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Lumbar spinal stenosis is defined as any type of narrowing of the spinal canal, nerve root canals, or intervertebral foramen. This narrowing can be caused by soft tissue, bone, or a combination of both. The resultant nerve root compression leads to nerve root ischemia and a clinical syndrome associated with variable degrees of low back, buttock, and leg pain.
The two main types of spinal stenosis are (1) congenital-developmental and (2) acquired spinal stenosis. In the most widely accepted classification, spinal stenosis is subdivided into two congenital-developmental subtypes and six acquired subtypes.
CONGENITAL-DEVELOPMENTAL STENOSIS
Idiopathic
Achondroplastic
ACQUIRED STENOSIS
Degenerative
Combined congenital and degenerative stenosis
Spondylolytic or spondylolisthetic
Iatrogenic (e.g., following laminectomy or spinal fusion)
Posttraumatic
Metabolic (e.g., Paget disease, fluorosis)
Acquired degenerative spinal stenosis is the most common type.
Pathologic changes in the lumbar disc and facet joints are responsible for the development of spinal stenosis. With the passage of time, biochemical and mechanical changes in the intervertebral disc decrease its ability to withstand cyclic loading. These changes predispose the disc to annular tears, loss of disc height, annular bulging, and osteophyte formation. A degenerative sequence also occurs posteriorly in the facet joint complex. Disc space narrowing increases loading on posterior facet and capsular structures leading to joint erosion, loss of cartilage, and capsular laxity. Ultimately, facet hypertrophy and osteophyte formation occur.
Osteophytes on the inferior articular process encroach medially resulting in central spinal canal stenosis . Ligamentum flavum hypertrophy and annular bulging further contribute to stenosis involving the central spinal canal.
Osteophytes on the superior articular process enlarge, resulting in lateral zone stenosis . Osteophytes may also form circumferentially at the vertebral margins at the attachment of the anulus in an attempt to autostabilize the motion segment. Portions of these osteophytes, termed uncinate spurs, may protrude from the subjacent vertebral endplate or disc margin into the lateral nerve root canal above and provide an additional source of lateral nerve root entrapment. Loss of disc space height can also decrease the cross-sectional area of the neural foramen and lead to symptomatic lateral zone stenosis.
Spinal instability may develop as a result of the degenerative process and lead to the development of degenerative spondylolisthesis, lateral listhesis, scoliosis, and complex spinal deformities.
Spinal stenosis may present at any age (e.g., congenital type). However, the acquired degenerative type of spinal stenosis typically becomes symptomatic in the sixth and seventh decades of life. The most common levels of involvement in the lumbar region are L3–L4 and L4–L5. Up to 15% of patients with degenerative lumbar spinal stenosis have coexistent cervical spinal stenosis (tandem stenosis).
The typical patient reports the gradual onset of low back, buttock, thigh, and calf pain. Patients may report numbness, burning, heaviness, or weakness in the lower extremities. The lower extremity symptoms may be unilateral or bilateral. Symptoms are exacerbated by activities that promote spinal extension such as prolonged standing or walking (neurogenic claudication). Maneuvers that permit spinal flexion such as sitting, lying down, or leaning forward on a shopping cart tend to relieve symptoms as these positions increase spinal canal diameter. Changes in bowel or bladder function due to lumbar spinal stenosis are uncommon but occasionally noted.
Common conditions that should be ruled out during assessment include:
Degenerative arthritis involving the hip joints
Peripheral neuropathy
Vascular insufficiency
Metastatic tumor
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