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[General Information | Pain or NO: The Research | Natural History | Grading the Spondylo | Classifications | X-ray Appearance | Diagnostic Techniques | Surgery Indications | Quiz ]
Another cause of spondylolisthesis in older people (usually around 60 years of age space [*4]) is degenerative change of the intervertebral disc in combination with the facet joints. This condition, called a degenerative spondylolisthesis, results from a failure of the degenerated facets (zygapophysial joints) to restrain the natural tendency of the affected vertebra to slide forward [*2,3]. Although the magnitude of forward slippage (anterolisthesis) is rarely greater than 15% [*4], the condition can become quite debilitating and necessitate surgery in patients who present with the conditions most common complaint: neural claudication [*5]. Although the ideology behind the facet joint failure is controversial, congenitally variations in facet plane orientation (i.e., more sagittally facing facets) and/or osteoporosis are two of the more popular theories [*11]. In general, problems with this forward slippage is that the delicate exiting nerve roots within the intervertebral foramen as well as the thecal sac itself can become compressed as the foramen and central canal are narrowed by the anterior slip. Another source of pain, arguably, for the non-degenerative spondylolisthesis is the actual breakage site within the pars interarticularis. In some cases, patients may present with a precursor to spondylolisthesis, which is called spondylolysis. This terminology simply means there is a fracture [134], defect, or weakening of the pars interarticularis, but no separation or forward slippage has yet occurred. How does this slip cause pain? Let's go a little deeper: In order to understand how spondylolisthesis causes pain, we have to understand a little bit about the anatomy of the lumbar spine. When two vertebrae are in perfect alignment, they create an exiting bony hole for the spinal nerve, which is called the neural foramen or intervertebral foramen (IVF). The IVF is the body's way of protecting the delicate spinal nerve and dorsal root ganglia, which also lives in the IVF. In order to achieve this perfect alignment, the vertebra above and below must have an intact posterior neural arch (the term posterior neural arch {or just neural arch or neural ring} includes the facets, pars interarticularis, lamina and spinous process). Any fracturing, congenital weakening, or congenital absence of any parts of the neural arch will result in a sliding of the body of the same vertebra forwards, which in turn can greatly reduce the size of the neural foramen. Obviously, if the neural foramen is reduced, it will "pinch" or irritate the delicate exiting nerve root and spinal nerve that lives within it, which will cause patient symptomatology. Which part of the posterior neural arch typically breaks? That would be the thinnest and most delicate portion of the neural arch; i.e., the pars interarticularis. Why does the pars interarticularis break? Significant trauma will fracture the pars because it is the weakest link. Another problem is the fact that in some patients the pars interarticularis is genetically weak and even more easily susceptible to stress fracture.. So in the unlucky individuals who were not blessed with good genes for neural arch building material, the pars may only be able to tolerate the 'activities of daily living' (135) and would be easily fractured with repeated loaded-flexion (136) and axial rotation. (139) Figure #6 demonstrates an isthmic grade 2 spondylolytic spondylolisthesis with a severe loss of disc height in a 28 year old patient with low back pain and some radiating lower limb pain that traveled to the knees. As you can see, there is a very visible pars defect (green arrow) that has allowed the L5 vertebra to translate (slid) forward by about 50% in relationship to the S1 segment/sacrum. In this particular patient, Flexion/Extension films revealed that this condition was stable, which means that the bone held its misalignment as the patient bent forward and then bent backwards. Grading the Spondylolisthesis: (Fig.#6) A system of slip classification developed by Leon Wiltse is what is mostly used in North America. The severity of spondylolisthesis may be classified/graded by noting the degree of anterior translation (forward slippage) of the top vertebral body in relationship to the bottom vertebral body: Slippage from 0-25% is called a Grade I spondylolisthesis; from 26-50% is called a Grade II; from 51-75% is called a Grade III; from 76-100% is called a Grade IV; and anything greater than 100% is called a Grade V spondylolisthesis or is given a special term: spondyloptosis. It is generally agreed upon that inheritance/genetics plays a "major role" in the development of a pars interarticularis defect, for the prevalence of spondylolisthesis is much greater within a family-tree of those affected when compared to the of the general public (8,240-242, 244). Wiltse has proposed that a hereditary defect or dysplasia in the cartilaginous model of the posterior neural arch is what predisposes folks to spondylo (245). Professor Nikolai Bogduk, who is the number 1 functional anatomist in the world and a two time Volvo Award Winner, has the following opinion on the origin of spondylolysis: "The biomechanical and epidemiological evidence points to pars defects as being an acquired fracture, either as a result of single, severe trauma or as a result of fatigue failure" (136,138,150,152,153)[126]. Occurrence Rate and Natural History: The Fredrickson Study: Fredrickson published the results of a fascinating investigation into the natural history of spondylolisthesis/spondylolysis (spondylo). The results of this study demonstrated that the majority of spondylos are detectable by age 12, and only 13% of these young spondyloses actually become symptomatic in the future. The study also demonstrated that once the patient was affected with the spondylodesis, it was pretty much with that patient for life (i.e., only 3% of the spondyloses actually healed with the passage of time). The other strange thing was that males were affected twice as frequently as the females [8]. The Specifics: in 1984, Fredrickson et al. x-rayed 500 asymptomatic six year-olds looking for spondylolisthesis and then followed the kids for over 20 years! Amazingly, all of the kids who were diagnosed with spondylolysis or spondylolisthesis all completed the 20 year study-none were lost! The entire group of kids were re-X-rayed every 4-5 years re-examined if pain developed. At age six, 4.4% (22/500) of the kids had either isthmic spondylolisthesis or spondylolysis on x-ray. By age twelve, 5.2% had the defect (85% participation rate, as some of the previously non-spondylo subjects were lost). This increased to 6% by age eighteen; however, the majority of the non-spondylo kids had dropped out of the study by this time (34% participation rate). From the aforementioned percentages, it can be calculated that about 66% of all spondylolistheses/spondylolyses occur by age twelve and are asymptomatic in the overwhelming majority of the cases. (8,502) The $64,000 question: did any of these patients have back pain? Between the ages of 14 and 27, four subjects developed back pain and one required surgery for a herniated disc that developed above the spondylolisthesis – none required surgery for spondylolisthesis. With regard to natural healing, only one subject's spondylolisthesis completely healed; however, that healing didn't manifest until the late 20s. Fredrickson also reviewed the spine x-rays of 500 newborns and could not find one single case of spondylolysis or spondylolisthesis; this finding had been previously verified by many other investigations. (204,208,211,224) In 10 of the kids, a spondylolysis developed between the x-ray intervals; none of these new pars defects were painful as the kids and their parents reported no back pain had occurred during that interval. In 7 of the 30 patients with spondylo, a progression of the slippage or initial slip occurred by age 16; again, the slippage appearance/increase was not associated with pain. The authors concluded that the "development of the pars interarticularis defect, with or without spondylolisthesis, does not cause pain in most patients." (8) THE DEFECT: In spondylolisthesis or spondylolysis, a "fibrous tissue" will form within the crack (defect) within the pars. (131) This "fibrous tissue" contains nerve fiber and pain-carrying free nerve endings (133) that contain neuropeptides (134); therefore, this tissue is theoretically capable of transmitting PAIN-signals to the brain [in layman's terms: this scar tissue like stuff that fills the crack in the back bone, has the potential to cause back pain.]
In Fig. #2 you can see that a "crack" or "pars defect" that has occurred within the pars interarticularis of the L5 neural arch. Because of the defect, the L5 vertebral body has slid forward by over 25% as measured against the sacral base below; anterior translation has occurred. This condition is called a "spondylolytic spondylolisthesis." Also notice that the thecal sac (yellow) has been kinked/irritated by the forward translation. The nerve roots (not shown) are also compressed and irritated. If severely symptomatic, a surgical procedure called a Fusion (ALIF, PLIF, or TLIF) may be indicated to realign the vertebrae and restore the lateral and central canals to their original size that accommodates the adjacent neural structures. In real life, the large and jagged "pars defect" is filled with a fibrous tissue that is, unfortunately, filled with nerve fiber that has the ability to carry pain signals to the brain. (133,134) Spondylolistheses are categorized or graded on the degree of forward slippage that has occurred. The bone/sacrum below is divided into four equal sections as noted in Figure # 3.
Also note the fibrotic tissue (green) that fills in the pars defect.
THE RESEARCH: DOES SPONDYLOLYSIS AND/OR SPONDYLOLISTHESIS CAUSE PAIN. [ Torgerson et al. | Fredrickson ] In 2003, Beutler and Fredrickson published the continued results of the ONLY prospective investigation into the natural history of spondylolisthesis / spondylolysis (“spondylo”) ever completed, which followed 30 subjects with confirmed youth-detected spondylolisthesis for more than 45 years! And the bottom line? The bottom line of this investigation was that the development of spondylolisthesis in childhood or early adulthood does not manifest into a serious pain syndrome or result in permanent disability. In other words, as compared to the general population, the group of spondylo patients were no more likely to undergo surgery or have chronic pain. They had the same quality of life as age matched non-spondylo patients did. In closing, the author stated, “The current study demonstrated that a unilateral pars defect is not associated with further slip or disability,” and “subjects with a bilateral pars defect follow a clinical course similar to that of the general population.” OTHER INVESTIGATIONS: Furthermore, it is common knowledge that spondylolysis and spondylolisthesis are seen with equal frequency in both asymptomatic people and symptomatic people (501,512), and the degree of forward slippage is in no way correlated with the degree of patient pain or disability. (16,46) More explicitly, in 1982 Libson and Dinari radiographically studied the occurrence rate (prevalence) of spondylolysis / spondylolisthesis in 936 asymptomatic (pain free) and 662 symptomatic (back pain suffering) military soldiers concurrently. They discovered that just as many pain-free soldiers had spondylolysis and/or spondylolisthesis on X-ray as did the soldiers who had symptomatic back pain, i.e., 10% of the asymptomatic soldiers and 9% of the symptomatic soldiers had spondylolysis/spondylolisthesis on radiograph. (501) However, in 1976, Torgerson et al. concluded, "Our findings indicate that this lesion [spondylolisthesis and spondylolysis] is often symptomatic.... Statistical interpretation indicated a significantly greater correlation between symptoms and the existence of spondylolysis and spondylolisthesis (p > 0.005). " The only problem with this investigation, which used x-ray to assess listhesis (forward slippage) and/or pars defect, was the fact that no oblique radiographs were made of the lumbar spine; therefore, this made iit extrememly difficult to assess the pars. This was probably the reason that the prevalance rate (4.7% and 1.4%) was so low in both groups. Other investigators have confirmed the prevalence rates in the aforementioned findings in pain-free people: Recently, in 2005 Beck et al. published the results of a very large investigation into the prevalence of spinal anomalies in patients with back pain. After studying the radiographs of 1004 patients presenting to a New Zealand chiropractic clinic for back pain, 7.8% had spondylolisthesis. (502) In 1966 a famous and often quoted investigation by Moreton investigated the prevalence (occurrence rate) of spondylolysis within 32,600 asymptomatic people who were X-rayed as part of a pre-employment screening. The prevalence of spondylolysis in this group of 18 to 35 year olds was 7.2%. (503) Other investigation have concluded this same prevalence rate. (8,512) The aforementioned investigation (512), prompted Professor Nikolai Bogduk, MD, researcher, author, and two-time Volvo Award winner to proclaim within the ‘Australasian Faculty of Musculoskeletal Medicine Guidelines’ that “finding a pars defect on a plain film does not constitute establishing a diagnosis of the patient's pain.” (500) Two other research giants, Schmorl and Junghans, have also proclaimed that pain specifically related to spondylolysis and/or spondylolisthesis does not exist. (27) However, in either spondylolisthesis or spondylolysis, the fibrous-filled defect that forms within the pars (131) certainly has the potential to generate back pain, for it contains both nerve fiber and pain-carrying free-nerve endings (133) that contain neuropeptides (134). CLASSIFICATION OF SPONDYLOLISTHESIS: The most widely used classification system was developed by Wiltse et al. back in 1976 (36) This system described five distinct types of spondylolisthesis: 1.) Dysplastic Spondylolisthesis: Congenital malformation of the sacrum or neural arch of L5. 2.) Isthmic Spondylolisthesis: Stress fracture, elongation, or acute fracture of the pars. 3.) Degenerative Spondylolisthesis: Long-standing arthritic process of the zygapophyseal joints. 4.) Traumatic Spondylolisthesis: Neural arch fracture excluding the pars region. 5.) Pathologic Spondylolisthesis: Bone disease - Paget's, Metastatic disease, or Osteopetrosis. 6.) Iatrogenic Spondylolisthesis: Man-made following lumbar spine surgery via LAIF or Laminectomy. Now, let us look at the more common forms of spondylolisthesis: DYSPLASTIC SPONDYLOLISTHESIS: (aka: Congenital Spondylolisthesis) This type of spondylolisthesis results from a congenital (from birth) malformation (aka: dysplasia or defective growth/development) of the neural arch of the vertebra and/or upper portion of the sacrum. More explicitly, the articular processes of the vertebrae are tipped too far forward, the facet joints are facing forward (sagittal or axial) instead of sideways (coronal), and/or there is a malformed sacrum with spina bifida that allows spondylolisthesis. Although fairly rare, 14-21% of all discovered spondylolisthesis are the result of the the aforementioned congenital malformations. (1) Isthmic spondylolisthesis, however, is four times more common. (40) When dysplastic spondylolisthesis occurs, it's usually quite severe. (40) Unlike the other forms of spondylolisthesis, the dysplastic variety has a possible genetic predisposition. More explicitly, Wynne-Davies et al. (2) X-rayed 147 first-degree relatives of patients with spondylolisthesis. The results indicated that 33% of the relatives also, unknowingly, had dysplastic spondylolisthesis. This is four-time higher than what would be expected in the normal population where 8% is the population prevalence for spondylolisthesis. (500,501,502,512) Other investigators have also reported a familial predisposition as well (3). ISTHMIC SPONDYLOLISTHESIS: (aka: Lytic Spondylolisthesis) SUB-TYPE A: (aka: Lytic Spondylolisthesis) Sub-Type A is the most commonly found type of spondylolisthesis in people under 50 years of age (40). It is believed that "biomechanical stress," such as repetitive mechanical strain from heavy work or sports, causes a fatigue fracture within the pars interarticularis (26) that in turns allows the defective vertebra to move forward in relationship to the sacrum or vertebra below. Figure #7 denotes such a condition: Yellow arrows point to a marked radiolucency (black area) through the pars interarticularis, which is highly indicative of a bilateral par fracture. The L5 vertebra has slide about 20% forward as indicated by the Red Arrow; therefore, this would be called a Grade 1 Isthmic Spondylolisthesis - Sub-type A. Interestingly, there does seem to be a familial predisposition for Isthmic spondylolisthesis, for 15% of first-degree relatives of people with Isthmic spondylolisthesis will also have spondylolisthesis (2); this 15% prevalence is double the natural occurrence rate of spondylolisthesis of 6-7%. (501,502,512) In a recent clinical guideline, Dr. Nikolai Bogduk MD, PhD, author, and Volvo Award Winner, stated, “The biomechanical and epidemiological evidence points to pars defects being an acquired fracture, either as a result of single severe trauma or as a result of fatigue failure (19,21,32,34,35).” (500) “The fibrous tissue that fills the defect may contain osseous debris that is evidence of its traumatic origin (17).” SUB-TYPE B: This type of Isthmic spondylolisthesis is characterized by a elongated pars without separation. It is believed that the elongation occurs secondary to "repeated, minor trabecular stress fractures of the pars." (26) Each time these possible sub-acute stress fractures occur and heal, the vertebral body is displaced farther and farther forward. Eventually, the pars may fail to heal and result as a full pars defect; therefore, it may be impossible to differentiate between Sub-Type A and Sub-Type B categories. SUB-TYPE C: These types of spondylolisthesis' are extremely rare and result from an acute pars fracture, often as result of traumatic lumbar hyperextension injury; displacement seldom occurs. (39) DEGENERATIVE SPONDYLOLISTHESIS: (aka: Pseudospondylolisthesis, nonspondylolytic spondylolisthesis) This is the most common form of spondylolisthesis in patients over 50 years of age and rarely occurs in those under 50. There is no fracture or elongation of the pars interarticularis and the neural arch is intact. The mechanisms of forward displacement are thought to involve a combination of "zygapophyseal joint arthrosis, disc degeneration, and remodeling of the articular processes and pars." (26,41) On X-ray, a widened "Pedicle-facet angle" is one of the tell-tale signs of degenerative spondylolisthesis. Finally, so some strange reason, Degenerative Spondylolisthesis has an affinity for affecting Females, at L4, who are over 40. [The 3 F's of degenerative spondylolisthesis.] This type of spondylolisthesis, which is extremely rare, results from a traumatically-induced fracture to the neural arch other than the pars region. The "Hangman's Fracture" in the cervical spine's second vertebra (Axis) is a common and often deadly example of such a traumatically induced phenomenon. This type of fracture is extremely rare in the lumbar spine. PATHOLOGICAL SPONDYLOLISTHESIS: Generalized or systemic disorders of bone may affect the neural arch of the spine and allow spondylolysis or spondylolisthesis to occur. Metastatic carcinoma (cancer), osteopetrosis, and Paget's disease are some of the more common disorders that may contribute to the formation of spondylolysis. (26) Iatrogenic (man-made) spondylolisthesis is a complication of lumbar anterior interbody fusion (LAIF), which ironically is often used to stabilize spondylolisthesis. Either the vertebrae above of below develops a pars fracture and possibly forward slippage from the extra stress placed upon that segment from the surgery. Laminectomy procedures, which are used for decompressing symptomatic disc herniations in the spine, will result in an overload of weight-bearing stress on the contralateral pars and, in some patients, result in a pars fracture. In 1994 Suh et al. described a technique for differentiating between a symptomatic pars defect and non-symptomatic pars defect. They simply anesthetized the suspect with lidocaine to see if this affected the patients pain. If so, then the pars was named a pain-generator and surgery proceeded. (154) Bogduk also described this 'pars block' in his recent book entitled "Medical Management of Acute and Chronic Low Back Pain." More explicitly, Bogduk stated the following: "The definitive test of whether a pars defect is symptomatic is to anaesthetise the [pars] defect. (154) Pars blocks are the only means available by which to determine whether or not a radiographically evident defect is a symptomatic or an asymptomatic one. Such a test is imperative in view of the high prevalence of defects in asymptomatic individuals." (126) As this disease progresses, symptomatology may become more severe. Patients may develop a classic knee bend/hip flex stance to compensate for tight hamstrings and paravertebral muscle spasm. The forthcoming are the indications for surgical stabilization [6]. 1.) persistent back and/or leg pain ( usually in a L5 distribution) that interferes with the normal daily function of the patient, who has failed conservative care ( physical therapy and bracing) and activity restriction. [Your Oswestry score had better be over 50 for at least a year in my opinion]. 2.) a worsening of the slip. For example, a grade 1 spondylolisthesis progressing into a grade 2 spondylolisthesis. 3.) A slip greater than 50%. In this case, it does not matter whether the patient has symptoms are not. 4.) There is a progressive loss of mobility--the patient is losing the ability to walk. There are also several contraindications for surgery of spondylolisthesis [6], but one that I want to mention here: reduction (that means trying to put the bones back in proper alignment) should never be attempted in patients in whom suffer a grade 5 spondylolisthesis (a.k.a. spondyloptosis). What do all you new experts think of this, Figure #8: Can't see it? Go here. I have drawn in some lines that should help you see it. Also note that the L5 disc is almost completely gone (discopathy). It's almost bone on bone between L5 and the sacral base.
REFERENCES: 1) Leone LD, Lamont DW. “Diagnosis and treatment of severe dysplastic spondylolisthesis.” J AM Osteopath Assoc 1999;99:326-8 2) Wynne-Davies R, Scott JHS. “Inheritance and spondylolisthesis – a radiographic family survey.” J Bone Joint Surg Br 1997;618:301-5 3) Saha MM, et al. "Osteopetrosis with spondylolysis: four cases in one family." Br Radiol 43:738, 1970. 5) Wiltse LL. "Spondylolisthesis: Classification and Etiology." Symposium of the Spine, Am Acad Orthop Surg 1969; 143. 6) St. John TA, Alber TJ. "Reduction of Spondylolisthesis with Pedicle Screw Fixation And Transforaminal Lumbar Interbody Fusion." In Surgical Techniques for the Spine; Haher TR, Merola AA; Thieme – New York 2003. 7) Batts M Jr. "The etiology of Spondylolisthesis." J Bone Joint Surg (Am) 21:879, 1939 8) Fredrickson BE, et al. "The Natural History of spondylolysis and spondylolisthesis." J Bone Joint Surg (Am) 66:699 1984 "We performed a prospective roentgenographic study to determine the incidence of spondylolysis, spondylolisthesis, or both, in 500 unselected first-grade children from 1955 through 1957. The families of the children with spondylolysis were followed in a similar manner. The incidence of spondylolysis at the age of six years was 4.4 per cent and increased to 6 per cent in adulthood. The degree of spondylolisthesis was as much as 28 per cent, and progression of the olisthesis was unusual. The data support the hypothesis that the spondylolytic defect is the result of a defect in the cartilaginous anlage of a vertebra. There is a hereditary pre-disposition to the defect and a strong association with spina bifida occulta. Progression of a slip was unlikely after adolescence and the slip was never symptomatic in the population that we studied." 10) Stewart TD. "The Age Incidence of Neural Arch Defects in Alaskan Natives, Considered from the Stand Point of Etiology." J Bone Joint Surg (Am) 1953; 35:937 11) Kettelkamp DB, Wright DG. "Spondylolysis in the Alaskan Eskimo." J Bone Joint Surg (Am) 1971; 53:563. 16) Turner RH, Bianco AJ. "Spondylolysis and Spondylolisthesis in Children and Teenagers." J Bone Joint Surg (Am) 53:1298, 1971 17) Eisenstein SM, Ashton IK, Roberts S, Darby AJ, Kanse P, Menage J, Evans H. Innervation of the spondylolysis "ligament". Spine 1994; 19: 912-916. 19) Cyron BM, Hutton WC. The fatigue strength of the lumbar neural arch in spondylolysis. J Bone Joint Surg 1978; 60B: 234-238. 26) Yochum TR, Rowe LJ. "Essentials of Skeletal Radiology" Baltimore; Williams & Wilkins; second edition: 1996: 27) Schmorl G, Junghans H. "The human Spine in Health and Disease, ed 2. New York, Grune & Stratton, 1971 31) Rowe GG, Roche MB. The etiology of separate neural arch. J Bone Joint Surg 1953; 35A: 102-110. 32) Hensinger RN. Spondylolysis and spondylolisthesis in children and adolescents. J Bone Joint Surg 1989; 71A: 1089-1107. 34) O'Neill DB, Micheli LJ. Postoperative radiographic evidence for fatigue fracture as the etiology in spondylolysis. Spine 1989; 14: 1342-1355. 35) Wiltse LL, Widell EH, Jackson DW. Fatigue fracture: the basic lesion in isthmic spondylolisthesis. J Bone Joint Surg 1975; 57A: 17-22. 36) Wiltse LL, Newman PH, Macnab I. "Classification of spondylolysis and spondylolisthesis." Clin Orthop Relat Res. 1976 Jun;(117):23-9. 37) McKee BM, et al. "Spondylolysis and spondylolisthesis in Children: A Review." J Can Assoc Radiol 1971; 22:100 39) Wiltse LL, et al. "Classification of spondylolysis and spondylolisthesis." Clin Orthop 117:23, 1976 40) Moe JH, et al. "Scoliosis and other Spinal Deformities," Philadelphia, WB Saunders, 1978. 41) Macnab I. "Spondylolisthesis with intact an intact neural arch-so called pseudospondylolisthesis." J Bone Joint Surg (Br) 32:325,1950 46) Friberg S. "Studies on Spondylolisthesis." Acta Chir Scand 82(Suppl):55, 1939. 126) Bogduk N, McGuik B. "Medical Management of Acute & Chronic Low Back Pain." vol 13 Amsterdam; Elservier: 2002 131) Roche MB. "The pathology of Neural-Arch Defects." J Bone Joint Surg 1949: 31A: 529-537 132) Ghelman B, Doherty JH. "Demonstration of Spondylolysis by Arthrography of the Apophyseal Joint." Am J Roentgenol 1978; 130:986-987 133) Schneiderman GA, et al. "The Pars Defect as a Pain Source: a Histological Study." Spine 1995; 20:1761-1764. "CONCLUSIONS. Free nerve endings believed to have nociceptive function were identified in all specimens. The finding of neural elements, including free nerve endings within the pars defect tissue, suggests that the pars defect may be a source of back pain in some patients with symptomatic spondylolysis." 134) Eisenstein SM, et al. "Innervation of the Spondylolysis 'Ligament'. Spine 1994; 19:912-916. "CONCLUSION. Spondylolysis of the lower lumbar vertebrae is a non-united childhood fracture of the arch of the vertebra, persisting into adult life. Symptoms of disabling low back pain appear in a minority of patients, usually for the first time in adulthood. This pain is considered to arise from several separate sources, one of which may be the spondylolysis ligament. The movement that the ligament allows at the fracture site may result in stimulation of the nerve endings both in the ligament and in the surrounding soft tissue." 135) Cyron BM, Hutton WC. "Variations in the amount and Distribution of Cortical Bone Across the Partes Interarticulares of L5. A predisposing Factor in Spondylolysis?" Spine 1979; 4: 163-167 136) Cyron BM, Hutton WC. "The Fatigue Strength of the Lumbar Neural Arch in Spondylolysis." J Bone Joint Surgery 1978: 60B:234-238. 138) Green TP, et al. "Spondylolysis: Bending of the Interior Articular Processes of Lumbar Vertebrae during Simulated Spinal Movements." Spine 1994; 19: 2683-2691. 139) Farfan HF, et al. "The Effects of Torsion on the Lumbar Intervertebral Joints: The role of Torsion in the production of Disc Degeneration." J Bone Joint Surg 1970; 52A: 468-497 150) Hensinger RN. "Spondylolysis and Spondylolisthesis in Children and adolescents." J Bone Joint Surg 1989; 71A:1089-1107 152) O'Neil DB, Micheli LJ. "Postoperative Radiographic Evidence for Fatigue Fracture as the Etiology in Spondylolysis." Spine 1989; 14:1342-1355 153) Wiltse LL, et al. "Fatigue Fracture: the Basic Lesion in Isthmic Spondylolisthesis." J Bone Joint Surg 1975; 57A: 17-22 154) Suh PB, Esses SI, Kostuik JP. "Repair of pars interarticularis defect. The prognostic value of pars infiltration." Spine. 1991; 16(8 Suppl):S445-8. "Ten patients with symptomatic spondylolysis or Grade I spondylolisthesis were treated with the Buck method. At follow-up, nine patients were graded as successful. All patients fused. Pain relief, level of function, and likelihood of return to work were higher in patients preoperatively selected by lidocaine infiltration of the pars defect. Pars infiltration gives an accurate prediction of successful outcome following pars repair." 204) Batts, Martin, Jr. "The Etiology of Spondylolisthesis." J Bone and Joint Sur. 1939; 21:879-884 208) Friberg, Sten: "Studies on Spondylolisthesis." Acta Chi. Scandinavica, Supplementum 55, 1939, 211) Hitchcock HH. "Spondylolisthesis. Observations on Its Development, Progression, 224) Rowe GG, Roche MB. "The Etiology of Separate Neural Arch." J Bone and Joint Surg; 1953; 35-A:102-110 240) Wiltse LL. "Etiology of Spondylolisthesis." Clin Orthop 1957; 10:48-59. 241) Wiltse LL. "Spondylolisthesis in Children." Clin Orthop 1961; 21:156-163. 244) Wiltse LL. "Fatigue Fracture: The Basic Lesion in Isthmic Spondylolisthesis." J Bone and Joint Surg 1975; 57-A: 17-22 245) Wynne-Davies, et al. "Inheritance and Spondylolisthesis. A radiographic Family Survey." J Bone and Joint Surg 1979; 61-B(3); 301-305 500) Professor Nikolai Bogduk, MD, Multiple Volvo Award Winner ‘Evidence-Based Clinical Guidelines for the Management of Acute Low Back Pain’ The Australasian Faculty of Musculoskeletal Medicine November 1999; Chapter 9 501) Libson E, Bloom RA, Dinari G. Symptomatic and asymptomatic spondylolysis and spondylolisthesis in young adults. Int Orthop 1982;6:259-261. 502) Beck RW, Holt KR, et al. "Radiographic anomalies that may alter chiropractic intervention strategies found in a New Zealand population." J Manipulative Physiol Ther. 2004 Nov-Dec;27(9):554-9. Conclusions: " Eight hundred forty-seven full-spine radiographs were included in the study. Anomalies were found in 68% of patients who had radiographs taken. The 5 most frequently occurring anomalies in descending order were degenerative joint disease (23.8%), posterior ponticle (13.6%), soft tissue abnormalities (13.5%), transitional segments (9.8%), and spondylolisthesis (7.8%). Other noteworthy occurrences because of their generalized status as absolute contraindications to adjustment are fracture (6.6%), malignant tumor (0.8%-3.1%), abdominal aortic aneurysm (0.8%) and atlantoaxial instability (0.6%)." 503) Moreton RD. "Spondylolysis." JAMA. 1966 Feb 21;195(8):671-4. " In 32,600 asymptomatic adults, the prevalence of a pars defect was found to be 7.2%." 512) Jensen MC, et al. “MRI imaging of the lumbar spine in people without back pain.” N Engl J Med – 1994; 331:369-373 [ Top ] © Copyright 2002 - 2012 All rights reserved - Douglas Gillard DC.
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Fig. #2 
Figure #3 demonstrates a Grade II spondylolytic spondylolisthesis. Note that the L5 vertebra has translated (slipped forward) by over 25%. This 35% slippage is categorized as a grade II spondylolisthesis. 
