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In Vivo studies

In Vivo studies. Kuslich et al:OCNA April 1991. The tissue of origin of low back pain and sciatica: A report of pain response to tissue stimulation during operations on the lumbar spine using local anesthesia.

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In Vivo studies

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  1. In Vivo studies Kuslich et al:OCNA April 1991. The tissue of origin of low back pain and sciatica: A report of pain response to tissue stimulation during operations on the lumbar spine using local anesthesia. Only the PLL, posterior and lateral annulus, and compressed nerve root produced pain consistently.

  2. Sinu Vertebral Nerve Size: 0.5 – 1mm Formed bilaterally and segmentally Sensory spinal branch from the ventral ramus and sympathetic branch from the grey ramus communicans which is the major contribution. Enter spinal canal through inter vertebral foramen passing just below the pedicle along with the segmental vessels, lying anterior to the nerve roots. Some time only multiple filaments (upto 6) are seen

  3. Sinuvertebral Nerve The nerve then sends transverse and descending branches to the same level disc and PLL and another branch which ascends along the PLL to the next level. These branches interdigitate with branches from the opposite side. The sinuvertebral nerve supplies only structures within the spinal canal. It innervates the anterior surface of the dura, the vessels in the anterior epidural space in addition to the PLL and posterior disc.

  4. Sinu Vertebral Nerve The nerve fibres penetrate the outer 3 layers of the annulus, for a distance of about 3 mm, and they are sparse. Disc surface, peridiscal tissues and PLL has a very rich network

  5. Sinu Vertebral Nerve Sympathetic fibres are vasomotor efferents and sensory fibres are proprioceptive and nociceptive. A delta and C fibres.

  6. Differential Innervation The lumbar vertebral endplate, particularly in its central area adjacent to the nucleus pulposus, is supplied with a neural pattern similar to the outer annulus. The anterior annulus and ALL is supplied by sympathetic fibres from the sympathetic trunk or grey ramus. The lateral side of annulus has the richest innervation, from the grey ramus and branches of the ventral ramus.

  7. The emerging concept is that disc, unlike other joints, is provided with a predominantly visceral type of nerve supply.

  8. Neural Sensitization ‘Peripheral sensitisation’ of the nerve endings take place by the pro-inflammatory mediators of the granulation tissue of the annular tears and also by the exposed nuclear material which can irritate the spinal root and the sinuvertebral nerve endings. The sympathetic afferents( mechanoreceptors and nociceptive) are also sensitised peripherally by efferent sympathetic fibres. The sympathetic afferents are also susceptible to ‘central sensitisation’ as in other visceral pains by ‘stress’ which will lower the pain threshold of the visceral afferents-in chronic discogenic pain.

  9. Neural Sensitization The pain response can be affected by local reflex mechanisms and also by the DRG satellite cells.

  10. Innervation of Pathological Disc In the degenerate disc the nerve fibres penetrate the outer half of the annulus and in some painful degenerate discs upto the inner third of the annulus. The fibres are seen in a perivascular position in the granulation tissue growing into the degenerate disc, neo-innervation.

  11. Origin of discogenic low back pain Injury or overload in a normal or aging disc Annulus fibrosus disruption or tear. Repair by Inflammation(ingrowth of macrophages and mast cells) Release of growth factors like bFGF and TGF b and cytokines like TNF a Proliferation and differentiation of cells in disc which produces fibrosis, neovascularisation and neoinnervation Disc degeneration and discogenic back pain.

  12. Discogenic low back pain The ingrowth of nerve endings to the deeper layers of the annulus is the cause of the chronic dull aching discogenic low back pain, which is exacerbated by mechanical loading of the disc. The principle of discography is increasing the intradiscal pressure stimulating these mechanoreceptors in the annulus.

  13. Disc deterioration and neuropathic pain In addition to the local pain responses described above leading to low back pain, disc degeneration also produces neuropathic pain by stimulating the cauda equina, the DRG or the roots distal to DRG with pain experience from the area of distribution of the nerve. This can be due to mechanical compression or inflammatory chemicals.

  14. Effects of nucleus pulposus It contain pro-inflammatory mediators like cytokines. Increases the discharge of nerve fibres, reduce the conduction velocity of the spinal nerve root, attract inflammatory cells , induce increased intraneural capillary permeability, and influence intraneural capillary blood flow, induce degeneration of nerve fibres. This nerve damage itself lead to macrophage stimulation.

  15. Molecular factors and biomarkers. Neurotrophins, such as nerve growth factor, brain derived neurotrophic factor and glial derived neurotrophic factor act at the level of DRG and nerve root and play role in chronic pain mechasnisms. Levels of S-100 protein and neurofilament have been found to be higher in the CSF of patients with disc herniation and sciatica, indicating axonal and Schwan cell damage.

  16. Outcome of discogenic sciatica& Pain generators

  17. Convergence and Referred Pain Visceral autonomic nervous system Somatic autonomic nervous system Pattern recognition by CNS to the somatic area Cardiac Pain referred to Lt shoulder

  18. After all, what is pain? Pain is an unpleasant sensory and emotional experienceassociated with actual or potential tissue damage or described in terms of such damage- International Association For The Study Of Pain 1979

  19. References J Randy Jinkin: the anatomic and physiologic basis of local, referred and radiating lumbosacral pain syndromes related to diseases of the spine. J Neuroradiol 31:163-80 (2004) M A Edgar . The nerve supply of the lumbar intervertebral disc. JBJS (2006) Peng B et al. possible pathogenesis of painful intervertebral disc degeneration. Spine 31(5) 560-566 (2006) Wiltse LL. The anatomy of the extradural compartments of the lumbar spinal canal- Peridural membrane and circumneural sheath. Radiologic Clinics of North America 38(6). 1177-1205 (2000) Mulleman D et al: pathophysiology of disc related low back pain and sciatica.II- Evidence supporting treatment with TNF-ά antagonists. Joint Bone Spine 73:270-277 (2006) Brisby H. pathology and possible mechanisms of nervous system response to disc degeneration. JBJS 88:68-71 (2006) .Bogduk N. The innervation of the lumbar spine. Spine 8(3) 286-93 (1983)

  20. It is now clear that if we can effectively treat the pain despite the underlying cause, it will be possible for patients to regain normal functioning. The key to more successful pain treatment is to understand the mechanisms that generate and maintain chronic pain. Nociception is essential for survival whereas pathological pain is maladaptive and often unresponsive to pharmacotherapy. Voltage-gated sodium channels, Nav1.1–Nav1.9, are essential for generation and conduction of electrical impulses in excitable cells. Human and animal studies have identified several channels as pivotal for signal transmission along the pain axis, including Nav1.3, Nav1.7, Nav1.8, and Nav1.9, with the latter three preferentially expressed in peripheral sensory neurons and Nav1.3 being upregulated along pain-signaling pathways after nervous system injuries. Nav1.7 is of special interest because it has been linked to a spectrum of inherited human pain disorders.

  21. Only when we have the tools to identify the mechanism responsible for the pain in a particular individual, and t h e n the capacity to reverse the mechanisms, will the management of neuropathic pain really advance. The onus on the clinician will then be to use the history, examination, investigation, and diagnostic tools as a way to identify the mechanisms that operate in their patients and use this information to select appropriate treatment.

  22. We highlight current theories about peripheral neuropathic pain and show that progress in management is contingent on targeting treatment not at the aetiological factors or the symptoms but at the mechanisms that operate to produce the symptoms. This approach will require substantial progress in our understanding of the pathophysiology of neuropathic pain, the development of accurate diagnostic tools to discover what mechanisms contribute to the pain syndrome in an individual, and effective treatments aimed specifically at the mechanisms.

  23. Neuropathic pain is a pathological pain The capacity to experience pain has a protective role: it warns us of imminent or actual tissue damage and elicits coordinated reflex and behavioural responses to keep such damage to a minimum. If tissue damage is unavoidable, a set of excitability changes in the peripheral and central nervous system establish a profound but reversible pain hypersensitivity in the inflamed and surrounding tissue. This process assists wound repair because any contact w i t h the damaged part is avoided until healing has occurred. By contrast, persistent pain syndromes offer no biological advantage and cause suffering and distress. Such maladaptive pain typically results from damage to the nervous system—the peripheral nerve, the dorsal root ganglion or dorsal root, or the central nervous system—and is known as neuropathic pain. Such syndromes comprise a complex combination of negative symptoms or sensory deficits, such as partial or complete loss of sensation, and positive symptoms that include dysaethesia, paraesthesia, and pain.

  24. ● The pathways of low back pain and radicular pain were clinically studied using a randomized control trial for L2 spinal nerve infiltration. ● The low back pain pathway was likely interrupted by L2 block in the treatment groups studied. ● The radicular pain pathway was interrupted for a short duration by L2 block in the clinical cases studied. ● The main afferent fibers of the low back pain pathway and part of those of the radicular pain pathway were thought to involve the L2 spinal nerve root, presumably via sympathetic afferents. ● An L2 block is useful in reducing LBP due to the disorders of L2 spinal nerve-innervated structures, such as the disc, facet joint, and sacroiliac joint. However, the therapeutic value of an L2 block may be occasionally insufficient to alleviate pain completely because of the short duration of its effect.

  25. It appears that only a small amount of investigation has been performed into the diagnostic accuracy of clinical tests to identify the tissue source of low back pain. There are tests for the disc and SIJ that have some diagnostic value but no test for the facet joint that appears informative. The usefulness of these tests in clinical practice, particularly for guiding treatment selection, remains unclear.

  26. There are inherent limitations in the accuracy of all diagnostic tests. The tests used to diagnose the source of a patient’s chronic low back pain require accurate determination of the abolition or reproduction of the patient’s painful symptoms.

  27. Examination of the back • 1 gait • 2 spine contours • 3 range of motion and rhythm • 4 reflexes • 5 strength • 6 root irritation signs • 7 root tension • 8 hip • 9 pulses 10 non organic signs

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