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95 Cards in this Set
- Front
- Back
T/F sensation of pain arises from excessive stimulation of same receptors generating other sensations
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False. nociception depends on specifically dedicated receptors and pathways
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Where do nociceptor cell bodies lie?
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Dorsal root ganglion (BODY) or trigeminal ganglion (HEAD)
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How do peripheral nociceptors terminate?
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Free nerve endings
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nociceptor axons are relatively (fast, slow)
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SLOW. usually they're unmyelinated
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What groups of axons do nociceptors fall into?
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Aδ (myelinated) or C fibers (unmyelinated)
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major ascending pathway for info about pain and temp
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spinothalamic tract
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another name for spinothalamic tract
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anterolateral (in contrast to mechnosensory pathway being the dorsal column-medial lemniscus system)
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what is dissociated sensory loss?
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A spinal cord lesion will result in diminished pain/temp sensation contralaterally, and diminished mechanosensory info ipsilaterally.
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Lissauer’s Tract
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Where the neurons from dorsal horn of spinal ascend several levels and spread out.
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absence of Lissauer’s tract is associated with
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Congenital lack of pain sensation in humans
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Where does the 2nd order neuron of pain pathway cross?
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Ventral white commissure of spinal cord
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After crossing the ventral white commissure, the axons ______
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axon ascends in the lateral funiculus or white matter
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Where are the cells of origin of the lateral spinothalamic tract?
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cells of origin of this tract are located in the contralateral dorsal horn of the spinal cord.
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Where does the 2ndary neuron synapse?
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VPL of thalamus
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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.
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2
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lesion at T2 in the lateral funiculus of the spinal cord will show what?
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T4 (and below) since that is where the axons originally entered the spinal cord.
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T/F It is Called the Lateral Spinothalamic Tract AFTER crossing in the spinal cord.
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T
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Where are the cell bodies of origin of lateral spinothalamic tract? (not first order cell bodies)
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Contralateral Dorsal Horn of the Spinal Cord
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Where does it project or terminate? Means where do those axons SYNAPSE?
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Ipsilateral VPL of thalamus.
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Head area is represented more (medial, lateral) in thalamus but (medial, lateral) in cortex.
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medial (VPM); lateral
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How does the affective/motivational component of pain arise?
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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.
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Pattern of dissociated sensory loss (contralteral pain & temp with ipsilateral touch) is a signature of _______
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spinal cord lesions
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What is the <b>dorsal column </b> pain pathway?
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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 |
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Drugs that block nociceptive synaptic transmission into the intermediate gray of the sacral spinal cord blocks what?
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the responses of neurons in the nucleus gracilius to noxious visceral stimuli
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What is midline myelotomy ?
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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.
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What does the Spinal Trigeminal Nucleus do?
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extends from the pons to C3 of the spinal cord and carries pain, temperature and some touch.
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Where do the afferents to the spinal trigeminal nucleus come from?
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All three branches of Trigeminal N.
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When neurons reach the Spinal Trigeminal Nucleus, what order are they?
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Second order, because there has already been one synapse in the trigeminal ganglion.
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From where does the Spinal Trigeminal Nucleus extend (what levels)?
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Pons to C3
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What is the spinal trigeminal tract?
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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.
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What other nerves (other than V) are associated with the spinal tract and spinal nucleus?
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CN VII (facial); CN IX (glossopharyngeal); and CN X (vagus) which makes sense because they all innervate some skin on the head region
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Where are the cell bodies of origin of the spinal trigeminal tract?
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Ipsilateral Cranial Nerve Ganglia of V, VII, IX, and X
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Where does the spinal trigeminal tract end/terminate?
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Ipsilateral Spinal Trigeminal Nucleus
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Where are the cell bodies of origin of the Ventral Trigeminothalamic Tract?
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Contralateral Trigeminal Nucleus
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Where does the Ventral Trigeminothalamic Tract end/terminate?
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VPM of thalamus
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What is Syringomyelia?
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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. |
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What are symptoms of Syringomyelia?
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Bilateral loss of pain and temperature at the level of the lesion (segments involved).
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Wallenburg / Lateral Medullary Syndrome
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lesion of the dorsolateral medulla (occlusion of posterior inferior cerebellar artery)
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Symptoms of Wallenburg/Lateral Medullary Syndrome?
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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 |
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Damage to what can cause Wallenburg syndrome?
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Posterior inferior cerebellar artery
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NOCICEPTION
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response to noxious stimuli and tissue damage (burn, cut, pin prick, crush).
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T/F/ stimulation of nociceptors does always results in the sensation of pain.
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F. Pain is the psychological construct; nociception is the physical
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What fiber type are Mechanosensitive nociceptors?
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Aδ
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What are Mechanosensitive nociceptors stimulated by?
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Squeezing, pressure.
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What are Mechanothermal nociceptors stimulated by?
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Excessive heat or cold
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What fiber type are Mechanothermal nociceptors?
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Aδ / Group III
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What are Polymodal nociceptors stimulated by?
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Wide range of thermal, mechanical, or chemical stimuli. Thought be an evolutionarily older system.
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What fiber type are polymodal nociceptors?
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C (slowest) / Group IV
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Why are the receptive fields of all pain-sensitive neurons relatively large, especially in thalamus and cortex?
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Presumably because the detection of pain is more important than its precise localization
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T/F nociceptive axons begin to discharge only when the strength of the stimulas reaches high levels
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T. This is in contrast to other receptors (eg., regular thermal receptors that do not fire any harder at extremely high levels)
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T/F Nociception requires special neurons, not simply greater discharge of neurons that respond to normal stimulus intensities
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T
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What are the two categories of pain perception?
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First pain (Aδ) and second pain (C)
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EPICRITIC vs PROTOPATHIC pain
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Epicritic - first pain
Protopathic - second pain |
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Causes first pain
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Aδ fibers / Group III
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Causes second pain
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C fibers / Group IV
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Description of first pain
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Sharp, well-localized, acute, rapid onset
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Description of second pain
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Duller, more diffuse, takes longer to happen, described as throbbing and burning. Occurs in chronic pain
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What are the layers of Lissauer's tract relating to pain?
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Layer I, II, and V
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What does Layer I (Nociceptor specific (NS) receive input from?
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Both A and C fibers
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What does Layer II (Substantia Gelatinosa (SG)) receive input from? What is in it?
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Mostly C fibers. but some Aδ 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 |
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What does Layer V (Wide Dynamic Range (WDR)) receive input from? What is in it?
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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
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Which layer are the following found in?
A) WDR B) NS C) Inhibitory interneurons |
A) Layer V
B) I C) II (Substantia gelatinosa) |
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painful stimulus causes firing of this cell. C fiber activity synapses onto it.
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Layer I - NS neurons
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This layer can modulate or stop painful activity. Anything that stimulates this slows down pain.
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Layer II - Substantia Gelatinosa layer - inhibitory interneurons
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These neurons interpret higher frequency/more stimulation as pain. At low frequencies they give sensation of course touch.
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Layer V - WDR
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What is the vanilloid receptor? (VR-1 or TRPV1)
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A specific receptor associated with nociceptive afferent endings. Found in both C and Aδ fibers and is activated by moderate heat.(~45C)
ALSO activated by capsaicin |
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What is the vanilloid-like receptor? (VRL-1 or TRPV2)
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Receptor with a higher threshold response to heat, NOT sensitive to capsaicin, and is found in Aδ fibers.
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Which receptor - TRPV1 (vanilloid) or TRPV2 (vanilloid-like) is
A) sensitive to capsaicin B) Found in Aδ fibers ONLY C) Found in both C and Aδ fibers |
A) TRPV1 / VR-1
B) TRPV2 / VRL - 1 C) TRPV1 |
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Which receptor- TRPV1 (vanilloid) or TRPV2 (vanilloid-like) is activated by a HIGHER temperature (>50C as opposed to ~45C)
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Vanilloid-like receptor
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What are the TRP channels?
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Transient-receptor potential channels. Known to comprise a large number of receptors sensitive to different ranges of heat and cold.
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Why did the nervous system evolve receptors that are sensitive to chili peppers (capsaicin?)
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They detect endogenous substances whose chemical structure resembles that of capsaicin.
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Other Modalities (other than pain) Mediated by the Anterolateral System
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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) |
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Itch is usually associated with ______ activating the free nerve endings.
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histamine
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What do cold and warm fibers respond best to?
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CHANGES in temperature - not absolute values.
For example, COLD FIBERS - respond best to decreasing skin temperatures (approx. 20 - 40 degrees C ) |
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What is difference in responding between cold fibers, warm fibers, and nociceptive fibers?
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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. |
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What is referred pain?
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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. |
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What is hyperalgesia?
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Following an injury, sensations that would normally be described as minor pain are described as more intense pain
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What causes hyperalgesia peripherally (at site of injury)?
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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.
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T/F Substances released by damaged tissue AND nociceptors contribute to inflammatory response
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T
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What is Substance P's and CGPR (calcitonin gene-related product)'s role in inflammatory response?
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Causes vasodilation, swelling, and histamine release from mast cells
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Damaged cells release cyclooxygenase (COX), which accelerates the synthesis of what?
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prostaglandins
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__________ sensitize the nerve fibers causing increased pain.
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Prostoglandins
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What are the central hyperalgesia/sensitization mechanisms?
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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. |
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Allodynia : defn
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Induction of pain by what is normally an innocuous stimulus. Typically occurs immediately after the painful event, can outlast stimulus by several hours.
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Windup : defn
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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”) |
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Neuropathic pain: defn
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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. |
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A sensation of pain from a body part that is not present (e.g. amputated limbs)
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Phantom pain
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What does stimulation of the <b>periaqueductal gray matter </b> induce?
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Analgesia; also inhibits activity of nociceptive projection neurons in dorsal horn
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T/F Descending projections have an overall inhibitory influence on nociceptive projection neurons in the dorsal horn (reduce pain).
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T. Release various NTs that modulate activity in the spinal cord projection neurons. A release of these sbustances is generally inhibitory.
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What is the Gate Theory of pain?
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Activation of mechanoreceptors (non-nociceptors) modulates the transmission of nociception to higher centers.
This happens because Aβ 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 |
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How do C fibers play in the Gate Theory of pain?
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C fibers INHIBIT the inhibitory interneurons (resulting in sensation of pain) while Aβ fibers ACTIVATE them, resulting in decreased sensation
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What's the significance of Endogenous Opioids?
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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. |
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enkephalins, endorphins, and dynorphins
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endogenous opioids
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_________ are found in synaptic terminals of local circuit neurons in the dorsal horn.
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Enkephalins
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What does Release of enkephalins into the prepsynaptic terminals of nociceptor fibers do?
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inhibits the activation of the pain projection neurons.
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