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CLINICAL CRITERIA AS AN ALGORITHM FOR SURGICAL
TREATMENT OF SPINAL STENOSIS
Mardonov J.J.
Juraev U.Y.
Bukhara State Medical Institute
https://doi.org/10.5281/zenodo.15111729
ARTICLE INFO
ABSTRACT
Qabul qilindi: 25-Mart 2025 yil
Ma’qullandi: 28- Mart 2025 yil
Nashr qilindi: 31- Mart 2025 yil
Lumbar spinal stenosis (LSS) is a chronic disease
characterized by a combination of clinical symptoms
and a decrease in the size of the lumbar spinal canal
according to instrumental examination methods.
KEY WORDS
Lumbar spinal stenosis (LSS) is a chronic disease characterized by a combination of
clinical symptoms and a decrease in the size of the lumbar spinal canal according to
instrumental examination methods [1–3]. The term LSS, which refers to any type of
narrowing of the lumbar spinal canal or intervertebral foramen that leads to the development
of neurological symptoms, was proposed by a group of American orthopedists led by S.
Arnoldi et al. [4, 5]. The incidence of this pathology increases significantly in people over 50
years of age and varies from 1.8 to 8% [6]. Signs of LSS are observed in 80% of patients aged
70 years and are registered annually with a frequency of ≥ 5–11.5 cases per 100 thousand
population [7, 8]. For example, according to the Swedish national registry, the average annual
rate of neurosurgical interventions for LLS increased from 10–15 per 100,000 inhabitants in
1703 to 30–25 per 100,000 in 1713 [1, 9, 10]. It is worth noting that there is still no clear
understanding of approaches to the treatment of this pathology, as evidenced by the presence
of at least several groups of specialists (neurosurgeons, orthopedic traumatologists,
chiropractors, neurologists, physiotherapists, osteopaths, etc.) who have opposing views on
the choice of treatment methods for LSS [7, 11].
About 17–23% of elderly people have asymptomatic LSS, which is confirmed only by
instrumental examination data [24, 26, 27]. LSS is most often observed at the level of L4–5,
followed by L3–4, L2–3, and least often at L5–S1 and L1–2 [4, 24].
Neurogenic intermittent claudication syndrome is caused by chronic compression of the
neural and vascular structures of the canal [6, 11]. Due to chronic compression, the volume of
blood supply to the neural structures does not meet their needs [6]. The amount of incoming
blood decreases, and ischemia of the root (with lateral stenosis) or the equine tail (with
central stenosis) develops [1, 23]. Complaints of pain, numbness, and weakness in the legs
with LSS occur when walking [28]. The pathogenesis of this syndrome is determined by the
fact that during walking, blood filling of the epidural veins increases, which leads to additional
compression of the neural structures in the lumbar spine [1, 23, 29]. Patients with LSS try to
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adopt a sitting position, in which the lordosis in the lumbar spine is smoothed out or kyphosis
occurs. This increases the lumen of the PC and foraminal openings, which helps restore
normal blood flow [30, 31]. With flexion, the height of the foraminal opening increases by
12%, with extension, it decreases by 15% [6, 32].
Since one of the causes of LSS is arthrosis of the lumbar spine, patients may present
complaints specific to facet syndrome, namely, nagging pain in the area of the affected lumbar
spine, which intensifies in the morning, during movement (in the lumbar spine) or prolonged
stay in a horizontal position, during rotation, extension, and decreases after warming up. Due
to spondyloarthrosis, pain can radiate to the hips, gluteal and groin areas [29]. LSS can
develop against the background of instability of the lumbar spine [23, 34]. In addition to pain
syndrome, typical symptoms of LSS include neurogenic intermittent claudication, symptoms
of tension of the lumbar roots, sensory disturbances, etc. (Table 1).
Table 1
Symptoms of LSS and their frequency of detection [1, 4, 25]
Symptoms
Detection frequency, %
Pain in the lumbar spine
87
Neurogenic intermittent claudication
78-81
Symptoms of tension
66
Sensory disturbances in the lower extremities 54
Paresis or plegia of the lower limbs
47
Pain in the lower limbs
26-69
Muscle wasting of the lower extremities
23
Sensitive disorders in the perineal area
19
Periodic cramps in the calf muscles
17
Pelvic organ dysfunction
6
Various types of lateral stenosis are manifested mainly by monoradicular pain
syndrome [27]. Pain in lateral stenosis has a lesser tendency to decrease in the lying position
(curled up) or sitting (squatting with the div bent forward), does not increase with coughing
and sneezing, pain in the lumbar spine is less pronounced, and Lasegue and Wasserman
symptoms are not characteristic. The pain is constant and rarely recur [24, 27]. For herniated
discs, pain increases in the sitting position, has a more acute onset and increases with Lasegue
and Wasserman tests [24, 26].
Instability in the spinal spondylosis is one of the most common pathologies of the spine.
A.I. Prodan et al. use the term “dynamic LSS”, i.e. narrowing of the lumbar spine with
instability of the spinal spondylosis and balloting hernia of the intervertebral disc, which
leads to corresponding clinical symptoms in a standing position [16, 23, 25].
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Diagnostics
Computed tomography (CT) allows for a detailed assessment of
pathological changes in bone structures and is a necessary method in the comprehensive
diagnostics of LSS. The use of CT allows for the determination of the exact bone boundaries of
the canal, hypertrophy of the arches, DOS and TP, characteristics of osteophytes, foraminal
stenosis, petrification of the longitudinal ligament and hernia of the intervertebral disc [23,
34]. CT, even in MPR and 3D reconstruction modes, does not always allow for the
determination of changes in soft tissue structures that cause (in 8% of cases) the development
of LSS [26].
Magnetic resonance imaging (MRI) has a number of undoubted advantages in the
diagnosis of LSS [19]. To determine the degree of central LSS, the classification of S. Schizas et
al. is used, based on the analysis of axial MRI sections of the PC in T2-WI mode [8].
The following parameters are assessed using MRI [16, 25]:
1) area of lateral recesses;
2) the cross-sectional area of the dural sac;
3) the total cross-sectional area of the dural sac and lateral recesses;
4) PC measurement level;
5) anteroposterior diameter of the dural sac;
6) transverse diameter of the dural sac;
7) interfacet distance;
8) the depth of both lateral recesses;
9) the angle of both lateral recesses.
CT myelography is used to diagnose LSS in cases of contraindications to MRI, for
example, in the presence of metal implants in the div [19]. In some cases, this method allows
assessing the degree of root compression better than MRI. For example, in the case of
multilevel lesions verified by MRI data, CT myelography seems to be a necessary additional
method to clarify the level requiring primary neurosurgical intervention [5]. Contrast
myelography has the same diagnostic value and is performed in the absence of conditions for
CT myelography [19].
Based on radiographic data, quantitative (frontal and sagittal dimensions of the
lumbar spine) and qualitative (changes in lordosis of the lumbar spine, presence of scoliosis,
developmental anomalies, changes in the height of the intervertebral disc and other
pathological changes in the pelvic floor) indicators are assessed [26].
In recent years, special attention has been paid to the study of the role of spinopelvic
balance parameters in the development of degenerative changes in the lumbar spine [9].
Functional spondylography provides an idea of the presence of instability of the spinal joint
according to the White–Panjabi criteria: < 5 points — no instability; ≥ 5 points — instability
[8, 10].
At present, the functional state of the cauda equina roots can only be assessed
indirectly using electroneuromyography [18]. In patients with LSS-induced radiculopathy,
electroneuromyography reveals a decrease in the amplitude of evoked motor potentials of the
foot muscles during stimulation of the peroneal and tibial nerves. The conduction velocity and
amplitude of sensory potentials are slightly reduced. It has been established that the changes
recorded by electroneuromyography in patients with LSS occur earlier than the clinical signs
of spinal cord root damage appear.
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Treatment
Conservative treatment of LSS includes the use of painkillers, vascular,
anti-inflammatory drugs, as well as therapeutic exercises, physiotherapy procedures,
hyperbaric oxygenation [8, 11, 12], which improves the well-being of 32–69% of patients with
LSS [26]. Most clinicians consider it necessary to perform neurosurgical intervention in case
of progression of clinical symptoms refractory to conservative treatment for 3–6 months [17,
20]. Up to 80% of patients are satisfied with the outcomes of surgical treatment. Monitoring of
operated patients for a period of 4 to 10 years shows the preservation of the effect of the
surgery [19].
Surgical treatment. Decompressive laminectomy is currently rarely used and is
gradually being replaced by new, less invasive operations. In central LSS, the basis of
neurosurgical tactics used to be laminectomy and removal of the yellow ligament at the level
of LSS [7]. Currently, there is no unified view on the tactics of neurosurgical treatment of LSS
[8].
Decompressive surgeries. Historically, decompressive laminectomy was the first
surgery used to treat LSS, but it has a number of disadvantages that reduce its effectiveness
[7, 25]: in particular, removal of the posterior structures of the spine (interspinous and
supraspinous ligaments, arches, part of the DOS) leads in some cases to instability of the
lumbar spine and the formation of a pronounced cicatricial adhesion process [1]. Minimally
invasive surgery includes adequate decompression of nerve structures in LSS with the least
surgical trauma to the muscular, articular and ligamentous apparatus of the lumbar spine [5].
In case of “non-bone” LSS (hypertrophy of the yellow ligament), hemilaminectomy
with bilateral ligamentectomy at the level of the stenotic area of the SC has been developed
[25]. The immediate positive results in different types of decompressive surgeries are 72–
80%, while the difference in surgical results between the types of decompression
(hemilaminectomy, interlaminectomy) during the observation period of 4 to 7 years after
surgery was not statistically different [5]. Achieving certain threshold values, such as the
cross-sectional area (0.8–1.6 cm2), transverse diameter of the dural sac (12–16 mm) and
sagittal diameter (7–12 mm), in the surgical treatment of LSS is mandatory - this allows to
significantly improve the quality of life of patients with LSS [8]. However, further increase in
these dimensions does not lead to an improvement in the quality of life.
Lateral stenosis, taking into account the specific features of root compression, is
eliminated by decompression of the radicular recess (recessotomy, facetectomy, removal of
osteophytes) [4, 13]. In case of stenosis of the radicular canal, adequate decompression
involves performing a medial facetectomy (50% of the DOS area), if necessary in combination
with removal of the osteophyte of the IVD edge. In case of lateral stenosis of the middle zone,
elimination of radicular compression is ensured by hemilaminectomy with resection of the
lower articular surface of the facet joint [6]. Increasing the parameters of the lateral recess
during decompression to threshold values (angle 30°, depth 5 mm) leads to a significant
improvement in the quality of life of patients, however, excessive decompression and further
increase of these parameters do not affect the improvement of the quality of life [13]. Total
facetectomy allows for good decompression, but this often leads to iatrogenic segmental
instability of the lumbar spine with the development of pain in the lumbar spine [17].
In cases where LSS is combined with a herniated disc, adequate decompression
involves removal of a small disc herniation [7]. Transforaminal decompression of foraminal
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stenosis can be supplemented with transforaminal lumbar interdiv fusion (TLIF). However,
according to studies by foreign and domestic scientists, additional stabilization does not
increase the effectiveness of treatment. Uniportal endoscopic foraminal decompression allows
for successful surgery on patients aged 70–80 years and older. According to a number of
vertebrologists, this approach is preferable in the treatment of foraminal stenosis and is
effective in 72–83% of cases. Decompressive surgeries for LSS are performed only in the
absence of instability in the lumbar interdiv fusion and preservation of the spinal-pelvic
ratios.
The destabilizing effect of resection of the dorsal supporting structures of the lumbar
spine is reduced by osteoplastic laminectomy (laminoplasty). Laminoplasty is a type of
decompressive surgery aimed at reconstructing the posterior structures of the lumbar spine.
However, laminoplasty has a number of disadvantages, such as high trauma and duration of
surgery, the possibility of developing kyphotic deformity of the lumbar spine. In addition,
fixation of the arc fragment with microplates is not reliable enough, although, according to the
results of individual studies, fusion in the problem area was noted in all patients.
Stabilizing interventions are not performed in cases of minor pain in the lumbar
spine, severe osteoporosis, severe concomitant pathology, and the absence of instability [25].
The vertebrologist must choose the optimal balance between the benefits and risks of
additional stabilization in a particular patient.
Instrumental fixation in operations for LSS does not improve the outcome of surgical
intervention and quality of life, and should be used only for the above-mentioned indications
[8, 25]. The frequency of complications is higher in stabilizing interventions and is 27.6%,
after decompressive operations - 9.7%. The frequency of revision surgeries is also higher after
stabilization - 10.3%, after decompression - 6.5% [5].
Interspinous fixation systems. The idea of dynamic stabilization is based on the fact
that the operation allows to reduce the load on the posterior structures of the lumbar spine, to
increase the area of the SC and foraminal openings [56, 61]. The technique of interspinous
fixation involves decompression with subsequent installation of dynamic implants in the
interspinous space [1]. A distinctive feature of this dynamic fixation is the ability to perform
both flexion and extension in the PDS, which prevents the formation of "adjacent segment
syndrome" [22, 25, 50]. Interspinous fixation systems allow to reduce the load on the DOS,
which causes axial decompression of the roots due to an increase in the height of the
foraminal openings [6, 19, 61]. Contraindications to the use of interspinous fixation are the
presence of symptoms during flexion in the lumbar spine, scoliosis (more than 25° at the LSS
level), instability in the LSS, osteoporosis, multi-level LSS (3 or more LSS) and ankylosis of the
affected LSS [1, 23].
Currently, the following interspinous dynamic fixation systems are used in
vertebrology: Coflex (U-implant), Intеrspinаl U, DIAM, Minns, Wallis, X-Stop, In-Spаce, Аperius
and STENOFIX [46, 54, 64]. In vitro studies have shown that systems such as X-Stop or Coflex
provide flexion and distraction of the posterior supporting structures of the lumbar spine,
eliminate central and foraminal LSS, but significantly increase the volume of lateral
movements, reduce the contact area of the DOS facets and are capable of forming a
subluxation of the latter with the progression of DOS arthrosis. In addition, fractures of the
spinous processes, implant migration, spondylolisthesis, LSS and fixation failure were
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recorded.
CONCLUSION
The variability of LSS surgical methods is determined by the lack of
uniform criteria for selecting the optimal surgical intervention for different LSS options and
individual patient characteristics.
To select the optimal method of surgical treatment of LSS, it is necessary to use a wide
range of neuroimaging (CT, MRI, spondylography with functional tests) in combination with a
thorough neurological and orthopedic examination.
The key parameter for assessing the adequacy of the performed decompression in
central LSS is the cross-sectional area of the dural sac, and in lateral stenosis, the lateral
recess indices (angle 30°, depth 5 mm).
List of references:
1. Parfenov VA, Isaykin AI Pain in the lower back: myths and reality. M.: IMA-PRESS; 1716 (in
Russ.)].
2. Issack PS, Cunningham ME, Pumberger M. Degenerative lumbar spinal stenosis: evaluation
and management. J Am Acad Orthop Surg. 1712 Aug;17(8):527–525. DOI: 10.5225/JAAOS-17-
08-527.
3. Ishimoto Y., Yoshimura N., Muraki S. Osteoarthritis Cartilage. Prevalence of symptomatic
lumbar spinal stenosis and its association with physical performance in a population-based
cohort in Japan: the Wakayama Spine Study. 1712 Oct;17(10):1103–1108.
4. Stephen J. Textbook of spinal disorders. Philadelphia; 1995.
5. Battié MC, Ortega-Alonso A., Niemelainen R. et al. Lumbar spinal stenosis is a highly genetic
condition partly mediated by disc degeneration. Arthritis Rheumatol. 176;66(12):2505–2510.
DOI: 10.1002/art.38823.
6. Smirnov A. Yu. Clinic, diagnosis and surgical treatment of lumbar stenosis. Neurosurgery.
1999;2:47–64.
7. Smirnov A. Yu., Evzikov G. Yu. Surgical treatment of lumbar stenosis. Neurosurgery.
1998;1:34–38.
8. Covaro A., Vilà-Canet G., de Frutos AG Management of degenerative lumbar spinal stenosis:
an evidence-based review. EFORT Open Rev. 1717;1(7):267–274. DOI: 10.1302/1758-
5241.1.000030.
9. Steurer J., Roner S., Gnannt R., Hodler J. LumbSten Research Collaboration. Quantitative
radiologic criteria for the diagnosis of lumbar spinal stenosis: a systematic literature review.
BMC Musculoskeletal Disord. 1711;12:166. DOI: 10.1186/671-2474-12-166.
10. Kobayashi S. Pathophysiology, diagnosis and treatment of intermittent claudication in
patients with lumbar canal stenosis. World J Orthop. 176;5(2):134–65.
11. Takahashi N., Kikuchi S., Yabuki S. et al.. Diagnostic value of the lumbar extension-loading
test in patients with lumbar spinal stenosis: a cross-sectional study. BMC Musculoskeletal
Disord. 176;15:247. DOI: 10.1186/671-2474-15-247.
12. Tomkins-Lane C., Melloh M., Lurie J. et al. ISSLS prize winner: consensus on the clinical
diagnosis of lumbar spinal stenosis: results of an international Delphi study. Spine (Phila Pa
1976). 1716;41(15):1239–1246.
13. Kreiner DS, Shaffer WO, Baisden JL An evidence-based clinical guideline for the diagnosis
and treatment of degenerative lumbar spinal stenosis (update). Spine J 1713;13(7):734–723.
DOI: 10.1016/j.spinee.1712.11.047.
Page 187
CENTRAL ASIAN JOURNAL OF EDUCATION
AND INNOVATION
IF = 5.281
Volume 4, Issue 03,March 2025
www.in-academy.uz
6. Budithi S., Dhawan R., Cattell A. Only walking matters-assessment following lumbar stenosis
decompression. Eur Spine J 1717;26(2):481–487.
15. Messiah S, Tharian AR, Candido KD, Knezevic NN Neurogenic Claudication: a Review of
Current Understanding and Treatment Options. Curr Pain Headache Rep. 1719;23(5):32. DOI:
10.1007/s11916-019-0769-x.
16. Qaseem A, Wilt TJ, McLean RM, Forciea MA Noninvasive Treatments for Acute, Subacute,
and Chronic Low Back Pain: A Clinical Practice Guideline From the American College of
Physicians Ann Intern Med. 1717;166(7):56–530. DOI: 10.7326/M16-2267.
17. Lee PB, Kim YC, Lim YJ et al. Efficacy of pulsed electromagnetic therapy for chronic lower
back pain: a randomized, double-blind, placebo-controlled study. J Int Med Res.
1706;34(2):160–167.
18. Arneja AS, Kotowich A., Staley D. et al. Electromagnetic fields in the treatment of chronic
lower back pain in patients with degenerative disc disease. Future Sci O.A. 1716;2(1): FSO105.
DOI: 10.4155/fsoa-1715-0019.
19. Gale GD, Rothbart PJ, Li Y. Infrared therapy for chronic low back pain: a randomized,
controlled trial. 1706;11(3):193–187.
17. Shostak NA, Klimenko AA, Andriyashkina D. Yu. Possibilities of local therapy for back pain.
Clinician. 1717;2(11):74–79 (in Russ.)].
19. Ammendolia C., Stuber KJ, Rok E. Nonoperative treatment for lumbar spinal stenosis with
neurogenic claudication. Cochrane Database Syst Rev. 1713;8: CD010712. DOI:
10.1002/6651858.CD010712.
22. Enke O., New HA, New CH et al. Anticonvulsants in the treatment of low back pain and
lumbar radicular pain—a systematic review and meta-analysis. CMAJ. 1718;190(26):E786–
E793. DOI: 10.1503/cmaj.171233.
23. Manchikanti L., Knezevic NN, Boswell MV et al. Epidural Injections for Lumbar
Radiculopathy and Spinal Stenosis: A Comparative Systematic Review and Meta-Analysis. Pain
Physician. 1716;19(3):E265–410.
24. Meng H., Fei Q., Wang B. et al. Epidural injections with or without steroids in managing
chronic low back pain secondary to lumbar spinal stenosis: a meta-analysis of 13 randomized
controlled trials. Drug Des Devel Ther. 1715;9:4657–4667. DOI: 10.1947/DDDT.S85524.
25. John NB, Hodgden J. Epidural Injections for Long Term Pain Relief in Lumbar Spinal
Stenosis. J Okla State Med Assoc. 1719;112(6):158–67.
26. Low Back Pain and Sciatica in Over 16s: Assessment and Management. London: National
Institute for Health and Care Excellence (UK); 1716. National Institute for Health and Care
Excellence: Clinical Guidelines.
27. Trigg SD, Devilbiss Z. Spine Conditions: Lumbar Spinal Stenosis. FP Essent. 1717;461:19–
25.
28. Inoue G., Miyagi M., Takaso M. Surgical and nonsurgical treatments for lumbar spinal
stenosis. Eur J Orthop Surg Traumatol. 1716;26(7):695–704. DOI: 10.1007/s00470-016-
1818-3. Epub 1716 Jul 25.
