Degenerative disease of the spine



Degenerative disease of the spine is a definition that includes a wide spectrum of degenerative abnormalities. Degeneration involves bony structures and the intervertebral disk, although many aspects of spine degeneration are strictly linked because the main common pathogenic factor is identified in chronic overload. During life the spine undergoes continuous changes as a response to physiologic axial load. These age-related changes are similar to pathologic degenerative changes and are a common asymptomatic finding in adults and elderly persons. A mild degree of degenerative changes is paraphysiologic and should be considered pathologic only if abnormalities determine symptoms. Imaging allows complete evaluation of static and dynamic factors related to degenerative disease of the spine and is useful in diagnosing the different aspects of spine degeneration.

Degenerative disease of the spine is a definition that includes a wide spectrum of degenerative abnormalities. Degeneration involves bony structures and the intervertebral disc, although many aspects of spine degeneration are strictly linked because the main common pathogenic factor is identified in chronic overload. During life the spine undergoes continuous changes as a response to physiologic axial load. These age-related changes are similar to pathologic degenerative changes and are a common asymptomatic finding in adults and elderly persons. A mild degree of degenerative changes is paraphysiologic and should be considered pathologic only if abnormalities determine symptoms. Imaging allows complete evaluation of static and dynamic factors related to degenerative disease of the spine and is useful in diagnosing the different aspects of spine degeneration.

  • Physiopathology

The causes of age-related and pathologic spine degenerative changes are multiple: traumatic, metabolic, toxic, genetic, vascular, and infectious. Trauma is the main pathologic factor, however, including chronic overload, chronic multitraumatism, and sequelae of acute trauma [1,2]. The concept of chronic duration trauma has the highest relevance, because degenerative disease of the spine is actually considered the consequence of overuse injury. Abnormal stresses, not sufficient to cause fracture, can be responsible for bone and disc damage if applied for long period. In most cases, the alterations involve the disc and the vertebral body because of the morphologic-functional relationship between these structures [3].


The distribution of axial load is responsible for the typical localization of spine degeneration. C5-6 and C6-7 levels are involved in most cases, because they are the sites of lordosis inversion. In the dorsal spine degeneration is rare, because this tract is less mobile and less involved in dynamic load. In the lumbosacral tract the most frequently degenerated levels are L4-5 and L5-S1, because they are the sites of the highest dynamic and static load [1,2,4]. The functional integrity of spinal curves is involved in degenerative changes. Spinal curves allow optimal redistribution of axial load. When curves are preserved, the spine is 30 times more elastic than a straight structure. If correct spine alignment is lost, an asymmetrical load distribution may cause focal or diffuse spine degeneration.

Because of overlap of imaging findings in age-related changes and degenerative changes, it is usually difficult to define whether abnormalities are paraphysiologic or pathologic. Evaluation of the presence of congruous symptoms and the severity of abnormalities is mandatory for a correct diagnosis [2,5,6].

Progressive involution of the spinal structures begins after the second decade and invariably determines some degree of vertebral and discal degeneration. The first sign of degeneration is the appearance of intranuclear clefts, which are virtually present in 100% of discs after 40 years [7]. Frequently in the adult population asymptomatic disc dehydration and radial fissures can be observed; in elderly persons a slight degree of osteochondrosis and other bony degenerative changes is normal and is considered paraphysiologic. The main difference between people with asymptomatic age-related changes and degenerative abnormalities is the presence of an abnormal axial load distribution in patients with degeneration. Overuse injuries develop pathologically at a younger age in these people than in the healthy elderly population [6].

  • Imaging methods: indications and techniques

Imaging plays an important role in the evaluation of degenerative spine. Indication for radiologic examination and technique should be evaluated in every case [8]. When a patient complains of typical back or monoradicular pain, there is no statistical risk in waiting 4 to 6 weeks before performing any radiologic examination. In many cases there is a high possibility of spontaneous pain regression, especially in cases of small acute herniations and extraspinal disorders, such as neuritis and muscular or insertional inflammation. Patients with a history of neoplasm, atypical pain, neurologic deficit, and other local or systemic symptoms should be evaluated earlier.

Plain films still play an important role in evaluation of the spine, because the examination is inexpensive and promptly available and gives a wide panoramic view of the spine. Direct information about bony structures can be obtained, and functional information about misalignment and vertebral stability can be obtained with upright dynamic films in flexion-extension and lateral bending [9].

When findings on plain films do not give sufficient explanation of symptoms, CT or MRI should be performed. If bony abnormalities are diagnosed or highly suspected, CT may be performed for a more complete evaluation. In elderly patients with low back pain or sciatica it is even more commonly accepted as a valid alternative to MRI [10].

Myelography is rarely performed and reserved for patients with contraindications to MRI or in whom subtle instability is suspected but not confirmed by other examinations. Discography is also reserved for selected patients before some interventional procedures or when the diagnosis of discogenic pain must be confirmed.



For accurate instability evaluation, plain films usually do not offer complete information. The main cause is absent direct visualization of cerebrospinal fluid and nervous structures. Weight-bearing CT and MRI are imaging alternatives. An axial loader is a hydraulic compressor that is placed below a patient’s feet and over the shoulders to apply a variable axial load on the spine. The device can be used with CT or MRI, and it simulates static mechanical forces acting on the spine in the upright position [11]. More recently, dedicated MRI units that allow examination with the patient in the upright position have been realized. These systems have the advantage of determining axial load by gravity, a patient’s weight, and spine morphology without artificial simulation [12,13]. With the same units, cervical dynamic flexion-extension evaluation is possible.


  • Bone structures
    • Vertebral osteochondrosis

Vertebral endplates bone marrow alterations are a common finding in patients with degenerative spine disease and are strictly associated with disc degeneration. To describe these changes, in 1985, Resnick [2] introduced the concept of vertebral osteochondrosis. This concept is considered an evolutionary process characterized by six phases: (1) disc thinning and hyaline degeneration, (2) chondral microfractures, (3) chondroblastic activation, (4) subchondral reactive neovascularization, (5) bony trabeculae demineralization, and (6) osteosclerosis.


Osteochondrosis is present in 19% of asymptomatic people [14]. It has been found in 50% of people who complain of low-back pain, however [15]. Reversible symptoms can be determined by acute inflammation in type I osteochondrosis, whereas other types are usually asymptomatic. Osteochondrosis is more frequent at levels at which the axial load is higher, such as L4-5 and L5-S1. The relationship with degenerative disc disease is probably caused by multiple factors, including common biomechanical factors, raised mechanical stresses on the endplates induced by disc dehydration, and disc metabolism changes. Other theories consider that the disc is an avascular structure supplied by diffusion from endplate cartilage; therefore, endplate alterations can induce disc trophism defects.

In 1988, Modic et al. [16] proposed a simple classification of vertebral osteochondrosis based on pathologic and imaging aspects. Modic type I (vascular pattern) is a discovertebritis or aseptic spondylodiscitis with bone inflammatory reaction associated with disc degeneration. In this phase, MRI signal of the endplates is low on T1-weighted and high on T2-weighted sequences. Modic type I can be reversible or can progress [17]. Modic type II (fatty pattern) is characterized by subchondral bone marrow changes with fatty marrow prevalence and demineralization. Endplate MRI signal is high on T1- and T2-weighted sequences. Modic type III (sclerotic pattern) is the final subchondral osteosclerotic evolution and is characterized by low signal on T1- and T2-weighted sequences. In this last case, plain films and CT clearly show endplate sclerosis. In almost all cases of vertebral osteochondrosis, MRI shows clear signs of disc degeneration. Sometimes more types are simultaneously found at the same level. In advanced cases, marginal traction osteophytes are frequently found. With MRI, differentiation between Modic types is usually possible. Diagnostic problems can be encountered in differential diagnosis between type I and infectious spondilodiscitis, however. In this case, gadolinium administration is useful, because in type I osteochondrosis disc enhancement is usually absent. In both cases subchondral enhancement can be registered.


  • Spondylosis

The most typical consequence of age- or load-related degeneration of the vertebral bodies is spondylosis deformans [2]. Spondylosis is found in 60% of women and 80% of men after the age of 50. In elderly people some degree of spondylosis is almost always found and can be considered paraphysiologic. When degenerative alterations are severe or symptomatic, they should be considered pathologic.

The classic sign of spondylosis is osteophytosis. Osteophytes are bony spurs that originate on the anterolateral aspect of the vertebral bodies a few millimeters from the margins of the disc space. They result from weakening and radial degeneration of the fibers of the annulus, with increased vertebral mobility and traction on Sharpey’s fibers determining subsequent osteogenic stimulation. Osteophytes usually follow Sharpey’s fibers. At the beginning they have a triangular shape and extend on the horizontal plane; in the more advanced phase they become hooked and grow vertically. Sometimes osteophytes develop on both sites of a disc space and grow until they fuse together to form a “bridge osteophyte” [2]. Although the most frequent site of osteophytosis is the anterolateral aspect of the vertebra, posterior osteophytes have higher clinical significance because of the possible compression of neural structures. Posterior osteophytes more frequently accompany osteophytes associated with osteochondrosis, microinstability, and disc degeneration. They are characterized by a bulky triangular shape and have a marginal location [6].

Plain films are adequate for the diagnosis of spondylosis and are helpful for the differential diagnosis between osteophytosis and other bony excrescences with different origin. CT and MRI can show the osteophytes, but they are useful for identifying other associated degenerative changes and establishing the relationship between bone and neural structures [7,10].


Schmorl’s node is a common sign of spinal degeneration that is often included in the spectrum of spondylosis, although it has a distinct pathogenesis. A Schmorl’s node is a herniation of the intervertebral disc through the endplate in the vertebral body and is a frequent incidental finding. Schmorl’s nodes are usually asymptomatic; however, in the acute phase they can determine temporary back pain. Imaging shows a central defect of the upper endplate of the vertebral body, often with a clear sclerotic rim. MRI best depicts the relationship between the herniated material and the disc, which is often dehydrated. Acute nodes can be hyperintense on T2-weighted sequences and can enhance after gadolinium administration.


Degenerative changes of the cervical spine typically involve the uncovertebral processes with formation of posterior osteophytes. Associated abnormalities are disc height decrease and disc bulging or protrusion. Plain films are useful for the evaluation of cervical uncoarthrosis; the examination should be completed with oblique projections because osteophytes often determine stenosis of the neural foramina and otherwise could be missed. MRI is required to identify disc herniations that can determine spinal canal stenosis and possible compressive myelopathy.

  • Facet joints

Facet joints are frequently involved in osteoarthritis. The typical imaging findings are joint space narrowing, subchondral sclerosis and cysts, osteophytosis, ligament thickening, intra-articular vacuum and joint fluid. Osteophytes can involve the whole facet that appears hypertrophic; however, they more often involve the articular surface of the superior facet of the lower vertebra, because the inferior is covered by the ligamentum flavum. Plain films can show the presence of degenerative changes; however, the anatomic complexity of this region requires CT or MRI for a complete evaluation of the degenerative process. Severe facet osteoarthritis can determine lateral recess and neural foramen stenosis; less frequently, canal stenosis can be observed. CT is more accurate for determining bony abnormalities, but MRI more clearly shows neural structures and soft tissues.


Facet joint osteoarthritis often leads to vertebral instability because of sagittal orientation of the articular rim and degenerative weakening of the capsule and the periarticular structures [18]. Abnormal orientation of the articular rim can be sometimes congenital and rarely asymmetric. In these cases facet joint osteoarthritis and instability develop earlier. Facet instability leads to anterior subluxation of the inferior facet of the upper vertebra or degenerative spondylolisthesis. Weight-bearing MRI can be useful in selected cases to diagnose facet joint instability, which appears as joint space widening and anterior slippage of the lower facet. Weight-bearing MRI also can show increased thickening of the ligamentum flavum during axial load caused by ligament laxity. This process can determine appearance of a stenosis only during axial loading [13]. The role of facet joints in back pain is often difficult to assess, because symptoms can be unspecific and imaging findings of degeneration are common [19]. In selected cases, nerve block or facet joint steroid and anesthetic injections are useful for diagnostic and therapeutic purposes, because they reduce pain for patients who have facet syndrome [20].

Rarely, patients with hyperlordosis and severe degenerative changes of the facet joints can develop Baastrup disease. This condition is characterized by interspinosus contact, with resulting inflammatory reaction and possible formation of pseudoarticulation.


Sometimes facet joint degeneration is complicated by synovial cysts. These formations originate from the joint and can keep or lose the connection with the joint. When they develop on the intracanalicular side of a joint, they can have compressive effects. Cysts can contain synovial serous fluid, more gelatinous material, air, or blood. The diagnosis and the connection with the joint can be confirmed by percutaneous CT or fluoroscopic-guided aspiration. After aspiration, the cyst can be filled with steroid and anesthetic and can be broken for curative purposes.


Facet joint synovitis has been recognized as a possible cause of facet syndrome. Typical MRI findings are intra-articular or pericapsular high signal on T2-weighted sequences and enhancement after contrast agent administration [7].

  • Spondylolysis and spondylolisthesis


Six types of spondylolysis have been defined: dysplastic, isthmic, traumatic, pathologic, iatrogenic, and degenerative (pseudospondylolysis). The most common kind of lumbar spondylolysis is the isthmic type, which is a typical pathologic condition of children, adolescents, and young adults. Isthmic spondylolysis can be defined as a defect of the pars interarticularis of the vertebra and it is considered a fatigue fracture produced by abnormal mechanical stresses on an otherwise normal bone. Spondylolysis is initiated by repetitive direct microtraumas, repeated contraction of agonist and antagonist muscles, and mechanical load of the body weight. These factors induce a stress response in the bone. The most common site of spondylolysis is L5 (81%) followed by L4 (14%). The prevalence of spondylolysis in the general asymptomatic population is approximately 3% to 7%, but it is higher in people who participate in sports activity [21,22].

Plain films are useful for diagnosing spondylolysis: a lateral view often allows identifying the isthmic lysis as a defect of the pars interarticularis with sclerotic borders, but the examination should be completed by 45° oblique view. On this projection, spondylolysis can be recognized for the classic sign of the “Scottish terrier’s collar.” Single-photon emission CT is sensitive for the detection of spondylolysis in the acute phase; older or asymptomatic lesions can be silent because of the absence of active bone reaction. CT is accurate for the detection of lysis, which appears as transverse isthmic fracture with irregular rim and sclerosis [21]. The examination should be performed with a reverse gantry angle (15%–25%) parallel to the axis of the isthmus; otherwise, differentiation between the lysis and normal facet joints can be difficult [23]. MRI is less sensitive and less accurate than CT; lysis can be distinguished on MRI as an interruption of the normal bony signal.

Spondylolysis often leads to spondylolisthesis, which is defined as anterior or posterior slippage of a vertebral body. In the elderly population, spondylolisthesis is frequent (approximately 4%) and is usually not related to spondylolysis but to severe degeneration of the interapophyseal joints. The typical sites of degenerative spondylolisthesis are L3-4 and L4-5 because of the more sagittal orientation of the joints. Anterior spondylolisthesis can be classified in four grades according to Meyerding’s classification. Degenerative spondylolisthesis is usually grade I (slippage below 25%). Posterior spondylolisthesis is a posterior subluxation of the body that is usually associated with facet joints and disc degeneration. This alteration is more frequent at more mobile spine segments, such as the cervical tract and upper lumbar levels. If spondylolisthesis is caused by isthmic lysis, the anterior slippage causes widening of the vertebral canal. Conversely, when spondylolisthesis has a degenerative origin the canal undergoes anteroposterior narrowing because of slippage of the posterior vertebral arch and facet hypertrophy [18,46].

Upright plain films are necessary for a correct diagnosis and grading of spondylolisthesis. Dynamic radiographs in hyperflexion, hyperextension, and lateral bending are useful for evaluating associated vertebral instability, which is characterized by loss of alignment of one of more vertebral lines. Radiographic signs of instability obtained with dynamic films are evidence of anterior or posterior vertebral slippage during motion or load, pedicle length variations, neural foramina narrowing, and loss of intervertebral disc height. Other associated signs are intradiscal vacuum and traction osteophytes. Conventional MRI can show spondylolisthesis, but its value is limited for functional information. MRI often shows “pseudobulging,” which usually occurs at the level of the lysis, and narrowing of the neural foramina. Axial loaded CT and MRI or upright MRI can provide functional information about vertebral stability and spine response to physiologic load conditions [24].

  • Degenerative stenosis


Degenerative changes can determine spinal stenosis, including central canal stenosis, lateral recess stenosis, and foraminal stenosis. Spinal stenosis is classified as congenital, acquired, or mixed. Congenital stenosis is more frequent in the lumbar tract. It can be part of a skeletal syndrome (eg, Morquio’s sign, achondroplasia, Down syndrome) or be idiopathic. The latter condition is characterized by shortness and thickness of the pedicles, shortness of laminae, or sagittal orientation of facet joints. Acquired stenosis is usually caused by degenerative bony and discal changes. They usually involve the cervical and lumbar tracts, whereas the thoracic spine is rarely affected. Mixed stenoses are caused by degenerative abnormalities in patients with a constitutionally narrow spinal canal [1].

The definition of central stenosis is subjective, although many studies tried to define stenosis on the basis of quantitative parameters. At the cervical level, an indicative value of early stenosis is a sagittal canal diameter <14 mm between C4 and C7. If the anteroposterior diameter is <11 mm, the patient usually experiences neurologic symptoms. Alternatively, stenosis should be considered if the ratio between canal sagittal diameter and body sagittal diameter is <0.8 mm. In the lumbar spine, normal median sagittal diameter is >15 mm. Moderate stenosis is established if the diameter is between 14 and 10 mm; severe stenosis is established if the diameter is <10 mm. In some cases, the sagittal diameter undergoes a slight narrowing because the transverse diameter can markedly decrease, and interpeduncular diameter should be considered. This diameter usually measures 17 to 19 mm at L1 and 20 to 23 mm at L5. Although measurement of canal diameters can be useful, its correlation with symptoms is low. Imaging evaluation is mainly based on subjective evaluation of canal morphology and the relationship between the dimensions of the containing and the contained structures.

All aspects of degenerative spinal disease contribute to spinal stenosis, and in most cases more factors are simultaneously present and variously combined. Disc bulging or herniations, spondylosis deformans, osteochondrosis with traction osteophytes, facet joint osteoarthritis, ligamentum flavum thickening, asymmetric facet joint orientation, and ligament calcifications can determine canalicular stenosis because of direct compression. Stenosis can be more evident in orthostatis when dynamic factors contribute to its genesis. This condition happens in patients with significant vertebral instability or spondylolisthesis [18].

Lateral recess stenosis is usually caused by hypertrophy and osteophytosis of the superior articular facet; less frequently the stenosis is caused by vertebral body osteophytosis or other degenerative changes. The stenosis can be isolated but usually involves the central part of the canal. The normal sagittal diameter of the lateral recess is >5 mm; when this space is <4 mm the recess is considered stenotic [7].


Foraminal stenosis is more common than lateral recess stenosis. It is usually caused by disc material and marginal osteophytes protruding into the foramen. Another common cause is narrowing of the disc space with subsequent anterosuperior slippage of the superior facet.

The role of imaging in spinal stenosis is to confirm the clinical diagnosis, identify the level of stenosis, establish causes, and guide treatment. Plain films are useful for measuring the diameter of the canal and evaluating bony abnormalities. Cross-sectional imaging is necessary for a complete balance of the entity and causes of spinal stenosis, however. CT is the gold standard for evaluation of bony abnormalities and is accurate for detecting posterior osteophytosis. The dural sac and the nervous structures are visible and their compression can be assessed. CT is useful for identifying calcifications of the ligamentum flavum and the posterior longitudinal ligament, which can play an important role in the genesis of stenosis, especially at thoracic level [25]. Calcifications can be missed easily by MRI, because degeneration of posterior arch structures is often homogeneously hyperintense because of the presence of marked fibrosis and bone sclerosis. MRI accurately depicts the disc pathology and shows nervous structures more clearly. At the lumbar level the hyperintense signal of cerebrospinal fluid on T2-weighted sequences offers a myelographic effect because of the high contrast resolution between the dural sac and the extradural structures. This effect can be stressed and myelo-MRI can be obtained; however, their clinical usefulness is limited. The best diagnostic sign is the reduction of the dimensions of the dural sac or the spinal cord, with hypertrophy of the surrounding bony and discal structures. Epidural fat is reduced or disappears on axial scan planes. On sagittal T2-weighted sequences, multiple anterior and posterior notches on the dural sac can be observed, the former caused by disc and vertebral body abnormalities and the latter caused by facet joint and ligamentum flavum thickening [25]. Vertebral body osteophytes are usually detected. They are often hypointense, however, and the distinction between osteophytes and the hypointense herniated disc can be difficult to make. In this case gradient echo (GE) T2-weighted sequences are useful because they enhance the intrinsic contrast between the disc (hyperintense) and the osteophyte (hypointense). Spinal stenosis. On CT, a bulky posterior marginal osteophyte (arrow) determines narrowing of the central canal and the lateral recess. Note anterolateral osteophyte (dotted arrow).

Figure 1. CT scan studies of the lumbar spine in patients with neurogenic claudication due to degenerative lumbar canal stenosis (A,B,C). Notice annulus bulging, ligamentum flavum hypertrophy, articular facet disease, and spinal vacuum phenomenon (B,C). D, CT myelography in a patient with degenerative lumbar canal stenosis, notice the trefoil appearance characteristic of central canal stenosis due to a combination of zygapophysial joint and ligamentum flavum hypertrophy.

A finding sometimes observed in patients with severe lumbar central canal stenosis is so-called “redundant nerve roots,” which present as enlarged and swollen aspects of cauda equina nerve roots. Redundant nerve roots are supposed to be caused by increased cerebrospinal fluid pressure and radicular venous congestion caused by the stenosis. The consequence would be radicular ischemic damage and edema [1]. Constitutional abnormalities that contribute to mixed stenosis are easily detected by imaging and must be reported for their implication on stenosis management.

In cervical and dorsal stenosis, MRI shows not only spinal degenerative changes but also disappearance of subarachnoid space and narrowing and compression of the spinal cord. MRI is helpful for diagnosing myelopathy, which appears as smooth, hyperintense areas on T2-weighted sequences. Rarely syringomyelic cavities are present. In compressive myelopathy, abnormal areas are usually located at the level of stenosis; however, sometimes they are found below the stenosis. These abnormalities are probably caused by ischemia, because increased cerebrospinal fluid at the stenotic level leads to reduced venous drainage and spinal cord venous congestion, which result in cord ischemic damage.

Dynamic plain films, weight-bearing CT, and MRI have been applied to the study of spinal stenosis [12]. Under axial loading or in an upright position, the stenosis can be more evident because of modifications of the intermetameric relationships induced by increased load, especially in patients with vertebral instability. In patients with kinetic-dependent instability and stenosis, the alterations can become evident only during weight-bearing or dynamic examination. Longitudinal hypermobility of the facet joints with anterior slippage of the articular processes is responsible for augmented central or lateral stenosis [18], which appears as increased degree of spondylolisthesis and increased protrusion of the articular processes into the canal. Disc herniations are sometimes more pronounced under weight bearing. Ligamenta flava hyperlaxity is another important cause of stenosis. It can appear more severe during weight-bearing examinations because narrowing of disc space determines shortening and thickening of the ligaments. Thanks to high signal of cerebrospinal fluid, myelographic semeiotic can be applied to upright MRI. Narrowing of perimedullary subarachnoid space and decrease of dural sac diameter during upright and dynamic examinations are important signs of stenosis.

Spinal canal stenosis: Pathology, anatomy and pathogenesis
  • Anatomy and pathology

The spinal cord in adults ends at the upper border of the L1 vertebral body and continues as multiple nerve roots, the cauda equina, that descend to their specific neural foramena, providing exit from the lumbosacral spinal canal. The spinal canal ranges from 15 to 23 mm in its anteroposterior diameter and is a triangular space bounded anteriorly by the dorsal surfaces of the bodies of the lumbar vertebrae and the disk spaces (covered by the posterior longitudinal ligament), medially by the pedicles that extend from the lateral margin of the vertebral body, posteriorly by the laminae of the vertebral arch and their covering, the ligamentum flavum; and the facet joints that are part of the posterior elements of each vertebral body. The vertebral bodies are connected to each other by the disks anteriorly and two facet or zygoapophyseal joints posteriorly. The disks are composed of a tough outer connective tissue annulus fibrosis and a soft, jelly-like center, the nucleus pulposus.

There are two major categories of lumbar spinal stenosis: congenital and acquired. The major contributors to narrowed lumbar canals on a congenital basis are short pedicles, thickened lamina and facets, and excessive scoliotic or lordotic curves. Patients who have these congenital anatomic changes have a small safety factor for the emergence of clinically significant lumbar spinal stenosis, which may be precipitated by further canal narrowing from later life–onset superimposed degenerative joint changes. Defects in cellular metabolism leading to retardation of cartilaginous growth and irregular intracartilagenous bone formation lead to congenital spinal stenosis in achondroplastic dwarfism, where there is significant narrowing of the spinal canal in all its dimensions, especially in the upper lumbar regions because of shortened pedicles, hypertrophied zygapophyseal joints, and thickened laminae.

The majority of cases of lumbar spinal stenosis, however, are acquired, and stem from degenerative or arthritic changes that affect the three-joint complex between lumbar vertebrae: the two zygoapophyseal (facet) joints posteriorly and the adjoining intervertebral disk anteriorly. The degenerative process begins most often with the disk and affects the articular processes secondarily. Initially, there is desiccation of the disk, narrowing of the disk space, rents or fissures in the annulus, disk bulging, and frank herniation of nucleus pulposus. This soon is followed by hypertrophic degenerative changes of the facets (osteophyte formation) and thickening of the ligamentum flavum. This results in central narrowing, so that the anteroposterior diameter is attenuated (typically to less than 12 mm), with compression of the cauda equina, and lateral narrowing (at the recesses), with root compression at the entrance of the intervertebral foramen. Spondylolysis (a defect in the pedicles, the pars interarticularis—congenital or acquired) may lead to spondylolisthesis, the anterior displacement of one vertebra relative to the one beneath it, further narrowing an already stenotic lumbar canal.

The spine is the site affected second most commonly in Paget’s disease, predisposing patients to spinal stenosis, occurring in one third of those who have spinal involvement. Pagetic spinal stenosis is brought about by bone remodeling of lumbar vertebrae, with bone expansion in all directions: posteriorly from the vertebral bodies, anterioromedially from the vertebral lamina, and medially from the pedicles. This leads to hypertrophic facet arthropathy and resulting spinal stenosis. Some cases of neurologic deterioration do not result from direct compression of neural elements, rather from spinal ischemia resulting from diversion of blood flow through remodeled hypervascular pagetic bone (referred to as the arterial steal phenomenon).

  • Pathogenesis

Three explanations are advanced to explain the phenomenon of neurogenic claudication, the cardinal manifestation of lumbar spinal stenosis. They are designated the postural, the ischemic, and the venous stasis (stagnant hypoxia) theories. The postural theory suggests that symptoms are explained by transient compression of the cauda equina (leading to sensory and motor axon dysfunction) by degenerated intervertebral disks and thickened ligamenta flava, when the lumbar spine is extended and lordosis is accentuated, either at rest or in the erect posture. In the ischemic theory, it is proposed that the metabolic demand of the cauda equina cannot be met during activity (eg, walking), that blood flow needs of the lumbosacral nerve roots are not met by the local vasculature that is compromised by lumbar spinal stenosis. Porter suggested the venous stasis theory: that the underlying mechanism of neurogenic claudication is inadequate oxygenation or the accumulation of metabolites in the cauda equina. He presented evidence from a porcine model that venous pooling of one or more nerve roots of the cauda equina between two levels of low pressure stenosis transitions to venous engorgement during exercise (walking), that in turn tends to prevent the expected arteriolar vasodilation response to activity, leading to nerve conduction failure with resulting symptoms of tiredness, weakness, and discomfort in the legs when walking.

  • Intervertebral discs
    • Pathophysiology

Degeneration of intervertebral disc is characterized by dehydration, fissures, bulging, and herniations. Degenerative disc disease is more common in the elderly population; however, acute herniations are frequent in the middle-aged population. Three main pathogenetic mechanisms are involved in degenerative disc disease:

1.Acute trauma, which leads to vertebral instability with alterations of spinal alignment that can accelerate degeneration. This mechanism is frequently related to the discovertebral degeneration observed after an acute cervical trauma.

2.Chronic static and dynamic overload, which causes chronic microtraumas. This is considered the most important factor leading to disc degeneration. It is also proven by the higher prevalence of disc herniations at levels of maximal axial load.

3.Decreased permeability of the endplates, which leads to dysfunction of fibroblasts and chondrocytes, with subsequent alteration of the keratin/chondroitin sulfate ratio. Matrix degeneration determines loss of nucleus pulposus water and consequent rigidity.

  • Classification and imaging

The first phase of disc degeneration is dehydration of the nucleus pulposus, which is caused by reduction of proteoglycans and is often associated with disc height decrease. Dehydration is well demonstrated by MRI because the disc becomes hypointense on T1- and T2-weighted sequences. In most cases disc dehydration is asymptomatic, but it indicates disc overload and often is followed by further degenerative abnormalities. In more advanced cases, degeneration progresses with wide destruction of the disc, extreme height reduction, and intradiscal gas formation. Gas frequently is observed on CT as an air density intradiscal area. MRI is less accurate for identifying gas, which appears as a hypointense area on all sequences.


Another common disc alteration is the intranuclear cleft, an early sign of disc degeneration caused by transverse rupture of nuclear fibers that appears as a hypointense transverse band inside the nucleus pulposus. This finding appears in all discs in the adult population after 40 years, and it is considered a paraphysiologic asymptomatic change.

Degenerative changes of the annular fibers may result in two types of fissures [7]: (1) circumferential fissures and (2) radial fissures. The former type consists of rupture of collagen bridges among annular fibers with annular weakness and preserved integrity of fibers. This alteration precedes the formation of annular bulging. On sagittal T2-weighted MRI, circumferential fissure appears as a focal hyperintense area into the external aspect of the annulus. Radial fissure is a linear rupture of annular fibers extending from the nucleus pulposus. Radial fissure can progress to more severe disruption and determine disc herniation. Rupture of inner thin, annular fibers leads to protrusion and rupture of thick peripheral fibers to herniation. On MRI, radial fissure appears as a hyperintense transverse band into the annulus. Radial and circumferential fissures have been found to determine microinstability and increased mobility of the discosomatic unit [26,27].


In the literature and in clinical practice, the definition of the forms of disc degeneration is often not univocal, because different terms are used for the same entity and vice versa. Recently, an attempt to define standard and uniform terminology was made [28]. According to the new nomenclature, in the bulging disc the contour of the outer annulus extends in the axial plane beyond the edges of the disc space over more than 50% of the circumference of the disc and usually less than 3 mm beyond the edges of the vertebral body. The bulging is defined as asymmetric if it is more evident in one section of the periphery of the disc but is not so focal as to be characterized as a protrusion. Disc herniation is defined as localized displacement of disc material beyond the normal margins of the intervertebral disc space. Disc herniation is classified as protrusion or extrusion.



Protrusion means that the greatest distance, in any plane, between the edges of the disc material beyond the disc space is less than the distance between the edges at the base in the same plane.

Extrusion means that any one distance between the edges of the disc material beyond the disc space is greater than the distance between the edges of the base in the same plane. When no contiguity exists with the parent disc, the extruded material may be characterized as sequester or free fragment.

Other definitions include the concept of migrated disc and contained herniation. In the migrated disc a portion of herniated disc material is displaced away from the tear in the outer annulus through which it has extruded. Contained herniation is defined as displaced disc tissue that is wholly within an outer perimeter of uninterrupted outer annulus or capsule. If the annulus is completely interrupted, the herniation can be defined as uncontained. When the herniation crosses the posterior longitudinal ligament, it can be defined as extraligamentous or transligamentous. This event is uncommon, and the fragment does not migrate for more than one level because of the strict adhesion of the Trolard’s ligament to the vertebral body in the midline. Relative to the axial plane, the herniation may be (1) central, (2) right-left central, (3) right-left subarticular, (4) right-left foraminal, or (5) right-left extraforaminal.

CT is accurate for the diagnosis of disc herniation and allows the differential diagnosis between bulging and herniation, the evaluation of dimensions and location of the herniated disc, and the detection of free fragments. The disc is hypodense but the nucleus pulposus cannot be exactly identified. CT is more accurate than MRI for the identification of calcified herniations and associated bony abnormalities, such as posterior accompanying osteophytes, which can be important for therapeutic decisions [7,10].

MRI is the technique most frequently used for the evaluation of disc herniation. The examination should comprise sagittal T1- and T2-weighted sequences and axial T1- and/or T2-weighted sequences. In the cervical tract, axial GE T2-weighted sequences are useful for differentiating osteophytes and disc material. MRI is the optimal diagnostic tool, comparable in sensitivity to myelo-CT, for the diagnosis of disc herniation. The principle of disc herniation diagnosis is the same with CT and MRI. The herniation is seen as a focal contour abnormality along the posterior disc margin with a soft tissue mass displacing the epidural fat and, sometimes, the dural sac and the nerve roots. The herniation is usually contiguous with the rest of the disc, but free fragments are possible [1,7,29]. The herniation is usually isointense to the rest of the disc on T1- and T2-weighted sequences. The herniation often is slightly or strongly hyperintense on T2-weighted sequences, however [7].


After gadolinium injection, many herniations have a thin peripheral enhancing rim caused by the inflammatory reaction [30]. Contrast injection is usually not necessary, however, but in select cases it can be useful for differential diagnosis between herniation and neurinoma. Contrast agent is more widely used in postoperative examinations, because it is useful for differentiating residual or recurrent herniations from scar tissue.


MRI is sensitive to the detection of early changes of the disc anatomy. This examination sometimes leads to an overinterpretation of the findings, giving pathologic meaning to paraphysiologic features and vice versa. Patient history and symptoms must be evaluated with care. Correlation with MRI findings is important to find out the reason for symptoms and give indication of surgery or other invasive treatments.

  • Natural history

Disc herniations usually have a favorable outcome. Long-term follow-up studies showed that regression or reduction of symptoms occurred in 71% to 95% of patients after 1 year, and stability or worsening occurred in 5% to 29% of patients [31,32,33]. Follow-up of surgically and non–surgically treated patients indicate that after a 5- to 10-year period, the success rate is similar [34,35,36]. Indications for surgery are actually selective because conservative treatment is usually effective.


Imaging studies with MRI follow-up 6 to 12 months after the diagnosis demonstrated that 63% of disc herniations may show a spontaneous volume reduction [31,37,38]. The causes of spontaneous reduction of herniated disc material are shrinkage caused by dehydration, fragmentation, and phagocytosis of the disc material. Shrinkage and fragmentation are related to matrix degeneration and loss of proteoglycans integrity; phagocytosis is induced by local inflammation with an immunomediated process, because nucleus pulposus is immunologically segregated [39].

MRI can be used for follow-up of nontreated disc herniations [30,40,41]. The main MRI findings useful to presume spontaneous regression of disc herniations after 6 months are [41] free fragments (100%), T2-weighted hyperintense herniation (83%), peripheral enhancement after gadolinium administration (80%), and recent clinical onset (75%). Among the types of herniations, protrusions are usually more stable than extrusions. Bulging disc history is different, because it usually does not undergo spontaneous anatomic regression and symptoms are more stable.

Finally, radiology is involved not only in the diagnostic phase of degenerative disc disease but also in the therapeutic phase [42]. Many minimally invasive interventional radiology techniques have been designed: automated discectomy [43], percutaneous laser disc decompression [44], coblation and intradiscal oxygen-ozone injection (chemiodiscolysis) [45]. All these technique offer a valid alternative to surgery, because at follow-up their success rate ranges from 70% to 80% [45]. Their potential complications are minimal and there is no risk of failed back surgery syndrome.


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[14] Jensen MC, Brant-Zawadzki MN, Obuchowski N, et al.. Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl J Med. 1994;331:69–73.

[15] Modic MT. Degenerative disc disease and back pain. Magn Reson Imaging Clin N Am. 1999;7:481–491.

[16] Modic MT, Steinberg PM, Ross JS, et al.. Degenerative disc disease: assessment of changes in vertebral body marrow with MR imaging. Radiology. 1988;166:194–199.

[17] Mitra D, Cassar-Pullicino VN, McCall IW. Longitudinal study of vertebral type-1 end-plate changes on MR of the lumbar spine. Eur Radiol. 2004;14:1573–1581.

[18] Jinkins JR. Acquired degenerative changes of the intervertebral segments at and suprajacent to the lumbosacral junction: a radioanatomic analysis of the nondiscal structures of the spinal column and perispinal soft tissues. Eur J Radiol. 2004;50:134–158.

[19] Helbig T, Lee CK. The lumbar facet syndrome. Spine. 1988;13:61–64.

[20] Murtagh R. The art and science of nerve root and facet blocks. Neuroimaging Clin N Am. 2000;10:465–477.

[21] Rossi F, Dragoni S. Lumbar spondylolysis and sports: the radiological findings and statistical considerations. Radiol Med (Torino). 1994;87:397–400.

[22] Harvey CJ, Richenberg JL, Saifuddin A, et al.. The radiological investigation of lumbar spondylolysis. Clin Radiol. 1998;53:723–728.

[23] Jayakumar P, Nnadi C, Saifuddin A, et al.. Dynamic degenerative lumbar spondylolisthesis: diagnosis with axial loaded magnetic resonance imaging. Spine. 2006;31:E298–E301.

[24] Congeni J, Mc Culloch J, Swanson K. Lumbar spondylolysis: a study of natural progression in athletes. Am J Sports Med. 1997;2:248–253.

[25] Yoshida M, Shima K, Taniguchi Y. Hypertrophied ligamentum flavum in lumbar canal spinal stenosis: pathogenesis, morphologic and immunohistochemical observation. Spine. 1992;17:1353–1360.

[26] Saifuddin A, McSweeney E, Lehovsky J. Development of lumbar high intensity zone on axial loaded magnetic resonance imaging. Spine. 2003;28:E449–E451.

[27] Haughton VM, Rogers B, Meyerand ME, et al.. Measuring the axial rotation of lumbar vertebrae in vivo with MR imaging. AJNR Am J Neuroradiol. 2002;23:1110–1116.

[28] Fardon DF, Milette PC. Nomenclature and classification of lumbar disc pathology: recommendations of the combined task forces of the North American Spine Society, American Society of Spine Radiology, and American Society of Neuroradiology. Spine. 2001;26:E93–E113.

[29] Milette PC, Fontaine S, Lepanto L, et al.. Differentiating lumbar disc protrusions, disc bulges, and discs with normal contour but abnormal signal intensity: magnetic resonance imaging with discographic correlations. Spine. 1999;24:44–53.

[30] Gallucci M, Bozzao A, Orlandi B, et al.. Does postcontrast MR enhancement in lumbar disk herniation have prognostic value?. J Comput Assist Tomogr. 1995;19:34–38.

[31] Bozzao A, Gallucci M, Masciocchi C, et al.. Lumbar disk herniation: MR imaging assessment of natural history in patients treated without surgery. Radiology. 1992;185:35–141.

[32] Saal JA. Natural history and nonoperative treatment of lumbar disc herniation. Spine. 1996;21:2S–9S.

[33] Bush K, Cowan N, Katz DE, et al.. The natural history of sciatica associated with disc pathology: a prospective study with clinical and independent radiologic follow-up. Spine. 1992;17:1205–1212.

[34] Komori H, Shinomiya K, Nakai O, et al.. The natural history of herniated nucleus pulposus with radiculopathy. Spine. 1996;21:225–229.

[35] Davis RA. A long-term outcome analysis of 984 surgically treated herniated lumbar discs. J Neurosurg. 1994;80:415–421.

[36] Postacchini F. Spine update: results of surgery compared with conservative management for lumbar disc herniations. Spine. 1996;21:1383–1387.

[37] Gallucci M, Bozzao A, Orlandi B, et al.. Follow-up of surgically treated and untreated disk pathology. Rivista di Neuroradiologia. 1995;8(s1):85–96.

[38] Delauche-Cavallier MC, Budet C, Laredo JD, et al.. Lumbar disc herniation: computed tomography scan changes after conservative treatment of nerve root compression. Spine. 1992;17:927–933.

[39] McCarron RF, Wimpee MW, Hudkins P. The inflammatory effect of nucleus pulposus: a possible element in the pathogenesis of low back pain. Spine. 1987;12:760–764.

[40] Kawaji Y, Uchiyama S, Yagi E. Three-dimensional evaluation of lumbar disc hernia and prediction of absorption by enhanced MRI. J Orthop Sci. 2001;6:498–502.

[41] Splendiani A, Puglielli E, De Amicis R, et al.. Spontaneous resolution of lumbar disk herniation: predictive signs for prognostic evaluation. Neuroradiology. 2004;46:916–922.

[42] El-Khoury GY, Renfrew DL. Percutaneous procedures for the diagnosis and treatment of lower back pain: discography, facet-joint injection, and epidural injection. AJR Am J Roentgenol. 1991;157:685–691.

[43] Bonaldi G. Automated percutaneous lumbar discectomy: technique, indications and clinical follow-up in over 1000 patients. Neuroradiology. 2003;45:735–743.

[44] Choy D, Ascher P, Ranu HS, et al.. Percutaneous laser disc decompression: a new therapeutic modality. Spine. 1992;17:440–443.

[45] Gallucci M, Limbucci N, Zugaro L, et al.. Sciatica: treatment with intradiscal and intraforaminal injections of steroid and oxygen–ozone versus steroid only. Radiology. 2007;242:907–913.

[46]. Metwally, MYM: Textbook of neuroimaging, A CD-ROM publication, (Metwally, MYM editor) WEB-CD agency for electronic publishing, version 9.1a January 2008


  1. انا عندى كسر قديم فى العمود الفقرى سنة 90 وتم تثبيته بجامعة اسيوط وبعد ثلاثة اشهر بدات الحركه والتحسن تدرجيا ولكن اثناء الحركه كسرة الشرائح والمساميير وتم رفعهم ولم يتم عمل شى اخر وعشت مع الالم حتى عام 2009 وبعد ذالك دخلت مستشفى عين شمس التخصصى وتم التثبيت الفقرات من الفقرة الثانيه الى الخامسه مرة اخرى زلكن قدر الله وما شاء فعل زاد اللم وقلت الحركه واى حركه فيها الم شديد وانا الان تعبان جدا وبعد عهرض الحاله على اساتذة العمود الفقرى كان الرى ان هناك تشوه فى الفقرات وانحناء امامى وضيق فى القناة وانا مش عارف اعمل العمليه مرة ثالثة ام لا افيدونى افادكم الله

    • الأخ الفاضل حلمى
      شفاك الله وعافاك
      يجب مناظرة الحالة وجميع الفحوصات حتى يتم إتخاذ القرار المناسب
      والشافى هو الله

  2. helo doc wanted to know is it bad to have L4-L5 disk dehydration with lft postero central disk protusion is seen compressing lft tranverse nerve root bilat facet arthropahty is also seen indicates lumbar spondylosis can physio help without doing surgery pls help thanks any suggestions

  3. Hello Sir .
    i want to discuss my fathers case with you he had a cervical spine attack due to which his left foot got turned.
    Please reply if you can help me i will send you his MRI reports copy and MRI images
    Thankyou very much..

    • You can call me at 002-02-33022907 at 4 pm daily except Thursday & Friday.

  4. anterior osteophytes are noted arising from c5-c6 vertebral bodies. eary degenerative changes are seen in the cervical spine.

    • Anterior osteophytes are neurologically insignificant.

      • I am 27 Years Guy having Lower Back bone Pain and below is my MRI L.S Spine Report. I need to know it in simple words what exactly does it means?? Also need suggestion that whether i should go for surgery or to have a P.T or Through medication??????? Plzzzz

        M R I L U M B O – S A C R A L S P I N E (Plain Study)


        • Early disk dessicatory changes are seen at L4-L5-S1 with normal disk height. Rest of the IV disk appears unremarkable.
        • Normal spinal curvature seen with normal vertebral alignment.
        • Mild to moderate central / right paracentral disk bulges and osteophyte complexes at L4-L5-S1; alongwith early facet joint hypertrophic changes; causing narrowing of inferior foraminal recesses and mild to moderate focal as well as bilateral exiting nerve roots compression (esp. at L4-L5).
        • No disk protrusion / herniation or spinal canal stenosis seen.
        • Posterior osteophytes are also visualized at L1-L2; causing minimal anterior thecal compression.
        • No evidence of vertebral collapse or paravertebral abnormality / collection seen.
        • Normal signal return from spinal cord with no evidence of cord ischemia / demyelination changes. Normal termination seen at L1 level.


         Mild to moderate central / right paracentral disk bulges and osteophyte complexes at L4-L5-S1; alongwith early facet joint hypertrophic changes; causing narrowing of inferior foraminal recesses and mild to moderate focal as well as bilateral exiting nerve roots compression (esp. at L4-L5).
         No disk protrusion / herniation or spinal canal stenosis seen.

      • you can have an appointment at
        daily from 3-6 pm Egypt time
        daily except Thursday & Friday.

  5. Wow, I really enjoyed this article. I just got my third MRI –two lumbar and one thoracic. I have had classic spinal stenosis sxs, since the birth of my daughter 15 years ago but MRI and Myelogram did not verify this dx. Now some mild foraminal stenosis is showing on MRI as well as some posterior spurs, end plate deformities due to schuermann’s disease, multiple bulges, arthritis, and ligamentous thickening. My doctor has been useless in figuring out why I have such significant pain in my lower back and left hip that radiates down my leg when I am laying down. I have also recently developed complete numbness on the bottom back of my left calf and heel that he cannot diagnose. This numbness and a significant increase in daily pain developed after I had microphlebectomy surgery on my left leg two months ago. I am at my breaking point here with daily constant pain. Any advice or direction you could provide would be so appreciated

    • you can have an appointment at
      daily from 3-6 pm Egypt time
      daily except Thursday & Friday.

  6. Hello sir,
    My cervical MRI says “signal alteration within the cord at C5-C7 levels suggestive of myelopathy” i dont have any symptoms of myelopathy though. Is this a confirmative test for myelopathy. if it is the beginning stage can i do something to stop it?


    • you can have an appointment at
      daily from 3-6 pm Egypt time
      daily except Thursday & Friday.

  7. Doc, can diffuse mild to moderate discogenic degenerative changes in lumbar spine cause a lot of pain?

  8. In 1998 I was diagnosed with Lumbar spindylothesis. Since then I have had several X-Rays due to my back being in pain on a daily basis. My recent x-ray showed “Modrate degenerative sponodylosis in the thoracic spine incidently noted”. What does this mean? The pain meds. I am taking (hydrocodne 10mgs) do not work I take the prescribed amount which equals 6 a day! I also take at least 6 Ibuprofen and 4 Excedrine. I’ve already had a doctor tell me my liver count was high, but never made an appointment. The last doctor that did a liver test in 2012 called me and said my liver count was normal “but quit drinking alcohol”. The thing is I havent had a drink since my early 20′s and I am 43. Could this be from taking to much hydrocodone and acetmentaphine? Your advise is grealty appreciated.


    • you can have an appointment at
      daily from 3-6 pm Egypt time
      daily except Thursday & Friday.

  9. Hello Doctor,

    I am a 41 year old, healthy female and I my recent MRI shows many issues that you discussed in this blog. I am at a loss of how to proceed–surgery or pain management? Physical therapy or chiropractor?

    My recent MRI report states the following findings, “There is 4 mm of retlisthesis of L5 on S1. There is marked reactive bone marrow change on the L5-S1 level. This is felt to be on a degenerative basis. No paraspinous mass is identified to suggest infections disctis. No evidence for pars fracture. The conus appears normal and terminates at T12-L1. The paravertebral soft tissues are intact.

    Would you be able to make an “informal” recommendation for a treatment plan for me based on the above findings?

    Thank you.

    • you can have an appointment at
      daily from 3-6 pm Egypt time
      daily except Thursday & Friday.

  10. Xray Impression:
    1. At least mild multilevel thoracolumbar spinal degenerative disc
    disease. This extends from T12-L1 through L5-S1.
    2. Transitional labeled L5 segment.
    3. No evidence of lumbosacral instability.

    Cervical spine 5 views:

    5 views of the cervical spine reveal evidence of degenerative disc
    disease at C4-C5 and C5-C6, and to a lesser extent at C6-C7. This
    consists of disc thinning and endplate spurring. There is a mild loss
    of normal upper to mid cervical lordotic curvature.

    Lateral flexion and extension views demonstrate no instability.

    1. Multilevel cervical spinal degenerative disc disease, most prominent
    at C5-C6 and C4-C5.
    2. No evidence of cervical instability.


    C4-C5 and C5-C6 moderate disc degeneration.

    C5-C6 moderate diffuse bulging annulus and moderate size left central
    disc osteophyte complex compresses ventral thecal sac and abuts
    ventral cord.

    C3-C4 and C4-C5 mild diffuse bulging annuli efface ventral thecal sac.

    Moderate size foraminal disc osteophyte complexes right C3-C4, C4-C5
    and bilateral C5-C6 cause moderately severe foraminal stenosis.

    No moderate or high-grade central canal stenosis.


    HISTORY: Bilateral hip pain, right leg pain and paresthesia

    Sagittal sequences of lumbar spine. Axial sequences from L1-L2 through
    L5-S1 disc spaces. Comparison is lumbar spine films 11/20/2013 and MRI
    lumbar spine 11/15/2002.

    Chronic mild compression superior endplate T11. Chronic Mild loss of
    normal lordosis at thoracolumbar junction. Large Schmorl node inferior
    endplate T12 stable since prior MRI. Small Schmorl nodes superior T11
    and L2. No marrow edema or bony lesion.

    Normal lumbar intervertebral disc space height with loss of normal

    T12-L1 noncompressive small central disc protrusion.

    L1-L2 normal intervertebral disc.

    L2-L3 mild diffuse bulging annulus mildly effaces ventral thecal sac
    and with hypertrophy of dorsal ligaments and facets causes borderline
    central canal stenosis.

    L3-L4 and L4-L5 no change in mild diffuse bulging annuli minimally
    effaces ventral thecal sac and hypertrophy of dorsal ligaments and
    facets, at L4-L5 with borderline central canal stenosis.

    L5-S1 no change in small central disc protrusion abutting ventral
    thecal sac. No central canal stenosis.

    Normal conus terminates at upper L1 level.


    L5-S1 no change in small central disc protrusion since prior MRI lumbar
    spine 2002.

    L2-L3, L3-L4 and L4-L5 mild diffuse bulging annuli.

    L4-L5 borderline central canal stenosis.

    With these results what would you recommend?
    I have lower and upper back pain
    Terrible hip pain
    Left leg/foot pain

    • you can have an appointment at
      daily from 3-6 pm Egypt time
      daily except Thursday & Friday.

  11. I am acting for a prisoner of war of the Japanese for 3 and a half years aged 18 to 21. He worked on the Burma railway carrying extremely heavy loads and while on only 500 calories a day – no protein – and beaten. Also in the mines. He was hospitalised at age 28 for back pain and has suffered back pain all his life. Would you consider his early trauma as POW as, on a balance of probabilities (obviously it cannot be totally proved), could be causative or contributory to his pain?

  12. Re the above comment, I have left an incorrect email address for response – should be .eu not dot.ey

  13. there is moderate left foraminal narrowing at C4-C5 on the basis of a disc osteophyte complex consisting of unconvertebral hypertrophy and disc bulge in 2012 I had a anti cervical disecetomy with fusin and allograft levels C5-C7 I also had a pinched nerve at level C4 before i had the surgery sound like to me they never fixed it anyway the rest of my report there is also mild foraminal narrowing at C7-T1 on the basis of the disc bulge I am having severe shoulder blade pain and the numbess is returned again is that pressing on a nerve what is foraminal narrowing mean I have been in pain for over 4 years and cant get any relief the pain doc i have now is worried about getting rid of my migraines and headaches I have something called Occipital Neuralgia :( I suffer on a daily basis non stop im sorry i had to write it again i sent the wrong email it is the second email

  14. Hello doctor

    i have had chronic pain in both my arms for 10 years now which has changed my life somewhat.

    I have had a recent mri. It says the followin:

    Mild degenerative disc change at c5 /6 & c6/7 with a small non-vertabral canal narrowing.

    Dr what does thismean. Does this condition have a name i can learn more about.

    Thank you dr

    • You need to be evaluated clinically & radiologically to know the source of your pain, which may not be discogenic.

    • you can take an appointment.

  15. Respected doctor
    I have chronic pain in my neck.Idid MRI at Islamabad Pakistan.The report reads as under
    Mild degree degenerative spondylitic and discogenic changes at lower cervical spine and c 6 -7 disc. No frank herniated disc spinal sterosis or abnormal MR cervical cord signal throughout cervical area.

    Kindly advise best possible treatment and d i have to visit you at egypt or get an appointment on telephone.
    Many Thanx

  16. I see this is a recent site that seems pretty informative on issues. I feel like I am a big mess with a terribly unstable back. The things that scare me most is that a few things are severe such as facet degen and bilateral forminimal narrowing, modic I and II changes, Grade 1 anterolisthesis. All thsi and I am only 37. I have never been in a accident but I actually wondered if this happened when I had my last child 9 years ago. It was a very hard delivery. I felt like I almost broke. i am experiencing severe leg pain that feels like my muscles are getting ripped right out of my leg. Its terrible and I cant seem to get a doctor to help me manage this pain properly even with the results of my MRI as well as giving me meds that can cause weight gain. im in PT trying to strengthen my core, but I cant lose any weight either. Im sure that doesnt help the matter.

  17. I have early lumbar spondylotic changes in L2 and L5, what can l do, please.

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