[Anatomical background of low back pain: variability and degeneration of the lumbar spinal canal and intervertebral disc].
The central and lateral lumbar canals constitute complex osteofibrous neurovascular tunnels, allowing movement and deformation of the spine without loss of their main configuration. Intervertebral discs play an important role in determining their configuration. Disc degeneration may alter or even threat the functional anatomical relationships between successive adjacent "juncturae" of the vertebral column. Shape and morphometric aspects of the bony neural canals reveal level dependency [39], inter-individual variation [11], and are particularly susceptible for changes with aging [49]. Articular tropism and other left-right differences may influence their morphology. In the epidural compartments behind the vertebral bodies, a sagittal membrane may totally or partly connect the deeper layer of the posterior longitudinal ligament (PLL) with the posterior midline of the vertebral body. This membrane is considered clinically significant in the prevention of movement of disc material from one side to the other at the level of the vertebral bodies [44]. Meningovertebral ligaments represent a heterogenous group of membranous formations, connecting the dura with the PPL and other elements of the spinal canal. They prevent the dura from moving away from the bony container. These ligaments may vary from loose areolar tissue to clearly individualised ligaments and from pure midsagittal septa to more laterally oriented attachments. A double cross vault structure between the PPL and the dura mater often extends from L3 to the end of the dural envelope [3]. A retrospective study of medial and paramedial attachments in CT- and MRT-scans confirmed the presence of a mediosagittal structure below L3 in 35% of the cases 7). It was hypothesized that meningovertebral ligaments may play a [7] role as a barrier to transverse displacement of extruded disc material [43]. The surrounding morphology renders the lateral neural canal its typical inverted teardrop shape [39]. The subpedicular notch of the upper vertebra provides the widest part and represents the neural foramen strictu sensu. The posterolateral aspect of two articulating vertebrae and the interposed intervertebral disc constitute the anterior wall. The morphology of the anteroinferior aspect of the intervertebral foramen strongly depends on the condition of the apophyseal rings and the intervertebral disc. The latter may show a slight physiological posterior bulging at lower lumbar levels. The posterior wall of the nerve root canal is represented by the ligamentum flavum, the pars interarticularis of the upper vertebra, and the superior articular facet of the vertebra below. Thickening of the ligamentum flavum must be considered in relationship to alterations of anterior components: trabecular reorganization and spreading of vertebrae in aging [49], and disc degeneration [38, 49]. Nerve root sleeves display a level dependent, variable oblique course from their emanation from the thecal sac towards the outer third of the neural canal [39]. The presence of anamalous lumbosacral nerve roots may result in considerable course alterations, originating from an abnormal high or low level emanation, conjoined nerve roots, a double set of nerve roots or anastomosis between nerve roots of adjacent levels [20]. Variation exists in the position of the dorsal root ganglia (DRG) relative to the intervertebral foramen. An intraforaminal position seems to be more common at L4 and L5 levels; an intraspinal position has to be expected for the S1 DRG. Intraspinal position of L4 and L5 DRG renders them more susceptible to compression from a superior articular facet or a bulging disc. Cases of extraforaminal positions of dorsal root ganglia have been reported at L4 and L5 levels [22]. On its recurrent course through the lateral canal, the sinuvertebral nerve(s) supplies the laterodorsal outer annulus of the intervertebral disc, the PLL, the anterior 2/3 of the dural sac and the anterior vascular plexus [4, 14]. Many blood vessels pass through the lateral neural canal: the anterior and posterior spinal canal branches, anterior and posterior radicular branches, and veins of the anterior and posterior internal vertebral venous plexus [9]. Per segment, one ore two thick and one to four thin sinuvertebral nerves (SVN) originate from rami communicantes close to the connection of the latter to the spinal nerve [14]. The extensive ramifications of the thin SVNs complete a thorough network at the floor of the central lumbar canal. A large part of it supplies the PLL. The PLL is assumed to play an important role in proprio- and nociception [34, 39]. It is probably one of the first structures to mediate nociceptive information from disc tissue [14]. After injection of neuronal tracers into the sympathetic trunk at L3-L4 in rats, labeled cells were found in higher DRGs as well as labeled nerve fibers in the dura mater at lower levels. These findings indicate both a segmental and a non segmental pathway of sensory innervation of the dura mater and a role of higher DRGs in mediating LBP [25]. In the neighborhood of the SVN, other small branches emanate from the rami communicantes and join the dorsal ramus and the segmental artery that enters the neural canal. The sympathetic nerve plexus inside the anterior longitudinal ligament and the SNVs provide a network of nerve fibers around the vertebral bodies and intervertebral discs. These pathways explain the sympathetic component of the innervation of a number of spinal structures. The dorsal ramus innervates the facet joints at the corresponding level and one below, before it gives off muscular and cutaneous branches.
van Roy
P
P
Institut für Experimentelle Anatomie, Freie Universität Brüssel, Belgien.
Barbaix
E
E
Clarijs
J P
JP
Mense
S
S
D000375:Aging; D018450:Disease Progression; D006801:Humans; D007403:Intervertebral Disc / Q000503:physiopathology*; D017116:Low Back Pain / Q000150:complications / Q000503:physiopathology*; D008159:Lumbar Vertebrae / Q000503:physiopathology*