DPT 581: Chronic Pain Management

• Chronic pain is managed in DPT 581: Medical Management I in Spring 2025 at Saint Joseph's University

Objectives

• The prevalence and economic impact of persistent pain are discussed
• Risk factors for developing chronic pain are identified
• Patient-reported outcome measures can help identify patients at risk of developing persistent lower back pain and disability
• Strategies to manage patients with persistent pain and maladaptive beliefs/behaviors can address activity effects

Pain Defined

• Pain involves unpleasant sensory and emotional experiences linked to actual or potential tissue damage

Acute vs. Chronic Pain

• Acute pain is a predictable response to injury, inflammation, or disease
• Duration of acute pain is linked to tissue healing times
• Mechanical factors can influence acute pain
• Acute pain may involve transient behavioral change and anxiety
• Chronic pain may or may not be associated with an injury
• The duration of chronic pain is longer than expected for tissue healing
• Non-mechanical factors, such as weather and emotions, can influence chronic pain
• Fear-avoidance behaviors and impaired pain beliefs are often components of chronic pain

Impact of Chronic Pain

• About 28% of US adults have chronic pain (68.7 million people)
• The estimated annual cost is between $560 to $635 billion
• LBP is the leading cause of activity limitation and missed work
• 5% of patients with LBP account for 75% of the money spent on treating it
• There is a 20%-65% rate of chronic pain recurrence over 1 year

Categories of Pain Mechanisms

• Nociceptive pain is caused by tissue injury or acute inflammation

• Local pain that responds predictably to mechanical loading is a clinical feature of Nociceptive pain

• Physical exams, palpation, PPIVMs/PAIVMs are methods used to assess Nociceptive pain

• Examples of Nociceptive pain: muscle strain, meniscus tear, clinical instability, fracture, and spondylosis

• Neuropathic pain originates from nerve injury such as spinal nerve root or peripheral entrapment

• Pain and paresthesias in dermatomal patterns, impaired strength/sensation/DTRs, and positive neurodynamic tests are clinical features of neuropathic pain

• Assessment is preformed via strength screen, sensory and DTR testing, and neurodynamics

• Examples of neuropathic pain: radiculopathy, fibular nerve entrapment, carpal tunnel syndrome, diabetic neuropathy, and trigeminal neuralgia

• Nociplastic pain stems from altered processing in the CNS

• Clinical features present like unpredictable and disproportionate pain provocation, diffuse tenderness in non-anatomical patterns, allodynia, hyperalgesia, and maladaptive psychology

• Assessment is performed via QST to test heat/cold, palpation, temporal summation, 2-point discrimination, and using the Central Sensitization Inventory

• Examples of nociplastic pain: chronic LBP, fibromyalgia, CRPS, phantom limb pain, and pain after CVA or SCI

Pain as an Output System

• Pain is produced from input from nociception, where stimuli that can damage tissue are received by the CNS
• The CNS perceives the stimulus as a threat or danger
• Pain involves complex processing by multiple brain areas

Nociceptors

• Nociceptors are free nerve endings with a high-threshold, slow conduction
• They respond to noxious stimuli that are mechanical, thermal, or chemical
• C Fibers are thin and unmyelinated
• Aδ Fibers are thin and myelinated

Processing Pain

• Structures involved in the processing of pain include: spinal cord, brain stem, thalamus, amygdala, insular cortex, somatosensory cortex, and cingulate cortex

Sensitization Types

• Peripheral sensitization increases responsiveness and reduces the threshold of nociceptive neurons in the PNS in response to stimuli in their receptive fields
• Central sensitization increases the responsiveness of nociceptive neurons in the CNS to normal or subthreshold afferent input

Peripheral Sensitization

• Tissue inflammation is a key aspect
• Pro-inflammatory cytokines such as IL-1, IL-6, and NGF (Nerve Growth Factor) are involved
• Neurogenic inflammation occurs through antidromic impulses and neuropeptide release at the injury site, resulting in vasodilation and stimulating immune cells
• This lowers threshold, increases excitability, and increases transmission to the CNS in nociceptors

Additional Information on Peripheral Sensitization

• There is an upregulation of existing ion channels
• New ion channels are produced on nerve terminals
• Increased sensitivity to inflammatory chemical mediators can result in more easily generated action potentials, and increase neurotransmitter release in the synaptic cleft at the dorsal horn of the spine
• This creates redness, primary hyperalgesia, and spontaneous pain

Abnormal Impulse Generating Sites (AIGS)

• AIGSs result from demyelination of axons and upregulation of ion channels in the axolemma
• This allows for neuron excitability at sites other than terminals
• Spontaneous ectopic impulses and orthodromic/antidromic firing occurs
• These sites of impulse generation are sensitive to mechanical, thermal, or chemical stimuli

Central Sensitization/Nociplastic Pain

• Involves altered pain processing in the CNS, maintained by PNS input
• Cortical reorganization and disinhibition(decreased descending inhibitory mechanisms) occurs
• Facilitation(enhanced descending facilitatory processes from PAG/RVM to the dorsal horn) happens
• Dorsal horn receptors become increasingly facilitated. This involves increased excitability, prolonged opening of ion channels, and expansion of receptor fields

Potential Consequences of Pain Neurotag on the Brain

• Amygdala changes can result in altered fear perception and avoidance
• Hippocampus may be impaired STM
• The Anterior Cingulate Cortex's functions of regulating blood pressure and heart rate could be impacted
• Reduced balance, coordination, and fine motor skill is found if the Cerebellum is effected
• Primary Motor Cortex changes will effect fine motor control
• Hypothalamus/Thalamus regulation of body temperature and eating/sleeping patterns is effected
• It becomes difficult to reason and make decisions if the Prefrontal Cortex is impacted
• Potential Spinal Cord effects are facilitation/disinhibition

Cortical Changes: Primary Somatosensory Cortex (S1)

• There is altered neuronal representation of the body
• People with chronic pain experience change
• A change in the shape/size relationship of the body map will change pain/disability
• Neglect or disuse of involved body parts can worsen
• Changes can occur in minutes

Cortical Changes: Primary Motor Cortex (M1)

• Discrete motor organization degrades
• Degree of "smudging" is correlated to pain intensity

Results of Changes

• Sensitization of PNS & CNS occurs
• Increased excitability as the threshold is reduced
• Expansion of receptor fields in periphery is found
• Primary and Secondary Hyperalgesia, Allodynia, and Temporal Summation are involved
• Changes can continue after healing

Chronic Pain is Complex!

• Epigenetic Factors: physical activity, psychological stress, environment, and behavior can influence chronic pain
• Neural Factors: include CNS & PNS adaptations
• Endocrine Factors: the hypothalamus, pituitary, adrenal axis(cortisol and epinephrine), and stress intolerance(increased symptoms in response to stress) have influence
• Immune Factors: immune cells & inflammatory mediators contribute to chronic pain

Biopsychosocial Model

• It recognizes that psychological, social, and biological components all have an effect on pain
• Biological processes: anatomy, physiology, tissue pathology
• Psychological: Thoughts, beliefs, and behaviors are impacted
• Social factors: Culture, occupation, and religion influence the experience of pain

Psychosocial Factors

• Yellow flags: emotional distress, pre-occupation with pain, pain catastrophizing, elevated fear-avoidance beliefs, kinesiophobia, low self-efficacy, incorrect beliefs about best strategies to treat pain, and incorrect beliefs about severity of injury and the impact of pain
• Blue Flags: Dissatisfaction with occupation or conflict with employer or colleagues

Common Clinical Presentations

• Common clinical signs include diffuse pain, hyperalgesia, allodynia, and impaired pain beliefs
• Fear, anxiety, and depression and common
• The patient presents fear-avoidance behavior which limits movement/activity, increased reliance on medication/assistive devices, and increased sensitivity to the stimulus of heat/cold/sound/light

Smart et al. (2012)

• Research identified cluster that was highly predictive of central sensitization: disproportionate/non-mechanical pain provocation patterns in response to multiple factors, and pain disproportionate to injury. Finally, they found maladaptive psychosocial factors

Patients Reported Outcome Measures (PROs)

• The 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), and Tampa Scale of Kinesiophobia (TSK) are all PROM tools used in research and practice

Biopsychosocial Approach: Interventions

• Top-down approaches include mindfulness, meditation, and sleep hygiene to address unhealthy pain beliefs and behaviors
• Pain Neuroscience Education and Graded Motor Imagery is helpful
• Movement/Exercise, Manual Therapy and Electromodalities, are also helpful

Interventions

• Treat identified impairments
• Emphasize active interventions and function/functional recovery instead of passive ones and focusing on pain
• Also educate: early and throughout treatment, provide reassurance, and limit anatomical descriptors to describe pain source

Cognitive-Behavioral Approaches to Intervention: Graded Activity & Graded Exposure

• These addresses modifiable risk factors
• Reinforce with positively with increasing the patient's activity level
• Also gradually expose those to situations of which they are fearful

Interventions: Pain Neuroscience Education

• Educate patients on the basic neurophysiological processes of pain in patient-friendly terms
• Avoid language describing pathologic tissue (e.g. "herniated disc", "degeneration”, “torn")
• Adjunct to movement-based interventions and improves fear of movement & pain catastrophizing

fMRI of Patient with Chronic LBP that received PNE

• People with lumbar HNP who received a 30' session of PNE had the fMRI obtained during performance of PPT
• Outcomes included: ↓ activation of PAG & cerebellum, and ↑ activation of M1

Clinical Data on PNE

• Research suggests that preoperative PNE will yield decreased utilization of healthcare at 1 & 3 years after lumbar surgery
• Studies find online and onsite PNEs help kinesiophobia but not perceived disability
• PNE should not be relied upon as the sole intervention
• PNE will reduce the rate of kinesiophobia & pain catastrophizing but not help pain or disability

Interventions: Graded Motor Imagery

• Treatment includes: Left / Right Discrimination, Explicit motor imagery, and Mirror therapy

Left/Right Discrimination

• There is a loss of being able to distinguish what side of the body the pain is on
• Training should use images of the involved body part: L vs R extremity, movement direction (i.e. RSB vs LSB), and uncommon positioning (e.g. upside down)
• Normal performance requires 80% accuracy and a 2.4-second response time

Explicit Motor Imagery

• This involves thinking of movement without actually moving
• When done, the areas of the brain associate with movement gets activated

Thearpy Through Mirrors

• Should progress to moving the involved side, starting without Begin with keeping involved side stationary & progress to moving involved side

Prognosis

• This is a difficult population because there effects on the physical and psychosocial traits
• Early identification is important. Prevention of it happening more so
• There is a low rate of full recovery as of 2023
• Treatment plans should be multimodal approach to exercise

Closing Thoughts

• Pain is a defense triggered when harm is about to happen, either really or perceived
• Long tern pain is caused changed in the brains functions
• The brains neuroplasticity is changed over time and can be reversed
• Patients need tailored treatment through the use of psychology, social activity, and the human anatomy work together for success