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Nociceptive Pain
Tissue is the issue
Localized pain
May be dull ache or throb at rest
No night pain, dysesthesia, burning, shooting, or electric sensation
Peripheral Neuropathic Pain
Nerve is the issue
History of nerve injury, pathology, or mechanical compromise, cancer
Pain referred in a dermatomal or cutaneous nerve distribution
Provoked with mechanical testing (neurodynamic testing)
Pins & needles or numbness
Nociplastic Pain
Pain disproportionate to nature of injury
Central sensitization
Unpredictable provocation & non-specific aggravating & easing factors
Widespread pain
Maladaptive psychosocial factors
Pain catastrophization, anxiety, & depression
How do you choose an intervention for your patient’s pain?
Subjective history, red flags, physical exam, outcome measures
Assess all biopsychosocial factors
Identify primary driving pain mechanism
Consider sound evidence
Choose best option for pt at that time
What are the main pain drivers of nociceptive pain?
Immuno-inflammatory cascade (classic)
Cytokines & chemokines
Edema
Post-op
What are potential biophysical agents to use for nociceptive pain?
Cold therapy
E-stim (NMES, TENS)
Low-Light Laser Treatment (LLLT) or Photobiomodulation (PBM)
What are the main pain drivers of neuropathic pain?
Immuno-inflammatory
Neurologic inflammation
What are potential biophysical agents to use for neuropathic pain?
E-Stim (TENS)
Low Light Laser Treatment (LLLT)
Gamma-Aminobutyric Acid (GABA)
Primary inhibitory NT of brain
Major inhibitory NT in SC (modulates ion channels)
E-Stim activates GABA → decrease pain
What are the main pain drivers of nociplastic pain?
Immuno-inflammatory (acute)
Neuro-inflammatory
Centrally mediated
Gate Control Theory of Pain
A-beta fibers = low threshold, fast, myelinated
Their activity activates inhibitory interneurons in dorsal horn → closes spinal gate → reduces/blocks pain transmission from C-fibers
C-fibers = high threshold, slow, unmyelinated
Their activity inhibits the inhibitory interneurons → opens gate → increases pain transmission to brain
Updated Gate Control Theory of Pain
Modulation is core concept
Primary afferents:
low-threshold C-fibers = mechanoreceptors
high-threshold A-delta & A-beta fibers = nociceptors
All primary afferents are excitatory
Dorsal horn complexity:
Multiple inhibitory + excitatory interneurons
Several distinct projection neurons send signals to different brainstem & brain nuclei
Non-neuronal cells actively contribute to pain processes
Descending modulation: brain exerts top-down control over spinal gating
Endocrine involvement: hormones help inhibit pain
Immune involvement: T-cells & macrophages release opioid peptides that contribute to analgesia
Cryotherapy
Use of cold as therapeutic agent
Locally → ice packs, ice massage, vapocoolant spray, gel packs
Broadly → non-local application
What are the general benefits of cryotherapy?
Decrease vascular permeability
Decrease pro-inflammatory cytokines
Increases anti-inflammatory cytokines
Decrease transmission velocity
Induce analgesia
Decrease oxidative stress
Nitrogen-Based Partial Body Cryotherapy
Liquid nitrogen used to cool a cylindrical shaped chamber
Gas enters from bottom at -150 - -200°
Whole Body Cryotherapy
Electric
Fresh, oxygenated air
Temperature maintained at -150°
Activates ANS → epi, norepi, & dopamine
Higher cellular activation & mitochondrial biogenesis
Lowers oxidative stress
Transcutaneous Neuromuscular Stimulation (TENS)
Reduces hyperalgesia → activates large diameter afferent fibers → CNS → activates descending inhibitory systems
High frequency → increase concentration of B-endorphins & methionine-enkephalin (CSF)
Low frequency → activates opioid, GABA, & serotonin by reducing dorsal horn neuron activity
Reduce central excitability
Low Level Laser Therapy (LLLT)
Laser = light amplification by stimulated emission of radiation
Molecular & cellular effects
NOT for nociplastic pain