Spinal Stenosis

Spinal Stenosis

Reference: JBJS 81-A, No. 4, April 1999, Instructional Course Lecture
– Garfin, Herkowitz, Mirkovic, San Diego, Michigan, Chicago

Main Message

Spinal stenosis is a syndrome that associates cauda equina compression with inflammation and pain (compression alone is not enough, as many asymptomatic people demonstrate compression). For those with severely disabling symptoms, operative care gives good results. The indications for operative care are a bit soft.

Points of Interest

Something we don’t understand about spinal stenosis is that the severity of symptoms is not necessarily associated with the magnitude of compression. ? Is it that we don’t understand the pathophysiology? Is our imaging insufficient?

Pathoanatomy

– the disc degeneration takes place over time; begins with degeneration and decreased production of proteoglycan in the nucleus, so that the water content of the nucleus diminishes and the ability to distribute stress is diminished and fissures/tears are formed in the annulus. The disc height decreases, as annular bulging, disc herniation, and early osteophyte formation is seen. Facet joints are then placed at increasing stress (although facet arthritis can precede disc degeneration) and degeneration leads to hypertrophy of the facet joint, thickening of the overlying capsule, and more osteophytes.
– if disc degeneration exceeds alteration to the facets, retrolisthesis may occur; as the facets erode, the subluxation reverses to more anterior listhesis.

– Degenerative changes are noted in most people over 60; but most who have evidence of mechanical nerve root compression do not have pain.

Pathophysiology

Nerve Compression
– alone, compression does not independently cause pain; there must be inflammation and irritation of the root. Compression of a normal nerve leads to paresthesia, sensory and motor loss, and reflex abnormalities, but pain usually does not occur. If an inflammed nerve, on the other hand, is compressed, then pain develops in addition to the objective signs.
– compression may be static or dynamic – flavum buckling, disc protusion, osteophyte impingment, nerve/vascular tethering
– the force of compression, duration of compression, and rate of compression are all important factors. Blood flow/ischemia is probably the final pathway, effecting changes in nerve root nutrition.

Clinically

– usually insidious onset
– classically, poain, numbness, and tingling in the posterior or posterolateral aspect of the limb. Exacerbated in extension, relieved in flexion. (Look at Table III for distinctions from vascular claudication).

Physical Examination

– specific motor deficits are uncommon, although weakness is a common complaint.
– watch for long tract signs – there may be a cause more cephalad in the cord!
– SLR is usually negative

Treatment

– severe debilitating neurological deterioration in patients managed nonoperatively is RARE
– operative treatment can usually be deferred, and a significant number may improve
– the decision to operate is based on symptoms and quality of life; the symptoms most amenable to treatment are the leg symptoms, not back pain.

Decompressive laminectomy and nerve root decompression – the standard procedure

– the controversy centers around when to add a fusion: Pre and Intraoperative considerations

Preoperative Structural Alterations
– degenerative spondylolisthesis – an indication for additional fusion; there is good evidence to support this concept, that after decompressing these, fusion is definitely recommended.
– scoliosis or kyphosis – factors to encourage arthrodesis are: 1. A very flexible curve. 2. documented progression. 3. Radiculopathy on the concavity. 4. Lateral slip. 5. Loss of normal lumbar lordosis (want to correct the sagittal alignment). 6. Failed surgery requiring further decompression (and destabilization). 7. Removal of 50% of the facet (renders the motion segment unstable).

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