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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 poste- rior 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, thick- ened 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 interver- tebral 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).

145

From: Arthroscopic and Endoscopic Spinal Surgery: Text and Atlas: Second Edition Edited by: P. Kambin © Humana Press Inc., Totowa, NJ

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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.

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.

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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 arthro- scopic 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 lat- eral 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 con- tributing 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 obtu- rator 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. How- ever, 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.

Lateral Recess Stenosis 147

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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,

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.

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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 postop- erative 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 pro- ceed with positioning of the cannulated obturator and working cannula, and comple- tion 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 ner- vous 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 invari- ably provides relief and enhances recovery time.

REFERENCES

1. Sachs B, Fraenkel J. Progressive ankylotic rigidity of the spine (spondylose rhizomelique).

J Nerv Ment Dis 1900;27:1–15.

2. Epstein JA, Epstein BS, Rosenthal AD, et al. Sciatica caused by nerve root entrapment in the lateral recess: the superior facet syndrome. J Neurosurg 1972;36:584–589.

3. Hoyland JA, Freemont JA, Jayson MIV. Intervertebral foramen venous obstruction: a cause of periradicular fibrosis? Spine 1989;14:538–568.

4. Olmarker K, Rydevik B, Holm S. Edema formation in spinal nerve roots induced by exper- imental graded compression: an experimental study on the pig cauda equina with special reference to differences in effects between rapid and low onset of compression. Spine 1989;14:569–573.

5. Parke WW. The significance of venous return impairment in ischemic radiculopathy and myelopathy. Orthop Clin North Am 1991;22:213–222.

6. Kambin P, Nixon JE, Chait A, et al. Annular protrusion: pathophysiology and roentgeno- graphic appearance. Spine 1988;13:671–675.

7. Kambin P, McCullen G, Park W, et al. Minimally invasive arthroscopic spinal surgery.

Instruct Course Lect 1997;46:143–161.

8. Schaffer JL, Kambin P. Minimally invasive spine surgery. Textbook Rheumatol Update 1994;9:2–12.

9. Kirkaldy-Willis WH, Paine KW, Cauchois J, McIvor G. Lumbar spinal stenosis. Clin Orthop 1974;99:30–50.

10. Yamada H, Oya M, Okada T, Shiozawa Z. Intermittent cauda equina compression due to narrow spinal canal. J Neurosurg 1972;37:83–88.

11. Kambin P, Casey K, O’Brien E, Zhou L. Transforaminal arthroscopic decompression of lateral recess stenosis. J Neurosurg 1996;84:462–467.

12. Kambin P. Arthroscopic treatment of spinal pathology, in Operative Arthroscopy, 2nd ed.

(McGinty JB, Casperi RB, Jackson RW, Poehling GG, eds.), Lippincott-Raven, Philadelphia, 1996, pp. 1227–1233.

Lateral Recess Stenosis 149

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13. Chiu J. Transforaminal endoscopic micro decompression of herniated lumbar discs and spinal stenosis. 22nd International Course for Percutaneous and Endoscopic Spinal Surgery, Jan 2004; ISMISS/SICOT, Zurich, Switzerland.

14. Knight MTN, Goswami A, Patko JT. Endoscopic foraminoplasty : a prospective study on 250 consecutive patients with independent evaluation. J Clin Laser Med Surg 2001;19:73–81.

15. Burton CV, Kirkaldy-Willis WH, Yong-Hing K, et al. Causes of failure of surgery on the lumbar spine. Clin Orthop 1981;157:191–199.

16. Ray CT. Transfacet decompression with dowel fixation: a new technique for lumbar lateral spinal stenosis. Acta Neurochir Suppl 1988;43:48–54.

17. Kambin P, O’Brien E, Zhou L. Arthroscopic microdiscectomy and selective fragmentectomy.

Clin Orthop 1998;347:150–167.

18. Jaffe RA, Rose MA. A comparison of local anesthetic effect of Meperidine Fentanyl and

Sufentanil on dorsal root axons. Anesth Analg 1996;83:776–781.

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