Spondylolysis and Spondylolisthesis

Published on 17/03/2015 by admin

Last modified 17/03/2015

Print this page

This article have been viewed 3898 times

CHAPTER 27 Spondylolysis and Spondylolisthesis

Suken A. Shah, MD, Faisal Mahmood, MD, K. Durga Nagraju, MD, DNB, Andrew H. Milby, MD

Spondylolysis is defined as a defect in the pars interarticularis of the posterior vertebral arch and is a common cause of back pain and disability.¹ In addition, spondylolysis may lead to instability of the spinal column and result in anterior translation of the vertebral body relative to the level inferior to the defect. This translation in the setting of spondylolysis is termed spondylolisthesis, from the Greek roots, spondylos, meaning “vertebrae,” and olisthesis, meaning “to slip.”² Even in the absence of symptoms from the pars defects themselves, spondylolisthesis may lead to clinically significant radiculopathy and progressive neurologic deficits secondary to nerve root impingement. Both conditions vary in their presentations and require judicious application of conservative and surgical treatment strategies.

The clinical syndrome of spondylolisthesis was first described in 1782 by the Belgian obstetrician Herbiniaux,³ before an understanding of its pathophysiology. Herbiniaux reported a bony prominence anterior to the sacrum that created an impediment to vaginal delivery in a cohort of his patients. In 1853, the German physician Robert⁴ reported on specific defects in the pars interarticularis; these defects were first labeled spondylolysis by Killian in 1854.² Killian² proposed that forces imposed by the body’s weight caused subluxation of the lumbosacral facets and subsequent vertebral body subluxation. A short time later, in 1855, anatomic studies by Robert and Lambl revealed that a neural arch defect typically preceded the subluxation.⁵ Robert freed the fifth lumbar vertebra successfully of surrounding soft tissue and showed that a neural arch defect was required for slippage to occur.⁶

In 1881, Neugebauer ⁷ detailed the clinical and anatomic manifestations of the deformity and suggested that lysis, elongation, and angulation of the pars interarticularis could lead to spondylolisthesis. In his travels through Europe in 1888, Neugebauer came across 10 specimens in which there was gross displacement of the fifth lumbar vertebra. He aptly termed this phenomenon spondyloptosis, from the Greek ptosis, meaning “falling off or down,” to indicate a vertebra that is completely dislocated. Neugebauer initially attributed the deformity to traumatic injury; however, he later proposed that it was due to a congenital abnormality of neural arch ossification. This theory of abnormal ossification was questioned by Lane, who, in 1893, posited that spondylolisthesis was due to modification of the interarticular part of the fifth lumbar vertebra by pressure from the inferior facet of L4 superiorly and from the superior sacral process inferiorly.

Pathophysiology

As understanding of spondylolisthesis progressed, classifications of common subtypes emerged. The most widely used classification system today was described by Wiltse.⁸^–¹¹ This system represents a further development of the classification described by Newman and Stone,¹² who, in 1962, reported the long-term outcomes of 319 patients with spondylolisthesis. In their series, spondylolisthesis was classified in terms of radiographic appearance and proposed etiology.

Wiltse separated spondylolisthesis into five main groups (Table 27–1). Type I, also known as congenital or dysplastic spondylolisthesis, is secondary to a congenital defect of the superior sacral facet or the inferior L5 facet or both with gradual anterior translation of the L5 vertebra. Type II, also known as lytic or isthmic spondylolisthesis, involves a defect in the isthmus or pars interarticularis. Type II is classified further into three subtypes: Type IIA represents a spondylolysis or a stress fracture of the pars region. Type IIB represents an intact but elongated pars caused by repeated stress and bony remodeling. Type IIC represents an acute traumatic fracture of the pars leading to anterolisthesis; this is the rarest of the subtypes. It is not the pars defect itself but the anterior translation that allows the lesion to be termed spondylolisthesis. Type III is degenerative in origin and is a disease of older adults that develops as a result of facet arthritis and remodeling. Such long-standing intersegmental instability can lead to either anterolisthesis or posterolisthesis. As the disease progresses, the articular processes may become more horizontally shaped, creating the potential for rotational deformity as well. Type IV is a post-traumatic disruption of posterior elements other than the pars (as in type IIC). This disruption is a gradual event and not an acute fracture-dislocation as seen in type IIC. Type V involves the destruction of the posterior elements in the setting of a pathologic process, such as malignancy, Paget disease, tuberculosis, or giant cell tumors. Additionally, an iatrogenic spondylolisthesis may occur after facetectomy.

TABLE 27–1 Spondylolisthesis Classification by Wiltse ¹⁸

Type	Description
I	Congenital dysplastic
II	Isthmic—defect at pars interarticularis
IIA	Spondylolytic—stress fracture of pars interarticularis
IIB	Elongation of pars interarticularis
IIC	Acute or traumatic fracture of pars interarticularis
III	Degenerative—long-standing intersegmental instability
IV	Post-traumatic—defects of posterior elements (aside from pars interarticularis)
V	Pathologic

Wiltse type I and type II constitute most cases, and these are the focus of this chapter. Although the classification schemes described allow for the systematic study of these disparate disease entities, they are of no proven prognostic value in the prediction of deformity progression.

The extent to which spondylosis depends on genetic or developmental factors is controversial. In 1982, Marchetti and Bartolozzi ¹³ divided spondylolisthesis into developmental and acquired subtypes. Developmental etiologies included elongation of the pars, lytic lesions, and traumatic events, whereas acquired etiologies included iatrogenic, pathologic, and degenerative conditions. In 1994, a revised classification system subclassified the developmental group further into high or low dysplastic. In these two subgroups, the pars interarticularis was described as being either osteolytic or elongated. Traumatic lesions were incorporated into the acquired group, and the iatrogenic etiology was relabeled as postsurgical (Table 27–2). Although developmental abnormalities of the posterior arch are typically insufficient to cause spondylolysis in the absence of other inciting factors, they may play a significant role in the predisposition to spondylolysis and subsequent spondylolisthesis.

TABLE 27–2 Spondylolisthesis Classification by Marchetti and Bartolozzi ¹³

Developmental
High dysplastic	Interarticular lysis
	Elongation of pars interarticularis
Low dysplastic	Interarticular lysis
	Elongation of pars interarticularis
Acquired
Traumatic	Acute or stress fracture
Postsurgical	Direct or indirect effect of surgery
Pathologic	Local or systemic pathology
Degenerative	Primary or secondary

A significant genetic predisposition is suggested by the observation that spondylolysis occurs in 15% to 70% of first-degree relatives of individuals with the disorder.¹⁴^–²² Spondylolisthesis also shows a strong familial association, with an incidence in first-degree or second-degree relatives of approximately 25% to 30%.^5,^9,^11,²³ A radiographic study by Wynne-Davies and Scott¹⁵ showed that dysplastic spondylolisthesis has a familial incidence of 33%, whereas the isthmic variant has a familial incidence of 15%. Compared with the incidence in the general population, this represents a fourfold and twofold increased familial risk in patients with dysplastic and isthmic spondylolisthesis. Wynne-Davies and Scott¹⁵ suggested a multifactorial autosomal dominant pattern of inheritance with incomplete penetrance. Wiltse²² suggested, however, that a cartilaginous defect in the vertebrae may be of autosomal recessive inheritance with varying expressivity. Additionally, the correlation between spina bifida occulta and spondylolisthesis strengthens the suggestion of a hereditary contribution.

In combination with developmental susceptibilities, certain activities are risk factors for spondylolysis because of the nature of the biomechanical stresses imparted on the pars interarticularis. Biomechanical analyses have shown that hyperextension and persistent lordosis increase shear stresses at the neural arch.²⁴^–²⁷ Wiltse and colleagues²⁸ hypothesized that most cases of isthmic spondylolysis should be considered fatigue fractures caused by repetitive load and stress as opposed to a single traumatic event, although a traumatic event may lead to completion of a fracture already in development. Farfan and colleagues²⁹ hypothesized that a single event leads to the initial microfracture in the pars, with fractures occurring as a result of repetitive overload. As a result of these biomechanical data, activities that involve hyperextension of the lumbar spine, such as gymnastics, weightlifting, diving, football, and volleyball, have been implicated as causative factors in the development of spondylolysis.^27,³⁰^–³²

Persistent lumbar lordosis may also increase susceptibility to spondylosis; Ogilvie and Sherman ¹⁴ reported a 50% prevalence of asymptomatic spondylolysis in patients with Scheuermann kyphosis. The tendency toward progression of slippage during adolescence and the observation that girls are several times more likely to have an increase in deformity are also suggestive of a hormonal role in the development of spondylolisthesis.²³

Epidemiology

The exact prevalence of spondylolysis is uncertain because it is asymptomatic in a large proportion of patients. Reports regarding the prevalence of spondylolysis are based primarily on painful or symptomatic spondylolysis or cases associated with listhesis. The prevalence in whites has been reported as 3% to 6% with a male-to-female ratio of 2 : 1.³³^–³⁵ Roche and Rowe³⁵ examined 4200 cadaveric specimens and found an overall prevalence of spondylolysis of 4.2%. Considerable ethnic variability exists in the prevalence of spondylolysis, with a lower prevalence in African Americans (1.8% to 2.4%) than in whites (5.6%).³⁶^–³⁹ The highest prevalence has been reported in the Eskimo population, with rates of 13% in adolescent patients and 54% in adults.⁴⁰ Although this prevalence may suggest a genetic predisposition, it has also been posited that Eskimos, who carry their infants in a papoose, place undue stress on the pars interarticularis.³⁶

The reported incidence of isthmic spondylolisthesis ranges from 2.6% to 4.4%.^5,⁴¹^–⁴³ In the largest prospective radiographic study, Fredrickson and colleagues⁴¹ evaluated 500 patients at age 6 years with a 20-year follow-up. A pars defect was appreciated in 4.4% of 6-year-old children. By age 12, 5.2% of the cohort were noted to have the defect (85% participation rate). This increased to 6% by age 18; however, most of the nonaffected patients had dropped out of the study (34% participation rate). Back pain had developed in only four of the patients, and one patient required an operative procedure to decompress a herniated disc at a level cephalad to the spondylolisthesis. Pars defects at L5 were noted to be bilateral in 78% of cases, with most of these progressing to spondylolisthesis. As a corollary to this study, Fredrickson and colleagues⁴¹ also evaluated 500 newborns and found no evidence of spondylolysis or spondylolisthesis. The only reported case of a pars lesion in a newborn has been published by Borkow and Kleiger.⁴⁴ Isthmic spondylolisthesis is rare in children younger than 5 years old, with only a few reported cases.^43,^45,⁴⁶

In spondylolysis, the pars interarticularis defect may be unilateral or bilateral. If the defect is bilateral, the chance of progression to listhesis is greater. The most common location of a spondylitic defect is L5 (85%),⁴⁷ and the defect may be observed as high as L2; multilevel defects are seen infrequently. Rarely, multiple defects may be seen at the same level. Ariyoshi and colleagues⁴⁸ reported a case of spondylolysis at three sites in L5 involving the bilateral pars interarticularis and the center of the right lamina.

The most common site of isthmic spondylolisthesis is at the L5-S1 level secondary to osteolysis at L5. Estimates show that this lesion is located at the L5 pars interarticularis in 90% of type II cases, at L4 in 5%, and in more cephalad vertebrae in the remaining 5% of cases.¹¹ Additionally, authors reported spina bifida occulta at the same level in 30% of patients with pars lesions. The incidence of spina bifida associated with spondylolisthesis has been reported to range from 24% to 70%.^9,^23,^49,⁵⁰ Age at presentation with isthmic spondylolisthesis follows a bimodal distribution. One peak occurs between the ages of 5 and 7 years, and the second occurs in the teenage years.^9,^19,^49,⁵¹ The incidence in athletes who subject themselves to excessive lumbar posturing, such as gymnasts, soccer players, pitchers, cricket bowlers, and divers, is higher than in the general population.⁵³^–⁶⁰

In pediatric patients, dysplastic and isthmic are the most commonly encountered subtypes, with the latter representing 85% of the cases. As with spondylolysis, isthmic (type II) spondylolisthesis is two times more frequent in boys than girls.³⁵ Dysplastic spondylolisthesis, similar to its isthmic counterpart, is also most commonly found at the L5-S1 junction. The incidence is two times higher in girls,^61,⁶² and based on more recent published reports, it accounts for 14% to 21% of total cases.^62,⁶³

History and Physical Examination

Spondylolysis may be discovered incidentally or may manifest with low back pain typically in the teenage years.⁶⁴ In approximately half of cases, the onset of low back pain is associated with a history of trauma or an inciting event.^23,^65,⁶⁶ Usually these patients complain of focal low back pain, only rarely radiating to the buttocks or posterior thigh, which becomes worse with activity or on hyperextension of the spine.^31,⁶⁷^–⁷⁰ Lifting and weight bearing can exacerbate the pain, and a forced lumbar extension often intensifies the symptoms. Neurologic involvement is rare in isolated spondylolysis. Medical professionals who have little experience with spondylolysis often assume the defect to be a sequela of trauma requiring immediate immobilization and surgical intervention. In these cases, it is the responsibility of the spine surgeon to offer reassurance that imminent neurologic compromise is highly unlikely.^71,⁷²

Physical examination of the lumbar spine reveals focal tenderness in acute cases and mild discomfort in chronic cases. Patients maintain a full range of forward flexion (unless the hamstrings are tight) that is usually painless, but hyperextension movement leads to an exacerbation of symptoms as does lateral bending or rotation. Other associated physical signs are an antalgic gait, increased lumbar lordosis, and hamstring tightness. A single-leg hyperextension test is used for the diagnosis and differentiation of unilateral spondylolysis from bilateral lysis. This test is performed by the patient bearing weight on one leg with the hip and knee of the other leg flexed, while hyperextending the lumbar spine. This maneuver is performed on both sides; asymmetrical low back pain indicates unilateral spondylolysis. Bilateral lesions show symmetrical or asymmetrical pain with this maneuver.^73,⁷⁴ The neurologic examination in isolated spondylolysis is generally normal, with radicular findings suggestive of foraminal stenosis owing to inflammation or instability.

Spondylolisthesis may manifest in a similar fashion but is also typically associated with hamstring tightness. This tightness manifests as a muscle spasm of the posterior thighs associated with a fixed flexion at the hip and knees. An increased popliteal angle is present on straight-leg raise. Increased popliteal angle is almost always observed universally, even in low-grade spondylolisthesis. Electromyographic and neurologic abnormalities are typically absent; this suggests that there is not a neurologic basis for the hamstring tightness, but that it likely results from the patient’s attempts to maintain global sagittal balance.^63,⁷⁵ Other authors hypothesize that tightness results as a sequela of chronic nerve root irritation from the instability and micromotion of the involved segment.⁷⁵^–⁷⁸ Patients often ambulate and stand with increased flexion at the hips and knees, also known as the Phalen-Dickson sign.⁷⁶ This flexed posturing increases as the amount of slippage increases. The patient may also exhibit a shuffled or short-stepped gait.⁷⁸

Patients with spondylolisthesis may initially present with focal neurologic deficits or radiculopathy, although this is uncommon. Bilateral radicular symptoms are more commonly observed than unilateral radiculopathy. Typically, the L5 root is involved with pain radiating to the buttocks and posterior thigh or weakness of the extensor hallucis longus. Constant loading of the pars defects may hinder bony healing, resulting in a fibrous union that may be a persistent source of pain. Local expansion of fibrocartilaginous scar tissue within the area of the pars defect may cause nerve root compression. Tension on the nerve root also increases with progression of olisthesis, increasing further the likelihood of radicular symptoms with disease progression.⁷² In higher grade subluxations, traction of the cauda equina over the sacrum may exist. This traction may lead to signs and symptoms of cauda equina compression, such as perineal paresthesia, decreased sphincter tone, and urinary retention. Additionally, traction of the cauda is thought to create a reflex spasm of the hamstrings.^79,⁸⁰

Higher grade spondylolisthesis results in a palpable step-off over the spinous processes. In isthmic spondylolisthesis, the step-off is typically found at the L4-5 junction, as the neural arch of the L5 vertebrae does not translate anteriorly with the body but remains within its geographic location in relation to the sacrum. In dysplastic spondylolisthesis, the neural arch is still attached to the vertebral body and slides anteriorly with the body, producing a palpable step-off that is typically appreciated at the lumbosacral junction. Lumbosacral kyphosis with a retroverted sacrum results in heart-shaped, flattened buttocks. In severe cases, the trunk appears grossly shortened, and the rib cage lies within close proximity to the iliac crests.

Scoliosis also may be associated with spondylolisthesis.^12,^25,⁸¹^–⁸⁵ The incidence has been reported to be 60%. Scoliosis may result because of a combination of hamstring and paraspinal muscle spasm, rotational deformity, or truncal asymmetry. If scoliosis is secondary to spondylolisthesis (nonstructural), it usually resolves after treatment of the olisthesis. The patient may also have an adolescent idiopathic curve with a low-grade spondylolisthesis that was detected incidentally on radiographic evaluation.

Radiographic Evaluation

Many imaging modalities may be useful in the diagnosis and evaluation of spondylolisthesis. Radiographic evaluation of spondylolisthesis begins with plain radiographs, including lateral, anteroposterior, and oblique views.⁸⁶ The anteroposterior view should be angled 15 degrees to the inclination of the L5-S1 disc (Ferguson view). This view not only allows for visualization of the presence of sacral spinal bifida, but also evaluates the size of the lumbar transverse processes and height of the disc.

The defect in isthmic spondylolysis is visualized as lucency in the region of the pars interarticularis. The lucency is commonly described as having the appearance of a collar or a “broken neck on the Scotty dog” seen in lateral oblique radiographs. A spot lateral view is able to identify only 19% of pars defects,^33,⁸⁷ whereas oblique lateral views can detect the pars defect in 84% of cases.⁸⁸ It is important to take right and left oblique views because pars defects may be unilateral in some cases, and the collar may be visible in only one projection.

Although oblique views are most sensitive in diagnosing spondylolysis, the lateral view is optimal for appreciating the degree of olisthesis in spondylolisthesis. The lateral view should be performed with the patient standing. Flexion-extension views may assess for the presence of associated instability. This subtle movement may be an important pain generator and is essential for further treatment planning. Additionally, these views show the extent of postural reduction of the lumbosacral angulation and translation that may be obtained without formal release.

Because the sensitivity of plain radiographs is limited, radionuclide (technetium 99mm) bone imaging may be a good option in cases of suspected spondylolysis with negative plain radiographs. A bone scan identifies pars interarticularis stress fractures that can be missed in oblique radiographs because a stress reaction may be present without a bony defect. Patients who have had a recent trauma or performed strenuous activity and are symptomatic have a bone scan showing increased uptake in the spondylolytic area; however, patients with chronic low backache can have normal bone scans if the defect is chronic, is sclerotic, and has lost its blood supply. Single photon emission computed tomography (SPECT) is more sensitive and provides more details than plain x-rays and technetium bone scan.^89,⁹⁰ A “hot” scan insinuates increased activity, and the patient may benefit from orthotic immobilization, whereas a “cold” scan suggests a chronic lesion that is not metabolically active and is unlikely to respond to immobilization alone.⁷²

Thin-cut axial computed tomography (CT) is highly accurate at visualizing osseous anatomy and is superior to plain radiography in its ability to show dysplastic facets and pars defects. CT may also be used after plain radiographs or bone scan to assess the healing potential of an identified pars defect.⁹¹ In addition to showing spondylolysis accurately, CT may identify changes in the apophyseal joints associated with degenerative and reverse spondylolisthesis and can show minimal degrees of spondylolisthesis by the presence of a pseudobulging disk.⁹²

Magnetic resonance imaging (MRI) is a highly sensitive imaging technique that allows for additional visualization of soft tissue and neural structures and is recommended in all cases associated with neurologic findings. MRI offers the distinct advantage of being able to image the spine in any plane without exposure to ionizing radiation. Sagittal thin slices (3-mm slice thickness for T1-weighted images and 4-mm slice thickness for T2-weighted images) are able to identify 95% of pars defects, with T1-weighted images being more sensitive than T2-weighted images.⁹³ In the early course of the disease, MRI helps in identifying the stress reaction at the pars interarticularis before the end-stage bony defect.^94,⁹⁵ In more acute presentations in which plain radiographs may be negative, a fat saturation technique can be applied to minimize signal from fat and to bring out signal from fluid structures such as bone edema. MRI also allows for evaluation the spinal cord and its associated elements with greater anatomic detail and without the procedural risks associated with CT myelography. MRI may show the degree of impingement of neural elements by fibrous scar tissue at the spondylolytic defect. Additionally, involvement of adjacent discs should be evaluated because abnormal biomechanics can lead to early degenerative changes at adjacent levels.

The most commonly used radiographic grading system for spondylolisthesis is the one proposed by Meyerding in 1932.^95a The degree of slippage is measured as the percentage of distance the anteriorly translated vertebral body has moved forward. On the lateral radiograph, a line is drawn along the posterior sacral border. A line perpendicular to this is drawn at the superior part of the sacrum. The anterior translation or displacement of the inferior border of L5 as a proportion of the width of S1 is expressed as a percentage. The Meyerding classification grades increasing olistheses from I to IV (Table 27–3). Spondyloptosis, in which the fifth lumbar vertebra has slipped forward over 100% of the gliding plane past the sacral promontory, is referred to as grade V. Spondylolysis without olisthesis is referred to as grade 0.

TABLE 27–3 Meyerding Classification *

Grade	Percentage of Slippage (A/B)
0	0 (spondylolysis)
I	0-25%
II	25%-50%
III	50%-75%
IV	75%-100%
V	Vertebral body completely displaced (spondyloptosis)

* Grades 0 and V were added later on.

Although the Meyerding classification system quantifies translational subluxation in the anteroposterior plane, it does not quantify the sagittal rotation of a vertebral body that may coexist in spondylolisthesis. This angular displacement is referred to as the slip angle, and as with the Meyerding grading system, the erect lateral radiograph is the basis for measurement. The slip angle is calculated by measuring the angle formed by the intersection of two lines: (1) a line perpendicular to the posterior cortex of the sacrum and (2) a line paralleling the inferior endplate of L5. In the normal spine, slip angle values should be close to zero. The slip angle quantifies the lumbosacral kyphosis and was shown by Boxall and colleagues ⁶³ to be the most useful tool in determining the risk of the progression in a skeletally immature patient. A slip angle greater than 55 degrees is associated with a high probability and increased rate of progression.

Sacral inclination or pelvic tilt refers to the vertical position of the sacrum. It is the angle formed by the intersection of two lines: (1) a line perpendicular to the floor and (2) a line parallel to the posterior cortex of the sacrum. Normal values are greater than 30 degrees. With an increasing slip, lumbosacral kyphosis is increased, and the sacrum is forced into a more vertical orientation decreasing the pelvic tilt.

In 1983, Wiltse and Winter ⁹⁶ proposed a classification that separated the tangential movement seen in low-grade slips (grade I and II) from the angular and tangential movement that was appreciated in high-grade slips (grade III or higher). The three measurements that were factored were degree of slip, vertebral wedging, and sacral rounding. These authors recommended the forward displacement of the fifth lumbar vertebra in relationship to the sacrum be measured as an actual percentage as first described by Taillard⁴² and later recommended by Laurent and Osterman.⁹⁷ It was stressed that even a small degree of progression should be measured, and this was not quantifiable on the Meyerding scale. Sacral tilt as described previously and sagittal rotation or slip angle were also used. The method for measuring slip angle, which Wiltse and Winter⁹⁶ termed sagittal rotation, was modified by measuring the angle formed by the intersection of two lines: (1) a line extending off the anterior cortex of the L5 vertebral body and (2) a line off the posterior border of the first sacral vertebrae. Wiltse and Winter⁹⁶ believed the endplates of the L5 and S1 bodies to be unreliable osseous structures secondary to osseous hyperplasia.

Conservative Management

Treatment of spondylolysis mainly focuses on pain relief, core muscle strengthening, and restoration of full lumbar range of motion. Achieving these goals enables the patient to return to normal activity without any restrictions. Management of spondylolysis depends on the severity of the symptoms and level of activity. Initial conservative management in the form of activity restriction and bracing (for pain relief) relieves symptoms in patients with spondylolysis. It is likely that most lesions do not heal with bone but become a stable fibrous union that remains relatively asymptomatic.

Conservative management of spondylolysis includes complete cessation of activity, rehabilitation with strengthening of the abdominal and paraspinal musculature, minimization of pelvic tilt, and perhaps antilordotic bracing.⁹⁸ Conservative management protocols also depend on several factors such as disease involvement (spondylolysis vs. spondylolisthesis), level and laterality of the defect (unilateral vs. bilateral pars defects), duration since injury (acute vs. chronic), and age of the patient.⁹⁹ Many authors prefer to use a total-contact, low-profile polyethylene orthosis, which is designed to maintain an antilordotic posture and extends from just below the nipples to 1 inch above the greater trochanter. The brace is worn for 23 hours/day for minimum of 3 to 6 months.¹⁰⁰ If clinical symptoms improve, the brace can be gradually weaned through a period of part-time wear.

Excellent clinical outcomes have been reported with a course of activity restriction and bracing that prevents repetitive hyperextension movements at the lumbar spine.¹⁰⁰^–¹⁰³ Good to excellent results with brace therapy have been shown in 80% of patients with grade 0 or I spondylolisthesis.^100,^104,¹⁰⁵ Bell and colleagues¹⁰⁴ showed prevention of increased slip angle and 100% reduction of pain in 28 patients with grade I or II spondylolisthesis after a mean brace treatment of 25 months. In a series of 82 symptomatic patients with various degrees of spondylolisthesis, Pizzutillo and Hummer¹⁰⁵ reported that nonoperative treatment of grade II or less was shown to relieve pain reliably in two thirds of patients. A study by Steiner and Micheli¹⁰⁰ showed radiographic evidence of healing pars defects in 12 of 67 patients with spondylolysis or grade I spondylolisthesis after treatment in a modified Boston brace. Excellent or good results were achieved in 78% with return to full activities. Patients with spondylolysis and grade I spondylolisthesis may return to full activity and sports with resolution of symptoms and documented lack of slip progression. Controversy exists regarding postbrace activity level for patients with grade II spondylolisthesis. The general consensus is that after successful brace treatment a child with grade II spondylolisthesis may return to sports that do not involve hyperlordotic posturing.^18,^26,²⁷

Patients with acute pars interarticularis fractures are best treated with immediate initiation of bracing for pain relief and restriction from athletic activity with continued mobilization for activities of daily living. Anderson and colleagues ¹⁰⁷ used clinical evaluation and SPECT imaging to compare the rate of response to early versus late initiation of bracing. In this study, patients with early bracing showed rapid relief of symptoms, a short bracing time, and rapid reduction of SPECT ratio. Patients showing a spondylolytic defect on plain radiography but whose bone scans were negative were determined to have inactive (terminal) spondylolytic defects, pseudarthrosis, or old unhealed fractures.^73,¹⁰⁸ Athletes with low back pain and increased uptake on SPECT scan at the pars interarticularis but no defect on radiographs typically respond to a period of rest and active rehabilitation; very few athletes develop defects or persistent back pain.¹⁰⁹

As the understanding of spinal biomechanics has progressed, Panjabi ¹¹⁰ posited the concept of specific training of lumbar muscles in chronic low back pain. According to his concept, specific training of muscles around the lumbar spine improves the dynamic stability and controls segmental spinal motion. The local muscular system that controls the lumbar spine consists of lumbar multifidus, internal oblique, and transverse abdominis.¹¹⁰ A randomized trial by O’Sullivan of 44 patients who were treated with two different protocols showed that a specific strengthening program was more effective than generalized back strengthening exercises.⁹⁸ Along with exercises that target specific core muscle groups with the spine in neutral position, strengthening of hip flexors and hamstring stretching are important and recommended.^100,^101,¹¹¹

Patients with low-grade dysplastic spondylolisthesis are less likely than patients with isthmic spondylolisthesis to respond to conservative measures,⁵ but conservative therapy is still recommended as the initial modality. The importance of radiographic and neurologic follow-up should be stressed to these patients because they are at a higher risk for slip progression owing to facet hypoplasia. Radiographic follow-up is recommended at least annually until skeletal maturity and more frequently during peak height velocity before puberty. Documentation of slip percentage, angle, sacral inclination, wedging, and pelvic tilt is recommended as part of proper documentation of progression of the deformity.