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.

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.

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

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.

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

Sinu Vertebral Nerve

• Sympathetic fibres are vasomotor efferents and sensory fibres are proprioceptive and nociceptive.

• A delta and C fibres.

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.

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

nerve supply.

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.

Neural Sensitization

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

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.

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.

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.

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.

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.

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.

Outcome of discogenic sciatica& Pain generators

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

After all, what is pain?

• Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage-

• International Association For The Study Of Pain 1979

References1. 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)

2. M A Edgar . The nerve supply of the lumbar intervertebral disc. JBJS (2006)3. Peng B et al. possible pathogenesis of painful intervertebral disc degeneration.

Spine 31(5) 560-566 (2006)

4. 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)

5. 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)

6. Brisby H. pathology and possible mechanisms of nervous system response to disc degeneration. JBJS 88:68-71 (2006)

7. .Bogduk N. The innervation of the lumbar spine. Spine 8(3) 286-93 (1983)

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.

Only when we have the tools to identify the mechanismresponsible for the pain in a particular individual, andt h e n the capacity to reverse the mechanisms, will themanagement of neuropathic pain really advance. The onuson the clinician will then be to use the history, examination,investigation, and diagnostic tools as a way toidentify the mechanisms that operate in their patients anduse this information to select appropriate treatment.

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

Neuropathic pain is a pathological painThe capacity to experience pain has a protective role: itwarns us of imminent or actual tissue damage and elicitscoordinated reflex and behavioural responses to keep suchdamage to a minimum. If tissue damage is unavoidable,a set of excitability changes in the peripheral and centralnervous system establish a profound but reversible painhypersensitivity in the inflamed and surrounding tissue.This process assists wound repair because any contactw i t h the damaged part is avoided until healing hasoccurred. By contrast, persistent pain syndromes offer nobiological advantage and cause suffering and distress. Suchmaladaptive pain typically results from damage to thenervous system—the peripheral nerve, the dorsal rootganglion or dorsal root, or the central nervous system—andis known as neuropathic pain. Such syndromes comprise acomplex combination of negative symptoms or sensorydeficits, such as partial or complete loss of sensation, andpositive symptoms that include dysaethesia, paraesthesia,and pain.

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

It appears that only a small amount of investigation hasbeen performed into the diagnostic accuracy of clinicaltests to identify the tissue source of low back pain. Thereare tests for the disc and SIJ that have some diagnosticvalue 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.

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

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