|Sciatica: Studies of symptoms, genetic factors, and treatment with periradicular infiltration|
The tissue origin of sciatic pain has been studied during decompression operations performed with local anaesthesia. In these studies, sciatic pain could be produced only by pressure on the compressed, swollen nerve root, or on the dorsal root ganglion (DRG). Pressure on normal nerve roots or on other tissue did not produce sciatica (Smyth & Wright 1958, Kuslich et al. 1991). The most common cause of nerve root compression is HNP (Mixter & Barr 1934).
Intervertebral disc is composed of lamellar anulus fibrosus (AF) encircling the central gelatinous nucleus pulposus (NP), and thin vertebral endplates. Collagens and proteoglycans (PG) are the primary structural components of the intervertebral disc macromolecular framework (Eyre & Muir 1976, Buckwalter 1995, Antoniou et al. 1996). The NP consists of a central core of a well-hydrated PG matrix entrapped in a loose, irregular meshwork of collagen fibers. The PGs consist of sulphated glycosaminoglycan side-chains (chondroitin and keratan sulphates) covalently bound to a protein core. The negatively charged sulphate and carboxyl groups attract cations (Na+, H+). Indeed, in children and young adults, water accounts for over 80% of the weight of the NP. Hyaluronic acid, long, nonsulphated glycosaminoglycan, binds multiple aggrecan molecules stabilized by a link protein, to form large PG aggregates (Eyre 1979). PGs account for 50 % of the dry weight of the NP from a child, whereas collagens account for about 20 % (Buckwalter 1995). Collagen II is the major collagen of human NP (~80 %), but collagen VI (~15 %), collagen IX (1–2%), collagen XI (3%) and traces of collagen III can also be found (Hukins 1988, Eyre et al. 1989, Buckwalter 1995).
The AF consists of 10–20 concentric lamellae of collagen fibres. The lamellae of the outer part of the AF are attached to the ring apophysis of the upper and lower vertebrae. The inner lamellae are attached to the end-plates. The content of collagen I increases (up to 80 %) towards the outer part of the AF and the content of collagen II towards the NP. Minor collagens of the AF include type V (3%), type VI (10%), type IX (1–2%) and traces of type III collagen (Eyre et al. 1989, Buckwalter 1995).
The end-plates consist of hyaline cartilage, which is approximately 1 mm thick. In contrast to articular cartilage, there are no collagenous connections directly anchoring the end-plates to the bone of the underlying vertebral bodies. The collagen fibers of the inner AF are attached to the end-plates. The cells of the cartilaginous end-plate are chondrocytic cells. The end-plate has a lower PG and water content, and a higher collagen content than do adjacent regions of the disc (Roberts et al. 1989). Its function is to serve as a semipermeable membrane to facilitate diffusion of solutes from the vertebra to the disc (Eyre 1979).
Human intervertebral discs undergo age-related degenerative changes, potential causes of which include declining nutrition, loss of viable cells, cell senescence, post-translational modification of matrix proteins, accumulation of degraded matrix proteins, and fatigue failure of the matrix (Buckwalter 1995). The onset of disc degeneration is not possible to observe in humans, but the process has been studied thoroughly in animal models. After incision of rabbit AF, acute herniation of the NP was produced, followed by progressive dehydration of the NP with a concomitant decrease in total uronic acid content (constituent of PGs) (Lipson & Muir 1981a, Lipson & Muir 1981b). Similar results (decrease of PG and water content in the NP) have been obtained in a pig model (Karppinen et al. 1995). The phenotype of the chondrocytes also seems to change after the injury; instead of producing collagen II, the chondrocytes begin to produce collagens I, III, IV and VI (Kääpä et al. 1994, Kääpä et al. 1995).
Mechanisms of disc injuries have been studied in animal and cadaver models. After the injury, progressive water and PG loss in the NP occurs (Karppinen et al 1995). In post-mortem analysis of human spine samples, three types of anular tears have been shown: concentric, transverse and radial tears (Yu et al. 1988b). Of these, concentric tears are not seen in MRI. Transverse, or rim lesions are suggested to be due to trauma rather than biochemical degradation, and they develop independently of nuclear degeneration (Osti et al. 1992). High-intensity zone (HIZ) lesions, which seem to associate with typical pain in discography, represent a combination of radial and circumferential tears (Aprill & Bogduk 1992).
Tears of the anulus are suggested to play an important role in the degeneration of the intervertebral joint complex (Osti et al. 1990). Radial ruptures are especially interesting as they precede disc degeneration (Yu et al. 1988a, Osti et al. 1992). Radial tears extending from the NP into the middle layers of the AF are associated with subjective pain in discography (Vanharanta et al. 1988a, Vanharanta et al. 1989, Moneta et al. 1994), and are also known to cause sciatic pain (Ohnmeiss et al. 1997).
Biomechanisms of disc herniation have been studied in cadaver spine segments. Hyperflexion injury caused an anular tear either centrally or on the side opposite the component of lateral bending where the AF was stretched the most (Adams & Hutton 1982). The fissure through which the nuclear pulp was extruded usually occurred at the boundary between the AF and the end-plate. Large central nuclear extrusions ruptured the posterior longitudinal ligament, whereas smaller extrusions either formed a bulge behind it or were deflected sideways and appeared on one or both posterior lateral margins of the disc (Adams & Hutton 1982). In the same study it was shown that the susceptibility of a disc to prolapse depends on age, degree of disc degeneration and spinal level. Slightly degenerated lower lumbar discs of people aged between 40 and 50 seemed particularly vulnerable (Adams & Hutton 1982). The same authors showed that even young discs can prolapse slowly over days or months by fatigue compressive loading of a flexed disc (Adams & Hutton 1985). Disc deterioration occurred gradually. Distortion of the posterior lamellae is first observed, then breaking through the lamellae, and thereafter gradual nuclear extrusion through posteriolateral anular fissures and disruption of anular lamellae (Adams & Hutton 1985). This gradual disc prolapse mechanism probably accounts for the non-dramatic disc herniation cases.
Nuclear extrusion usually occurs posterolaterally, at the weak point of the dorsal AF (Farfan et al. 1970, Adams & Hutton 1985). At this point, the structures prone to irritation by the HNP are nerve roots. At each lumbar level, a pair of dorsal and a pair of ventral nerve roots leave the dural sac just above the level of each intervertebral foramen, taking with them an extension of dura and arachnoid mater called the dural sleeve (Figure 1A). Later, dorsal and ventral roots at both sides converge at the outlet of the root canal, giving rise to a spinal nerve (Olmarker 1991, Bogduk 1997a).
The dorsal root transmits sensory fibres from the spinal nerve to the spinal cord, whereas the ventral root largely transmits motor fibres, along with some sensory fibres, from the cord to the spinal nerves. The diameter of large myelinated axons (Aδ and Aβ fibers) ranges between 1.5 and 16 µm, while the unmyelinated nociceptor axons (C fibres) range between 0.4 and 1.6 µm (Olmarker 1991, Bogduk 1997a). The soma of ventral roots lie in the ventral horn of the spinal cord, whereas the soma of the afferent dorsal roots lie in the dorsal root ganglia (DRG). A DRG typically lies at the distal end of the dorsal root inside the apex of the dural sleeve, directly inferior to the pedicle and close to the nerve root axilla (Cohen et al. 1990).
The nerve roots differ from peripheral nerves as they are enclosed by the thin root sheath, cerebrospinal fluid and meninges. The axons of the peripheral nerves, on the other hand, areenclosed by the epineurium and the perineurium (Olmarker 1991). Moreover, the arteriolar and venular networks are less developed in the nerve roots (Figure 1B), and there is no regional blood supply to the intrinsic vasculature, as in peripheral nerves. These anatomical circumstances make nerve roots more vulnerable to mechanical stress than peripheral nerves. The findings in the porcine model indicate that diffusion from the cerebrospinal fluid can not compensate completely for compression-induced effects on the blood flow in the intrinsic vessels (Olmarker et al. 1990). DRG is an exceptional neural tissue as it is covered by a tight capsule with a blood-nerve barrier less well developed than in the nerve root vessels (Seitz et al. 1985), which makes it more prone to the closed compartment syndrome (Rydevik et al. 1989).
Figure 1. A) Cross-section of the spinal cord with a ventral (VR) and dorsal (DR) spinal nerve root. The cell bodies of the motor axons are located in the anterior horn of the gray matter of the spinal cord, whereas the cell bodies of the sensory axons of the dorsal root are located in the dorsal root ganglion (DRG). The ventral and dorsal nerve roots blend just caudal to the DRG, and form the spinal nerve (SN). Nerve roots are covered with root sheath (RS), a continuation of the pia mater covering the spinal cord. The spinal cord and nerve roots are floating freely in the cerebrospinal fluid (CSF) in the subarachnoid space. D=dura. B) Schematic drawing of vascular supply to the spinal cord and nerve roots. The nervous system branch of the segmental artery (SA) joins the nerve root and forms a ganglionic plexus (GP) in the DRG and caudal nerve root arteries (NRA) running in cranial direction. From the vaso corona of the spinal cord, cranial arteries run in caudal direction in the nerve roots. (Reproduced with permission from, Olmarker K, Thesis, Gothenburg 1990).
Other causes of sciatica can be divided into intraspinal or extraspinal. Intraspinal causes include spondylosis and osteoarthritis with encroachment upon the intervertebral foramina (Schellinger et al. 1987). Lateral lumbar spinal canal stenosis due to osteoarthritis can be divided into entrance zone, mid zone and exit zone stenosis (Lee et al. 1988). The most common cause of entrance zone stenosis is hypertrophic osteoarthritis of the facet joint, particularly involving the superior articular process, whereas exit zone stenosis is caused typically by a subluxed facet joint or by an osteophytic ridge along the superior margin of the disc. However, mid zone stenosis is clinically the most important entity, because the DRG occupies a large part of the mid zone. Two common causes are osteophyte formation under the pars interarticularis where the ligamentum flavum is attached, and fibrocartilagenous or bursal tissue hypertrophic at a spondylolytic defect (Lee et al. 1988). Spondylolisthesis is occasionally responsible for sciatica, and symptoms are usually bilateral (Kikuchi & Hasue 1988). Zygoapophyseal joint cyst, on the other hand, produces unilateral symptoms (Reust et al. 1988). Other intraspinal processes causing sciatica include tumors, abscesses and tuberculosis (Elliott & Schutta 1971).
Extraspinal causes can be differentiated into diseases of the lumbosacral plexus and lesions of the sciatic nerve or its branches. Lesions of the lumbosacral plexus usually produce symptoms of more than one segment, and often the pelvic condition responsible for lumbosacral pain overshadows sciatica. In disease of the sciatic nerve, pain is not usually a prominent symptom (Elliott & Schutta 1971). Diseases of the lumbosacral plexus include pelvic tumors (Bickels et al. 1999), intrapelvic aneurysm (Dudeney et al. 1998), and endometriosis (Dhote et al. 1996). Disease of the sciatic nerve can be caused by compression of the nerve as in hamstring (Puranen & Orava 1991) and piriformis syndromes (Hanania & Kitain 1998), or by vascular compromise as in diabetes (Naftulin et al. 1993). A rare cause of sciatica is cervical and thoracic spinal cord compression (Ito et al. 1999).
Physicians have to recognize nondermatomal pain which is synonymous with referred pain from the mesenchymal structures (bones, joints, ligaments and bursae) of the lumbosacral spine, the pelvis and the lower extremity. Referred pain is deep, dull, boring and aching. It follows the distribution of the myotomes and sclerotomes (Elliott & Schutta 1971, Bogduk 1997a), as opposed to dermatomally distributed radicular pain.