L17 - NEUROSCIENCE: PAIN PRINCIPLES IN MSK PRACTICE

Question 1

Definition of pain + key concepts

Answer 1

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

Question 2

BPS model of pain + implications of MSK practice

Answer 2

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

Question 3

Different types of pain & description of each
Why important to differentiate it

Answer 3

• 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

Question 4

Epidemiology of pain in MSK disorders

Answer 4

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.

Question 5

Neuroscience of pain: overview of pathways

Answer 5

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

Question 6

Nociceptive pain mechanisms:
- Definition
- Types of nociceptors
- Subtypes of pain

Answer 6

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

Question 7

Mechanical pain:
- Definition
- Mechanism
- Mechanical nociceptors
- Agg & easing factors
- Location
- Examples

Answer 7

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

Question 8

Inflammatory pain:
- Definition
- Mechanism
- Inflammatory mediators

Answer 8

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

Question 9

Ischemic pain:
- Definition
- Mechanism
- Clinical characteristics
- Examples

Answer 9

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.

Question 10

Rehabilitation considerations

Answer 10

Rehabilitation considerations
- Tailor intervention to pain mechanisms
- Monitor for overlapping pain types

Question 11

Neuropathic pain mechanisms:
- Definition
- Mechanisms
- Neuroimmune interactions
- Clinical features

Answer 11

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

Question 12

Nociplastic pain mechanisms
- Definition
- Mechanisms
- Neurochemical changes
- Functional brain changes
- Clinical features

Answer 12

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)

Question 13

Neuroplasticity in pain:
- Synaptic plasticity
- Structural plasticity
- Cortical reorganization
- Epigenetic modifications
- Implications for rehab

Answer 13

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.

Question 14

Definition of chronic pain

Answer 14

Chronic pain = pain persisting beyond normal healing time
- Can involve nociceptive, neuropathic, nociplastic, or mixed mechanisms.

Question 15

Chronic pain vs Nociplastic pain
- Key distinctions
- Clinical significance
- Assessment challenges

Answer 15

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.

Question 16

Different pathways of nociplastic pain

Answer 16

Ascending pathways
Thalamic processing
Cortical processing
Descending modulation

Question 17

Description of ascending pathways

Answer 17

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.

Question 18

Description of thalamic processing

Answer 18

Thalamic processing
- Ventral Posterolateral Nucleus (VPL)
o Sensory-discriminative aspects.
- Medial Thalamic Nuclei:
o Affective-motivational aspects.

Question 19

Description of cortical processing

Answer 19

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.

Question 20

Description of descending modulation

Answer 20

Descending modulation
- Periaqueductal Gray (PAG):
o Initiates pain inhibition.

• Rostral Ventromedial Medulla (RVM):
  o Modulates pain signals through ‘on’ and ‘off’ cells.

Question 21

Sensitization: overview & significance in pain

Answer 21

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

Question 22

Description of peripheral sensitization + clinical manifestation

Answer 22

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

Question 23

Description of central sensitization + clinical manifestations

Answer 23

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

Question 24

Overview of pain pathways: neurotransmitters involved & description of each

Answer 24

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.

Question 25

Importance of pain assessment:
- Purpose
- Approach
- Holistic perspective

Answer 25

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.

Question 26

Subjective assessment of pain + pain qualify descriptors

Answer 26

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

Question 27

Objective assessment of pain

Answer 27

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.

Question 28

Pain assessment tools:
- Application
- Benefits

Answer 28

Application
- Administered during the subjective assessment.
- Interpreted alongside clinical findings.

Benefits
- Improves diagnostic accuracy
- Enhances communication among healthcare providers.

Question 29

Assessment of nociceptive pain

Answer 29

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.

Question 30

Description of McGill Pain Questionnaire

Answer 30

• 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

Question 31

Assessment of neuropathic pain

Answer 31

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.

Question 32

Description of pain detect questionnaire

Answer 32

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

Question 33

Description of LANSS

Answer 33

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

Question 34

Description douleur neuropathique 4

Answer 34

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

Question 35

Assessment of nociplastic pain:
- Common tools
- Clinical indicators
- Testing methods

Answer 35

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.

Question 36

Description of CSI

Answer 36

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

Question 37

Description WPI

Answer 37

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

Question 38

Treatment principles

Answer 38

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

Question 39

Treatment of mechanical pain:
- interventions
- goal
- patient education

Answer 39

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

Question 40

Treatments to inflammatory pain:
- interventions
- goals
- pharmacological options
- patient education

Answer 40

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

Question 41

Treatment for ischemic pain:
- intervention
- referral
- goals
- patient education

Answer 41

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

Question 42

Treatment for neuropathic pain:
- interventions
-goals
- patient education

Answer 42

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

Question 43

Treatment for nociplastic pain:
- intervention
- goals
- patient education

Answer 43

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

Question 44

Pain éducation:
- purpose
- strategies
- topics to cover
- benefits

Answer 44

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.

Question 45

Cognitive behavioral therapy:
- principles
- techniques
- applications in pain management
- evidence
- integration into practice

Answer 45

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

Question 46

Neuromodulation & innovation techniques: description

Answer 46

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.

Question 47

Neuromodulation & innovation techniques:
- considerations
- integration into practice
- Evidence base

Answer 47

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.