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Patofisiologi Lumbal Spinal Stenosis

Spinal stenosis results from the narrowing of the spinal canal and lateral recesses due to age-related degeneration including disc collapse, spur formation, and thickening of ligaments. This compresses the spinal cord and nerve roots. Movement further injures the spinal cord from static and dynamic compression. The proposed mechanisms for neurogenic claudication include cauda equina ischemia due to dilation and congestion of epidural veins during movement, as well as axonal injury and fibrosis. Pain may also originate from compression of dorsal root ganglia containing pain-mediating substances.

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224 views2 pages

Patofisiologi Lumbal Spinal Stenosis

Spinal stenosis results from the narrowing of the spinal canal and lateral recesses due to age-related degeneration including disc collapse, spur formation, and thickening of ligaments. This compresses the spinal cord and nerve roots. Movement further injures the spinal cord from static and dynamic compression. The proposed mechanisms for neurogenic claudication include cauda equina ischemia due to dilation and congestion of epidural veins during movement, as well as axonal injury and fibrosis. Pain may also originate from compression of dorsal root ganglia containing pain-mediating substances.

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okkiems
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Lumbal Spinal Stenosis

Pathophysiology
The pathophysiology of spinal stenosis is related to cord dysfunction
elicited by a combination of mechanical compression and degenerative
instability. With aging, the intervertebral disk degenerates and collapses,
leading to spur formation. This most commonly occurs at C5-6 and C6-7. A
relative decrease in spinal motion occurs at these levels with a concomitant
increase in spinal motion at C3-4 and C4-5. The spine responds to
physiological stresses with bone growth at the superior and inferior margins
of the vertebral body (osteophytes). Osteophytes can form anteriorly or
posteriorly. Posterior osteophytes narrow the intraspinal diameter and also
cause lateral recess stenosis. This results in spinal cord or nerve root
impingement. Furthermore, arthritic degeneration causes formation of
synovial cysts and hypertrophy of the facet joints, which further
compromise the patency of the spinal canal and the neural foramina.

Spinal stenosis results from progressive narrowing of the central spinal


canal and the lateral recesses. The essential content of the spinal canal
includes the spinal cord, the cerebrospinal fluid (CSF) of the thecal sac,
and the dural membranes that enclose the thecal sac. In the absence of
prior surgery, tumor, or infection, the spinal canal may become narrowed by
bulging or protrusion of the intervertebral disc annulus, herniation of the
nucleus pulposus posteriorly, thickening of the posterior longitudinal
ligament, hypertrophy of the facet joints, hypertrophy of the ligamentum
flavum, epidural fat deposition, spondylosis of the intervertebral disc
margins, uncovertebral joint hypertrophy in the neck, or a combination of 2
or more of the above factors.

The resultant degeneration and abnormal motion lead to instability with


anterolisthesis or retrolisthesis (subluxation of vertebral bodies out of the
normal cervical alignment). Therefore, the cord tends to be compressed
from spur formation at C5-6 and C6-7 and compressed from listhesis at C3-
4 and C4-5. Often, this is accompanied by posterior canal compromise
from ligamentum flavum hypertrophy.

The cord is subject to further injury from repetitive dynamic injury during
normal neck movements. These static and dynamic compressive forces on
the cord lead to spinal cord injury and the clinical myelopathic syndrome.
Proposed mechanisms for development of neurogenic claudication (NC) include
cauda equina microvascular ischemia, venous congestion, axonal injury, and
intraneural fibrosis. Ooi and colleagues myeloscopically observed ambulation-
provoked cauda equina blood vessel dilation with subsequent circulatory stagnation
in patients with LSS who have NC. [22] They proposed that ambulation dilates the
epidural venous plexus, which, amidst narrow spinal canal diameter, increases
epidural and intrathecal pressure. Such elevation of pressure ultimately compresses
the cauda equina, compromises its microcirculation, and causes pain.

Another pain generator may be the dorsal root ganglion (DRG), which contains pain-
mediating neuropeptides, such as substance P, that possibly increase with
mechanical compression. The DRG varies spatially within the lumbosacral spine,
with L4 and L5 DRG in an intraforaminal position and S1 DRG located intraspinally.
Such foraminal placement may predispose to stenotic compression with subsequent
radicular symptomology.

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