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Neurophysiology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Pain

A

An unpleasant sensory and emotional
experience associated with actual or potential tissue
damage. (IASP)
Learned through experience early in life and is subjective

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2
Q

Percieved pain

A

is likely to damage tissue

Is an experience that we associate with actual or potential danger

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3
Q

Pain vs. Nociception

A

Pain: a concious experience. From brain activity in response to a noxious stimulus. Engages sensory, emotional, and cognitive processes of the brain

Nociception: Process by which information about a noxious stimulus is conveyed to the brain. The total sum of neural activity that occurs prior to cognitive processes that allow for the identification of a sensation as pain. Nociception alone is not sufficient to cause pain (weird, right?)

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4
Q

Nociception

A

Neural process of encoding noxious stimuli. Consequences can include autonomic responses (BP change) or behavioral responses (motor withdrawal reflex)

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5
Q

Nociceptor

A

A high threshold sensory receptor of the peripheral somatosensory nervous system that is capable of transducing and encoding noxious stimuli

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6
Q

Noxious stimuli

A

Stimulus that is damaging or threatening to damage tissue

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7
Q

-algia

A

localized percieved pain without presuming its cause
“lumbalgia”
Hyperalgesia or hypoalgesia

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8
Q

Antalgic/analgesic

A

Pertaining to the reduction of pain perception

Paresthesia: an abnormal sensation, whether spontaneous or evoked

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9
Q

Decreased Sensation terms

A

Hypoesthesia: Decrease in senstivity to stimulation, excluding the special senses
Hypoalgesia: Decrease in pain in response to a typically noxious stimuli
Anesthesia: Absence of all sensation
Analgesia: Absence of all pain in response to stimulation which would typically be painful

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10
Q

Increased Sensation terms

A

Hyperesthesia - Increased senstivity to stimulation excluding the special senses
Hyperalgesia - Increased pain from a stimulus that typically provokes pain
Allogesia - Pain from a stimulus that does not typically provoke pain

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11
Q

General features of Nociception

A

Mediated by neural networks that are homologous across all mammalian species.
Must be able to react and detect noxious and potentially harmful stimuli

Engages multiple interacting mediating mechanisms
Neural systems, neurohormonal systems, neuroimmune systems

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12
Q

The Paradox of Pain

A

Adaptiveness: The experience of pain is important for survival and serves as a warning sign despite appearing negative
Lack of clear cortical representation: Noxious stimuli activate several regions of the cortex and interpersonal variation is present
Presence of descending pain control mechanisms: cognitive and emotional factors can effectively suppress or amplify the experience of pain

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13
Q

Rene Descartes and the Mind-Body model

A

Asserted that the mind and the body are two seperate things with the body as a machine controlled by the soul
Pain is spirits that travelled through nerves and to the brain that is the seat of the mind. Therefore pain is a construct of the mind.. with ghosts

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14
Q

Biomedical Model

A

Informed by Descartes theory

Each disease process results from a unique pathoanatomical/pathophysiological lesion

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15
Q

Biopsychosocial Model

A

Current
Pain perception is neither phsiological or neuroanatomical
Pain is a conscious experience that can engage the sensory, cognitive, and emotional networks of the brain.

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16
Q

Goals of the biopsychosocial model

A

Explain the multidimensional nature of the pain experience
Emphasize the complexity and interdependence of the components which contribute to the experience of pain
Provide health professionals with an explanation for the components of pain

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17
Q

(Biological) Biopsychosocial

A

NMS components and other related processes

Anatomy, neuroanatomy, inflammatory processes, genetics, family history, age, sex, race, pre-existing medical history

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18
Q

(Psychological) Biopsychosocial

A

Attitudes, belief, behaviors and coping, perceptions, cognition/thought patterns, emotional state

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19
Q

(Social) biopsychosocial

A

Social context of health that has to do with external pressures and constraints on behavior and functioning
Previously learned information regarding health, disease, and pain
Cultural background
Social support and interactions
Family influence and support
Financial influences
Workplace environment

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20
Q

Temporal categories of pain

A

Transient Nociceptive pain - an unpleasant sensation in response to noxious stimuli that does not injure tissue
Acute Pain - Unpleasant sensation in response to tissue injury/inflammation. recurrent acute pain is pain that returns in distinct episodes

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21
Q

Transient Nociceptive Pain

A

Temporary discomfort without tissue damage
Sensations of first pain (Ad fibers) and second pain (C fibers)
Serves as an early warning sign
Triggers pain avoiding behaviors

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22
Q

Acute Pain

A

Clinically significant acute pain elicited by tissue damage and inflammation that activates Nociceptive afferent neurons at the site of local damage
Local tissue damage and inflammation temporarily alters the response of peripheral nociceptors as well as their central connections
Injury induced physiological changes produce hypersensitivity
Signals the presence of tissue damage and activates physiological and behavioral mechanisms

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23
Q

Chronic Pain

A

Persistent pain that is not amenable to specific remedies

Persists after the trigger event beyond normal expectations for healing

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24
Q

Taxonomy of nociceptive pain

A

Normal tissue, Well localized pain. 1st and 2nd pain

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25
Q

Taxonomy of acute pain

A

Inflamed, increased excitation or decreased inhibition of nociceptors, peripheral and central sensitization of PNS and CNS. Increased pain sensitivity, hyperalgesia, allodynia.

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26
Q

Taxonomy of chronic pain

A

Injury to nervous system. Modification fo pain afferents in the PNS. Rewired networks/assemblies, circuits in the CNS. If prolonged similar pain symptoms to Acute

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27
Q

Two functional categories of pain

A

Nociceptive

Neuropathic

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28
Q

Nociceptive pain

A

Further divided into Somatic, visceral, and inflammatory
transient pain that occurs with a mechanical, temperature, or chemical noxious stimulus.
Subcategory should be identified.
INFLAMMATORY nociceptive pain is associated with tissue repair

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29
Q

Neuropathic pain

A

Divided into neurogenic and functional pain
From a nervous system disorder
Treatment will depend on wether or not the injury results from peripheral (ie. diabetic neuropathy) or central. central component may develop following peripheral pain

Functional neuropathic pain is a dysfunction of the central nervous system that can enhance the perception of pain through excitation of neural systems or through the inhibition of endogenous pain control mechanisms (fibromyalgia and post-stroke central pain syndrome)

30
Q

Nociceptive Somatic Pain Calssification

A

(fracture, laceration)
Superficial or deep pain, nociceptive reflex, & autonomic response.
Mechanical, thermal, or chemical stimulation

31
Q

Nociceptive visceral pain

A

(colitis)
Constant or cramping, not well localized, & autonomic response.
Distention of viscera

32
Q

Nociceptive Inflammatory pain

A

Sponataneous diffuse pain, hyperalgesia, allodynia

Assocaited with tissue lesions and inflammation

33
Q

Neuropathic Neurogenic

A

(neuralgia, spinal injury, thalamic injury)
Spontaneous sharp electrical pain, hyperalgesia, & allodynia.
Hyperactivation or loss of pain inhibitor.

34
Q

Two principles for the evaluation of pain

A

Patient is the only authority for pain evaluation

Pain evaluation should be evaluated in the terms of its impact on the person as a whole

35
Q

Quantifiable components of the pain experience

A

Pain intensity: FACES scale, Visual Analog Scale, Oral Pain Scale, LOCQSMAT
Physical capacity: preventing from doing certain activites
Spatial attributes: Where is the pain
Psychological component: Is the pain affecting your mood/emotional well-being? (Beck Depression scale, SBST, Patient Health Questionarre-9, Fear-Avoidance)

36
Q

Neurological Events of Nociception

A

Transduction - Converting noxious stimuli into eletrical stimulation
Transmission - Transmit electrochemcial impulses to various nervous system regions
Modulation - Altering the perception of noxious stimuli by peripheral or central mechanisms
Perception - Concious experience of pain created by the interpretation of nociceptive information by higher cneters of the CNS

37
Q

Sensory Transduction

A

Noxious stimuli to electircal signals

Nociceptor properties
Free nerve endings of specialized afferent fibers
Primary cell bodies of neurons carry pain information from the BODY are located in the DORSAL ROOT ganglia
Primary cell bodies of neurons carry pain information from the FACE are located in the TRIGEMINAL ganglia

All nociceptive neurons utilize glutamate and substance P as primary neurotransmitter
Peripheral nociceptors are characterized by properties of their fibers (myelinated Ad and unmyelinated C fibers)

38
Q

Myelinated Nociceptors

A 
(20%) 
Ad fiber group
Large myelinated groups (1-5um)
Conduct at ~20 m/s
Bimodal: respond to noxious mechanical and thermal stimuli
Small receptive fields
Project to lamina I of spinal cord grey

Respond to: Greater than 10g of pressure, Heat >45 degree Celsius or less than 11 degrees

39
Q

Unmyelinated Nociceptors

A

(80%)
C fibers
Small axons in Remak bundles (diameter 0.2-1.5um)
Conduct at -2m/s
Polymodal: respond to mechanical, thermal & chemical stimuli
Large receptive fields
Project to Lamina II and III of spinal cord grey

Respond to the same stimuli as myelinated in addition to chemical substances

40
Q

How inflammation can increase the perception of pain

A

Modifying the degree of nociceptor activation/excitation
Results in increased transmission of nociception information and enhanced perception of pain

Sensitization of nociceptors
Increased responsiveness to stimuli (heat, chem, mech)
Results in hyperalgesia and allodynia
Cellular mechanisms on injured and nearby non-injured fibers (Increased expression of Na ion channels; receptor upregulation along afferent fibers)

41
Q

Entry of afferent fibers into the spinal cord

A

Ab fibers assume dorsomedial position

Ad & C fibers assume ventrolateral position

42
Q

Nociceptive neurons in dorsal horns

A

Nociceptive specific (those that are activated only by Ad fibers and those that are activated only by Ad and C fibers)
Interneurons that are mainly inhibitory and release GABA
Wide Dynamic Range neurons (non-nociceptive specific)

43
Q

Wide Dynamic Range neurons

A

Receive afferent contact from Ab, Ad and C fibers and respond to both noxious and innocuous stimuli
Receive inhibitory contacts from interneurons
Receive efferent contacts from descending pathways
Utilize glutamate as main NT
Have large convergent receptive fields
Receive input from viscera, muscles and joints
Can be sensitized via central sensitization mechanisms

44
Q

Peripheral Sensitization

A

Increased sensitivity of a nociceptor to stimuli
Results in hypersensitivity and allodynia

From increased expression of Na channels and receptor upregulation

May occur with exposure to inflammatory mediators
repeated application of a noxious stimuli

45
Q

Central sensitization

A

Can sensitize Wide-Dynamic range neurons
Hyperactive ciceptors can exhibit increased signal frequency following activation (hyperalgesia)
Has a lower excitation threshold which can result in allodynia
Can reduce the effectiveness of endogenous pain modulators mechanisms through the disinhibition of typically inhibitory interneurons
Enhanced release of ATP can activate local glial cells which release cytokines and other irritating molecules

There is a dynamic increase in the receptor field of dorsal horn neuron

46
Q

K ions and histamine

A

Escape from damaged cells

Activate polymodal nociceptors

47
Q

prostaglandins

A

Synthesized from enzymes released by substrates created by tissue damage

Sensitize nociceptors by:
Increasing cAMP levels within Nociceptive neurons
Phosphorylation of Na ion channels (this decreases the depolarization level)

48
Q

Bradykinin, 5HT, and ATP

A

Arrive following plasma effusion or lymphocyte migration

Activate and sensitize nociceptors

49
Q

Substance P, Calcitonin gene-related peptide

A

Secreted by nociceptor activity

Contribute to the inflammatory response by initiating release of other substances

50
Q

Generation of LTP of WDRs

A

Normal generation of ATP
Ligand binding to both NMDA and AMPA receptors (Ligand is glutamate)
Depolarizes the postsynaptic WDRs neuron membrane
Removes Mg ion blocking the ion channel of the NMDA receptor
Intracellular Na ion influx into the WDR neuron

51
Q

4 mechanisms of LTP of WDR

A

Increased postsynaptic excitability of the postsynaptic membrane due to the phosphorylation of ion channels
Increased glutamate release from the presynaptic neuron: following the released the retrograde messenger NO
Enhanced/sustained EPSP depolarization resulting in an increase of AMPA receptors on the WDR neuron
Changes in gene transcription due to activation of intracellular STPs

52
Q

Temporal Summation of WDRs

A

High frequency repetitive Nociceptive stimulation will result in temporal summation of the Nociceptive afferent impulses from C and Ad fibers.
Perception of 2nd pain is increased
Wind up (increasing fire rate of dorsal horn neurons)
Spinal sensitization (central)

53
Q

Spatial summation of WDRs

A

Stimulation of a large surface area will stimulate an equally large number of nociceptors, thereby increasing the Nociceptive afferent impulses
Nociceptive stimulation will be perceived to be of higher intensity on a larger surface than on a smaller one

54
Q

First pain

A

Sharp pain
By fast conducting Ad fibers
Localized
Not long lasting

55
Q

Second Pain

A 
If the noxious stimulus continues
Dull pain
Slow C fibers
Less well-localized
Long lasting
56
Q

Primary hyperalgesia

A

Occurs at injury site
Local vasodilation, followed by edema, swelling, & release of inflammatory mediators
Peripheral sensitization of nociceptors

57
Q

Secondary hyperalgesia

A

Occurs at uninjured tissue beyond
Increased receptive field of WDR neurons
Central sensitization of WDR

58
Q

WDR Neuron changes

A

Increased impulse frequency from sensitized nociceptors (hyperalgesia)
Lowered activation threshold and increased impulse frequency to innocuous stimuli - allodynia
Increase in WDR receptive field - Pain region expansion (secondary hyperalgesia/pain radiation)
Progressive EPSPsize increase and impulse frequency with repeated noxious and innocuous stimuli - Chronic pain

59
Q

Neuropathic pain definition

A

Chronic intense perceived pain that arises from mild to no stimulation

60
Q

Visceral referred pain (development)

A

Pain sensation is often referred from a visceral structure to a somatic structure that originated from the same embryonic segment (dermatome pattern)

61
Q

Convergence-projection theory of referred pain

A

Afferent sensory inputs from somatic and visceral tissues converge on nociceptive dorsal horn neurons at the same spinal cord level
Fibers ascend together in the spinothalamic tract and synapse on the same ventral posterior lateral nuclei within the thalamus
These thalamus neurons send projections to higher cortical regions

Higher central nervous system receiving these thalamic inputs are often unable to distinguish stimuli from visceral receptors from stimuli from somatic receptors.
Difficulty in identifying source of nociceptive input. discomfort in internal organ manifests as cutaneous pain

62
Q

Visceral nociceptive pathway

A

Occurs via nociceptive fibers within autonomic nerve bundles

Pain sensation is referred to the surface often far from the organ of nociceptive origin

63
Q

Parietal pathway of pain

A

Nociception is conducted directly to local spinal nerves from parietal peritoneum. pleura, and pericardium
sensations are localized directly over the origin of nociception

64
Q

Bottom up pain modulation

A

Transitory pain sensation suppression via non-noxious peripheral sensory stimulation
Effects last as long as non-nociceptive stimulation persists.

65
Q

gate control theory of pain

A

R melzack and P Wall
Proposed a bottom up modulation mechanism in which the spinal cord contained a neurologic pain gate which could be shut in order to avoid pain

Non-noxious stimuli can activate peripheral mechanoreceptors. Collaterals of these large non-noxious sensory fibers can facilitate inhibitory GABA-ergic interneurons (within substantia gelatinosa; lamina II) which synapse on and inhibit WDRs
This prevents fibers from signaling to WDRs

66
Q

Top down modulation of pain mechanisms

A

Systems originating in various regions of the cerebral cortex and other higher processing regions send projections as part of descending systems that modulate the transmission of ascending pain signals (the descending analgesic system)
these regions send projections to the dorsal horn of the spinal cord to influence WDR neurons, either directly or indirectly through the action of inhibitory interneurons
Can be either inhibitory of facilitative

67
Q

Regions involved in top down modulation of pain

A

somatosensory cortex
Hypothalamus
Thalamus (mediodorsal nuclei)
Amygdala
Pariaqueductal grey (stimulation of the PAG in rodents eliminates pain perception)
Brainstem Nuclei: locus coeruleus (NE/NA), raphe nuclei (5-HT), Ventral tegmental area (DA)

68
Q

Graded Motor Imagery

A

A technique that involves gradual activation of the motor system and associated cortical regions without causing perceived pain in patients displaying hypersensitivity as well as amputees with phantom limb pain

69
Q

Mirror therapy

A

Utilizes the visual recreation of movement of a lost limb by moving the intact limb in front of a mirror and has been utilized to combat PLP

70
Q

Targets of the nociceptive pathway

A

Thalamic nuclei targets (VPL/ VPM/ Mediodorsal, etc.)
S-S cortex: sensory discriminative aspect (what/ where/ when/ how strong)

Limbic structures/reticular formation: affective emotional aspect (unpleasantness)
Anterior cingulate gyrus and insula

Neurophysiology (3 decks)

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