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26 Lumbosacral Decompression

and Foraminotomy

Trevor Bebchuk

Pathophysiology allowing it to bulge within the spinal canal at L7 and S1, also
Degenerative lumbosacral stenosis (DLSS), also known as cauda known as IVD protrusion or Hansen type II disc disease
equina disease or syndrome and lumbosacral compression, is a [1–5,7–9,11–14]. These changes lead to or add to the instability at
common cause of pain and pelvic limb dysfunction in dogs [1–5]. the lumbosacral space, resulting in subluxation of the vertebral
It may be especially prevalent among military working dogs [6]. endplates and facetal joints between L7 and S1. As a response to
The clinical signs, including difficulty rising and going up and instability, the dorsal longitudinal ligament, the interarcuate liga-
down stairs, reluctance to jump and, in some cases, neurological ments, and the facetal synovial capsules hypertrophy. This insta-
deficiencies of the pelvic limb(s), are primarily a result of com- bility also leads to new bone formation (spondylosis deformans)
pression of the cauda equina, the seventh lumbar nerve (L7), and along the ventral aspect of the L7 and S1 vertebral endplates and
vascular supply to the cauda equina and nerve roots [1–5,7]. The facetal joints. Together, these changes cause compression of the
disease occurs secondary to the high mobility at the lumbosacral
joint primarily in dorsoventral flexion and extension but also in
lateral flexion, extension and rotation. This mobility places a large
amount of stress on the lumbosacral disc space as this is the con-
nection between the relatively flexible lumbar spine and the rigid
sacrum and pelvis. These forces are complex and concentrated on
the connectors and stabilizers of the joint: the intervertebral disc
(IVD), facetal synovial joints, dorsal and ventral longitudinal liga-
ments, interarcuate ligaments, interspinous ligaments, and per-
ispinal fascia and muscles (Figure 26.1) [1–5,7–9]. In addition, the
presence of anatomical malformations of the structures in the
lumbosacral region (e.g., sacralization of the seventh lumbar ver-
tebrae, lumborization of the first sacral vertebrae, malarticulation
of the diarthrodial joints at the L7–S1 junction) can contribute to
changes in the three‐dimensional motion pattern of the lumbosa-
cral junction. Even without these changes, there may be certain
breeds that have an inherent abnormal motion pattern at L7–S1
[10,11]. While the exact pathophysiology and progression that
leads to DLSS is unknown, it is thought to follow a specific
sequence of events. Chronic repetitive microtrauma and aging
causes the nucleus pulposus to desiccate, altering the shock‐
absorbing biomechanics of the IVD and leading to greater forces Figure 26.1 Schematic of the lumbosacral joint. Note the L7 nerve root exit-
being absorbed by the annulus fibrosus. The annulus fibrosus sub- ing the intervertebral foramen and the proximity to both the intervertebral
sequently weakens and develops small tears in the dorsal portion, disc and the facetal joint. Source: Smith et al. [58].

Current Techniques in Canine and Feline Neurosurgery, First Edition. Edited by Andy Shores and Brigitte A. Brisson.
© 2017 John Wiley & Sons, Inc. Published 2017 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/shores/neurosurgery

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