Spinal degeneration is the result of primary or secondary spondylo-arthritis and disc degeneration (1). Although there are some who associate the onset of degeneration involving the intervertebral disc and facet joints with facet joint arthritis, the general belief is that it occurs as a result of disc degeneration (1,2). The disc structure begins to degenerate in the third decade, water loss occurs in the nucleus pulposus, the disc height decreases with annular tears, the facet joint distance is prolonged, the spine becomes prone to abnormal movement and instability as a result of ligament laxity and becomes open to trauma. With the addition of inflammatory factors to recurrent traumas, cartilage becomes thinner, annular tears grow, facet joint synovitis occurs, cartilage goes to destruction and osteophytes develop. Posterior movement of the disc structures causes narrowing of the spinal canal, hypertrophy develops in the facet joints, and the ligamentum thickens. Result; It is degenerative stenosis (1-3).

Disc degeneration

Intervertebral disc, which is one of the main reasons for the onset of spinal degeneration, has an avascular structure. It consists of chondrocyte and fibroblast-like cells within the extracellular matrix. Disk; It includes two main regions: nucleus pulposus (NP) and Annulus Fibrosis (AF). While chondroblasts and type-2 collagen are mostly organized in the gelatinous structure of the NP in the inner region of the disc, the basic structure of AF in the lamellar structure is mostly composed of fibroblasts surrounded by type-1 collagen. It synthesizes the appropriate matrix in which both cell groups are located. In the lower and upper parts of the disc (endplate); There are chondrocyte cells that synthesize hyaline cartilage surrounded by a thin cortical bone (1).

Disc degeneration is characterized by NP dehydration along with AF rupture and clefts in the endplate area that can turn into fractures. With annulus degeneration, collagen loses its fibril organization and undergoes myxomatous degeneration. The number of lamellae increases, cell distribution deteriorates, and clusters occur. While NP loses water, it loses its height, cavities form and expand posterolaterally. Endplate degeneration progresses with subchondral sclerosis and calcification in the hyaline cartilage. All this causes the disc to become thinner, to lose its elasticity, and to not be able to distinguish between the nucleus and annular region. Disc hernias with the nucleus remaining in the annular ligament (Contained-NP containing) and material protruding out of the disc (noncontained-NP content) It can be divided into. Annular tears are often very large in an uncontrolled hernia. Degeneration is at an advanced stage (1).

At the cellular level, disc degeneration begins with increased cellular mating and groupings in the NP region. The distribution of the basic proteins of the cytoskeleton, Actin and Vimentin, is disturbed. The cell loses its shape. Gap connections are reduced with connexins 43 and 45, which provide intercellular connection. In addition to all these mechanical reasons, nutrient and oxygen diffusion in cells is metabolically reduced (1).

Diffusion occurs through the posterior and anterior vertebral vessels. Factors such as enplate calcification, narrowing of the lamina cribrosa pores and decreased local blood flow reduce diffusion. Matrix synthesis is disrupted by increasing the amount of lactate by anaerobic metabolism. Martrix degradation increases and gradient molecules accumulate. With the addition of genetic, systemic factors and smoking, necrosis increases, NP becomes hyalinized, the annulus weakens with disorganization, proteoglycan distribution will change, and water retention decreases (1).

Matrix proteins undergo changes in the degenerated disc. Proteoglycans provide the viscoelastic structure by holding water and increase the tensile-compressive strength of the disc. Chondroitin sulfate and keratan sulphate are predominant proteoglycan, they aggregate by binding to hyaluronate molecules. Aggrecan, the largest aggregate molecule, is mostly found in AF. Versican, decorin, biglycan, fibromodulin and lumican, which are more in the fetal disc, are also available. Link proteins stabilize proteogiers as glycoproteins. Chondroitin sulfate synthesis is disrupted by degeneration, leaving its place to keratan sulphate. This leads to a decrease in water retention in the NP structure and deterioration of the gel consistency. In addition, water depletion reduces diffusion at the molecular level. Collagen and matrix connections provide the mechanical strength and stability of the disc. Collagen Type 2 increases resistance to compressive forces. This stability, which is protected by cross-links, is disrupted by the replacement of types 1, 2, 3 and 5 collagen by degeneration, by type 1, 4 and X In advanced levels of degeneration, anaerobic respiratory cross-links are disrupted and stability is removed. Fibronectin osteoarthritis is a glycoprotein containing collagen-glycoprotein-integrin and membrane protein binding points with increased itte release. In recent years, it has been found that while decreasing proteoglycan synthesis in NP in degenerate disc, it increases proteoglycan synthesis with an adverse effect in AF and its release is high in annulus repair. It has been observed that fibronectin fragments inhibit chondrocyte-derived aggrecan production and increase metalloproteinases responsible for cartilage breakdown. A link between polymorphism in the Aggrecan gene and disc degeneration has been determined. Sequence differences in protein chains are held responsible in degenerate discs. Chondromodulin-1 (ChM-I) is thought to have a role in chondroprotective effect by preventing vascularization and fibrosis change in early degeneration of the disc. This molecule is secreted during the gestational period, the growth plate due to cartilage provides the development of chondrocytes. It is thought to be secreted also in mature NP and AF cells. Inflammatory such as nitric oxide (NO), interleukin-1B (IL-1)., Interleukin-6 (IL-6)., Tumor necrosis factor alpha (TNF-oc)., Prostaglandin E2 (PGE2)., Matrix metalloproteinase (MMP) Other tissues are also affected by the spontaneous increase of mediators in disc cells. Proteoglycan synthesis is inhibited in joint cartilage. Cartilage degradation begins with the increase in IL1. While MMP increases this degradation, exogenous NO, IL-6 and PG-E2 increase inflammation. Phospholipase activation by migration of CD68 cells during neovascularization is the main cause of pain and destruction at this stage. This mechanism may explain the inflammatory mechanism of disc-induced facet joint degeneration (1).

Mechanical effects in disc degeneration cause endplate damage, increased intra-disc hydrostatic pressure to increase NO amount and decrease proteoglycan synthesis and decrease water retention. Vibration reduces the amount of intracellular aggrecan. The related increase in MMP-1 causes matrix degradation. In addition, vibration disrupts ATP controlled flow in Ca channels. Result; disruption of cell nutrition, reduction of martyx production, degradation and degeneration (1).

Externally, the effect of growth factors on degeneration has been demonstrated. These effects are of varying intensity at different stages from apoptosis to matrix organization. The presence of LacZ and Luciferase markings in degenerated discs has shown that genetic transition in degeneration can occur regardless of age and gender. It is claimed that gene transfers with adenoviruses may eliminate the genetic factors, perhaps the main cause, of disc degeneration in the future. Masuda et al, recombinant human osteogenic protein-1 (rHOP-1) increased cell and matrix proteoglycan synthesis on the radar with its mitogenic effect. Because of the similar effects of growth factors, they may be used in treatment (1).

In short, disc degeneration develops due to extrinsic, intrinsic and genetic reasons. Deciding the stage of this condition resulting in stenosis in the spinal functional subunit should constitute the main framework in determining treatment options.

Pathological anatomy of the lumbar degenerated spine Spinal canal stenosis may develop in the central, lateral dead-end and pedicular regions in the coronal plane (Figure 1).

Figure 1: Schematization of the anatomical localizations of degenerative stenosis. While lateral stenosis is classified as subarticular, foraminal and extraforaminal, central stenosis may occur at the pedicular disc and intermediate levels. (Inspired by Kuslich (27)).


In the sagittal plane, narrowing may be at pedicular, intermediate and disc levels (3,4).

Lateral stenosis; It can occur in three stages, including the entrance of the spinal nerve to the foramen (subarticular), foramen and exit (extraforaminal). The first part described is the most cephalic located, superior articular facet medial and inferior location. It has only anterior and posterior osseous wall. Medial and lateral are normally open. The middle part contains the foramen, under the pars interarticularis of the lamina and the pedicle. The anterior wall forms the vertebral body. Pars interarticularis makes the posterior wall, pedicle lateral wall. The medial wall opens into the spinal canal and is normally open. The exit part is surrounded by the intervertebral foramen. The disc is located in the anterior, and the lower part of the facet joint is located laterally. (3-5).

Anatomical classification of the degenerative spine made the therapeutic classification necessary with the growing need for planning treatment. Hansraj stenosis; It handles in two parts as simple or typical and complex. In the typical definition of stenosis, cases without instability or with first-degree spondylolisthesis and scoliosis of less than 20 degrees are understood. These patients often only benefit from decompression therapy. Complicated cases may need to be combined with decompression therapy, as well as fusion and instrumentation (5,6).


It usually becomes symptomatic in older ages. It is more common in women. L3-4, L4-5 levels are the most frequently affected segments. Cervical involvement is detected in 5% of the patients (2). Patients describe hip, thigh, leg, foot pain along with back and waist pain. Bilaterate involvement is common. Neurological claudication, increased pain when walking and standing, decreased pain when lying down and extending the legs, and increased pain with concussion are typical. Posture is slightly flexed.

With the increase in pain, functional capacity gradually decreases and walking distance becomes shorter. Daily business starts to disrupt. Pain can be questioned with various scales. Visual analog pain grading system VAPS is one of the most widely accepted scales (7). Work disability can be scored by the work disability score (WL-26). Under the Deyo core set title, he gathered the interrogation suggestions targeting spinal diseases in six groups and created a useful system. In recent years, the numerical expression of the impact on functional capacity in spinal diseases can be made using disability scoring systems such as Oswestry. Scores such as SF-36 that question general health status are useful before surgery (6,7). These applications should be queries that the patient can easily understand. Roland disability questionnaire, which has been translated into Turkish and its validity has been determined statistically, is a specific and sensitive test for low back pain (8).

The need for analgesics and response to analgesics should be recorded. This can give an idea about the degree of stenosis. Bladder functions must be questioned.

Flattening, paravertebral spasm, increased pain with movement and decreased range of motion in extension can often be detected in lumbar lordosis. Flexion width has decreased but is accompanied by pain. The straight leg raising test is usually negative. Decrease in motor power can be detected in provocative tests. Although sensory impairment can sometimes be selective in the relevant dermatome, it is generally not sensitive because minor sensory changes are expected at these ages (6-9).


Radiologically, disc space reduction, osteophytes, facet hypertrophy are pathognomonic. The defect in the pars interarticularis should be noted in terms of spondylolysis and narrowing of the pedicle spaces in terms of congenital stenosis. The borders of the foramina should be examined, the hypertrophy of the facet joints and the relationship of osteophytes on the wing should be evaluated.

must. The presence of scoliosis, kyphosis, hyperlordosis, sacralization and lumbalizations that disrupt the spine mechanics should be questioned in flexion-extension and standing dynamic radiographs. It is involved in the etiology of foraminal stenosis of a fibrocartilage-like structure in spondylolysis. Listesis rate should be graded by standard indicators. The psoas shadow and the robustness of the pedicles should be noted (9,10).

Tomographic evaluation maintains its importance in understanding osteophyte organization. Lateral dead-end and foraminal structures limited by bony structures can be clearly evaluated. Magnetic resonance imaging (MRI) has greatly reduced tomography and myelographic examinations. With MRI, the channel relationship of disc structures, intradiscal pathologies and fibrous tissues that cause foraminal stenosis can be evaluated better. MRI is the most sensitive evaluation method in disc degeneration. However, CT-myelogram is as valuable as MRI for preoperative planning in cases with metal implants and MRI application is contraindicated (5,9-11).

In laboratory tests, neuroflament specific to nerve injury and proteins such as 5-100 have been shown to increase in the cerebrospinal fluid (CSF) and blood. It was found that the amount of total protein, albumin, IgG, IL-8 increased in CSF and the amount of ApoE increased in both CSF and plasma (5).

Discography is the most effective diagnostic method that enables a dynamic decision to clarify the disc pathology and to plan the treatment. Discography provides the clinical relationship of the location of the annular tear and point targeting convenience in the treatment of complicated radicular symptoms. Anesthetic agent and steroid injection into the disc can provide therapeutic effect and assist the physician in differential diagnosis. White and Pancabi measured the disc pressure and showed the effects of pathological loads on the disc. Disc pressure dynamic measurement can be used as a reference in elucidating mechanical problems.

The objective contribution of the EMG test, which is the most commonly used electrodiagnostic test, is indisputable. It fully reveals the radicular level of the lesion. Working with evoked sensory potentials is more sensitive. Electrodiagnostic tests do not show the decompression or treatment site. However, the surgical intervention area should be decided by comparing it with other diagnostic tests. The perop must be repeated to confirm the diagnostic discography intervention site. Selective root blocks can be used to separate the cause of pain in multi-segment stenosis (5,9-12).

The diagnostic algorithm guides in planning treatment. The flow chart should primarily separate low back pain and non-mechanical pain due to medical diseases. Conservative treatment and pain that does not respond to rest necessitate re-initiation of differential diagnostic steps.

Differential diagnosis

Disc hernias should be evaluated very well in differential diagnosis. Usually in the stenotic degenerated spine the disc shows a slight overflow. Symptoms should not be attributed to disc disease and limited to discectomy or medical therapy.

The medical evaluation flow chart that separates medical and non-mechanical low back pain should be followed carefully (9).

If cauda equina syndrome develops acutely, extensive disc herniation may be considered. Spinal cord tumors, primary and metastatic bone tumors, infections and fractures should be considered in the differential diagnosis (2).

It is the vascular claudication, which is the most clinically involved condition. This type of pain increases with walking, in contrast to stenosis, when lying down, and decreases when standing. A careful vascular examination makes diagnosis easier. EMG is required for differential diagnosis in patients with diabetic neuropathy (2).


Anti-inflammatory therapy is the first step in degenerative lumbago. Treatment for reflex muscle spasm supported by muscle relaxants can be combined with physical therapy. In resistant cases, epidural steroids and anesthetics may facilitate transition to functional therapies (13,14). Combinations of gababentin or amiltriptyline give significant results in cases where epidural injection is applied (13). Successful results of calcitonin use in degenerative luminopia have been reported (10). Cases who do not respond conservatively, have neurological dysfunction (bladder, radicular motor deficit, etc.), and whose functional disability is found to be low, may be referred to surgical treatment. Surgery should reduce pain, increase mobility and prevent neurological deficit. Adequate decompression and preservation of joint and pedicle structures to ensure stability are the basis of treatment. Today’s surgery can be summarized as maintaining anatomical integrity, providing decompression and avoiding fusion as much as possible. Minimally invasive procedures meet these needs with increasingly developing techniques. Strictures that can be treated with wide bone resections with percutaneous surgeries and scopic interventions can be easily reached, vital vascular nerve structures

Decompression and fusion can be applied through. Open surgical decompression operations were performed under spinal anesthesia, reducing pulmonary complications. However, the occurrence of conditions that will increase the possible CSF pressure (coughing, etc.) may lead to large and difficult dural tears (11).

Surgical treatment: 1. The location of the stenosis, 2. the number of involved segments, 3. stability, 4. degenerative spondylolisthesis, 5. previous surgical treatments, recurrence and iatrogenic reasons, and 6. accompanying scoliosis and kyphosis are regulated by evaluating parameters. Surgical treatment flow chart is summarized in Figure 2 (11).

Non-fusion techniques and disc surgery

Disc degeneration and reduced disc height are the main causes of spinal degeneration. Maintaining the disc height before facet joint involvement occurs can prevent lumbar degeneration. It is possible to reduce disc damage and pain due to injury by repairing the damage. Various treatment methods are used for the annulus and nucleus (15,16).

The first attempt to target the nucleus in disc surgery was performed in 1963 by Lyman W. Smith with kimopapain injection. After the injection of chymopapain into the nucleus, it decomposes the proteoglycans contained in the nucleus, decreasing its volume and providing decompression. However, it has a damaging effect on neural tissues. Deaths due to transverse myelitis, paraplegia, and anaphylactic shock have been reported (11,15).

Techniques targeting the nucleus in disc herniations containing nuclei can be grouped under the heading Nucleoplasty. In the early 1990s, laser discectomy and nucleotomy, which were popular with local anesthesia, became one of the safe and effective treatments with a short rehabilitation period (17).

Using similar equipment and energy in annuloplasty, this time it was aimed to evaporate the nucleus water content. In this way, the pressure in the posterior annulus is reduced. It is necessary to be more selective than annuloplasty in patient selection.

Arthrocare Perc-D Coblation device, one of the options in nucleoplasty, vaporizes the nucleus with bipolar radioenergy by mechanically giving localized energy. Approximately six channels are opened to the nucleus to provide decompression. The nucleus turns into plasma form with its water content and is taken out of the cannula (17-20).

The use of thermal energy in nucleus decompression has been provided by radiowave Radionics probes. In short, in the treatment referred to as PIRFT, the heat effect of the energy is utilized. Unlike annuloplasty in nucleoplasty, the temperature reaches 70-80 degrees. The contribution of this energy to annular denervation is controversial and the pain reduction mechanism has not been explained yet (17,19).

In laser nucleoplasty technique, the evaporation effect of energy and the heat effect are reflected on the nucleus as ° rent. The nucleus is broken down by laser energy.

Intradiscal electrothermal therapy (IDET) is a treatment intervention for annulus. It is referred to as “annuloplasty” as it is aimed to treat annulus rupture in this way. In 1997, Saal and Saal treated the tears in annular defects with the help of thermal wire. The basis of treatment should be stabilized collagen fibrils as in arthroscopic capsulography. Thermal effect can be obtained from electrothermal, radio wave or laser energies. Symptoms regress with thermal effect, collagen stabilization and annulus denervation. When 42 ° C is exceeded in heat therapy, neural structures are damaged (17).

“The narrowing of the disc space is the beginning of the process in the degenerative spine.” his discourse has revealed his materials replacing the disc. Facet instability, foraminal narrowing and subsequent degenerative conditions are secondary to narrowing of the disc space. Artificial nucleus replacements Artificial Nucleus Replacement (ANR) have been tried to regain this distance. Injection of polymethylmethacrylate and silicone materials into the nucleus cavity resulted in disappointment. The metal nucleus results he described Fernstrom in 1966 are still controversial. It has been observed that reactive bone formation and resorption continue in the silicon-dacron composite implant in Urbaniak chimpanzees. The ideal material described by Edeland in 1981 should have vital functions such as water permeability as well as nucleus-like skin-sil responses. A nucleus-like effect was created by using hygroscopic thixotropic gel such as hyaluronic acid with high molecular weight polyethylene fiber encapsulated impregnated with ray and gobbin polymeric material. The cadaver biomechanical studies of the horseshoe shaped lumbar intervertebral disc prosthesis (LIDP) implanted by Hou et al anterior paramedian retroperitoneal intervention have been completed. The elastomer reinforced polyurethane nucleus modified by Sulzer Spine-tech company, the Hydrogel nucleus developed by Rao and Higham in 1991 that can be sent from the 5 mm cannula, and finally the Ray modification (Prosthetic Disc Nucleus PDN), which includes a hydrogel polyethylene sheath. Its main purpose is to provide physiological response of the nucleus to the loads, as well as the disc height. The most important technical problem in disc prostheses is the sizing difficulty. If the disc prosthesis is smaller or larger than normal, it will cause problems (17,19).

Decompressive attempts

It is planned according to the development area of ​​the stenosis. The aim is to eliminate the pressure without disturbing the stability of the spine. Interventions that will create instability should be determined by fusion applications (Figure-2).



Central canal stenosis: The stenotic segment is treated with decompressive lumbar laminectomy. Decompression starting from the maximum constriction zone should be extended caudally and cephalicly. Instability should be prevented by protecting the medial facet joint. Decompression is terminated by making sure that the nerve root is relaxed. If there is any sensation in the dura, superior facet medial can be included in the excision (4,10,11,16,18,20).

In lateral canal stenosis, the nerve root can be treated with unilateral laminotomy. Stenosis at the entrance requires medial facetectomy. Facetectomy should be sufficient to provide 1 cm medialization of the nerve. In the stenosis of the middle part, the dorsal root is under pressure. Decompression can be performed by performing total facetectomy to include the pars area. Fusion and instrumentation are required to ensure stability. Hypertrophic facet welding in the exit section! ‘ There is compression of osteophytes and osteophytic margins around the disc. The Witse paraspinal approach is used for decompression of this area with open techniques. The area is reached with transverse protrusion excision. The success and patient satisfaction of minimally invasive techniques such as foraminoscopy is higher. Mr Knight et al. Provides fusion decompression in minimally invasive foraminoscopic decompression treatments. (4,10,11,16,18,20). Knight et al. It reports successful results by applying annuloplasty and nucleoplasty in the same session as well as decompression with the combined use of laser and radiowave energies (12).

Multiple laminotomies can be performed at multiple levels in mild to moderate stenosis, preserving structures such as Spinoz protrusion in the midline.

Expansive Lumbar Laminoplasty provides decompression by preserving the technical stability applied for the first time by Tsuji et al. (11).

In distraction laminoplasty, the lumbar canal is decompressed by preserving the maximum bone. The medial facet and inner regions of the lamina are removed with the aid of distraction instruments (11).

Distraction devices such as spinous protrusion x-stop and PEEK reduce compression in the area of ​​constriction caused by the ligamentum flavum by indirect decompression. It can be applied under local anesthesia (11).

Dynamic intervertebral disc prostheses are a developing technique as an alternative to fusion from non-fusion techniques. Since Edeland, there are disc prostheses anchored to the bone, designed either constrained or nonconstrained, such as total joint prostheses that allow movement. The main purpose of these implants, whose validity is discussed with animal and biomechanical experiments such as the caustic design, is to protect the spine motion by preserving the disc height (21).

Fusion surgeries

These are interventions that maintain stability by providing arthrodesis.

It is applied in posterior instrumentation, pedicle screw fixation, wide decompression causing instability and multi-level laminectomies. It is used to provide a corrective effect and prevent progression in the presence of spondylolisthesis and mechanically impaired spine such as scoliosis. Distraction and alignment correction after extensive decompression may contribute to decompression. Arthrodesis reduces pain and prevents progression. Since the fusion will be achieved by rigid fixation, it can be combined between the posterior elements as well as the vertebral bodies. The necessity of the integration is to ensure fusion and maintain the stability until fusion. Various studies comparing pseudoarthrosis rates advocate that pedicle screw fixation should leave its place to selective fusion other than spondylolisthesis, scoliosis and multi-segment decompression (2-4,10,11,22).

Interbody fusion

It can be applied posteriorly or anteriorly. It provides selective fusion opportunity. Apart from open surgery, it can be applied scocopically (10,11,22). In addition to being popular especially in scopic decompression surgeries that require fusion, it has become one of the indispensable techniques combined with posterior applications with wide decompression. Lumbar interbody fusion (LIF) technique, which has developed rapidly since Cloward (1950), can be applied to the posterior and anterior. Posterior LIF is classified according to the entrance corridor: Paramedian intervention (PLIF), transforaminal intervention (TL1F) (23). Both techniques can be applied as percutaneous, minimally invasive or open (4,22,24,25). Implant; It is a titanium cylinder with a cancellous-like structure like the Bagly and Kuslich design (BAK), which is called cage (4). Transforaminal application with grade 1-2 spondylolisthesis neurolo

It is the ideal treatment option in cases without jik deficits (25). Provides disc height in the foraminal area and reduces foraminal stenosis.

Anterior LIF can be performed transperitoneally or paramedian retroperitoneally or laparoscopically (26-29). AL1F scope application is advantageous compared to PLIF applications in terms of not causing dural damage. While PLIF allows decompression and fusion together, the dura and nerve damage risk is higher. Like posterior applications, ALIF restores disc height and provides decompression in the formaninal region following discectomy, but it is considered as a disadvantage that facet nipertrophy and osteophyte organizations do not ‘eliminate’ (27):


Back pain is resolved despite treatment at the rate of ° / 087. Any treatment that starts without defining the stage of the pathology may increase the symptoms of the patient. Therefore, physiopathological staging should be done very well. Decompressive attempts to cause instability in a stable spine may cause the symptoms to worsen. Fusion surgery can also reduce patient satisfaction when not performed on site. The limits of minimally invasive interventions are clear. In cases that require extensive decompression, traditional surgical methods should not be avoided (30).

After making sure that the degenerative spine is responsible for pain and dysfunction, the degree of lumbar degeneration and disc pathology should be established. Degeneration is a progressive process but can be slowed down. Conservatively or surgically recovered healthy disc distance will delay stenotic spine disease. Stenosis surgery has now been demonstrated with its clear benefits and harms. The current approach should be to discuss conservative, genetic, and surgical, especially mini-mal invasive techniques that preserve disc distance before degeneration begins.

Current Medical Journal (April 2004-Volume 9 Issue: 4)


  • Chung SA, Khan SN, Diwan AD. The molecular basis of intervertebral disk degeneration. Orthop Clin N Am 2003;34: 209-19.
  • Whiffen JR, Neuwirth MG. Spinal stenosis in Spinal surgery. Ed Bridwell KH, DeWald RL. Vol 2 (25). Lippincott Co Philadelphia; 1991,S:637-656.
  • White AA, Pamjabi MM. Clinical Biomechanics of the spine. Part 4 349-362 Lippincott Co Philadelphia; 1990
  • Kuslich SD. Lumbar degenerative disc disease-axial back pain Posterior In Vaccaro AR, Albert T] ed. Master Cases Spine Surgery. Thieme NewYork; 2001, 5:93-99.
  • Brisby H. Nerve root injuries in patients with chronic low back pain. Orthop Clin N Am. 2003;34: 221-30.
  • Boden SD. Outcome assesment after spinal fusion. Orthop Clin N Am. 1998;29(4).: 717-28.
  • Schaufele MK, Boden SD. Outcome research in patients with chronic low back pain. Orthop Clin N Am. 2003;34: 231-7.
  • Küçükdeveci AA, Tennant A, Elhan AH, Niyazoglu H. Validation of the Turkish Version of the Roland-Morris Disability Questionnaire for Use in Low Back Pain. Spine 2001; 26(24)., 2738h
  • McCowin PR, Borenstein D, Wiesel SW. The Current Approach to the Medical Diagnosis of Low Back Pain. Orthop Clin N Am. 1991;22 (2). 315-25.
  1. Spivak MJ. Degerenative Lumbar Spinal Stenosis. (Current Concepts Review).. J Bone Joint Surg . 1998; 80-A
  2. Sengupta DK, Herkowitz HN. Lumbar spinal stenosis treatment strate­gies and indications surgery. Orthop Clin N Arn. 2003;34: 281-95.
  3. Knight M, Goswami A. Management of isthmic spondylolisthesis with posterolateral endoscopic forarninar decompression. Spine 2003;15; 28(6).: 573-81.
  4. Pirbudak L, Karakurum G, Satana T, Karadasli H, Topalhan M, Oner U, Gulec A. Epidural Steroid Injection and Amitriptyline in The
    Management of Acute Low Back Pain Originating frorn Lumbar Disc Her­niation. Arthroplasty Arthroscopic Surgery 2003;14(2).:89-93.
  5. Freedman MK. Axial low back pain. Nonoperative approach. In Vac­caro AR, Albert TJ ed. Master Cases Spine Surgery Thieme NewYork; 2001,5:78-83.
  6. Herkowitz Current status of percutaneous discectomy and chemonucleolysis. Orthop Clin N Ara 1991;22(2). 327-32.
  7. Hasea RJ. Lumbar spinal stenosis:surgical considerations. J South Ort­hop Assoc 2002 11(3). 127-34.
  8. Sagi HC, Bao QB, Yuan HA. Nucrear Repracement Strategies. Orthop Clin N Am 2003;34: 263-67.
  9. Kwon BK, Vaccaro AR, Grauer JN, Beiner J. Indications, techniques and outcomes of posterior surgery for chronic low back pain. Orthop N Anı 2003;34:297-308.
  10. Davis TT, Sra P, Furier N, Bae H. Lumbar intervertebral thermat ther­ Orthop Clin Am 2003;34:255-62.
  11. McCuiloch JA. Lumbar spinal stenosis without instability. in Vaccaro AR, Albert TJ ed. Master Cases Spine Surgery Thieme NewYork; 2001,S:100-8
  12. Kostuik JP. Alternatives to spinal fusion. Orthop Ciin N Am 1998;29(4).: 701-14.
  13. Brislin B, Vaccaro AR. Advances in posterior lumbar interbody fusion. Orthop Clin N Am 2002;33: 367-74.
  14. Moskowitz A. Transforaminal lumbar interbody fusion. Orthop Clin N Am 2002;33:359-66.
  15. Mathews HH. Percutaneous interbody fusions. Orthop Clin N Am 1998;29(4).: 647-63.
  16. Moskovitz PA. Minimal invasive posterolateral lumbar arthrodesis. Orthop Clin Am 1998;29(4). 665-78.
  17. Burkus (K. Intervertebral Fixation: CIinical results with anterior cages. Orthop Clin N Am 2002; 33: 349-57.
  18. Kuslich SD. Lumbar Degenerative disc disease-axial back pain an­terior approach. In Vaccaro AR, Albert T] ed. Master Cases Spine Surgery Thieme NewYork; 2001,85-92
  19. Silcox III HD. Laparoscopic bone dowel fusions of the lumbar spine. Orthop Clin N Am 1998; 29(4).: 665-693.
  20. Zdeblick TA. Laparoscopic spinal fusion. Orthop Clin N Am 1998;29 (4). 635-45.
  21. Diwan AD, Parvartaneni H, Cammisa F. Faifed degenerative lumbar spine surgery. Orthop Clin N Am 2003;34: 309-324.