Managing Chronic Pain: Objectives and Impact

Objectives of Managing Chronic Pain

• Discuss prevalence and economic impacts
• Identify risk factors
• Discuss use of relevant outcome measures for LBP and disability
• Discuss management strategies regarding activity

Understanding Pain

• Pain is an unpleasant sensory and emotional experience linked to actual or potential tissue damage.

Acute and Chronic Pain

• Acute Pain
  • Predictable response to injury, inflammation, or disease
  • Duration correlates with tissue healing
  • Can be influenced by mechanical factors
  • May involve transient behavioral changes and anxiety
• Chronic Pain
  • Connection with injury is possible
  • Significantly longer durations than expected for tissue healing
  • Influenced by non-mechanical factors like weather and emotions
  • Fear-avoidance behaviors and beliefs are often present

Impact of Chronic Pain

• Roughly 28% of US adults live with chronic pain, about 68.7 million people.
• Estimated annual cost is between 560to560 to 560to635 billion,
  • This is greater than the combined costs of cardiovascular disease, cancer, and diabetes.
• A main cause of activity limitation and missed work is lower back pain (LBP)
  • 5% of lower back pain patients account for 75% of the costs.
  • Recurrence rates range from 20–65% each year.

Categories of Pain Mechanisms

• Nociceptive

  • Cause: Tissue injury or acute inflammation
  • Clinical Features: Localized pain with predictable responses to mechanical loading
  • Assessment: Physical exams, palpation, PPIVMs/PAIVMs (accessory motion testing)
  • Examples: Muscle strain, meniscus tears, clinical instability, fractures,spondylosis

• Neuropathic

  • Cause: Nerve injury; spinal nerve root or peripheral entrapment
  • Clinical Features: Pain and paresthesias in dermatomal patterns; weakness, sensory changes, altered reflexes.
  • Assessment: Strength/sensory tests; neurodynamic tests
  • Examples: Radiculopathy and nerve entrapment such as carpal tunnel, diabetic/trigeminal neuralgia

• Nociplastic

  • Cause: Altered processing in the central nervous system (CNS)
  • Clinical Features: Unpredictable, disproportionate pain; diffuse tenderness; allodynia, hyperalgesia.
  • Assessment: Quantitative sensory testing, palpation, temporal summation
  • Examples: Chronic/fibromyalgia, CRPS, Phantom limb/CVA pain

Pain as an Output

• Nociception acts as a stimulus that has potential to damage tissue.
• Results in a perceived threat/danger by the Central Nervous System.
• Pain is more than just nociception since involves processing in multiple areas of the brain.

Understanding Nociceptors

• Free nerve endings
• High-threshold: sensitive to strong stimuli
• Slow-conducting: transmit signals at a lower rate
• Respond to noxious stimuli, which can be:
  • Mechanical: related to pressure or deformation
  • Thermal: related to temperature changes
  • Chemical: related to irritants
• Fiber Types:
  • C Fibers: thin, unmyelinated
  • Aδ Fibers: thin, myelinated

Sensitization

• Peripheral
  • There is increased responsiveness and reduced threshold of nociceptive neurons in the PNS.
• Central
  • Increased responsiveness of nociceptive neurons in the CNS to normal afferent input.

Peripheral Sensitization Details

• Related to tissue inflammation,
  • Mediated by cytokines (IL-1, IL-6, NGF).
• Neurogenic inflammation:
  • Antidromic impulses and neuropeptides release at injury leading to vasodilation and immune cell stimulation.
• Nociceptor effects:
  • Decreased threshold
  • Increased excitability
  • Increased transmission to CNS
• Results in:
  • Upregulation of existing ion channels
  • Production of new ion channels on nerve terminals
  • Increased sensitivity to inflammatory mediators
• Clinical signs include:
  • Redness, primary hyperalgesia, and spontaneous pain.

Abnormal Impulse Generating Sites (AIGS)

• Result from demyelination, upregulation of ion channels.
• Increased excitability in neurons
• May cause spontaneous ectopic impulses
  • Orthodromic & Antidromic firing, stimulates CNS and neurogenic inflammation.
• May be sensitive to pressure, temperature, or chemicals.

Central Sensitization Characteristics

• Altered pain processing in the CNS which is
  • Maintained by input from the peripheral nervous system (PNS).
• Shows decreased descending inhibitory mechanisms and enhanced descending faciliatory processes.
• Facilitated dorsal horn receptors:
  • They show increased excitability, prolonged opening of ion channels, and expanded receptor fields.

Potential Consequences on the Brain due to Pain

• Amygdala: Altered fear perception and avoidance behaviors.
• Hippocampus: Impaired short-term memory.
• Anterior Cingulate Cortex: Dysregulation of blood pressure and heart rate, impaired concentration, and indecisiveness
• Cerebellum: Decreased balance, coordination, and fine motor skills
• Primary Motor Cortex: Impaired fine motor control.
• Hypothalamus/Thalamus: Body temperature dysregulation and altered eating or sleeping patterns.
• Prefrontal Cortex: Difficulty with analytical tasks and decision-making.
• Spinal Cord: Facilitation or disinhibition of signals

Cortical Changes due to Chronic Pain

• Primary Somatosensory Cortex (S1)
  • Changes in neuronal representation of the body occur
  • There are differences chronic pain patients
  • Correlation exists between the shape/size of the body map and the level of pain/disability.
  • Issues Worsens with disuse and neglect of body
  • Impaired perception of body parts.
  • Changes occur rapidly, even within minutes
• Primary Motor Cortex (M1)
  • Loss of precise motor organization
  • Degree of smudging correlates with the intensity of pain

Results of Changes

• PNS and CNS become sensitized.
  • Reduced threshold for activation.
  • Increased excitability of neurons.
• Result in expansion of receptor fields in the periphery
• Primary and Secondary Hyperalgesia
• Allodynia can result
• Temporal Summation
• Effects can continue after the original injury has healed.

Chronic Pain Factors

• Complex: can involve
  • Epigenetic, neural, endocrine, and immune factors.
• Epigenetic factors include:
  • Physical activity, psychological stress, and environmental factors.
• Endocrine factors relate to the
  • Hypothalamus-Pituitary-Adrenal Axis and increased sensitivity to stress.
• Immune factors include
  • Immune cells and inflammation.

Biopsychosocial Model

• Biological Processes: Anatomy, physiology, and tissue pathology.
• Psychological Factors: Thoughts, beliefs, and behaviors.
• Social Factors: Culture, occupation, and religion.

Psychosocial Flags

• Yellow Flags
  • Emotional distress, preoccupation with pain, pain catastrophizing, elevated fear-avoidance beliefs, and kinesiophobia.
  • Low self-efficacy and incorrect beliefs about treatment and pain severity.
• Blue Flags
  • Dissatisfaction with occupation and conflict with employers or colleagues.

Common Clinical Presentations of Chronic Pain

• Diffuse Pain
• Hyperalgesia & Allodynia
• Impaired Beliefs: catastrophizing pain or believing work/activity is harmful.
• There is also Anxiety & Fear-avoidance behavior resulting n
  • Limited movement/activity
• Increased reliance on medication/assistive devices
• Sensitivity to stimuli (heat, cold, sound, light)

Identifying Central Sensitization

• Central sensitization shows disproportionate, non-mechanical pain patterns.
• Involves widespread non-anatomic pain/tenderness and psychosocial factors.

Outcome Measures for Chronic Pain

• Tools to assess;
• Fear-Avoidance Beliefs Questionnaire (FABQ)
• STarT Back Screening Tool
• Orebro Musculoskeletal Pain Questionnaire (OMPQ)
• OSPRO Yellow Flag (OSPRO-YF) Assessment Tool
• Central Sensitization Inventory (CSI)
• Tampa Scale of Kinesiophobia (TSK)

Biopsychosocial Approach Interventions

• Top-Down Approaches:
  • Mindfulness, meditation, sleep hygiene
  • Pain Neuroscience Education
  • Graded Motor Imagery
• Bottom-Up Approaches:
  • Movement/Exercise
  • Manual Therapy
  • Electromodalities

Interventions for Patients

• Always treat identified impairments
• Use active interventions
• Emphasize function and minimize focus on pain.
• Educate patient, reassure, encourage activity, and limit anatomical terms for problem.

Cognitive-Behavioral Techniques

• Target modifiable risk factors through graded activity.
• Positively reinforce increasing activity levels.
• Use graded exposure, gradually exposing the patient to fearful situations.

Pain Neuroscience Education (PNE)

• Involves teaching patients neurophysiological processes of pain in patient-friendly
• Avoids language that relates to tissue damage when explaining conditions;
  • ("herniated disc", "degeneration”).
• PNE appears most beneficial as an adjunct to traditional movement-based interventions.
• In studies, shown to improve fear of movement and catastrophizing.

fMRI with PNE

• Study showed:
  • Patients receiving PNE experienced decreased activation of the periaqueductal gray (PAG) and cerebellum
  • Increased activation of the motor cortex (M1).

Effect of PNE on Pain

• Preoperative PNE shown to decrease healthcare utilization after lumbar surgery.
• Studies show incorporating it as part of treatment can reduce kinesiophobia.

Graded Motor Imagery

• Involves a sequential process of;
  • Left/Right Discrimination
  • Explicit Motor Imagery
  • Mirror Therapy in order.

Left/Right Discrimination

• First step of a graded motor imagery program.
• It addresses the loss of recognizing painful body part laterality.
• Uses images,
  • Differentiating left from right limb
  • Assessing movement direction
  • Uncommon limb positions
• Performance is expected to be above 80% accuracy with a response time around 2.4 seconds.

Explicit Motor Imagery

• The second part of a graded motor imagery
• Activates areas of the brain associated with motor function by
• Imagining body part static, involved body part moving, performing task

Mirror Therapy

• The third part of graded motor imagery
• Involves use of mirror to create virtual imagery of the affected limb performing tasks.

Prognonsis

• Physical & psychosocial factors affect outcomes.
• Early identification and prevention of chronicity is best.
• Full recovery is rare, multimodal treatment is best.

Closing Thoughts on Chronic Pain Management

• Pain is an output when the body feels threatened
• It is a complex condition influenced by neuroplastic changes.
• Neuroplasticity offers the opportunity to potentially reverse pain processing.
• Utilize a holistic approach via the biopsychosocial model.
• Physical therapy should be multimodal, include both “top-down” and “bottom-up” approaches.