L17 - NEUROSCIENCE: PAIN PRINCIPLES IN MSK PRACTICE Flashcards
Definition of pain + key concepts
Definition of pain
Pain = unpleasant sensory & emotional experience associated with or resembling that associated with, actual or potential tissue damage
Key concepts
- Subjectivity of pain
- Multidimensional nature
o Sensory-discriminative
o Affective-motivational
o Cognitive-evaluative components
BPS model of pain + implications of MSK practice
Bio-psycho-social model of pain
- Biological factors: Include tissue damage, inflammation, nerve injury & genetic predispositions. These are physical aspects of pain.
- Psychological Factors: Encompass emotions like anxiety & depression, cognitive processes such as attention & memory, beliefs & attitudes about pain & coping strategies. For instance,
catastrophizing thoughts can amplify pain perception.
- Social Factors: Involve cultural influences, social support systems, family dynamics, work
environment & socioeconomic status. Social isolation or stress at work can exacerbate pain
experiences.
Implications for MSK Practice:
- Holistic assessment and management
Different types of pain & description of each
Why important to differentiate it
- Nociceptive Pain: Arises from actual or threatened damage to non-neural tissue & involves activation of nociceptors. It’s typically associated with acute injury & serves protective function.
o Mechanical
o Inflammatory
o Ischemic - Neuropathic Pain: Results from lesion or disease affecting somatosensory nervous system. It often presents as burning, shooting pain & may be accompanied by sensory deficits.
- Nociplastic Pain: Refers to pain arising from altered nociception without clear evidence of actual or threatened tissue damage or disease of somatosensory system. Central sensitization = key mechanism here.
Importance of Differentiation:
- Guides assessment & treatment strategies
Epidemiology of pain in MSK disorders
Epidemiology of pain in MSK disorders
- Global Burden of MSK Pain
- Prevalence of Common Conditions
o Low back pain: 7.5% of global population suffers from LBP at any given time. This
equates to about 577 million people globally.
o Osteoarthritis: 528 million people worldwide
o Neck pain: 288 million people affected by neck pain globally at any given time. Annual
prevalence of neck pain approximately 15% to 20% among adults.
- Impact on Quality of Life
- Economic Costs: MSK pain leads to significant healthcare costs & loss of productivity due to work absenteeism.
Neuroscience of pain: overview of pathways
Overview of pain pathways
- Transduction: Activation of nociceptors
- Transmission: Afferent pathways to spinal cord
- Modulation: Spinal cord processing & descending inhibitory/facilitatory pathways
- Perception: Thalamus & cortical areas
Nociceptive pain mechanisms:
- Definition
- Types of nociceptors
- Subtypes of pain
Definition
= Arises from actual or threatened damage to non-neural tissue & involves activation of nociceptors.
Typically associated with acute injury & serves protective function
- Pain due to activation of nociceptors by noxious stimuli
Types of nociceptors:
- Mechanical
- Thermal
- Chemical
- Polymodal
Mechanical, ischemic & inflammatory
Mechanical pain:
- Definition
- Mechanism
- Mechanical nociceptors
- Agg & easing factors
- Location
- Examples
Mechanical pain
Definition
= Pain resulting from mechanical deformation of tissues
Mechanism
- Activation of mechanical nociceptors due to physical forces.
- Involves stretch, compression, or tension exceeding physiological limits.
Mechanical nociceptors
- A-delta & C fibers respond to high-threshold mechanical stimuli
- Mechanosensitivity ion channels (ex : Piezo1, Piezo2)
Clinical characteristics
- Quality of pain: Sharp, stabbing, or shooting.
- Location: Localized to area of mechanical stress
- Behavior:
o Provoked by movement, load, or specific positions
o Alleviated by rest or unloading.
Table
Examples: Ligament sprain, muscle strain, disc herniation
Inflammatory pain:
- Definition
- Mechanism
- Inflammatory mediators
Inflammatory pain
Definition
= Pain associated with tissue inflammation due to injury or infection
Mechanism
- Activation & sensitization of nociceptors by inflammatory mediators
- Peripheral Sensitization:
o Lowered activation threshold of nociceptors
o Increased responsiveness to stimuli
Inflammatory mediators
- Prostaglandins, bradykinin, cytokines, histamine
- Upregulation of TRPV1 channels & Nav1.8 sodium channels
Ischemic pain:
- Definition
- Mechanism
- Clinical characteristics
- Examples
Definition
= Pain resulting from insufficient blood flow, leading to hypoxia & metabolite accumulation.
Mechanism
- Activation of metabolic nociceptors due to accumulation of metabolites
- Metabolic Byproducts:
o Lactic acid, ATP, protons activating ASICs (acid- sensing ion channel) & purinergic receptors
Clinical Characteristics
- Quality of Pain: Cramping, squeezing, deep aching.
- Location: Corresponds to ischemic tissue.
- Behavior:
o Worsens with activity
o Relieved by rest or restoring blood flow.
- Associated Signs: Pallor, coldness, muscle weakness
Examples: Peripheral arterial disease, angina pectoris.
Rehabilitation considerations
Rehabilitation considerations
- Tailor intervention to pain mechanisms
- Monitor for overlapping pain types
Neuropathic pain mechanisms:
- Definition
- Mechanisms
- Neuroimmune interactions
- Clinical features
Definition
= pain arising as direct consequence of lesion or diseases affecting somatosensory system
Mechanisms
- Peripheral sensitization: ectopic discharges, upregulation of sodium channels (Nav 1.7, Nav 1.8)
- Central sensitization
o Increased excitability of dorsal horn neurons
o NMDA receptor activation leading to calcium influx & gene expression changes
- Disinhibition
o Loss of inhibitory interneurons
o Reduced GABAergic & glycinergic inhibition
- Structural reorganization
o Sprouting of A-beta fibers into nociceptive lamina (lamina II)
Neuroimmune interactions
- Activation of glial cells (microglia, astrocytes)
- Release of pro-inflammatory cytokines (TNF-alpha, IL-1beta)
Clinical features
- Quality of pain: burning, shooting, electric shocks or lancinating
- Location: follows nerve or dermatomal distribution
- Sensory abnormalities: paresthesia (tingling), dysesthesia (unpleasant sensations), hypoesthesia (numbness)
- Signs of sensitization
o Allodynia: pain from non-painful stimuli
o Hyperalgesia: exaggerated response to painful stimuli
o Hyperpathia: delayed & explosive pain response
- Autonomic changes: skin color changes, temperature alterations
- Diagnostic tools :
o Quantitative sensory testing
o Nerve conduction studies
Nociplastic pain mechanisms
- Definition
- Mechanisms
- Neurochemical changes
- Functional brain changes
- Clinical features
Definition
= Pain arising from altered nociception despite no clear evidence of tissue or nerve damage.
Mechanisms
- Central Sensitization:
o Increased excitability & synaptic efficacy of central neurons
o Involvement of NMDA receptors & calcium-dependent pathways
- Altered Descending Modulation:
o Impaired inhibitory pathways from brainstem (PAG, RVM)
o Enhanced facilitatory pathways increasing pain transmission
Neurochemical Changes:
- Imbalances in neurotransmitters (e.g., increased glutamate, decreased GABA).
- Elevated levels of substance P and brain-derived neurotrophic factor (BDNF).
Functional brain changes:
- Altered connectivity & activity in pain-processing regions (insula, ACC, prefrontal cortex)
- Gray matter volume changes in chronic pain conditions.
Clinical features
- Quality of Pain: Widespread, diffuse, deep aching.
- Location: Poorly localized, often bilateral, may involve multiple regions.
- Associated Symptoms:
o Somatic: Fatigue, sleep disturbances, stiffness.
o Cognitive: Difficulty concentrating, memory issues (“fibro fog”).
o Autonomic: Sensitivity to light, sound, temperature
- Psychological Impact:
o High prevalence of anxiety, depression, stress-related disorders
- Diagnostic Considerations:
o Exclusion of nociceptive & neuropathic pain causes.
o Use of tools like the Central Sensitization Inventory (CSI).
o Application of diagnostic criteria (ex: ACR criteria for fibromyalgia)
Neuroplasticity in pain:
- Synaptic plasticity
- Structural plasticity
- Cortical reorganization
- Epigenetic modifications
- Implications for rehab
Synaptic Plasticity:
- Long-Term Potentiation (LTP):
o Persistent strengthening of synaptic connections
o Involves NMDA receptor activation, calcium influx & kinase pathways
- Long-Term Depression (LTD):
o Persistent weakening of synaptic strength.
o Potential target for reversing central sensitization.
Structural plasticity:
- Dendritic Spine Remodeling:
o Changes in spine density & morphology affecting synaptic efficacy
- Neurogenesis & Gliogenesis:
o Altered patterns in response to chronic pain.
Cortical Reorganization:
- Somatotopic Map Changes:
o Altered representation of body parts in the somatosensory cortex.
o Associated with phantom limb pain & complex regional pain syndrome.
Epigenetic Modifications:
- DNA Methylation & Histone Modification:
o Influence gene expression related to pain sensitivity.
Implications for rehabilitation
- Activity-Dependent Plasticity:
o Therapeutic interventions can harness neuroplasticity to reverse maladaptive changes.
- Use of Non-Invasive Brain Stimulation:
o Techniques like transcranial magnetic stimulation (TMS) to modulate cortical excitability.
Definition of chronic pain
Chronic pain = pain persisting beyond normal healing time
- Can involve nociceptive, neuropathic, nociplastic, or mixed mechanisms.
Chronic pain vs Nociplastic pain
- Key distinctions
- Clinical significance
- Assessment challenges
Nociplastic Pain = Subtype of chronic pain with predominant central sensitization.
Key distinctions
- Not all chronic pain is nociplastic.
- Chronic pain may have ongoing peripheral input or nerve damage.
Clinical significance
- Identifying nociplastic pain is essential for selecting central-targeted therapies
Assessment Challenges:
- Overlapping symptoms require thorough evaluation.
Different pathways of nociplastic pain
Ascending pathways
Thalamic processing
Cortical processing
Descending modulation
Description of ascending pathways
Ascending Pathways
- Spinothalamic Tract:
o Transmits pain & temperature to thalamus.
o Divided into lateral (sensory-discriminative) & medial (affective-motivational) pathways.
- Spinoreticular Tract:
o Projects to reticular formation, influencing arousal & autonomic responses. - Spinomesencephalic Tract:
o Projects to the midbrain, including the PAG, involved in pain modulation.
Description of thalamic processing
Thalamic processing
- Ventral Posterolateral Nucleus (VPL)
o Sensory-discriminative aspects.
- Medial Thalamic Nuclei:
o Affective-motivational aspects.
Description of cortical processing
Cortical processing
- Primary Somatosensory Cortex (S1):
o Localization and intensity.
- Secondary Somatosensory Cortex (S2):
o Integration of sensory information. - Insular Cortex:
o Interoceptive awareness, emotional aspects. - Anterior Cingulate Cortex (ACC):
o Emotional and cognitive aspects of pain.
Description of descending modulation
Descending modulation
- Periaqueductal Gray (PAG):
o Initiates pain inhibition.
- Rostral Ventromedial Medulla (RVM):
o Modulates pain signals through ‘on’ and ‘off’ cells.
Sensitization: overview & significance in pain
Sensitization Overview:
- Peripheral Sensitization
o Increased responsiveness of peripheral nociceptors
- Central Sensitization
o Enhanced excitability of neurons within the central nervous system (CNS)
Significance in pain
- Contributes to chronic pain development
- Alters pain perception & processing
Description of peripheral sensitization + clinical manifestation
Table
Clinical manifestation of peripheral sensitization
- Primary Hyperalgesia:
o Increased sensitivity to painful stimuli at injury site
- Allodynia:
o Pain in response to normally non-painful stimuli (e.g., light touch)
- Protective Role:
o Promotes guarding behaviors to facilitate healing
- Temporal Aspects:
o Generally acute & resolves with tissue healing
Description of central sensitization + clinical manifestations
Table
Clinical manifestation of central sensitization
- Secondary Hyperalgesia:
o Increased pain sensitivity beyond the injury site
- Widespread Pain:
o Pain in multiple body regions
- Allodynia:
o Pain from non-nociceptive stimuli (ex: light touch, clothing)
- Enhanced Temporal Summation:
o Increased pain with repeated stimulation
- Associated Symptoms:
o Fatigue, sleep disturbances, cognitive difficulties, mood disorders
Overview of pain pathways: neurotransmitters involved & description of each
Excitatory neurotransmitters:
- Glutamate:
o Acts on AMPA and NMDA receptors.
o Key in synaptic plasticity and central sensitization.
- Substance P:
o Binds to NK1 receptors.
o Involved in neurogenic inflammation and pain transmission.
- Calcitonin Gene-Related Peptide (CGRP):
o Vasodilator, contributes to neurogenic inflammation.
Inhibitory Neurotransmitters:
- GABA:
o GABA_A & GABA_B receptors reduce neuronal excitability
- Glycine:
o Inhibitory neurotransmitter in the spinal cord.
Modulatory Neurotransmitters:
- Serotonin (5-HT):
o Can be inhibitory or facilitatory, depending on receptor subtype.
- Norepinephrine (NE):
o Generally inhibitory in the spinal cord via alpha-2 adrenergic receptors.
- Endogenous opioids
o Enkephalins, endorphins, dynorphins.
o Activate opioid receptors to inhibit pain transmission.
Neurotrophic factors:
- Brain-Derived Neurotrophic Factor (BDNF):
o Released from neurons and glia.
o Modulates synaptic plasticity & central sensitization.
Cytokines and Chemokines:
- Interleukins (e.g., IL-1beta, IL-6), TNF-alpha:
o Pro-inflammatory mediators enhancing neuronal excitability.
Importance of pain assessment:
- Purpose
- Approach
- Holistic perspective
Importance of pain assessment
- Purpose:
o Accurate diagnosis.
o Development of effective treatment plans.
o Monitoring progress and outcomes.
- Approach:
o Comprehensive and systematic.
o Incorporates subjective and objective data. - Holistic Perspective:
o Considers biological, psychological & social factors.
Subjective assessment of pain + pain qualify descriptors
Subjective assessment
- Pain History:
o Onset: Sudden or gradual
o Duration: Acute or chronic.
o Intensity: Use of pain scales (e.g., VAS, NRS).
- Quality & Pattern:
o Descriptors (e.g., sharp, burning, aching).
o Temporal pattern (constant, intermittent). - Aggravating & Relieving Factors:
o Activities, positions, medications.
Pain quality descriptor
- Nociceptive Pain: Sharp, aching, throbbing
- Neuropathic Pain: Burning, tingling, electric shocks
- Nociplastic Pain: Diffuse, deep aching, persistent
- Use of Pain Descriptors: Guides differential diagnosis
Objective assessment of pain
Objective assessment
- Physical Examination:
o Inspection: Posture, alignment, swelling, atrophy.
o Palpation: Tenderness, tissue texture, temperature changes.
o Range of Motion (ROM): Active and passive movements, noting limitations and pain.
- Neurological Examination:
o Sensory Testing: Light touch, pinprick, vibration, proprioception.
o Motor Testing: Muscle strength grading (Oxford scale).
o Reflexes: Deep tendon reflexes, pathological reflexes. - Special Tests:
o Orthopedic Tests: To identify specific tissue involvement.
o Neurodynamic Tests: Assess nerve mobility and sensitivity. - Functional Assessments:
o Gait analysis.
o Balance and coordination tests.
o Functional movement patterns.
Pain assessment tools:
- Application
- Benefits
Application
- Administered during the subjective assessment.
- Interpreted alongside clinical findings.
Benefits
- Improves diagnostic accuracy
- Enhances communication among healthcare providers.
Assessment of nociceptive pain
Common Measures:
- Visual Analog Scale (VAS): Measures pain intensity on a continuum.
- Numeric Rating Scale (NRS): Rates pain intensity on a numerical scale (usually 0-10).
- McGill Pain Questionnaire: Evaluates qualitative aspects of pain.
Quality of Life Measures:
- SF-36 Health Survey: Assesses overall health and well-being.
Description of McGill Pain Questionnaire
- Purpose: Assess qualitative aspects of pain
- Structure: Descriptive words categorized into sensory, affective, evaluative
- Administration: Patient selects words that describe their pain
- Scoring: Pain Rating Index (PRI)
- Interpretation:Provides a comprehensive pain profile
Assessment of neuropathic pain
Common Tools:
- Pain DETECT Questionnaire : Assesses neuropathic pain components.
- Leeds Assessment of Neuropathic Symptoms and Signs (LANSS): Combines symptom
assessment & sensory testing.
- Douleur Neuropathique 4 (DN4): Short questionnaire for neuropathic pain screening.
Description of pain detect questionnaire
n DETECT Questionnaire
- Purpose: Screen for neuropathic pain features
- Structure: 9 items: 7 symptom descriptors, 2 pain pattern items
- Administration: Self-administered questionnaire
- Scoring: Total score ranges from -1 to 38
- Interpretation:
o ≤12: Neuropathic pain unlikely
o 13-18: Uncertain
o ≥19: Neuropathic pain likely
Description of LANSS
Leeds Assessment of Neuropathic Symptoms and Signs (LANSS)
- Purpose: Identify neuropathic pain based on symptoms and signs
- Structure: 5 symptom items, 2 clinical examination items
- Administration: Combination of patient questionnaire and sensory testing
- Scoring: Total score out of 24
- Interpretation: ≥12 indicates likely neuropathic pain
Description douleur neuropathique 4
Douleur Neuropathique 4 (DN4)
- Purpose: Quick screening for neuropathic pain
- Structure: 10 items: 7 symptoms, 3 clinical examination findings
- Administration: Conducted by clinician
- Scoring: Each positive item scores 1 point
- Interpretation: Score ≥4 suggests neuropathic pain
Assessment of nociplastic pain:
- Common tools
- Clinical indicators
- Testing methods
Nociplastic pain
Common Tools:
- Central Sensitization Inventory (CSI)
- Widespread Pain Index (WPI)
- Symptom Severity Scale (SSS)
Clinical Indicators:
- Allodynia
- Hyperalgesia
- Hyperpathia
- Wide-spread pain
Testing Methods:
- Quantitative Sensory Testing (QST): Measures thresholds for thermal, mechanical & vibration
stimuli.
- Temporal Summation: Repeated stimuli leading to increased pain perception.
- Conditioned Pain Modulation (CPM):Evaluates the efficiency of descending inhibitory pathways.
Description of CSI
Central Sensitization Inventory (CSI)
- Purpose: Assess symptoms related to central sensitization
- Structure: Part A: 25 self-report items
- Administration: Patient rates frequency of symptoms over the past 3 months
- Scoring:
o Each item scored 0 (never) to 4 (always)
o Total score out of 100
- Interpretation: Scores ≥40 indicate significant central sensitization
Description WPI
Widespread Pain Index (WPI): symptom severity scale
- Purpose: Assess widespread pain and symptom severity
- Structure:
o WPI: Counts number of painful body regions (0-19)
o SSS: Rates severity of fatigue, sleep, cognitive symptoms (0-12)
- Administration: Patient self-report
- Interpretation: Combined scores aid in diagnosing conditions like fibromyalgia
Treatment principles
Treatment principles
- Nociceptive Pain: Interventions targeting tissue healing & reducing nociceptor activation.
- Neuropathic Pain: Approaches focusing on modulating nerve function & reducing neural
hyperexcitability.
- Nociplastic Pain: Strategies addressing central sensitization & enhancing neuroplastic
Treatment of mechanical pain:
- interventions
- goal
- patient education
Interventions:
- Manual Therapy: pain modulation
o Joint mobilizations
o Soft tissue techniques
- Exercise Therapy: pain modulation and resilience
o Strengthening
o Flexibility exercises
Goals:
- Restore normal biomechanics
- Reduce mechanical stress
Patient education
- Posture correction
- Activity modification
Treatments to inflammatory pain:
- interventions
- goals
- pharmacological options
- patient education
Interventions:
- Physical Modalities:
o PEACE & LOVE
o POLICE
- Therapeutic Exercises: do not aggravate
o Gentle range of motion
Pharmacological Options:
- NSAIDs (as prescribed)
Goals:
- Reduce inflammation
- Prevent stiffness
Patient Education:
- Importance of adhering to anti-inflammatory strategies
Treatment for ischemic pain:
- intervention
- referral
- goals
- patient education
Interventions:
- Exercise Therapy: Graded walking programs
- Lifestyle Modifications:
o Smoking cessation
o Dietary changes
Referral:
- Vascular specialist
Goals:
- Improve circulation
- Enhance endurance
Patient Education:
- Risk factor management
Treatment for neuropathic pain:
- interventions
-goals
- patient education
Interventions:
- Pharmacological Management:
o Anticonvulsants
o Antidepressants
- Physical Therapy:
o Desensitization Techniques: Gradual exposure to stimuli to reduce hypersensitivity.
o Neural Mobilization: Improve nerve mobility and reduce compression.
o Transcutaneous al Nerve Stimulation (TENS): Modulate pain signals.
Goals:
- Reduce pain intensity
- Improve nerve function
Patient education
- Pain management strategies
- Coping skills
Treatment for nociplastic pain:
- intervention
- goals
- patient education
Interventions:
- Exercise Therapy:
o Aerobic conditioning
o Graded activity
- Psychological Approaches:
o Cognitive Behavioral Therapy
o Mindfulness techniques
Goals:
- Modulate central sensitization
- Enhance quality of life
Patient education
- Understanding pain mechanisms
- Importance of active participation
Pain éducation:
- purpose
- strategies
- topics to cover
- benefits
Purpose:
- Enhance patient understanding of pain mechanisms.
- Correct misconceptions and reduce fear.
Strategies: Pain In Motion
- Use metaphors and analogies (e.g., “alarm system”).
- Provide clear explanations of central sensitization.
- Use visual aids and educational materials.
Topics to Cover:
- Difference between hurt and harm.
- Role of the nervous system in pain.
- Importance of active participation in recovery.
Benefits
- Reduces catastrophizing and fear-avoidance.
- Empowers patients to engage in rehabilitation.
Cognitive behavioral therapy:
- principles
- techniques
- applications in pain management
- evidence
- integration into practice
Cognitive Behavioral therapy
Principles:
- Thoughts, feelings, and behaviors are interconnected.
- Changing maladaptive thoughts can alter emotional and behavioral responses.
Techniques:
- Cognitive Behavioral Therapy (CBT):
o Cognitive Restructuring: Identify and challenge negative thought patterns.
o Behavioral Activation: Encourage engagement in meaningful activities.
o Exposure Therapy: Gradual exposure to feared movements or activities.
- Acceptance and Commitment Therapy (ACT):
o Focus on accepting pain while committing to actions aligned with personal values.
- Mindfulness-Based Stress Reduction (MBSR):
o Mindfulness practices to reduce stress and improve emotional regulation
Applications in Pain Management:
- Reduces catastrophizing and fear-avoidance.
- Improves coping strategies and self-efficacy.
Evidence
- Proven effectiveness in reducing pain intensity & disability.
Integration into practice
- Can be delivered by trained physiotherapists.
- Collaboration with psychologists for comprehensive care
Neuromodulation & innovation techniques: description
Neuromodulation & innovation techniques
Transcutaneous Electrical Nerve Stimulation (TENS):
- Mechanism: Stimulates nerves to modulate pain signals, based on the gate control theory.
- Application: Electrodes placed over painful areas, delivering low-voltage electrical currents.
Acupuncture:
- Mechanism: Insertion of fine needles stimulates endogenous opioid release & modulates pain pathways.
- Dry Needling: Targets trigger points in muscles to reduce pain and improve function.
Virtual reality (VR) therapy
- Mechanism: Immersive environments distract from pain and promote engagement in therapy.
- Applications: Used for pain distraction, motor rehabilitation, and exposure therapy.
Emerging Technologies:
Non-Invasive Brain Stimulation:
- Transcranial Magnetic Stimulation (TMS): Modulates cortical excitability.
- Transcranial Direct Current Stimulation (tDCS): Alters neuronal firing patterns.
Neuromodulation & innovation techniques:
- considerations
- integration into practice
- Evidence base
Considerations:
- Evidence of Efficacy: Varies by modality; ongoing research is expanding the knowledge base.
- Patient Suitability: Not all patients may be candidates; consider contraindications.
Integration into Practice:
- Use as adjuncts to traditional therapies.
- Monitor patient responses and adjust as needed.
Evidence Base:
- Some modalities have strong support (e.g., TENS for certain conditions), while others are
emerging and require further research.
