Final Exam Flashcards
Pain
An unpleasant sensory and emotional
experience associated with actual or potential tissue
damage. (IASP)
Learned through experience early in life and is subjective
Percieved pain
is likely to damage tissue
Is an experience that we associate with actual or potential danger
Pain vs. Nociception
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?)
Nociception
Neural process of encoding noxious stimuli. Consequences can include autonomic responses (BP change) or behavioral responses (motor withdrawal reflex)
Nociceptor
A high threshold sensory receptor of the peripheral somatosensory nervous system that is capable of transducing and encoding noxious stimuli
Noxious stimuli
Stimulus that is damaging or threatening to damage tissue
-algia
localized percieved pain without presuming its cause
“lumbalgia”
Hyperalgesia or hypoalgesia
Antalgic/analgesic
Pertaining to the reduction of pain perception
Paresthesia: an abnormal sensation, whether spontaneous or evoked
Decreased Sensation terms
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
Increased Sensation terms
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
General features of Nociception
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
The Paradox of Pain
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
Rene Descartes and the Mind-Body model
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
Biomedical Model
Informed by Descartes theory
Each disease process results from a unique pathoanatomical/pathophysiological lesion
Biopsychosocial Model
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.
Goals of the biopsychosocial model
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
(Biological) Biopsychosocial
NMS components and other related processes
Anatomy, neuroanatomy, inflammatory processes, genetics, family history, age, sex, race, pre-existing medical history
(Psychological) Biopsychosocial
Attitudes, belief, behaviors and coping, perceptions, cognition/thought patterns, emotional state
(Social) biopsychosocial
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
Temporal categories of pain
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
Transient Nociceptive Pain
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
Acute Pain
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
Chronic Pain
Persistent pain that is not amenable to specific remedies
Persists after the trigger event beyond normal expectations for healing
Taxonomy of nociceptive pain
Normal tissue, Well localized pain. 1st and 2nd pain
Taxonomy of acute pain
Inflamed, increased excitation or decreased inhibition of nociceptors, peripheral and central sensitization of PNS and CNS. Increased pain sensitivity, hyperalgesia, allodynia.
Taxonomy of chronic pain
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
Two functional categories of pain
Nociceptive
Neuropathic
Nociceptive pain
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
Neuropathic pain
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)
Nociceptive Somatic Pain Calssification
(fracture, laceration)
Superficial or deep pain, nociceptive reflex, & autonomic response.
Mechanical, thermal, or chemical stimulation
Nociceptive visceral pain
(colitis)
Constant or cramping, not well localized, & autonomic response.
Distention of viscera
Nociceptive Inflammatory pain
Sponataneous diffuse pain, hyperalgesia, allodynia
Assocaited with tissue lesions and inflammation
Neuropathic Neurogenic
(neuralgia, spinal injury, thalamic injury)
Spontaneous sharp electrical pain, hyperalgesia, & allodynia.
Hyperactivation or loss of pain inhibitor.
Two principles for the evaluation of pain
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
Quantifiable components of the pain experience
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)
Neurological Events of Nociception
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
Sensory Transduction
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)
Myelinated Nociceptors
(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
Unmyelinated Nociceptors
(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
How inflammation can increase the perception of pain
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)
Entry of afferent fibers into the spinal cord
Ab fibers assume dorsomedial position
Ad & C fibers assume ventrolateral position
Nociceptive neurons in dorsal horns
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)
Wide Dynamic Range neurons
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
Peripheral Sensitization
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
Central sensitization
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
K ions and histamine
Escape from damaged cells
Activate polymodal nociceptors
prostaglandins
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)
Bradykinin, 5HT, and ATP
Arrive following plasma effusion or lymphocyte migration
Activate and sensitize nociceptors
Substance P, Calcitonin gene-related peptide
Secreted by nociceptor activity
Contribute to the inflammatory response by initiating release of other substances
Generation of LTP of WDRs
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
4 mechanisms of LTP of WDR
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
Temporal Summation of WDRs
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)
Spatial summation of WDRs
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
First pain
Sharp pain
By fast conducting Ad fibers
Localized
Not long lasting
Second Pain
If the noxious stimulus continues Dull pain Slow C fibers Less well-localized Long lasting
Primary hyperalgesia
Occurs at injury site
Local vasodilation, followed by edema, swelling, & release of inflammatory mediators
Peripheral sensitization of nociceptors
Secondary hyperalgesia
Occurs at uninjured tissue beyond
Increased receptive field of WDR neurons
Central sensitization of WDR
WDR Neuron changes
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
Neuropathic pain definition
Chronic intense perceived pain that arises from mild to no stimulation
Visceral referred pain (development)
Pain sensation is often referred from a visceral structure to a somatic structure that originated from the same embryonic segment (dermatome pattern)
Convergence-projection theory of referred pain
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
Visceral nociceptive pathway
Occurs via nociceptive fibers within autonomic nerve bundles
Pain sensation is referred to the surface often far from the organ of nociceptive origin
Parietal pathway of pain
Nociception is conducted directly to local spinal nerves from parietal peritoneum. pleura, and pericardium
sensations are localized directly over the origin of nociception
Bottom up pain modulation
Transitory pain sensation suppression via non-noxious peripheral sensory stimulation
Effects last as long as non-nociceptive stimulation persists.
gate control theory of pain
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
Top down modulation of pain mechanisms
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
Regions involved in top down modulation of pain
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)
Graded Motor Imagery
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
Mirror therapy
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
Targets of the nociceptive pathway
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
