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Lateral Recess Stenosis of Lumbar
Spine Foraminoplasty
Parviz Kambin, MD
INTRODUCTION
In 1900, Sachs and Fraenkel (1) described the diagnosis and treatment of lateral
recess stenosis as an entity. Epstein et al. (2) further clarified it as a distinct clinical
entity. The availability of computed tomography (CT) and magnetic resonance imaging
in recent years has facilitated visualization of the content of the lateral recess and diagnosis
of this pathological condition (Fig. 1).
The nerve root canal begins from the nerve root sheath and terminates when the exiting
root emerges from the foramina. The superior facet, capsular ligamentous complex (Fig. 18
in Chapter 2) forms the posterior boundary or roof of the lateral recess. Expansion of the
posterior longitudinal ligamentum to the foramen, the intervertebral disc, and the posterior surface of the adjacent vertebral bodies forms the ventral or anterior surface of the
foramen. The exiting root occupies the pedicular notch superiorly.
Degenerative changes in the facet joints associated with synovial hypertrophy, thickened and fibrotic facet capsules, and ligamentum flavum complex (Fig. 2) contribute to
the narrowing and stenosis of the lateral recess. In addition, marginal osteophytes arising
from the vertebral bodies, combined with posterior bulging and protrusion of the intervertebral disc, cause further restriction, thus adding tension and compression on the exiting
nerve root and its vascular structures. It has been shown that interference with the
venous return of the nerve root causes chronic edema of the root, which may become
associated with intra- and perineural fibrosis (3–5). The pathophysiology of the bulging
annulus or protrusion has also been described (6–8).
With the advancement of aging, dehydration and collagenization of the nucleus pulposus,
combined with tear and disorganization of the annular fibers, plays an important role in
the development of abnormal protrusion of the intervertebral disc (Fig. 17A in Chapter 2).
CLINICAL PRESENTATION
Patients with spinal stenosis are usually seen in the physician’s office with signs and
symptoms of neurogenic claudication and, at times, complaining of numbness or a feeling
of pins and needles in the lower extremities (9,10).
From: Arthroscopic and Endoscopic Spinal Surgery: Text and Atlas: Second Edition
Edited by: P. Kambin © Humana Press Inc., Totowa, NJ
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Fig. 1. Preoperative axial CT scan study of a 60-yr-old male presented with signs and symptoms
of bilateral lateral recess stenosis. Note degenerative changes of the facet joints, narrowing of
the foramen, bulging of the annulus.
Fig. 2. Schematic drawing demonstrating how posterior marginal osteophytes from vertebral
bodies combined with inflamed and hypertrophic facet capsules contribute to stenosis of nerve
root canal.
The symptoms are diminished when the patient sits or reclines. This is in contrast to
vascular claudication, for which the symptoms subside when the patient stops walking.
Individuals with lateral recess stenosis have a tendency to bend forward while walking.
Extension of the lumbar spine invariably is associated with pain. Neurological examination
usually is not revealing; no reflex abnormality, sensory deficit, or positive tension signs
are found.
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SURGICAL MANAGEMENT
The evolution of minimally invasive spinal surgery and the availability of microbipolar
electrocoagulators, radiofrequency probes, and flexible-tip microinstruments have permitted
access to both the ventral and posterior boundaries of the neural canal. Reshaping of the
dimensions of the lateral recess via resection of the compressive elements under arthroscopic illumination and magnification has become a standard operative procedure
among minimally invasive spine surgeons.
As early as 1988, my colleagues and I used mechanical tools successfully for removal of
posterior osteophytes and resection of fibrotic and bulging annulus for the treatment of lateral recess stenosis (11,12). Subsequently, we were able to utilize a radiofrequency probe
for vaporization of the inflamed facet capsules and the ligamentum flavum that were contributing to the clinical manifestation of lateral recess stenosis. In recent years, laser
lights via a flexible-tip working scope have been used for ambulatory treatment of spinal
stenosis (13,14).
Arthroscopic access to the lateral recess requires further lateralization of the skin
entry site. This allows insertion of the cannula in the foramen and provides access to the
compressive elements on both the ventral and dorsum of the nerve root foramen. When
in doubt, particularly when surgery is being attempted in the upper lumbar spine, it is
advisable to secure a preoperative prone CT scan study from the surgical site. This will
ensure safety of the content of the abdominal cavity and its vital structures.
The needle is positioned at the midpedicular line as observed in the anteroposterior
fluoroscopic examination. This step is followed by introduction of the cannulated obturator and positioning of the working cannula (see Chapter 3). Under arthroscopic
control, mechanical tools may be used for removal of annular protrusion and marginal
osteophytes that are arising from the vertebral plates adjacent to the intervertebral disc
(Fig. 3). We have used a prebent radiofrequency probe for vaporization of the articular
capsule and inflamed synovial tissue.
RESULTS
The outcome of a prospective study of 40 consecutive patients who underwent
arthroscopic foraminal decompression of the lateral recess stenosis was published in
1996 (11). The reported outcome of patients who underwent arthroscopic decompression
of lateral recess has been compatible or better than the reported result following extensive
open operative procedures (15,16).
DEVELOPMENT OF DYSESTHESIA
Approximately 4 to 5 d following the surgical procedure, patients began to experience
a burning sensation or hypersensitivity of skin to touch affecting the involved extremity
(17). At times, patients are unable to use covers on their legs after this type of surgery.
This subjective complaint of hypersensitivity usually is not associated with objective
neurological deficit. Reflex abnormality, weakness, atrophy, or sensory deficit is not
usually found. The dermatomal distribution of the dysesthesia at times is not clear. However, it may follow the pattern of sensory nerve supply of a given nerve root at the site of
the surgical procedure. The etiology of this disturbing complication is attributed to
manipulation, excess heat, or trauma to the nerve root ganglia.
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Fig. 3. (A) Intraoperative arthroscopic view of lateral recess of patient shown in Fig. 1. Note
how the osteophytes that are arising from the vertebral body of the proximal segment contribute
to the development of root canal stenosis. (B) The fibers of the bulging annulus are seen distal to
the above osteophytes.
MANAGEMENT OF DYSESTHESIA
The operating surgeon has the responsibility to prepare and warn the patient of
potential development of dysesthesia following surgery. This reduces or prevents the
undue anxiety that invariably accompanies this organic disorder. In our experience,
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intraoperative injection of diluted fentanyl solution around the nerve root ganglia at
the onset of the operative procedure reduces the incidence of development of postoperative dysesthesia.
Following proper positioning of the patient and insertion of an 18-gage needle
into the foramen, a mixture of 1 cc of fentanyl and 3 cc of saline solution is injected
into the foramen. Within a few minutes following the injection, the surgeon may proceed with positioning of the cannulated obturator and working cannula, and completion of the operative procedure. Bathing of the root ganglia in the fentanyl solution
will have a tendency to alter the sensitivity of the root ganglia to external stimulation.
Fentanyl-induced antinociceptive effect is supraspinally mediated. It interacts with
opioid receptors that are present in the dorsal ganglia and dura and the central nervous system (18).
In addition, it is advisable to inject a diluted solution of a steroid compound into the
foramen prior to withdrawal of the instruments. Postoperatively the majority of patients
respond favorably to the use of oral nonsteroidal anti-inflammatory medications and
analgesics within 4–6 wk. However, when the presenting symptoms are severe, under a
strict sterile environment, the patient is positioned prone on the operating room table
and the 18-gage needle is reinserted into the foramen according to the previously
described steps. Injection of the steroid compound around the nerve root ganglia invariably provides relief and enhances recovery time.
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