Richard Bartley MSc MCSP, Betsi Cadwaladr University Health Board, Wales
Only a few studies on nerve root compression exist. Olmarker et al, in 1990, experimented with porcine nerve roots. Balloons were attached to the nerve roots and inflated to different pressures. Light pressure (10 mg) compromised venous blood flow, nutritional supply and nerve conduction, whilst moderate pressure (up to 50 mg) was associated with the formation of oedema and substantial reduction in axonal transport. High pressure completely stopped motor and sensory conduction.
Garfin et al, in 1995, analysed the effects of compression on nerve roots in pigs. Graded compression of more that 75 mg for two hours induced electrophysiological alterations in afferent and efferent conduction. Pressure beyond these parameters caused irreversible damage to the nerve roots, particularly to the afferent (sensory) fibres.
This may be explained by the structure of the nerve root. The outer layer of a nerve, the epineurium, acts as a buffer to any mechanical interface. It is less well developed in a spinal nerve root compared to a peripheral nerve and therefore offers less protection to mechanical force (Murphy 1977).
A peripheral nerve also contains a deeper layer providing tensile strength and the elasticity, the perineum, which is absent in a spinal nerve root. This may explain why blood flow and nerve conduction can be impeded at relatively low pressure.
Compression also effects the blood flow to the spinal nerve roots and will interfere with transmission to and from the spinal cord to the lower limbs (Garfin et al, 1995). The blood supply of the spinal nerve root takes the form of a network of capillary beds, supplied by arterioles that enter the epinerium at various points along the nerve. The mid-zone between the point of entry of the arterioles is relatively hypovascular (Parke 1985). In addition, the lymphatic network of the spinal nerve root is relatively poor (Sunderland, 1968).
These two factors combined can prevent the removal of inflammatory agents from the nerve when injured by mechanical compression or stretching. Longitudinal tension may also induce conduction failure and ischaemia. If there is increased tension, as when a nerve root is displaced by a disc hernia, this normal motion may be restricted leading to irritation and inflammation of the nerve as it is stretched during attempts to elongate and deviate along its course (Spencer et al, 1983). Kwan et al, 1992, showed that spinal nerves fail at 15-23% strain. This tension may also effect blood flow and conduction but the effects of stretching compared to compression is less well studied.
There is some evidence to show that the proteoglycans present in the nucleus pulposus of the intervertebral disc, may have a toxic effect on nerve root tissue if they escape the confines of the disc and infiltrate the neural canal and spinal nerve roots. The spinal nerve lacks a smooth membrane called the perilemma, which is present in peripheral nerves. This acts as a diffusion barrier preventing chemical irritants coming into contact with the nerve itself (Kristensson & Olsen, 1971).
Marshall, 1977, subjected lung tissue of guinea pigs to an isolated human proteoglycan and this produced a marked reaction of bronchospasm followed by oedema of the lung. This was further confirmed by the ability of cortisone, when injected into the neural space, to reduce the symptoms of nerve root pain.
Two other important experiments highlight the importance of autoimmunal reactions to disc material. McCarron et al, 1987, injected autogenous nuclear material into the neural canals of four dogs and normal saline into another four dogs. Following autopsy analysis the control group that received the saline resulted in no inflammatory response which was in marked contrast to the group that received the nuclear material.
Bobechko and Hirsch, 1965, inserted material from the nucleus pulposus of a series of rabbit lumbar discs into pouches behind the animal's right ears. A similar pouch was made behind the left ears but no nuclear material was placed in these. No histological changes were noted between the left and right pouches but the right primary lymph nodes were invariably larger adjacent to the right pouches compared to those on the left. This experiment showed, that at least in rabbits, material from the nucleus pulposus will produce an auto-immune reaction when it is exposed to tissue outside the disc.
The results of these experiments have implications for the understanding of nerve root pain secondary to herniated disc. They suggest that proteoglycans from the nucleus pulposus are antigenic and will cause irritation, oedema and nociceptive responses when a spinal nerve root is exposed to them. These research findings suggest that mechanical forces alone cannot explain sciatica. However the investigation of the histological states of injured nerve roots is not yet possible and the use of radiological investigations, such as MRI, remain the mainstay of clinical practice at this time.
References
Garfin SR, Rydevik B, Lind B & Massie J: Spinal nerve root compression. Spine 1995: 20; 1810-1820
Kristensson K, Olsson OH: The perineurim as a diffusion barrier to protein traces: differences between mature and immature animals. Acta Neuropath. 1971; 17: 127
Kwan MK, Wall EJ, Massie J, Garfin SR: Strain, stress and stretch of the peripheral nerve. Acta Orthop Scand 1992; 63: 267-272
McCarron RF, Wimpee MW, Hudgkins PG: The inflammatory effect of the nucleus pulposus. Spine 1987; 12: 759-764
Murphy RW: Nerve roots and spinal nerves in degenerate disk disease. Clin Ortho & Rel Research 1977; 129: 46-60
Olmarker K, Rydevik B, Holm S: Edema formation in spinal nerve roots induced by experimental, graded compression. Spine 1989; 14: 569-573
Parke WW, Watanabe R: The intrinsic vasculature of the lumbosacral spinal nerve roots. Spine 1985; 10: 508-515
Spencer DL, Irwin GS, Miller AJ: Anatomy and significance of fixation of the lumbosacral nerve roots in sciatica. Spine 1983; 8: 672-679
Sunderland S: Blood supply of peripheral nerves: practical considerations. Arch Neuro. Psychiatr 1945; 54: 25