Lumbar Spine Pathology 4 PDF

Lumbar Spine Pathology 4 Leanna Blanchard, PT, DPT Guided Learning DPTD 851 Musculoskeletal Practice Management I  Learning Objectives At the end of this lesson, students will be able to: Describe the pain neuroscience associated with low back pain Describe th...

Lumbar Spine Pathology 4 Leanna Blanchard, PT, DPT Guided Learning DPTD 851 Musculoskeletal Practice Management I  Learning Objectives At the end of this lesson, students will be able to: Describe the pain neuroscience associated with low back pain Describe the neurophysiologic changes often associated with chronic low back pain Implement interventions specifically to address altered nociception Primary Hyperalgesia When injury to a tissue occurs, a few things happen at the site of injury: Release of ATP and protons Mast cells release histamine, 5-HT, prostaglandins Macrophages release cytokines, growth factors, bradykinins, and COX-2 Primary afferent neurons release substance P and CGRP We call this “inflammatory soup” Results in primary hyperalgesia Costigan and Woolf (increased nociceptive response) Primary Hyperalgesia The “inflammatory soup” causing primary hyperalgesia sensitizes the nociceptive neurons (peripheral sensitization) Nociceptor has a reduced threshold Nociceptor has increased excitability Primary hyperalgesia is only local to the injury Requires ongoing stimulus to maintain hyperalgesia Example When we push on a facet joint (UPAs) of someone without back pain, it does not hurt, or may only hurt a bit at very end range If someone has an injury to the facet tissues, resulting in primary hyperalgesia, when we apply our UPA, it may now be painful, or require less pressure (stimulus) to evoke the pain Secondary Hyperalgesia and Central Sensitization Say that facet joint does not get treated, and the patient continues to move into pain provoking positions/activities This results in repeated stimulation of the peripherally sensitized nociceptors Continued input to the dorsal horn of the spinal cord results in: Increased excitability of the ascending nociceptive pathway Decreased descending inhibition of nociception These CNS changes (central sensitization) may result in secondary or even widespread hyperalgesia Pain may now persist even once the stimulus at the facet joint is removed This video describes the process of central sensitization well: https://youtu.be/Te_8IS_4E7o?si=OPZj_1Px7PAJDHiT D’Mello and Dickenson Allodynia Allodynia may be present in patients with neuropathic and nociplastic pain types Example of potential neuropathic pain = lumbar radiculopathy Example of potential nociplastic pain = fibromyalgia Presence of allodynia indicates alteration of CNS processing of nociceptive stimuli Potentially also indicates sensitization of A-beta neurons in the PNS Heterosynaptic Facilitation Another potential central mechanism behind secondary hyperalgesia and allodynia is heterosynaptic facilitation Pathways adjacent to the injured/primary area synapse in the same region of the spinal cord May result in hyperalgesic spread of symptoms to non- injured areas (regional, mirror- image, widespread) Courtney et al, 2017 May result in allodynia if normally non-nociceptive fibers undergo this facilitation Neurogenic Inflammation Results when primary afferents behave differently after injury C fibers begin to act efferently – releasing inflammatory mediators to the injured tissue Substance P, calcitonin gene- related peptide (CGRP) Results in further sensitization and latent pain Latent pain = delayed pain Julius and Basbaum 2001 Hypoesthesia Both vibration detection and two-point discrimination (measures of potential hypoesthesia) may be decreased in those with chronic LBP Grey lines/areas indicate impaired VDT A: absent at S1 and S2 centrally, R L5 B: improved at S1 and S2, some residual loss Geletka et al, 2012 at R L5 Two point discrimination This example provides evidence of altered CNS Solid black lines indicate width at which patient could discriminate 2 separate points processing in a patient with LBP of contact The smaller the line, the better the Also provides evidence that PT interventions can ability to discriminate 2 points improve this altered CNS processing! Improved from figure A to B Exercise-based treatment Hypoesthesia Hypoesthesia may be the result of C fibers overriding A- beta fibers C fiber hyperexcitability Inhibits A-beta processing Results in impaired vibration detection threshold and impaired light touch sensation (both forms of hypoesthesia) Geletka et al, 2012 How do we know if someone with LBP has a centrally mediated pain component? Heightened intensity of pain that does not seem proportional to stimulus Altered threshold of pain outside the primary area Secondary or widespread hyperalgesia Pain ramps up easily – recall temporal summation Latent pain We use our quantitative sensory testing (QST) measures! Recall from 742… Pressure pain threshold Allodynia assessment Vibration detection threshold Mechanical detection threshold Temporal summation and conditioned pain modulation Transcutaneous Electrical Nerve Stimulation (TENS) Reduces central excitability, activates central inhibition Repetitive TENS use results in cumulative and longer lasting effect High vs Low Frequency TENS have similar but different effects (see next slide) TENS effects are dose-dependent – need to dose appropriately to have effects!  Transcutaneous Electrical Nerve Stimulation (TENS) High Frequency (50-100 Hz) Low Frequency (