PT 506 Exam 1 | Verified with 100% Correct Answers

PT 506 Exam 1 | Verified with 100% Correct Answers What population is less likely to receive analgesic pain medication, regardless of SES? African Americans Who gets prescribed opioids more easily? patients with higher SES Who is more likely to be uninsured or underinsured? Impoverished individuals, minorities 2011 IOM Report's goal Outline a plan addressing need for cultural transformation to prevent, assess, understand and treat pain of all types Significant barriers to adequate pain care includes individual and systems level What is the leading reason to seek medical care? Acute pain What is the significance of pain? Interrupts your day-to-day activities Quite alarming Makes you want to change your behavior Pain=reaction to noxious elements Early 20th century: pain Specific pain fibers, pathways, and a pain center in the brain 1950's pain pain is related to extent of tissue damage/injury 1960's pain changed to research related to pain and theories: gate control theory (wall and melzack) 1990's- present pain pain neuromatrix proposed by melzack Intensity theory Plato (c. 428 to 347 B.C.): pain is defined not as a unique experience, but as an "emotion" that occurs when a stimulus is intense and lasting Cartesian dualistic theory Descartes (): pain could be the result of physical injury or psychological injury, but the two did not influence each other Specificity theory Early theory that proposed that injury activates specific pain receptors and fibers that project pain along special pain pathways to pain center (eg: heat pain goes to heat pain pathway) Pattern theory Early theory that proposed pain would result from patterned input from sense organs in the skin Gate control theory (melzack) The spinal cord has a “gate” mechanism that can modulate pain signals before they reach the brain. Small nerve fibers (A-delta, C fibers) carry pain signals → their activity tends to open the gate → more pain gets through. Large nerve fibers (A-beta fibers) carry non-painful input like touch, pressure, vibration → their activity tends to close the gate → less pain gets through. The brain can also influence the gate → descending signals can either open it (increasing pain, e.g., stress, fear) or close it (decreasing pain, e.g., distraction, relaxation). Club analogy for gate theory. Think of the spinal cord gate like the bouncer at a nightclub. Pain signals (small fibers: A-delta & C fibers) are like rowdy people trying to push into the club. If lots of them show up → the bouncer lets them in → the gate opens → you feel more pain. Touch/pressure signals (large fibers: A-beta fibers) are like calm VIPs who help keep order. When they show up, the bouncer listens to them → the gate closes → fewer rowdy people get in → pain decreases. The brain is like the club manager calling the bouncer. If the manager says “let them in” (stress, anxiety, focus on pain) → the gate opens more. If the manager says “keep them out” (distraction, relaxation, positive mood) → the gate closes more. The big takeaway: pain isn’t just about how many “rowdy guests” (pain signals) show up — it’s about how the bouncer (spinal gate) and the manager (brain) decide who gets through. What could the gate control theory not account for? Phantom limb pain, chronic pain, pain variability between similar pain presentations Melzack and Pain Neuromatrix The most notable theory of pain: Neuromatrix = a large, widespread network of neurons that consists of loops between the thalamus and cortex as well as between the cortex and limbic system How many components of the neuromatrix theory 4 Body-self neuromatrix Cyclical The Brain Activation of an action neuromatrix Body-self neuromatrix component of the neuromatrix neural network in the brain containing somatosensory, limbic, and thalamocortical components; integrates multiple sources of input resulting in the cognitive, affective, and sensory perceptions of pain Cyclical component of the neuromatrix processing and synthesis of stimuli which produces a neurosignature The brain component of the neuromatrix sentient neural hub: converts neurosignatures into awareness Activation of action neuromatrix provides: awareness of the output overt action pattrn of morements to achieve desired goals achieve homeostasis in face of stress Analogy for Neuromatrix: Neuromatrix = the whole nightclub operation (the staff, the crowd, the manager, and the vibe of the place). Four Components: Cyclical processing and synthesis → “Club Atmosphere” The club constantly takes in cues (music, lighting, crowd behavior) and creates a unique vibe (neurosignature) each night. Similarly, the brain constantly processes sensory, emotional, and cognitive inputs and produces a neurosignature (your personal “pain fingerprint”). The brain converts neurosignatures into awareness → “Club Experience” Guests don’t just hear music separately or see lights separately — they experience the whole atmosphere of the club. Likewise, the brain integrates the neurosignature and turns it into a conscious experience of pain (or not pain). Action neuromatrix → “What the club does”The club responds to its vibe in 3 ways: Awareness of output → The club knows if the vibe is good or bad (brain recognizes pain is present). Overt action patterns → If the crowd gets rowdy, security steps in; if chill, people dance. (You limp, guard an injury, or move differently.) Homeostasis under stress → The club adjusts (lowers the music, adds security, opens a new bar). (The body tries to restore balance under stress via hormones, endorphins, etc.) Inputs → “What shapes the club vibe” Cognitive-evaluative: The club’s reputation and past events (your memories, expectations, personality, culture). Sensory-discriminative: Tonight’s live details — music, crowd size, lighting (sensory input from nerves, vision, balance, internal organs). Motivational-affective: The mood of the staff & manager (stress hormones, immune system, emotions, limbic system). Definition of pain (IASP) An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage. Definition of chronic pain (IASP) Pain that lasts or recurs for longer than 3 months Six key notes associated with the definition - Pain is always a personal experience that is influenced to varying degrees by biological, psychological, and social factors. - Pain and nociception are different phenomena. Pain cannot be inferred solely from activity of sensors. -Through their life experiences, individuals learn the concept of pain. - A person's report of an experience as pain should be respected. - Although pain usually serves an adaptive role, it may have adverse effects on function and social and psychological well-being. - Verbal description is only one of many behaviors to express pain; inability to communicate does not neglect the possibility that a human and nonhuman animal experiences pain. What activates nociceptive afferent fibers? Noxious stimuli Hyperalgesia Increased pain from a stimulus that usually causes pain Allodynia Pain due to a stimulus that does not normally provoke pain Dysesthesia Unpleasant abnormal sensation (usually pain) spontaneous or provoked Paresthesia abnormal sensation of numbness and tingling without objective cause Glutamate A major excitatory neurotransmitter; involved in memory. Interacts with NMDA and AMPA receptors Lamina I aka Marginal layaer Contains A delta and C fibers Project to the thalamus responds to intense cold and a variety of noxious stimuli (some innocuous stimuli as well) Lamina II Also known as substantia gelatinosa Contains A delta and C fibers Project to the brain stem and thalamus Selective response to noxious stimuli Lamina III and IV Contains A Beta fibers Project to the brain stem and thalamus respond to light touch Lamina V Contains A beta, A delta fibers, and C fibers from somatic and visceral tissues Projects to the brain stem and thalamus Responds to a wide variety of noxious stimuli Lamina VI Contains large-diameter fibers from muscles and joints Projects to the brain-stem and thalamus Respond to non-harmful joint movement Why is it significant that one CNS neuron connects to ~1000 other neurons? It allows amplification, integration, and plasticity of signals — meaning one pain input can spread widely, be shaped by emotion/memory, and adapt over time (basis for pain modulation and central sensitization) Ion channels can be dormant, on but inactive, or active (same thing with synapses). How might this, along with extensive neuron innervation, impact synaptic transmission? Plasticity → Dormant channels/synapses can be recruited with repeated use or injury (basis for learning or chronic pain). Modulation → Inactive-but-primed states allow quick up- or down-regulation (e.g., “gating” pain). Amplification or dampening → Extensive connectivity means small local changes (like opening a few Na⁺ channels) can either spread widely or be suppressed depending on what’s active. Variability → Explains why the same stimulus doesn’t always feel the same (context, emotion, prior experience can shift which channels/synapses are on). Role of axo-axonic synapses & presynaptic inhibition in pain? Inhibitory axon terminals modulate nociceptor terminals → ↓ Ca²⁺ entry → ↓ neurotransmitter release → dampened pain signal (basis of gate control). How do axo-axonic synapses fit into Gate Control (SG & T-cells)? Peripheral nociceptors (Aδ and C fibers) synapse onto T-cells. Normally, they release glutamate, substance P, CGRP → excite the T-cell → pain signal ascends. Aβ touch fibers (large diameter) activate SG interneurons. These SG interneurons form axo-axonic synapses on the nociceptor terminals. They release inhibitory transmitters (GABA, glycine, enkephalins). This causes presynaptic inhibition: ↓ Ca²⁺ influx in nociceptor terminal → ↓ excitatory transmitter release. Result: T-cell is less excited → pain transmission is reduced = “closing the gate.” Descending central control can further modulate SG cells. Brain can tell the SG to ramp up inhibition (e.g., in stress-induced analgesia) or reduce it (e.g., anxiety, attention to pain). Simplified Flow (Gate Control in Terms of Synapses) Small fibers (C, Aδ) → excite T-cells → open gate → pain. Large fibers (Aβ) → activate SG → inhibit nociceptor terminals (axo-axonic presynaptic inhibition) → close gate → less pain. Brain input (central control) → can reinforce SG inhibition or weaken it, depending on context. What does DCML (Dorsal Column Medial Lemniscus System) pathway deal with? Fine touch/proprioception Synapse on dorsal horn of interneuron, goes up What does the ALS (anterolateral system) system deal with? Pain/temperature (nociception) Synapses on dorsal horn of interneuron and crosses over DCML pathway from bottom to top Lumbar dorsal colum medial lemniscus -- Cervical dorsal colum medial lemniscus -- Dorsal column nuclei--medial lemiscus--thalamus--somatosensory cortex ALS pathway Anterolateral funiculus -- Medullar RF -- Medullary RF--pontine RF--periaqueductal grey matter--thalamus--somatosensory cortex Spinothalamic tract Origin: Lamina I & V neurons (nociceptive-specific, thermosensitive, wide dynamic range) (located in the spine) Destination: Thalamus → then to somatosensory cortex. Function: The classic pain pathway → carries info about location, intensity, and quality of pain (“sharp/dull, hot/cold”). spinoreticular tract Origin: Lamina VII & VIII (polysynaptic pathway, goes through interneurons in the dorsal horn). Destination: Reticular formation (RF) and thalamus. Function: Controls arousal, alertness, and modulation of pain. Explains why pain can keep you awake or make you hyper-alert. spinomesenphalic tract Origin: Lamina I, IV, V. Destination: Midbrain → mesencephalic RF, periaqueductal gray (PAG), amygdala (via parabrachial nucleus). Function: Involved in the emotional/affective dimension of pain (“this hurts and it makes me anxious or fearful”). Also key for descending pain modulation via PAG. spinohypothalamic tract Origin: Lamina I, V, VIII. Destination: Hypothalamus. Function: Links pain to autonomic & endocrine responses (↑HR, ↑BP, sweating, stress hormone release). Cervicothalamic Tract Less emphasized, but: Origin: Upper cervical spinal cord neurons. Destination: Thalamus. Function: Provides an alternative pathway for nociceptive information from the neck/upper body to reach higher centers. How are nociceptive stimuli transmitted to the brain, and where do they ultimately terminate? Nociceptive stimuli travel simultaneously along multiple ascending tracts (e.g., spinothalamic, spinoreticular, spinomesencephalic, spinohypothalamic, cervicothalamic). Depending on the tract, signals synapse in the brainstem, thalamus, or both. All sensory information ultimately terminates in the primary sensory cortex (S1) for perception of pain. What happens at the synapse during nociception? 1. Presynaptic nociceptor releases neurotransmitters (glutamate, Substance P, CGRP). 2. These bind to postsynaptic receptors in the dorsal horn (lamina I/II). 3. Causes ion channel opening → depolarization of the postsynaptic neuron. 4. If threshold is reached, an action potential is generated. 5. The signal is then sent along ascending tracts (e.g., spinothalamic) to the brain for pain perception. What does it mean that nociceptors send an “afferent barrage” that is necessary but not sufficient for pain? Nociceptors send action potentials to the dorsal horn, but pain depends on second-order neuron sensitivity. The number of active receptors/ion channels (few = little effect, many = strong excitation) determines whether pain is actually perceived. What are AMPA receptors and their role in pain? AMPA receptors are located on the post-synaptic cleft 1. When a peripheral nociceptor is activated by a noxious stimulus, it releases glutamate (excitatory) at its synapse in the dorsal horn. 2. Glutamate binds to AMPA receptors on second-order neurons (T cells in Lamina I/II) 3. This causes Na+ influx -- depolarization -- can generate an action potential if the threshold is reached, sending a signal to the brain How do AMPA receptors work with central sensitization? After injury or inflammation, more AMPA receptors may be inserted into the membrane or exsisting ones may become more responsive. This makes the second-order neurons more excitable, contributing to hyperalgesia (more pain from the same stimulus) or allodynia (pain from normally non-painful stimuli) NMDA receptor a specialized glutamate receptor that is activated with postsynaptic depolarization (due to sodium influx from AMPA receptors) - controls a calcium channel that is normally blocked by Mg2+ ions -Mg2+ ion moves and opens the channel when depolarized - This causes an influx of Ca2+ (due to the release of substance P) and more Na+ to allow for further depolarization in the post-synaptic terminal involved in long-term potentiation Substance P binds to ______ and causes _____ Substance P is released from the central terminal of the afferent nociceptive fiber, and it binds to Neurokinin receptors (NK-1 G protein-coupled receptors). Activation of NK-1 receptors causes a cascade of chemical reactions that release intracellular stores of Ca++, as well as inhibiting the effects of GABA, glycine and endorphin receptors (inhibitors) Sodium channels now stay open longer! How is excitability of the neuron enhanced?