Background

Lumbar spinal stenosis (LSS) implies spinal canal narrowing with possible subsequent neural compression. LSS is classified by anatomy or etiology. Anatomic subclassifications include central canal and lateral recess stenosis. The classification of lumbar stenosis is important because of the implications of the underlying etiology and because it affects the therapeutic strategy, specifically the surgical approach.

• Central canal stenosis, commonly occurring at an intervertebral disk level, defines midline sagittal spinal canal diameter narrowing that may elicit neurogenic claudication (NC) or pain in the buttock, thigh, or leg. Such stenosis results from ligamentum flavum hypertrophy, inferior articulating process (IAP), facet hypertrophy of the cephalad vertebra, vertebral body osteophytosis, vertebral body compression fractures and herniated nucleus pulposus (HNP). Abnormalities of the disk usually do not cause symptoms of central stenosis in a normal-sized canal. In developmentally small canals, however, a prominent bulge or small herniation can cause symptomatic central stenosis. Large disk herniations can compress the dural sac and compromise its nerves, particularly at the more cephalad lumbar levels where the dural sac contains more nerves.
• Lateral recess stenosis (ie, lateral gutter stenosis, subarticular stenosis, subpedicular stenosis, foraminal canal stenosis, intervertebral foramen stenosis) is defined as narrowing (less than 3-4 mm) between the facet superior articulating process (SAP) and posterior vertebral margin. Such narrowing may impinge the nerve root and subsequently elicit radicular pain. This lateral region is compartmentalized into entrance zone, mid zone, exit zone, and far-out stenosis.
  • The entrance zone lies medial to the pedicle and SAP, and, consequently, arises from facet joint SAP hypertrophy. Other causes include developmentally short pedicle and facet joint morphology, as well as osteophytosis and HNP anterior to the nerve root. The lumbar nerve root compressed below SAP retains the same segmental number as the involved vertebral level (eg, L5 nerve root is impinged by L5 SAP).
  • The mid zone extends from the medial to the lateral pedicle edge. Mid-zone stenosis arises from osteophytosis under the pars interarticularis and bursal or fibrocartilaginous hypertrophy at a spondylolytic defect.
  • Exit-zone stenosis involves an area surrounding the foramen and arises from facet joint hypertrophy and subluxation, as well as superior disk margin osteophytosis. Such stenosis may impinge the exiting spinal nerve.
  • Far-out (extracanalicular) stenosis entails compression lateral to the exit zone. Such compression occurs with far lateral vertebral body endplate osteophytosis and when the sacral ala and L5 transverse process impinge on the L5 spinal nerve.

Amundsen and colleagues found concomitant lateral recess stenosis in all cases of central canal stenosis; consequently, in his study, pure central stenosis without lateral stenosis failed to exist.

Parenthetically, Keim and colleagues mention the following simplistic LSS anatomical classification scheme:

• Lateral, secondary to SAP hypertrophy
• Medial, secondary to IAP hypertrophy
• Central, due to hypertrophic spurring, bony projection, or ligamentum flavum/laminar thickening
• Fleur de lis (clover leaf), from laminar thickening with subsequent posterolateral bulging

LSS arises from the following primary and secondary etiologies:

• Primary stenosis encompasses congenital malformations and developmental flaws. Congenital malformations include incomplete vertebral arch closure (spinal dysraphism), segmentation failure, achondroplasia, and osteopetrosis. Developmental flaws include early vertebral arch ossification, shortened pedicles, thoracolumbar kyphosis, apical vertebral wedging, anterior vertebral beaking (Morquio syndrome), and osseous exostosis. Primary stenosis is uncommon, occurring in only 9% of cases.
• Secondary (acquired) stenosis arises from degenerative changes, iatrogenic causes, systemic processes, and trauma. Degenerative changes include central canal and lateral recess stenosis from posterior disk protrusion, zygapophyseal joint and ligamentum flavum hypertrophy, and spondylolisthesis. Iatrogenic changes result following surgical procedures such as laminectomy, fusion, and diskectomy. Systemic processes that may be involved in secondary stenosis include Paget disease, fluorosis, acromegaly, neoplasm, and ankylosing spondylitis.

Pathophysiology

Disk desiccation and degenerative disk disease (DDD) with resulting loss of disk height may induce segmental instability. Such instability incites vertebral body and facet joint hypertrophy. Cephalad vertebral body IAP hypertrophy promotes central spinal canal stenosis. Further canal volume loss results from HNP, ligamentum flavum hypertrophy, and disk space narrowing.

Alternatively, the caudal vertebral body SAP contributes to lateral recess and foraminal stenosis. Indeed, facet hypertrophy between L4 and L5 vertebrae may impinge the L4 nerve root in the foramen and the L5 proximal nerve root sheath in the lateral recess.

Jenis and An eloquently describe foraminal stenosis pathoanatomy, characterized by disk desiccation and DDD, which narrows disk height, permitting the caudad SAP to sublux anterosuperiorly. Such subluxation decreases foraminal space. Continued subluxation with resulting biomechanical disruption provokes osteophytosis and ligamentum flavum hypertrophy, further compromising foraminal volume. Anteroposterior (transverse) stenosis ultimately results from narrow disk height and hypertrophy anterior to the facet; specifically, the SAP and posterior vertebral body transversely trap the nerve root. Furthermore, in vertical (craniocaudal) stenosis, posterolateral vertebral endplate osteophytes and a lateral HNP may impinge the spinal nerve against the superior pedicle.

The 2 lower motion segments (L3-L4, L4-L5) are most commonly affected by degenerative stenosis. These segments are in a transition zone from the rigid sacrum to the mobile lumbar spine. Also, the posterior joints in this area have less of a sagittal orientation, which affords more rotation, and are therefore more vulnerable to rotatory strains.

Dynamic foraminal stenosis implies intermittent lumbar extension-provoked nerve root impingement from HNP, osteophytosis, and vertebral body slippage. Such dynamic stenosis with associated intermittent position-dependent symptoms may not manifest on imaging studies, thereby confounding diagnosis. Other factors promoting development of LSS include shortened gestational age, and synovial facet joint cysts with resulting radicular compression. Adult degenerative scoliosis, secondary to DDD-induced instability with subsequent vertebral rotation and asymmetric disk space narrowing, promotes facet hypertrophy and subluxation in the curve concavity. Degenerative spondylolisthesis, when combined with facet hypertrophy, causes both central canal and lateral recess stenosis.

Frequency

United States

LSS remains the leading preoperative diagnosis for adults older than 65 years who undergo spine surgery. The cost of more than 30,000 LSS surgeries performed in 1994 exceeds 1 billion dollars.

The incidence of lateral nerve entrapment is reportedly 8-11%. Some studies implicate lateral recess stenosis as the pain generator for 60% of patients with symptomatology of failed back surgery syndrome.

Incidence of foraminal stenosis increases in lower lumbar levels because of increased dorsal root ganglion (DRG) diameter with resulting decreased foramen (ie, nerve root area ratio). Jenis and An cite commonly involved roots as L5 (75%), L4 (15%), L3 (5.3%), and L2 (4%). The lower lumbar levels maintain greater obliquity of nerve root passage, as well as higher incidence of spondylosis and DDD, further predisposing patients to L4 and L5 nerve root impingement.