Week 1 IPS Summary PDF

1.2 the patients voice the impact of pain subjective • considerations: 1. depression 2. anxiety 3. impaired phys ed 4. impaired mental fxn 5. impaired socialization can create burdens both personally and • socioeconomically -course aims to emphasize the challenges of measuring the impact of...

1.2 the patients voice the impact of pain subjective • considerations: 1. depression 2. anxiety 3. impaired phys ed 4. impaired mental fxn 5. impaired socialization can create burdens both personally and • socioeconomically -course aims to emphasize the challenges of measuring the impact of pain the patients voice: impact of pain the impact of pain is very hard to measure 2 commonly used outcome tools: 1. McGill Pain questionnaire 2. the National Initiative on Pain Controls quality of Life Scale. • shortcomings of these assessment tools- +imprecise nature of numeric pain rating scales and interchangeable qualitative adjectives describe an individual's pain. • - impact of pain is best expressed through a pt's own words. 1. loss a. employment b. social and family roles c. ‘self’ d. fxn 2. stigma - being stereotyped usually no consideration for either psychological or social factors of pain in assessment or treatment. ex: pt is looked at like they are difficult or drug seeking • contributes to an undertreatment of pain and indirectly devalues and excludes our patients w/in their society. the pts voice: therapeutic alliance • 1. strong therapeutic alliance may improve pain outcomes agreement on the goals of treatment 2. agreement on tasks 3. :bw provider and pt development of a bond made up of reciprocal positive feelings : collaborative agreement thats built on trust and empathy according to Rando and [UNKNOWN]1981 paper, relationship of power involved in working alliance a verbal exchange that includes high • levels of involvement on part of the pt enhances the Therapeutic Alliance. key for promoting pt involvement: • humor, clear words, active listening and subjective info the pt’s voice: listening “ as practitioners, we need to give pts the time and permission to tell their story” -Neilsen et al, 2009 • john et al.. in 1999, promoted that understanding an illness begins w understanding an illness as it is lived by the pt summary: • pain is multifaceted and complex 1.3 Intro to Pain Science Pain: unpleasant sensory & emotional experience associated w/ actual Pain is subjective & doesn’t or potential tissue damage always mean tissue damage!! highlights biological, psychological & social components of pain • noxious stimulus: stimulus damaging/threatening damage to normal tissue nociception: neural process of encoding a noxious stimulus nociceptive pain: pain arising from actual or threatened damage to tissue bc activation of nociceptors neuropathic pain: pain caused by injury or disruption of the somatic neural system nociplastic: pain from altered nociception w/ no evidence of actual injury causing the activation of peripheral nociceptors or evidence for lesion of somatosensory system causing pain in class definition: this involves more experience/emotions bc not direct soft tissue or neurological pathology 3 primary categories of pain • nociceptive pain • neuropathic pain • nociplastic pain Pain is not nociception • pain is a sensation or perceived experience Nociception • encoding of noxious stimulus by nervous system Nociception Analogy nociception = switch that causes pain • - switched on the electrical impulses can pass - ONLY if threshold reached Pain • protective mechanism • only mechanism we are aware of that protects us • pain is subjective & needed for survival pain is modulated by info internally/externally associated w/ perceived threat/danger • - pain depends on balance of danger & safety - bioplastic system: escape restrictictions of own genome and adapt - danger detection sensors have adjustable sensitivity - danger transmission system has adjustable sensitivity can be why difficult to find pain relief Summary 1. nociception & pain different 2. 3 primary categories of pain 3. pain is a protective mechanism, can be modulated by internal processes of the body as result of both external and internal stimuli 1.4 neuroscience basics grand theories of pain grand theories of pain: its personal biomedical model product of ancient western philosophical thought that looks to understand the biological origin of an illness biopsychosocial model categorizes the potential influences on pain onto those that occur in the biological, psychological and social domains ex: how we think, feel or act (behavior) biomedical model lens • body can be fixed w medicine and surgery (standpoint of treatment) • model looks at health and pain purely as physiological bio-psycho-social domains interaction and intersection of • these 3 domains is where a persons health can be captured grand theories of pain: sensory and emotional “ an unpleasant sensory and emotional experience associated w or resembling, actual or potential tissue damage” what this course considers are the general characteristics of pain. • pain is always felt • pain can only occur in a live animal. • painful stimulus is one that necessarily triggers pain. • we can fear pain and that pain doesnt predicate or is determined by an external injury. the basics interactive dimensions of pain -malzak and casey, 1968 • author propose that there is a dynamic neural relationship bw sensation, motivation and cognition to account for pain related behaviors. • our experience of pain and what we do in response to pain. • our behavior is determined by discriminative info we receive from our sensory system, our emotional responses to pain, as well as cognitive processing by our higher central nervous system. primary categories of pain 1. nociceptive pain : pain that arises from actual or threatened damage to tissue bc of activation of nociceptors 2. neuropathic pain : pain caused by injury or disruption of the somatic neural system 2. nociplastic pain : pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain summary: 1. biomedical and biopsychosocial theories in pain offer 2 different frameworks for the management and treatment of pain. 2. understanding the characteristics of pain is a useful clinical tool that will help the clinician and patient better understand pain. 3. theoretically, the three primary categories of pain vary both in their origin and in their mechanism in causing pain. 1.5 Musculoskeletal Nociception Nociception: neural process of encoding noxious stimulus for transmission to CNS Noxious stimulus: stim strong enough to threaten perceived health of body Nociceptor: high threshold sensory receptor of peripheral somatosensory nervous system to transduce and encode noxious stim EX: receptor in soft tissue that encodes for noxious stim Process of stimulus hitting threshold • receptors (activators): turn on/produce AP & & Modes of nociception (what activates receptor) • mechanical stim • thermal stim • chemical stim - - - • type of stim • magnitude • -- environment of receptor I I Y & I & Transduction? Idk he didn’t describe what this is T stimulus - 7 = tip: when identifying the nociceptor - ↓ 1111111 ↓ receptor ↓ receptor activated creating an AP if magnitude is enough W AP to brain through CNS REMEMBER key points 1. di nociceptors in both somatic/visceral structures pain signal - soft tissue, bone/joints, visceral structures 2. nociception involves both PNS & CNS 3. nociception = input to CNS from PNS ex: moment of high adrenaline - nociception doesn’t produce an experience of pain every time don’t feel pain even tho noxious AP 4. Pain is an OUTPUT of the CNS if certain requirements are met sent to CNS this due to Gate 5. 5 steps of nociception control or central mechanisms nociception inhibition 5 steps of nociception 1. transduction: terminal nerve fibers/receptors depolarized/activated 2. conduction: AP travels across peripheral afferent sensory n, 1st order NS: afferent n. * Peripheral * CNS: reach dorsal horn neuron, synapse of dorsal horn of SC - this is technically part of transmission 3. transmission: AP in dorsal horn -> brain 4. modulation: nervous system inhibits & facilitates nociceptive AP 5. perception: converting nociceptive input to localized unpleasant pain 1 summary TCTMP (sing it to 1. nociception = general process to encode a noxious stimulus remember hehe) 2. nociceptors produce AP in response to stimuli 3. 3 modes of nociception: mechanical, thermal, chemical 4. 5 steps of nociception 1.6 nociception: unpacking transduction 5 steps 1. transduction 2. conduction 3. transmission 4. modulation 5. perception transduction begins when terminal neural fibers are depolarized by a receptor • when a receptor translated an arriving stimulus from outside or inside the body - an action potential • terminal nerve fibers reached depolarized by a receptor - a nociceptor nociceptors • typically high threshold unspecialized sensory receptors, or “free” nerve endings, associated w A-delta and C fibers unpacking transduction: freenerve endings unpacking transduction high threshold high—more stimulus is needed to activate, noxious; threshold of possible tissue injury (B) • magnitude of stimulus is a characteristic of every receptor activated in our body. • depending on the magnitude of stimulus, certain thresholds may be met for either non-noxious or noxious stimulus low—less stimulus is needed to activate, non-noxious; threshold for basic sensory information (A) fxnally, non-noxious and noxious receptors are not mutually exclusive. unpacking transduction: A-delta and C fibers A-alpha- fastest A-beta- faster encode non-noxious information, which includes things like proprioception, touch and pressure. A- delta (type 1 and 2)- fast encode for noxious mechanoreceptors C- slowest -these types of fibers have receptors associated with encode for noxious and non-noxious thermoreceptors thermo, chemo and mechanical receptors - much more diverse, and they can encode for both heat and cold damage to our tissue. A-delta and C fibers : commonly associated with noxious stimuli to cns summary 1. transduction begins when terminal neural fibers are depolarized by a receptor. 2. high threshold receptors are classically recognized as noxious stimulus receptors, while low threshold receptors provide information on basic sensory information. 3. free-nerve endings are characteristic of nociceptors. 4. Aδ and C fibers are thought to be fiber-types that carry noxious stimulus. 1.7 Specialized Sensory Receptors Most tissues: sensory nerve cells that respond to changes in homeostasis translate stimuli into AP -> CNS -> perceived as sensation • 4 Types of Specialized Receptors • meissner corpuscles • pacinian corpuscles • merkel discs • ruffini corpuscles all have specialized organ attached to neural fiber for transmitting info from periphery to CNS Free nerve ending/Nociceptor: no specialized ending Meissner Corpuscles Pacinian Corpuscle • low freq • high freq • skin indentation with movement • depression/deep pressure in soft tissue • discriminative touch • proprioception Merkel Discs • light touch indentation • tactile acuity/info on object characteristics - shape/surface texture Ruffini Corpuscle • low freq • slowly adapting • latent info on mechanical pressure (stretch) Nociceptive modulation: specialized receptors can produce antinociceptive effects • • peripheral stimulus inhibits/decreases noxious AP mainly ruffini - ex: rubbing spot that hurts will help Fxn/Sensitivity of receptor can change based on state of neuron or environment • can lead to mechanical sensitivity: tactile allodynia - ex: following injury, inflammation causes them to become non-noxious stim translated - to noxious stim bc threshold lowered sensitized (threshold lowers) Summary • 4 primary specialized sensory receptors • each receptor activated by a set of specific sensory stimuli • provide sensory info, can drive nociceptive modulation (inhibition/facilitation) 1.8 nociceptor activation nociceptor activation: 3 primary types 1. mechanical nociceptors 2. thermal nociceptors - extreme heat/cold 3. chemical nociceptors - arthritis, inflammation, sun burn in the event that a receptor is activated by one, two, or more types of poly is throwing the stove! stimulus, it is known as polymodal. • nociceptor activation: mechanical and mechano-insensitive nociceptors mechincal nociceptors (mechano-sensitive) • 1. heat 2. cold -commonly thought to be polymodal thermal nociceptors mechano-insensitive nociceptors • - normally dormant nociceptors that become nociceptively competent, ( become sensitive to noxious stimulus following an injury) -believed that this is tied to inflammation and the chemical sensitivity characteristic of this kind of receptor and is associated with a type of sensitization called peripheral sensitization. nociceptor activation: sources 1. skin; superficial somatic refers to soft tissues of the body, while visceral 2. joints: deep somatic 3. Somatic tissue structures refer to organs and blood vessels muscles: deep somatic 4. visceral: visceral 2 different structures in the body that are thought to carry nociceptors: somatic tissue and visceral structures • primary nociceptors is based on those that innervate the skin. muscle tissue: have a greater quantity of receptors that are sensitive to mechanical stimulus. (why we know when an object is sharp nociceptor activation: physiology Ion channels which are proteins found in the cell wall of our sensory receptors convert thermomechanical or chemical energy into an action potential. • many of these ion channels respond to voltage changes at the cell membrane. this can be facilitated by protons, including potassium and hydrogen, as well as others and inflammatory meters, for example, body kinases and prostaglandins. nociceptor: damage releases chemicals from cells surrounding these types of receptors. • as a result of the injury, new substances are made as these chemicals interact with intercellular fluids. these chemicals can then turn on specialized channels located in the cell membrane of nociceptors. if the right type and amount of chemicals are released, these nociceptors will generate an action potential. common substances that activate nociceptors or chemicals like substance P, histamine, nerve growth factors and potassium. after an action potential is generated, it travels to the dorsal root ganglia and eventually the dorsal horn of the spinal cord and synapses on second quarter and interneuron processes through a process called nociceptive conduction. worth noting that substances like substance P are significant factors in chemical sensitization at the level of the nociceptors. • these chemicals can decrease our thresholds of pain -hyperalgesia. this means we experience pain faster and in greater intensity, and cause other physiological changes in tissue local to cellular damage, amounting to vascular dilation, swelling, and redness. summary 1. the three primary type of nociceptors are mechano-, chemo- and thermonociceptors. 2. each type of nociceptor has a primary stimulus that best activates it. 3. nociceptors are found in both somatic and visceral tissue. 4. ion channels found in our sensory receptors convert thermal, mechanical or chemical energy into an action potential. In class notes neuropathic- type of pain neuroplastic- how pain changes over time becomes more sensitive bc NS changes practice matching the definition! Noxious stimulus & Nociceptor relationship • nociceptor creates AP after stimulation of noxious stimulus • doesn’t always produce pain!! why? experience detection Nociception & Pain • nociception encodes noxious stim vs pain is an experience that MAY be caused by nociception pain = produced by brain Answer doc • activity identify type of pain • neuropathic • nociceptive • nociplastic • nociception or neuropathic depending on how deep • neuropathic • nociplastic Synchronous Session One Faculty Name PT, PhD Jeffrey Foucrier PT, DPT Orthopedic Clinical Specialist Synch Session Expectations Present – Engaged – Inclusive Announcement The Graduate Degree Programs is seeking a notetaker this semester for this course, specifically for the on-site clinical skills lab. The notetaker will be paid $150 at the end of the semester after notes for each day of the on-site clinical skills lab have been submitted to the Office of Student Affairs. One key requirement will be submitting notes in a timely manner, generally 24 hours after the class takes place. If interested, please reach out to the me at [email protected] for more information. As a part of this, please include a sample of your notes from the first week of class. Week One Anatomy of Pain Science – Part One 1. Introduction to Pain Science: 1. Common Terms / Categories associated with Pain 2. Characteristics of Pain 2. Grand Theories of Pain 3. Modes of Pain 4. 5 Steps of Nociception (Information Processing) 5. Nociceptive and Non-Nociceptive Receptors 6. Nociceptor Activation (Transduction) Activity: Matching 1. Nociceptive Pain 2. Noxious Stimulus a) b) 3. A stimulus that is damaging or threatens damage to normal tissues. Neural process of encoding noxious stimulus. Nociplastic Pain c) 4. Nociception 5. Neuropathic Pain d) e) Pain that arises from actual or threatened damage to tissue because of activation of nociceptors. Pain caused by injury or disruption of the somatic neural system. Pain that arises from altered nociception despite no clear evidence of actual or threatened tissue damage causing the activation of peripheral nociceptors or evidence for disease or lesion of the somatosensory system causing the pain. Activity: Waterfall – Describe relationships Noxious Stimulus and Nociceptor • <Enter Text> Nociception and Pain • <Enter Text> nociceptor receive and create • action potentials after bring nociception encodes noxious stimulus • pain is an experience that MAY be caused by nociception stimulated by noxious stimulus pain is a product (conclusion) or experience, NOT data Activity: Practical Application – Name the Type of Pain • Pain originating from shingles Nociception • Nociplastic Neuropathic Nociplastic Pain originating from a muscle strain Nociception • Neuropathic Pain not mediated by nociception or neuropathic processes Nociception Neuropathic Nociplastic Activity: Practical Application – Name the Type of Pain • Pain originating from a deep muscle laceration Nociception • Nociplastic Neuropathic Nociplastic Pain arising from diabetic neuropathy Nociception • Neuropathic pathology of NS Pain described as originating from factors such as sleep, mood, and memory Nociception Neuropathic Nociplastic Activity: Waterfall – Characteristics of Pain • <Enter Text Here> What does it all mean? protective, anxiety, subjective, awareness, bio, emotional, neurological, acute, chronic, physical, always felt, dull, an experience, physical-dull-achy-sharp, multifactorial, • Point One: normal experience • Point Two: protection • Point Three: biophysosocial, constant, radiating, threat to self, normal, somatic vs visceral, needed for survival, ext and int stim, makes us human, describes as a story, phantom pain, threshold vs tolerance variable- controlled by both external and internal variables Activity: Roleplay – Explain the Following Concepts to Dr. Stern… Case One: Biopsychosocial Model 3 components makes up our behavior Case Two: Biomedical Model more of a bio or psychological • dismisses the pt • fix it w meds or surgery only Activity: Discussion – Nerve Types ache after injury mechanoreceptors 1. more chemical response in soft tissue trauma What are the differences between Aδ and C fibers? 1. Structure 2. Speed 3. Function A delta- larger, C- smaller in diameter more myelinated feel pain/danger/noxious stimulus faster than others • A delta = faster, impulses transferred faster A delta theeen C fibers a delta and c fibers can be free nerve endings 2. What are the modes of nociception? 1. How are these different than types of pain? mechanical, chemical, thermal —the kind of data we are receiving modes how stimulates body, if there is threshold then pain types of pain felt: soft tissue, nervous system. neither (nociplastic?) burning - neuropathic msk - nociceptive neither - nociplastic Activity: Discussion – Non-Nociceptive Receptors Clinical Application What is the relationship between non-nociceptive receptors and nociception? kinda lost me here SAME we need to the differences and what they encode for Image modified from Moseley and Butler’s Explain Pain Supercharged Activity: Break Out Rooms - Nociceptors 1. Explain the roles of the following receptors? 1. Mechanical nociceptors 2. Thermal nociceptors 3. Chemical nociceptors 4. Polymodal Nociceptors 5. Mechano-Insensitive pain after the injury, like getting a cut then area around that cut hurts, increases sensitivity to trauma (form of sensitization) 2. In what types of tissues will you find these receptors? 3. From lecture, name one tissue that DOES NOT have these receptors? 4. Distinguish between types and pain, as well as sources and modes of nociception. Vascular tissue - has some but way less neural tissue- why you can do open brain surgery Week 1: Check-Point Take-Aways review!! Key Points: • Difference between nociceptors and non-nociceptors • Specialized receptors • Characteristics of pain • Read assigned articles Meeples [email protected] [email protected] Note: We may not have had time to cover all activities. Please go through these on your own time to help you study for our assessments and Check-Points. © All rights reserved.