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Neuro Quiz 4 Final > 58 Pain > Flashcards

58 Pain Flashcards

1
Q

What is Referred Pain?

A

Perception of pain in an area different than the source.

Common phenomena with pain from deep musculoskeletal or visceral structures.

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2
Q

What is Hyperalgesia?

A

Magnification of pain perception to normally minimally painful stimuli

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3
Q

What is Allodynia?

A

Perception of pain from a non-painful stimuli
ex: touching a sunburn
Similarities with Dysthesia.

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4
Q

What is Hyperesthesia?

What is Dysthesia?

A

Hyperesthesia is a magnified sensation of any type

Dysesthesia is a distorted, magnified and unpleasant sensation to normal stimuli (this is similar to Allodynia)

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5
Q

What is Neuropathic pain?

A

Pain originating from the nervous system itself that is not explained by stimuli
Includes sensations of burning, stabbing, or shooting pain.

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6
Q

What is the difference between Nociceptive and Neuropathic pain?
Why is this relevant pharmacologically?

A

Nociceptive is normal pain from tissue damage.
Neuropathic is due to nervous system malfunction.
Different Tx and pharmocology works for each.

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7
Q

Describe the basic construction of a Nociceptive the two basic pain receptors.
What do each detect?

A

MECHANORECEPTORS: High threshold, usually with free nerve endings
CHEMORECEPTORS: detect tissue metabolites (released with tissue damage) as well as inflammatory mediators and neuromodulators

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8
Q 
As pain stimuli for chemoreceptors, what are examples of...
Tissue metabolites (3)?
Neurotransmitters and modulators (2)?
Tissue cell products (3)?
Inflammatory mediators (3)?
A

Tissue metabolites - potassium, acids, ATP
Transmitters/neuromodulators - substance P, norepinephrine.
Tissue cell products - histamine, bradykinin, nerve growth factors
Inflammatory mediators - prostaglandins, cytokines, leukotrines

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9
Q

What is Substance P (SP)?

A

a neuropeptide - a substance that functions as a neurotransmitter and as a neuromodulator.

Substance P is released from the terminals of specific sensory nerves, it is found in the brain and spinal cord, and is associated with inflammatory processes and pain.

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10
Q

Chemical mediators…

Some directly activate & some sensitize fibers
Some cause release of other algetic substances
Some recruit other elements to an inflammatory reaction

Peripheral nerve fibers are modified by stimuli…

PGE2, bradykinin, and NGF activate G-protein mechanisms that phosphorylate ion channels

Protein Kinase A (cAMP-dependent) and C (calcium dependent) phosphorylate transient receptor potential ion channels (TRPV1)

A

.

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11
Q

What are afferent Pain fibers (Alpha Numeric Greek system)?

A 
A delta (faster)
C fibers (slow and unmyelinated)
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12
Q 
What are the qualities of afferent nerve fibers A-delta and C fibers?
Adaption speed?
Conduction speed?
Purpose?
Effect is where?
A

Both: slow adapting and slow conduction
A-detla: 15 m/s (quick withdrawal from pain)
C: 1 m/s (confirmation or denial of pain)
Release neurotransmitters both in CNS and peripheral end of PNS which contributes to vasodilation and swelling at tissue and may affect neuroplasticity (via neurotrophic factor BDNF)

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13
Q

What is the Zone of Lissauer?

A

When pain sensory fibers reach the nervous system via the DRG, they collateralize and spread over several segments up and down the spinal cord via the Zone of Lissauer. This means that pain the input is not highly focused in the spinal cord.

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14
Q

In what layers (3) do C fibers terminate in the spinal cord?

A

Layer I
Layer IV
Layer V

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15
Q

What do A-beta fibers detect?

What is their relationship to pain fibers?

A

Convey normal touch, pressure, and proprioception
Can inhibit pain fibers (note: enkephalin interneurons also modulate pain sensation. These are in the spinal cord)
This is why rubbing a painful area can diminish pain

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16
Q

What are MARGINAL vs WIDE DYNAMIC pain transmission neurons?
What layer of the spine are each located?
What do each transmit?

A

MARGINAL aka nociceptive specific neurons are in LAYER 1 and transmit SHARP STINGING pain that enables you to LOCALIZE the pain, rather than intensity.

WIDE DYNAMIC pain transmission are in LAYERS 4 and 5 and receive highly CONVERGENT information via DENTRITES IN ALL LAYERS that relays the INTENSITY of pain rather than location. Contributes to REFERRED PAIN.

Both transmit to the spinothalamic tract.

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17
Q

What pain neurons contribute to REFERRED PAIN?

A

WIDE DYNAMIC neurons receive info from all layers of the dorsal spinal cord that converge from many areas of the body.

18
Q

Examples of referred pain include pain to the left side of the neck, jaw or arm from hard pain, to the shoulders from diaphragm pain or the mid thoracic region from upper abdominal pathology. In orthopedics, it’s well known that hip fractures often are felt as knee pain.

A

.

19
Q

Why is the location of head pain less diagnostic than pain characteristics, aggravating and alleviating, and accompaniments of pain?

A

Pain entering with the trigeminal nerve terminates in the spinal nucleus of the trigeminal in an overlap with upper cervical sensory nerves. Therefore, problems with the upper neck or back of the head can be felt in the front or vice versa.

20
Q

Pain withdrawal reflexes are mediated through ____ neurons.

A

Interneurons.

21
Q

Because of the importance of pain, what are the four partially redundant pathways that transmit pain in the spine?
Which is the most direct?

A

NEOSPINALTHALAMIC TRACT
Paleospinalthalmic Tract
Spinoreticulothalamic Tract
Propriospinal Tract

22
Q

What are the two sets of neurons that involved in the neospinothalamic tract?

A 
Marginal cells (precise location, but not intensity of pain)
Wide Dynamic Range (WDR) cells (intensity, but not location of pain)
23
Q

What are the termination sites of the neospinothalamic pathway?

A

Main: Ventral Posterolateral Thalamus and Somatosensory cortex

Also in the brainstem which affects autonomic functions (ex: sweating, HR, Paleness, nausea in response to pain)
Medulla: Reticular Formation
Pons: Parabrachial Nuclei and Reticular Formation
Midbrain: Periaqueductal Gray

24
Q

What types of neurons are involved with Paleospinothalamic pathway?

A

Mostly Wide Dynamic Range (WDR)

25
Q

What are the termination sites of the Paleopsinothalamic pathway?

A

Nonspecific (Intralaminar nuclei) thalamic nuclei that project broadly over the cortex
Affects many areas of the brain including mood and attention
Also projections in the brainstem affecting autonomic funtions in response to pain.

26
Q

Question for Swenson: Do paleo and neo both affect intralaminar nuclei of the thalamus?

A

.

27
Q

Note: Pain can cause arousal from sleep.

A

.

28
Q

What are two ASCENDING neurons that modulate pain sensation?

A

A-beta sensory nerves in the PNS

29
Q

What are interneurons that modulate pain in the spine?

A 
Enkephalin interneurons (activate opiate receptors)
GABA interneurons
Glycine interneurons
30
Q

What are the neurotransmitters used by ASCENDING A-beta neurons that modulate pain?

What are the neurotransmitters used by DESCENDING neurons that modulate pain?

A

Asceding A-beta: GABA and/or GLYCINE interneurons

Descending: 5-HT and Norepi descend and activate enkephalin and GABA interneruons

31
Q

What are the steps of the descending pathway for pain control?

A

Wide variety of inputs (spinothalamic tract, amydala, hypothalamus, frontal cortex, insular cortex, reticular formation, and cetecholamine nuclei, such as the locus ceruleus) all target the PERIAQUEDUCTAL GRAY&raquo_space; glutamine to activate ROSTRAL VENTROMEDIAL MEDULLA and NUCLEUS RAPHE MAGNUS&raquo_space; 5-HT synapses with neurons in the DORSAL HORN

Note: the RVMM and the Raphe also synapse with the medullary catecholamine nuclei that release norepi onto the dorsal horn

32
Q

Which steps in the descending pain modulating pathway contain Enkephalic interneurons (opiate receptors)?
Which has the most opiate receptors of anywhere in the nervous system?

A

PERIAQUEDUCTAL GRAY
Rostral Ventromedial Medulla
Dorsal Horn of of the spine

33
Q

What are mechanisms that are targeted for therapeutic agents for pain control?

A 
Opioids (cause tolerance and dependence)
Serotonin
Norepinephrine reuptake inhibitors
Voltage Gated Calcium Channels (alpha2delta subunit)
Sodium Gated Channels
34
Q

What are drugs used to modify pain via Voltage Gated Calcium Channels?

A

Gabapentin and Pregabalin

35
Q

What is the role of the Thalamus in pain modulation?

A

Damage to sensory pathways that innervate the Thalamus (DE-AFFERENTIATION) results in diminished sensitivity and loss of inhibitory functions including the death of inhibitory interneurons.
This can cause distressing pain and numbness that is difficult to treat.

36
Q

Explain the physical correlations between physical pain and emotional suffering.

A

Both physical pain and emotional suffering activate the ANTERIOR CINGULATE CORTEX and medial frontal lobes.

People with pain often have depression. People with depression often have pain.

37
Q

What is the role of the MEDIAL FRONTAL LOBE in pain perception?

A

Becomes active at the threshold of pain.

Appears to help determine how one is going to react to pain.

38
Q

What is Facilitation in neuroscience?

A

Plasticity due to interneurons facilitating excitatory potentials

39
Q

How are the mechanisms for plasticity in pain neurons similar to hippocampal neurons?

A 
Very similar.
Presynaptic enhancement via short-term and long-term plasticity via PKA activity
Postsynaptic AMPA (fast reacting) NMDA (slow reacting blocked with Mg) glutamine receptors
40
Q

Quick review of plasticity with AMPA and NMDA…

A

Glutamine activates AMPA
Na enters cell
Depolarization releases the Mg ion blocking NMDA
NMDA allows Ca into cell
Ca causes post-synaptic remodeling with upregulating AMPA receptors

Neuro Quiz 4 Final (4 decks)

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