In the late 1800s and early 1900s, there were multiple studies attempting to identify the cause and incidence of spondylolysis, which was thought to be a major factor in causing spondylolisthesis, especially at the junction of the fifth lumbar vertebra and sacrum. After examining 101 museum specimens in 1888, Neugebauer introduced the anomalous ossification theory as the cause of spondylolysis. He postulated that there were two centers of ossification for each half of the posterior neural arch, and the failure of fusion between these two anomalous centers of ossification was the cause for spondylolysis. However, this conjecture was discredited by numerous studies in the early 1900s showing that there was no evidence of accessory centers in the neural arches.

In 1906, Mall inspected 60 embryos less than 100 days old and found no evidence of accessory centers in the neural arches [6]. In 1931, Theodore Willis, from Western Reserve University in Cleveland, Ohio, examined 1,520 human skeletons and found spondylolysis in 79 specimens, or an incidence of 5.2 % of all involved specimens [7]. Like Mall, Willis did not find any evidence of anomalous ossification centers. During the same year, Russell Congdon of Washington State and Henry Meyerding of The Mayo Clinic studied different human populations in an attempt to define the nature of spondylolysis and its association with spondylolisthesis. Congdon evaluated 200 skeletal remains of American aborigines obtained in the Columbia River region and found that bilateral separation of the neural arch was found in ten subjects, or 5 % [8]. In those 5 % with bilateral spondylolysis, nearly 50 % of those subjects displayed spondylolisthesis. Meyerding, in a retrospective case series, looked at 121 patients with spondylolisthesis [3]. Unlike earlier reports, the author found that the condition was more common in males (62 %) than females. Additionally, he introduced the concept of trauma appearing to be a significant factor in the etiology of spondylolysis as approximately 38 % of patients in this series ascribed the cause to trauma. Nevertheless, Meyerding still believed that congenital defects and the apparent instability of the lumbosacral joint may serve as additional factors in creating spondylolysis.

In 1932, Norman Capener tried to explain the pathogenesis of spondylolysis, along with demographics relating to spondylolisthesis, through 34 cases of patients with spondylolisthesis [5]. Like Meyerding, he found that males were more affected than females (53–47 %). Also relating to the trauma concept introduced by Meyerding, Capener described the deleterious effect of the sacrum on the fifth vertebra. He believed that the sacrum acts as a wedge, particularly the posterosuperior apex of the sacrum, which is then driven upwards and splits the fifth lumbar pars interarticularis, creating two portions of the vertebra (Fig. 1.2). Spondylolisthesis, or slipping of the anterior vertebral body with its superior facets, then ensues with continual wedge-like effect of the sacrum as it further displaces the anterior and posterior portions of the fifth vertebral level. He also provided possible reasons that could limit the amount of slippage as he noticed that in the majority of cases, the displaced body comes to a final position of rest after making only a moderate amount of movement. The iliolumbar ligaments can provide checkreins to excessive anterior displacement by the vertebral body, while the bony buttress from the proliferation of bone on the anterior surface of the sacrum can also stop the slippage progression of the L5 vertebra.

From 1939 to 1951, more studies were performed to discern the incidence and etiology of spondylolysis. In 1939, Martin Batts, from the University of Michigan, studied 200 fetal spines and did not find a single instance of double ossification center as mentioned by Neugebauer [9]. Likewise, in 1951, Maurice Roche and George Rowe of Washington University in Saint Louis, Missouri, did not find any consistent association of accessory ossification center with spondylolysis after examining 53 stillborn human fetuses and 20 human embryos [10]. Roche and Rowe also inspected 4,200 human skeletons taken from the Terry Anatomical Collection at Washington University and the Todd Collection at Western Reserve University. They discovered that the incidence of neural arch separation was 4.2 % [11]. Moreover, they further delineated the incidence based on race and sex. Males were more affected than females (6.4–2.3 %), and Caucasians were more likely affected compared to African-Americans. Interestingly, Eskimos have the highest rate, up to 50 %, of developing spondylolysis among different races.

Thus, up to this point, although a congenital factor may still play a large role in creating spondylolysis, the accessory ossification theory had been widely rejected by numerous studies. Consequently, other authors have continued to attempt to explain its etiology. In 1957, Wiltse theorized that the pars lesion may result from congenital weakness [12]. In 1959, Nathan, after inspecting 450 skeletons, ascribed the condition of spondylolysis and its resultant spondylolisthesis to the “pincer effect,” and that the presence of preceding bone abnormalities or congenital defects of the pars interarticularis would seem unnecessary for the production of the pars defect [13]. Accordingly, the pars lesion derives from its position between the inferior articulating process of the cephalad vertebral level and the superior articulating process of the caudad level, causing a “pincer grasp” (Fig. 1.3). Continuous compressive effect of these two articular processes on the pars interarticularis can ultimately cause a fracture of the pars. Nathan also explained why spondylolysis commonly occurred at the fifth lumbar and sacrum junction. Due to its inherent hyperlordotic position compared to the upper lumbar spine, the lower lumbar levels transmit more compressive forces to their posterior neural arches, lending to the “pincer effect.”

In 1976, Wiltse et al. described one of the more useful classifications of spondylolysis and spondylolisthesis that is commonly used today [14]. The classification distinguishes the multifactorial factors causing these conditions. Type 1 is due to the dysplastic predisposition of the bony architecture of the vertebrae. A congenital deficiency of the superior sacral facet or the posterior neural arch of the fifth lumbar vertebra can allow forward slippage of L5 on S1. Type 2, called isthmic spondylolisthesis, is the most frequent and more commonly involves L5 and S1, is associated with a defect in the pars interarticularis. This defect can be due to chronic stress fracture, an elongated but intact pars due to chronic stress, or acute pars fracture. Type 3 is secondary to the degenerative process and is commonly found at L4 and L5. Unlike its isthmic counterpart, women are more affected than men. Chronic degenerative changes in the discoligamentous complex lead to intersegmental instability of the facet joints and disc space. Types 4 and 5 are less common, but each involves traumatic or pathologic factors, respectively.

In 1979, Wynne-Davies and Scott studied the relationship of inheritance and spondylolisthesis [15]. They followed 147 first-degree relatives of 47 patients with either dysplastic or isthmic spondylolisthesis in Edinburgh. They found that the dysplastic form had a higher proportion of affected relatives (33 %) than the isthmic type (15 %). Due to the higher genetic association in the dysplastic group, they emphasized that affected siblings and children can be identified at an early age.

In 1984, Fredrickson et al. performed a prospective roentgenographic study on 500 first-grade children and made conclusions that align with contemporary beliefs regarding this topic. They reported the incidence of spondylolysis with or without spondylolisthesis to be 4.4 % at the age of six compared with 6 % when reaching adulthood [16]. Although the progression of slip is highest during adolescence, the authors stated that it was unlikely in adulthood. Additionally, they found that spondylolisthesis did not exist at birth.

In 1782, Herbiniaux described the first case of spondylolisthesis when he discovered difficulty with labor and delivery due to pelvic outlet obstruction associated with the condition. Neugebauer, in the late 1800s, documented a case series of his encounters with spondylolisthesis. In his description of the first clinical case of spondylolisthesis in Freiburg, Germany, Neugebauer portrayed the clinical examination of a female who had undergone an unfortunate delivery and was “attacked with the most violent pains in the right hypogastrium” [17]. His examination of the patient included: “there was a slight lordotic sinking in of the lumbar vertebra, which was more noticeable when the patient laid prone,” “the spinal column can be easily felt through the abdominal walls with quite moderate pressure,” and “projecting from the anterior surface of the sacrum for about the thickness of a vertebra, immediately behind the vaginal portion, was a hard prominence, which was apparently the last lumbar vertebra.”

In 1905, Bradford and Lovett added to the clinical diagnosis of spondylolisthesis [18]. “A disturbance of equilibrium resulting in a faulty carriage, which was shown chiefly by a sharp increase in the lower lumbar curve in even the mildest cases. The spine curved forward sharply from the sacrum, and this gave undue backward prominence to the crest of the ilium and the buttocks. The appearance at first glance was the same as that in cases of double congenital dislocation of the hip.”

Capener, in 1932, further described the clinical features of spondylolisthesis [5]. “A shortened trunk in which the lower ribs were depressed, sometimes almost into the pelvis, was associated with a rotation of the pelvis upon a transverse axis so that the sacrum appeared more vertical. There was a small hollow behind the lumbar spinous processes, and at the lower end of this hollow there was a bony projection, which in the commonest type of spondylolisthesis was the tip of the spinous process of the fifth lumbar vertebra. A peculiar waddling gait may be observed. This was due to hyperextension of the hips secondary to the pelvic rotation.”

Phalen and Dickson, in 1961, made a significant contribution to the understanding of the muscular imbalance around the hips [19]. They described a case in which a boy “walked on his tarsal pads and thrusted his pelvis violently forward to overcome posterior muscle spasm.” The spasm was due to the excessively tight hamstring muscles, which kept the pelvis and the trunk tilted backward and limited the amount of hip flexion. “To pick something from the floor, the child must squat down beside it, since, even with the knees flexed he could not flex his back and hips sufficiently to permit him to bend forward and to reach the floor with his hands.”

Before radiographs were introduced in 1895 by Wilhelm Rontgen, Pott’s disease was a common differential diagnosis with low back pain. But with radiographic evaluation, especially the lateral view, spondylolisthesis can be easily differentiated from other etiologies of lower back pain. Associated spondylolysis can be viewed on the lateral or oblique radiographs. Computed tomography (CT) later on aided in cases where spondylolysis was difficult to see on plain radiographs.

In order to quantify the severity of the slippage, Meyerding, in 1938, developed a grading system in which the superior endplate of the first sacrum was divided into four quarters [20]. The amount of slippage of the fifth lumbar vertebra on the sacrum corresponded to: grade 1 is slippage of the L5 vertebral body up to 25 % of the sacral endplate’s anteroposterior width; grade 2 is up to 50 %; grade 3 is up to 75 %; grade 4 is up to 100 %; and grade 5 is more than 100 % (spondyloptosis). Taillard, in 1954, described a grading system as percentage of displacement of the cephalad vertebral body on the caudad body based on the standing lateral radiograph, which was a modification of the Meyerding classification [21]. In 1983, in addition to quantifying translational displacement, Wiltse standardized terminologies and their methods of measurement related to spondylolisthesis deformity [22]. These included slip angle, sacral inclination, lumbar lordosis, rounding of the first sacral vertebra, sacral slope, lumbosacral joint angle, and lumbosacral angle. The details of these terminologies are beyond the scope of this chapter as they are likely to be mentioned in other chapters.

Although the vast majority of patients with spondylolisthesis can be treated conservatively, those who display intractable pain or neurological deficits warrant surgical treatment. In the past, nonoperative treatment consisted of prolonged bedrest and casting, which were not tolerated well [23]. Nonoperative treatment used to involve traction on head and feet in a position of recumbency [4]. The feet were elevated to 35–40° in relation to the torso, with countertraction placed on the head and axillae. Once reduction was accomplished, the patient was placed in a double spica cast extending from the axillae to include both legs for about 6–8 weeks. The cast was reinforced with a steel-back for support.

It was not until the early 1900s that surgery was deemed as a viable option for those who failed conservative treatment. Russell Hibbs and Fred Albee, both of whom were from New York, simultaneously presented the first form of posterior spinal fusion that was later used by many surgeons for spondylolisthesis. Interestingly, both initially devised this surgical technique for deformities caused by Pott’s disease. In 1911, both surgeons described methods of fusing the spine, through a posterior midline approach, by partially cutting the local bony elements (spinous processes and laminae) to create a fusion bed and applying the local osteotomized bone over the desired vertebral levels to obtain fusion [24, 25] (Fig. 1.4). In Albee’s technique, the spinous process was split and the tibial graft was placed between the halves of the spinous process. Because early posterior spinal fusion did not involve instrumentation to provide stability while the fusion was taking place, Albee and others tended to keep the patients on a fracture bed for 5 weeks, after which a long plaster-of-Paris jacket molded over the buttocks was applied for an additional 2 months [4].