same spinal cord segment. The visceral and somatic pain fibers converge on the same population of nociceptive neurons in the spinal cord and since somatic pain normally predominates, the brain interprets the activity in this pathway as arising from the somatic source even though it is from a visceral structure.

Question 30

What are some examples of referred pain involving the trigeminal nerve?

Answer 30

1) Tooth pain from one tooth is felt as pain in another 2) Pain from actual tooth is felt as a headache 3) Infections of the ears and sinuses can cause the sensation of a toothache 4) Angina is felt as a tooth ache or jaw pain

Question 31

What is the gate control theory?

Answer 31

Perception of pain is not simply due to activation of nociceptors, but is the outcome of modulation of both nociceptive and non-nociceptive inputs. According to the gate theory of pain, inhibitory interneurons regulate the transmission of ascending nociceptive information at the level of the second order neuron, allowing modulation of the signal (both increases and decreases in activity are possible). This modulation can explain phantom limb pain, as well as the success of TENS treatment and the actions of opioid analgesics.

Question 32

Stimulation of certain brain regions, especially the __________________________________, produces profound analgesia with no loss of tactile sensibility.

Answer 32

Periaqueductal gray

Question 33

What is analgesia?

Answer 33

Loss of pain

Question 34

T/F - Analgesic action of IV injected or ingested opiates is due to direct action on the CNS not peripheral receptors even though peripheral nociceptive endings do express opiate receptors.

Answer 34

True

Question 35

What are the 3 classes of endogenous opioid peptides?

Answer 35

1) Beta-endorphin from proopiomelanocortin precursor of pituitary 2) enkephalins from proenkephalin precursor 3) dynorphin from prodynorphin precursor (least potent analgesic)

Question 36

What are the 3 major classes of opiate receptors?

Answer 36

Mu, delta, and kappa

Question 37

Nearly all the clinical effects of opiates are mediated by ___ receptors.

Answer 37

Mu

Question 38

______________ is a potent agonist of the mu receptor.

Answer 38

Morphine

Question 39

The most clinically used opiate antagonist is ______________ which binds specifically to mu receptors.

Answer 39

Naloxone

Question 40

T/F- Opiate action is probably due to disinhibition of the periaqueductal grey neurons.

Answer 40

True

Question 41

Injections of __________ into subarachnoid space of the spinal cord (intrathecal injection) alleviates labor pain.

Answer 41

Opiates

Question 42

Descending serotonergic and noradrenergic fibers synapse directly on spinothalamic neurons and on _______________-containing interneurons.

Answer 42

Enkephalin-containing - Directly suppresses spinothalamic neurons - Indirectly suppresses spinothalamic neurons through activation of enkephalin-containing interneurons