Pain Lecture Spring 2025 PDF

Pain Theory and Mechanisms PT 8313 – Spring 2025 Emily Blum, PT, DPT, OCS Contributions by: Ann Nicholson PT, DPT, and Joe Signorino, PT, DPT Objectives Verbalize the importance of pain in the context of therapeutic modalities Recall to the foundation of pain sci...

Pain Theory and Mechanisms PT 8313 – Spring 2025 Emily Blum, PT, DPT, OCS Contributions by: Ann Nicholson PT, DPT, and Joe Signorino, PT, DPT Objectives Verbalize the importance of pain in the context of therapeutic modalities Recall to the foundation of pain sciences Differentiate various types of pain Verbally explain the mechanisms for pain perception Describe the therapeutic implications of physical agents What IS pain? What does pain mean to you? Who is in more pain? Who is in more pain? How about now? What if an injury occurs in this situation? What if an injury occurs in this situation? So, What IS pain? COMPLEX interaction of both physical and psychological processes “…an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” – International Association for the Study of Pain, IASP Pain can be experienced without the presence of tissue damage Subjective and an individualized experience What WAS Pain? Pain was “sent to the brain” One direction of pain signals (peripheral to central) Tissue damage = harm Modern Pain Experience Nail Through the Boot Guy Quiz Question 1 Can pain be experienced WITHOUT the presence of tissue damage? A. Yes B. No C. What. Pain Science The Pain Neuromatrix The Pain and Movement Theory Reasoning Model The Pain Neuromatrix Theory In human beings, a “pain matrix” has evolved that enables interplay between bottom-up processing of tissue pain sensations as danger signals and top-down regulation of the nociceptive information by the brain. This interplay produces the brain’s summary “opinion” as to its safety. The neuromatrix proposes that the output patterns of the body-self neuromatrix activates perceptual, homeostatic and behavioral programs after injury, pathology or chronic stress. Pain, then is produced by the output of a widely distributed neural network in the brain rather than directly by sensory input evoked by injury, inflammation or other pathology. The Pain Neuromat rix Theory The Pain and Movement Reasoning Model Man Ther 2014 Jun;19(3):270-6.doi:10.1016/j.math.2014.01.010. Epub 2014 Feb 7 The Pain and Movement Reasoning Model “…pain is accepted as an OUTPUT subsequent to complex interactions of homeostatic systems.” Physical therapists need to understand complexities of pain to create effective management strategies Pain is NOT unidimensional – like once believed Physiological, cognitive, emotion and social input all have an influence on pain Three types of pain: Local/Nociceptive Neuropathic/Regional Influences Central/Central Modulation Pain in Physical Therapy #1 reason why individuals seek out PT – but not the only reason Often contributes to objective impairments Leads to functional limitations Associated with participation restrictions (think ICF) Documenting Pain BODY CHART NPRS or VAS Pain Pressure Threshold  ▪ Numerous physical agents produce analgesic effect ▪ Analgesia = acting to relieve pain Pain and Therapeut ▪In order to address pain – you and the patient must understand it! ic Modalities ▪Various physical agents have different physiologic effects, some better suited for different pain conditions  1. Maximize healing associated with the underlying pathology that is contributing to the pain experience Treatment (if applicable) Goals for 2. Modify patients’ pain perception Pain - Recognize this may NOT only be physical but cognitive 3. Maximize function Pain Receptors: Nociceptors Free nerve endings Bead-like appearance Present in almost all types of tissue Activated by chemical, pressure/mechanical, temperature, light touch, noxious stimuli When activated, release substance P, prostaglandins and leukotrienes https://i.pinimg.com/originals/1e/80/ba/1e80ba0050fa040237aa0a1f53d42ce4.jpg Types of Nociceptors: Afferent Nerve Fibers C fibers A-delta fibers Most sensitive to high-intensity Account for ~80% of pain-transmitting mechanical stimulation or fibers thermal Small, unmyelinated, transmits slowly – 1.0 to 4.0 m/sec2 Small-diameter, myelinated, transmits more rapidly – 30 Pain typically described as dull, m/sec throbbing, aching, burning, tingling, tapping Pain typically described as sharp, stabbing, pricking Slow-onset, long-lasting Quick-onset, short-lasting Difficult to localize Afferent Nerve Fibers: First Order Neurons Pain Classifications Based on: 1. Time (acute vs persistent) 2. Mechanisms: Local/Nociceptive Neuropathic/Regional Central sensitization Acute Pain Often able to identify specific onset or associated event Mediated through rapidly conducting pathways and linked to increased CNS activity Muscle tone HR BP Skin conductance Hormonal changes Generally well-localized and identified mechanism of injury/onset Acute Pain Can resolve once tissue healing occurs or the threat of damage passes (Pain not perceived when trying to survive) Can be accompanied by cardinal signs of inflammation Warmth, redness, swelling Often responds well to tissue-specific rehab I.E ankle sprain, small burn, etc. Persistent (Chronic) Pain May result from acute injury or insidious onset Often associated with no acute tissue damage Think neck pain that gradually worsens over weeks while studying Typically, > 3-6 months of symptom duration ~1/3 of population thought to have persistent pain https://www.youtube.com/watch?v=ikUzvSph7Z4&t=72 s Persistent Pain Often meets the following criteria: Enduring or recurrent pain Pain persisting longer than is typical for an associated condition, or associated with an intermittent or chronic disease process Pain that has responded inadequately to appropriate and/or invasive care Pain associated with significant impairment of functional status Persistent Pain -Cyclical Quiz Question 2 How is persistent pain defined? A. Can resolve once tissue healing occurs or the threat of damage passes B. Can be accompanied by cardinal signs of inflammation C. Pain persisting longer than is typical for an associated condition D. Typically less than 3-6 months of symptom duration Types of Pain Nociceptive/Local: pain related to activation of peripheral receptive terminals of primary afferent neurons in response to mechanical/pressure, pain/noxious, chemical or thermal stimuli Neuropathic/Regional: pain arising from a primary lesion or dysfunction in the peripheral nervous system Central (sensitization): pain arising from a dominance of neurophysiological dysfunction within the CNS  2012, 5 items in a diagnostic cluster JMMT Pain localized to the area of injury/dysfunction Clear, proportionate mechanical/anatomical nature to aggravating and easing factors Usually intermittent and sharp with movement/mechanical provocation May be a more constant dull ache or throb at rest Absence of: Pain associated with other dysesthesias (or abnormal sensation) Night pain/disturbed sleep Antalgic postures/movement patterns Pain variously described as burning, shooting, sharp or electric- shock-like Presence of the cluster has high levels of classification accuracy: Sensitivity: 90.9 (95% CI: 86.6-94.1) Specificity: 91.0 (95% CI: 86.1-94.6)  3 items in the diagnostic cluster 2012, JMMT Pain referred in a dermatomal or cutaneous distribution History of nerve injury, pathology, or mechanical compromise Pain/symptom provocation with mechanical/ movement tests (active/passive, neurodynamic) that move/load/compress neural tissue Presence of the cluster has high levels of classification accuracy: Sensitivity: 86.3 (95% CI: 78.0-92.3) Specificity: 96.0 (95% CI: 93.4-97.8)  2012, 4 items in a diagnostic cluster JMMT Disproportionate, non-mechanical, unpredictable pattern of pain in response to multiple/non-specific aggravating/easing factors Pain disproportionate to the nature and extent of injury or pathology Strong association with maladaptive factors (ie negative emotions, poor self-efficacy, etc) Diffuse/non-anatomic areas of tenderness on palpation Presence of the cluster has high levels of classification accuracy: Sensitivity: 91.8 (95% CI: 84.5-96.4) Specificity: 97.7 (95% CI: 95.6-99.0) Sensitization (the Basics) Lowering of the nociceptive firing threshold Which means nociceptive messaging is activated EARLIER than under normal conditions Increased magnitude of response to stimuli - categorized generally as peripheral vs. central https://img.medscapestatic.com/article/754/961/754961-fig2.jpg /Threshold Central Hyperexcitable pathways - increased Sensitization sensitivity to things that are not normally painful International Association for the Study of Pain (IASP) – Impaired inhibition of pain “Increased responsiveness of nociceptive neurons in the central nervous system to Associated with hyperalgesia and their normal or subthreshold afferent input” allodynia Centrally mediated pain – the pain experience is no longer associated with a mechanical, chemical, thermal and/or noxious stimuli  Central Pain Syndrome A neurologic dysfunction caused by damage or dysfunction to the CNS. The syndrome can be caused by: Stroke Tumors Epilepsy MS Parkinson’s SCI or TBI Pain is constant and made worse with touch, movement, emotions or temperature changes (usually cold) Pain can also be…Referred! Pain is felt at a location distant from its source Usually 3 options: 1) from a nerve to its area of innervation 2) from one area to another derived from the same dermatome 3) from one area to another derived from the same embryonic segment Referred Hip Pain The hip joint is the primary tissue involved, but these images are possible pain patterns that a patient can report Pain Referred from Viscera Pain Theory Review Sensation/ perception of pain is then Messages sent created as an to the CNS via OUTPUT if peripheral brain nerves, reaches Stimulation of determines somatosensory peripheral sensory input cortex and nociceptive is a threat consciousness structures Pain Perception Pain is an individualized experience! Can be influenced by a variety of factors: Physiological mechanisms of pain receptors Neurotransmitter levels Motivation Behavior Physiological and emotional state  The Sensory Exam Why perform a sensory exam prior to using any modalities for someone who has pain? To determine location and quality of sensory impairment To determine how sensory deficit affects movement To provide a justification for therapeutic intervention To assure patient safety To establish goals and select intervention https://static.seekingalpha.com/uploads/2015/5/14/saupload_AIS_2BScale.jpg The Peripheral Nerve Sensory Exam (review) Distal 🡪 proximal Random/unpredictable Superficial 🡪 deep 🡪 combined cortical Superficial = pain (Sharp/dull), temperature (water), light touch (cotton, finger sweep), pressure (skin indentation) Deep = Kinesthesia (awareness of direction DURING motion), proprioception (joint position at rest), vibration (tuning fork) Combined Cortical = Steriognosis (object discrimination), tactile location, two point discrimination, double simulation, graphesthesia (letter in hand), barognosis (weight recognition), texture recognition (texture variances) PNN Sensory Exam: Order of Exam (Review) 1. Full explanation of the purpose of the testing 2. Assist patient in finding relaxed comfortable position 3. Request that the patient refrain from “guessing” if they are uncertain of the correct response 4. Trial run demonstration prior to administration of test 5. Occlusion of vision (consider timing and method)  So …what does this mean when creating a treatment plan and including therapeutic modalities? Clinical Implications Physical agents can help to down modulate pain transmission Often work through stimulating non-nociceptive tissues to regulate pain impulses to the brain (think over riding “the system”) Gate Control Theory of pain modulation Can also help with tissue relaxation, breaking the pain-spasm-pain cycle Knowing as much as possible about the pain and pain science can help specify your treatment approach Clinical Implications Modalities can be PART OF a comprehensive treatment approach in combination with other interventions Think “adjunct intervention” to primary care plan Modalities vs. pharmacological agents (adverse effects?) Rarely effective in “fixing” pain itself – modalities can help modulate pain and offer temporary relief The root problem needs to be addressed with primary intervention Resources for you and your patients Why Do I Hurt? – Adriaan Louw Explain Pain – Butler and Moseley The Body Keeps Score - Bessel Van Der Kolk When the Body Says No – Gabor Maté