The lumbosacral spine is the caudal end of the human axial skeleton and connects the pelvis to the body. The lumbar thecal sac in the central canal contains a bundle of lumbosacral nerve roots known as cauda equina. Each lumbar nerve emanates from the dural sac and exits the spinal canal beneath the pedicle at its corresponding vertebral level through the intervertebral foramen. The intraforaminal and extraforaminal parts of the lumbar nerve are referred to as lumbar exiting nerve. The primary disease of nerve roots is uncommon. The radiculopathy caused by exiting nerve compression or injury can result from various pathologies along its course. Degenerative spondylopathy is the most common etiology of lumbar radiculopathy, including intervertebral disc disease, spondylolisthesis, and facet arthropathy [1]. These degenerative diseases usually lead to traversing nerve root compression in the spinal canal. The lumbar exiting nerve root compression is infrequent. However, the unique anatomy of the lumbosacral junction makes the L5 exiting nerve vulnerable to compression.

The anatomy at the L5–S1 level is different from the other levels, especially extraforaminal regions. The L5–S1 level is the junction between the lumbar spine and pelvis. The relationship between the pelvic bone and the lumbosacral spine affects the surgical corridor at the lumbosacral junction. The iliac crest height and lordosis can cause a steeper trajectory angle in the axial and coronal plane at the L5–S1 level during posterolateral approaches of the L5 exiting nerve [2]. It is mandatory to master the related anatomies at the lumbosacral junction to avoid failures or complications during the surgery. Therefore, the current paper will provide an overview of the anatomy and pathology, mainly concerning the L5 exiting nerve.

The L5 exiting nerve root leaves the spinal canal through the lumbosacral foramen to the anterior sacrum. Before exiting the spinal canal, the L5 traversing nerve root originates from thecal sac and travels in the spinal canal. The L5 nerve then enters the L5–S1 intervertebral foramen underneath the L5 pedicle and is referred to as the intraforaminal L5 exiting nerve. The intervertebral foramen is a natural orifice between the lateral sides of the L5 vertebra and sacrum. The pedicles are rostral and caudal boundaries of the intervertebral foramen. The maximum internal transverse pedicle diameter was at the L5 level with a mean of 8.95 mm (range, 7.10–11.21 mm) [3]. The ventral boundary comprises the intervertebral disc and parts of the posterior vertebral body. The zygapophyseal joint dorsal to the intervertebral foramen forms the dorsal boundary of the foramen. The facet orientation measured by the angle between the facet joint and the sagittal plane increases toward the caudal level [4]. Therefore, the facet joint orientation becomes more coronally oriented at the L5–S1 level, meaning less mobility in the rotation direction but more mobility in the flexion and extension direction. The diameter of the lumbar intervertebral foramen is widest at the L5–S1 level. The mean transverse and sagittal diameters are 10.1±0.7 mm and 22.6±0.4 mm, respectively [5]. The intervertebral foramen is largest at the L5–S1 level, but the high iliac crest can sometimes offset the advantage during the transforaminal approach [6].

The extraforaminal lumbar exiting nerves are located in the L1 to L5 level intertransverse space. The L5 transverse process, ala of sacrum, and iliac crest border the L5–S1 extraforaminal space. Compared with the rostral level, the L5–S1 intertransverse space is the smallest, and its dimension is about 13.2 mm in width and 13.4 mm in height in the coronal plane [7]. The extraforaminal L5 exiting nerves travel to the anterior sacrum through the lumbosacral tunnel in the intertransverse space. The lumbosacral tunnel extended from the extraforaminal zone of the L5–S1 intervertebral foramen to ala of the sacrum. The floor of the tunnel is the anterior-superior surface of the sacral ala. The medial boundary of the tunnel is the lateral L5 vertebral body and L5–S1 intervertebral disc. The lumbosacral ligament delineates the lateral border, and the roof is only present proximally, constituted by the inferior surface of the L5 transverse process [8] (Figure 1). After going out from the tunnel, a ventral ramus of the L5 exiting nerve will join the branch of the L4 exiting nerve to form the lumbosacral plexus.

The spinal nerves are composed of ventral and dorsal roots. The dorsal root carries sensory fibers responsible for nerve impulses from peripheral receptors. Dorsal root ganglion (DRG) has a cluster of sensory neuron cell bodies and is closely associated with spinal radicular pain. DRG is more susceptible to mechanical injuries or chemical irritations than the nerve itself. The location of the DRG varies significantly among different spinal nerve segments. About 95% of L5 DRGs are located at the intraforaminal L5 nerve, as reported in a magnetic resonance imaging (MRI) study [9]. Another cadaveric study reported that the extraforaminal type of DRG is more common in the L5 nerve (33%) than in other lumbar or thoracic nerves [10]. This may imply the higher incidence of L5 radicular pain caused by extraforaminal pathologies.

The arterial supply at the L5 level also differs from the L1 to L4 level. The abdominal aorta gives rise to 4 lumbar segmental arteries, which extend dorsolaterally around the middle of the vertebral body at the L1 to L4. The L5 segmental arteries bifurcate from the median sacral artery [11]. However, segmental arteries were identified in less than 10 % of patients at the L5 in a lower lumbar computed tomography (CT) angiographies study. The L5 level also receives arterial supply from the branches of the iliolumbar arteries (Figure 2). The previous study reported that the most frequent pattern of the L5 blood supply was the combination of the branches of the L4 segmental artery and the spinal branches of the iliolumbar artery [12]. Therefore, the risk of massive bleeding due to injury to the segmental artery is relatively low during the L5–S1 paraspinal or extraforaminal approaches.

The most common pathology that causes L5 exit nerve compression is degenerative spondylopathy, such as spondylolisthesis or herniated intervertebral disc [13]. Other etiologies, including hypertrophy of the L5 transverse process, metastatic tumor invasion, sacral fracture, sacroiliac joint injury, inflammation, infection, and lumbosacral transitional vertebrae, are infrequent [14]. Primary neoplasm such as schwannoma arising from lumbar nerve root is rare [15,16]. The curvature of the spine changes from lumbar lordosis to sacral kyphosis at the L5–S1 level. Besides, 75% of flexion and extension mobility occurs at the lumbosacral joint. Therefore, the loading force increases at the transitional zone, especially in flexion posture. The biomechanic features lead to a higher incidence of intervertebral disc degeneration, facet arthropathy, and spondylolisthesis at the L5–S1 level. Osteophyte formation at the posterior vertebral body's margins may accompany intervertebral disc degeneration. The bulging disc, osteophytes, or spine misalignment may cause impingement on the L5 exiting nerve.

The L5 exiting nerve compression can result from a far-lateral disc herniation of the L5–S1 intervertebral disc (Figure 3). The L5–S1 disc herniation is generally in the spinal canal and causes S1 traversing nerve root compression. The extraforaminal herniation is rare by 3%–11% of all disc herniations [17]. Though the far-lateral disc herniation is more often in the upper lumbar levels, symptomatic far-lateral disc herniation requiring surgery occurs most commonly at the L5–S1 level [18]. The reasons are the unique anatomical features at the L5–S1 level, such as broad pedicles and lumbosacral tunnel. Besides, DRGs can be located at the extraforaminal part of the L5 exiting nerve. Therefore, the L5 exiting nerve is vulnerable to a herniated disc in the extraforaminal zone.

Far-out syndrome, first reported by Wiltse et al. [19] in 1984, is referred to as L5 exiting nerve radiculopathy due to extraforaminal compression. Their report introduced 2 types of patients and surgical approaches for the far-out syndrome. Type 1 is the most common in older adults with degenerative scoliosis. The tilting L5 vertebra causes the L5 transverse process to tip toward the ala. Type 2 is in the younger adult population with isthmic spondylolisthesis and at least 20% slip [19]. As the vertebral body slips forward, the transverse processes move in both anterior and caudal directions. The listhesis makes the L5 transverse process settle down against the sacrum. Two types of L5 transverse process displacement compress the L5 exiting nerve. Moreover, the narrowed extraforaminal space can cause an L5 exiting nerve by a protruding osteophyte or herniated disc.

The extraforaminal L5 exiting nerve compression can result from lumbosacral transitional vertebra (LSTV) (Figure 4). LSTV is a congenital anomaly in which a hypertrophic L5 transverse process fuses with varying degrees to the ala of the sacrum [20]. There are 4 types of LSTV in Castellvi classification. Type I is a hypertrophic transverse process in a triangular shape, measuring at least 19 mm in width. Type II is incomplete fusion with pseudarthrosis between the enlarged transverse process and the sacral ala. Type III is the complete fusion between the enlarged transverse process and the sacral ala. Type IV is a mixture of type II on one side and type III on the other. Bertolotti stated that LSTV may cause low back pain due to arthritic changes occurring at the site of pseudoarthrosis [21]. Therefore, Bertolotti syndrome has been referred to as low back pain due to the LSTV. Only a few studies reported L5 exiting nerve compression in LSTV. A retrospective case series reported that 13% of patients with LSTV had neural compression by osteophytes from the pseudoarthrosis detected by MRI and CT images. All these patients are Castellvi type II of LSTV. Furthermore, 70% of patients with radiological evidence of neural compression were symptomatic [13]. The extraforaminal L5 exiting nerve should be carefully evaluated in all symptomatic patients with an LSTV.

The L5 exiting nerve radiculopathy can result from intraforaminal or extraforaminal region compression. The anatomy of the lumbosacral junction, especially the extraforaminal space, differs from the other rostral levels. Therefore, extraforaminal exiting nerve compression can be more symptomatic at the L5–S1 level. The anatomical features also affect the decision to use the surgical approach. It is mandatory to comprehensively understand the L5 exiting nerve pathology and associated regional anatomy before surgical planning.