Disc Herniation & Radiculopathy Facts:

 

  1. 76% of the disc herniations and 26% of disc bulges show partial or complete resolution on repeat scanning. (1) 46% will have 75-100% resorption and 36% will show a 50-75% decrease in herniation size. The largest extrusions demonstrate the greatest degree of resorption and contained herniations demonstrate the least. (1)

 

1. Bush K. Cowan N, Katz De, et al. The natural history of sciatica associated with disc

pathology: A prospective study with clinical and independent radiographic follow-up.

Spine 1992;17:1205-12.

 

  • It is postulated that once the nuclear material is exposed to the vascular

environment of the epidural space, cellular mechanisms contribute to resorption. (38)

These disc later demonstrate desiccation on follow-up MRI studies (37)

 

37. Saal JA, Saal Js, Herzog RJ. The natural history of lumbar intervertebral disc

extrusions treated non-operatively. Spine 1990;15:683-6.

38. Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase

A2 activity in lumbar disc herniations. Spine 1990;7:674-8.

 

·       Additionally, 90% of patients respond to conservative care with no statistical difference in those with neurologic weakness, size of herniation or presence of extruded or fragmented disc. (2)

 

2. Saal AJ, Saal JS. Nonoperative treatment of herniated lumbar intervertebral disc with

radiculopathy. An outcome study. Spine 1989;14:431-7.

 

  • Small, contained herniations frequently create severe pain and large extrusions and sequestrations can be painful or painless. The factors that determine the pain producing capability is unclear and may be related to its chemical potential more than its anatomic characteristics. (36)

 

36. Saul JS. The role of inflammation in lumbar pain. Spine 1995;16:1821-7.

 

  • Annular damage leads to the escape of nuclear material, which causes an inflammatory reaction, local nociceptor stimulation, potential nerve injury and subsequently pain. When this occurs by fissures reaching the outer disc annulus, which has a nerve supply, it may serve to explain back and somatic referred pain into the lower limb (i.e. internal disc disruption syndrome). When the fissure extends though the annulus, the inflammatory process leads to radicular limb pain. This process may explain those instances of severe radicular pain occurring in the absence of gross neural compression – that is chemical radiculitis. (95)

 

95. Macnab I. The mechanism of spondylogenic pain. Pain 1971;89-95.

 

 

 

  • Consistent with the findings that sensory fibers are the most susceptible to compression, they are the first fibers to be injured and the last to recover. (40) Recovery of the efferent (motor) conduction system after compression is usually more complete than the afferent (sensory) nervous system. (52).

 

40. Saul JA. Natural history and nonoperative treatment of lumbar disc herniation. Spine

1996;21 (24S)2S-9S.

52. Rydevik BL, Pedowitz RA, Hargens AR, et al. Effects of acute, graded compression

on spinal nerve root function and structure. Spine 1991;16:487-93.

 

·       Additionally, demonstration of radicular symptoms and signs can develop without significant nerve root compression (56). Conversely, radicular findings may improve or even resolve despite the persistence of focal compressive lesions. (57)

 

56. Jaffrey D, O’Brien JA. Isolated intervertebral disc resorption: a source of mechanical

and inflammatory back pain. Spine 1986;11:397-401.

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57. Boden SD, Davis DO, Dina TS, et al. Abnormal magnetic-resonance scans of the

lumbar spine in asymptomatic subjects: a prospective investigation. J Bone Joint

Surg 1990;72:403-8.

 

  • Compression of normal spinals nerve results in neurologic symptoms such as paresthesias and motor loss but pain is absent unless an inflammatory response also occurs. (58) This suggests the importance of the role of inflammation in radicular pain.

 

58. Garfin Sr, Rydevik B. Lind B, et al. Spinal nerve root compression. Spine

1995;20:1810-20.

 

  • Exiting nerve roots and their nutrient vessels lack a perineurium and have a poorly developed epineurium, rendering them particularly vulnerable to mechanical and chemical injury. Mechanical injury may occur directly from compression of the neural tissue itself or more commonly, indirectly from a disturbance of the blood and nutrient supply to the nerve (23).

 

23. Rydevik B, Brown M., Lundborg G. Pathoanatomy and pathophysiology of nerve

root compression. Spine 1984;9:7-15.

 

 

  • Additionally the threshold of firing of nociceptors will be

lowered by inflammation. (41)

 

41. Tal M, Devor M. Ectopic discharge in injured nerves: comparison of trigeminal and

somatic afferents. Brain Research 1992;1:148-51.

 

  • In patients with disc herniations, it has been shown that elevated levels of

phospholipase A2, tumor necrosis factor-alpha, prostaglandin E2, and inflammatory cytokines may directly or indirectly stimulate the nerve root and that inflammatory reactions may play an important role in causing sciatica. (48) Phospholipase A2 has neurotoxic properties and propagates an inflammatory cascade via liberation of arachidonic acid resulting in chemotactic and non-cellular mediated responses through leukotrienes and prostaglandins. (49). Levels 1000x normal are found within the nucleus pulposus of herniated discs. (38)

 

48. Takahashi H, Suguro T, Okazima Y, et al. Inflammatory cytokines in the herniated

disc of the lumbar spine. Spine 1996;21:218-24

49. Franson RC, Saal JS, Saal JA. Human disc phospholipase A2 activity is

inflammatory. Spine 1992;17(S):129-32.

38. Saal JS, Franson RC, Dobrow R, et al. High levels of inflammatory phospholipase

A2 activity in lumbar disc herniations. Spine 1990;7:674-8.

 

  • Nerve impairment can persist from an initial injury

(mechanical or chemical) or from repeated injury. Repeated injury can potentially lead to neurophysiologic changes in the central nervous system. Central sensitization refers to an enhanced responsiveness of the central nervous system to afferent input and is defined as a decreased threshold, an increased response to suprathreshold stimuli and ongoing spontaneous activity in the dorsal horn. After nerve injury, inflammatory mediators such as IL-b, PLA2, etc may act directly or induce the production of known algesic mediators, which sensitize dorsal horn neurons, resulting in central sensitization. (46)

 

46. Woolf CJ, Walters ET. Common patterns of plasticity contribution to nociceptive

sensitization in mammals and aplysia. Trends Neurosci 1991;14:74-78.

 

 

 

 

 

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