Spondylolisthesis

• Spondylolysis is a fracture or defect of the pars interarticularis, the thin bridge of bone that joins the upper and lower joints of a vertebra; spondylolisthesis is the forward slip (or much less often backward or sideways slip) of one vertebra on the one below it.
• The two conditions are on a continuum, not two separate diseases. A pars fracture most often stays on one side. When the fracture or defect involves both sides, the back of the vertebra is no longer anchored and the vertebral body can slide forward.
• The typical patient is an adolescent athlete in a sport that repeatedly hyperextends and rotates the lower spine, especially gymnastics or American football. The symptom is a one-sided ache in the lower back or buttock that appears with sport and settles with rest.
• The forward slip is measured with the Meyerding system: grades I and II (less than 50% of the vertebral body slipped) are low grade and usually settle without surgery; grades III to V are high grade and usually need surgery.
• Back pain is only part of the story. Tight hamstrings, a step that feels uneven to the examiner, and sometimes neurogenic leg pain or neurogenic claudication mark more advanced disease.
• Plain lateral and oblique radiographs start the work, computed tomography (CT) shows bone best, and magnetic resonance imaging (MRI) finds an early stress injury before the bone has broken. Treatment is first activity restriction, then strengthening; surgery is reserved for failures and for high grade slips.

By the end of this page you should be able to:

1. Explain the difference between spondylolysis (a pars lesion) and spondylolisthesis (a slipped vertebra), and why one may follow the other.
2. Describe the pathophysiology of a pars stress fracture in an adolescent athlete and recognise gymnastics and football among the risky sports.
3. Grade a slip with the Meyerding system from a lateral radiograph, distinguishing low grade from high grade.
4. Interpret the clinical pattern of back pain, hamstring tightness and neurogenic symptoms, and elicit it on examination.
5. Choose and interpret the imaging studies: lateral and oblique radiographs, flexion and extension views, CT, MRI and bone scan.
6. Outline conservative management (activity restriction, physiotherapy, the disputed role of bracing) and the indications for direct repair or fusion.

The two words are Greek: spondylos (vertebra) with lysis (loosening) in the first and olisthesis (slipping) in the second. ^[1] They are not alternatives. A single vertebra can carry a pars defect for life without ever slipping, while a slip can occasionally occur without a visible pars fracture. ^[3] The picture is simple: the pars is the weakest link between the body of the vertebra in front and the joints and lamina behind it. While one side still holds, the segment is stable. When both sides fail, the vertebral body can slide forward under the pull of gravity, body weight and spinal lordosis. ^[1]

Nearly all clinically relevant disease sits at two adjacent levels. About 95% of spondylolysis occurs at L5, where the shear between the inferior articular process of L4 and the superior articular process of S1 is concentrated. ^[1] The second most common level is L4. ^[3] L5 on S1 is the classic childhood slip level. In adult life the picture shifts to L4 on L5, because degeneration, not fracture, drives the disease. ^[5]

The modified Wiltse classification divides spondylolysis and spondylolisthesis by aetiology. ^[4][6] It is the most useful frame for the clinic, because the type predicts the age, the severity and the management.

Isthmic slips (type II) are the childhood and adolescent disease. Degenerative slips (type III) are the adult disease and are discussed below as the contrast. ^[6]

A separate, older classification by Marchetti and Bartolozzi divides disease into developmental (high or low dysplastic, with or without elongation or lysis) and acquired (traumatic, post-surgical, pathological, degenerative). It is more prognostic than the Wiltse system but harder to use at the bedside and has not entered routine use. The Spinal Deformity Study Group (SDSG) system adds pelvic and spinal sagittal balance to the Meyerding grade; it is more complete but less reliable in everyday practice. ^[5]

Spondylolysis and spondylolisthesis are very different in how common they are.

• Spondylolysis affects between 6 and 8% of the adult population. It is rare in young children, and its prevalence increases steadily with age (and with weight-bearing) up to about 18 years, after which it plateaus. ^[1][6]
• Spondylolisthesis, the slip, is less common than the defect itself. About 3.1% of people are affected, and 4 to 6% of children. ^[6]
• Most people with either condition never know: only 23% report symptoms before the age of 20, and 2.5 to 3.5% of children who have pelvic CT or MRI for unrelated reasons are found to have spondylolysis or isthmic spondylolisthesis incidentally. ^[6]
• In cadaveric and screening series the prevalence runs from 4.4% of 6-year-old children to about 6% of young adults. ^[3]

Athletes are the exception that defines the topic. Spondylolysis explains close to 47% of back pain in adolescent athletes, as against about 18% in their non-athletic peers. ^[1] The condition has been reported in 30% of football (soccer) and baseball studies, in up to 44% of hockey players, 40% of tennis and diving athletes, and up to about 50% of cricket fast bowlers, rugby players and American football players. ^[1][4] Early investigators described a female-to-male ratio favouring males, but as girls and young women entered competitive sport, especially gymnastics, the female prevalence has risen fourfold. ^[1]

Other risk factors besides sport matter:

• Spina bifida occulta is found in 92.6% of elementary-school-age children with L5 spondylolysis in one series, and carries a 3.7-fold increase in risk. ^[1]
• Scheuermann's kyphosis brings a 30 to 50% incidence, probably through the increased lumbar lordosis. ^[1]
• Scoliosis and other spinal malalignment add risk. ^[6]
• Genetic loading is strong: 15% (and in some reports up to 70%) of people with spondylolysis have a first-degree relative with the same lesion. ^[6]
• In the United States the condition is most common in white males (prevalence about 6.4%), followed by African American males, white females and African American females. ^[1] Alaskan Native heritage also confers increased risk. ^[6]

The accepted mechanism is a stress fracture from cumulative microtrauma in a person with a susceptible spine. ^[1] Competitive sport is the leading environmental factor; the sport matters because of the forces, not because of the ball. Sports that combine repetitive lumbar extension with rotation and axial loading are the dangerous ones. The list repeated across sources includes gymnastics, football, (American) football, soccer, tennis, baseball, rowing, cricket fast bowling, rugby, hockey, diving, wrestling, pole vaulting, racquet sports and weightlifting. ^[2][4]

Structural and biological modifiers control who gets hurt:

1. A larger pelvic incidence produces a larger lordosis, which sends more anterior shear through the pars and raises the risk. ^[3]
2. Ligamentous laxity and the hormonal environment of adolescence (and of pregnancy) may contribute.
3. The growth spurt between 10 and 15 years is the window in which the defect forms and in which a defect most often turns into a slip. ^[1][6]
4. Ossification of the lumbar growth plates after the age of 20 is the reason that slips rarely progress in adult life. ^[2]

The adult (degenerative) contrast. Degenerative spondylolisthesis is a disease of ageing. Average age of presentation is in the sixth and seventh decades; most cases occur at L4 on L5 and the slip is almost always Meyerding grade I or II. Women are affected roughly six times as often as men. ^[5][6] In a prospective study of 142 previously healthy women, 12.7% developed degenerative spondylolisthesis over eight years. ^[6] The cause is not a fracture but attrition: disc degeneration, facet joint arthrosis, horizontalisation of the facet orientation and laxity of supporting ligaments allow the vertebra to creep forward. ^[6] Because the spinal canal, rather than a mobile segment, is the problem, the dominant clinical picture is spinal stenosis rather than a loose motion segment.

The sequence is best understood as five steps.

Step 1: shear on the pars. At L5 the inferior articular process of L4 and the superior articular process of S1 form a pincer. In a spine with a large lordosis, repetitive extension and rotation repeatedly load the pars interarticularis between them. Ward and colleagues found shorter transverse interfacet distances at L3-S1 in patients who later developed spondylolysis, consistent with greater shear in the lumbar spine. ^[1]

Step 2: a stress fracture that behaves like any other. The pars breaks first on its ventral surface. ^[3] MRI can show marrow oedema (a stress reaction, Hollenberg type 1) before a visible crack exists; CT then shows a hairline (early) or wider (progressive) defect. ^[3][4] The defect may be one or two sided; if it is unilateral the other side often carries a reactive sclerotic pedicle. ^[1]

Step 3: healing or non-union. Unilateral and acute lesions heal well with rest. Bilateral lesions go on to a non-union in about a third of cases, leaving a fibrous or cartilaginous bridge rather than bone. ^[1][2]

Step 4: slip. When both pars are deficient the posterior arch is disconnected from the vertebral body. Up to 70% of people with bilateral pars defects progress to isthmic spondylolisthesis, most often between the ages of 10 and 15. ^[6] The natural history series of Fredrickson and colleagues (45-year follow-up) and of Beutler showed that slippage largely stops once growth is complete. ^[2][3]

Step 5: what the slip does to the patient. Because the central canal in isthmic disease usually stays wide, pure spondylolysis produces pain without nerve compression. Nerve root impingement arrives later, with age and disc degeneration. ^[3] High grade slips are the exception and can compress the L5 roots and the cauda equina. ^[3]

The degenerative disease has its own sequence: facet joint arthrosis and subluxation, plus disc narrowing and ligament failure, let the vertebra slide forward, often a few millimetres at a time. The central canal narrows as it does, which is why neurogenic claudication is the defining symptom of adult disease. ^[6]

Most spondylolysis is silent. About 87% of cases are asymptomatic and are found incidentally or only after a fracture is suspected for another reason. ^[1]

When symptoms are present they are recognisable. The classic athlete's story is:

• localised or one-sided lower back or buttock ache that begins after a training load increase, a change of sport or a specific repetitive skill such as a back handspring, a vault, a serve or a fast bowl run-up;
• pain brought on by extension of the lumbar spine and by the sport, relieved by rest. Sitting is usually comfortable, which helps to separate this from discogenic pain;
• morning stiffness after a session;
• a stooped or antalgic gait in severe cases, because tight hamstrings hold the pelvis in retroversion;
• hamstring tightness that the patient notices as loss of knee extension and that the examiner measures. ^[1]

Pain that worsens at rest, at night, or while sitting is atypical and should redirect the search toward sacroiliac disease, malignancy, infection or a progressive slip. ^[1]

Neurological findings are uncommon in youth. Pure isthmic disease rarely produces a neurological deficit. ^[1][6] The appearance of a radiculopathy (usually L5) suggests either disc degeneration on a long-standing defect or a high grade slip. Cauda equina symptoms are possible in severe slips and require urgent referral. ^[1][6]

The adult degenerative picture is different. ^[5][6]

Adult patients may also present without pain at all: up to a third of elderly patients with degenerative spondylolisthesis are asymptomatic and the slip is an incidental radiological finding. ^[6]

Inspection begins with standing alignment. Look for an exaggerated or flattened lumbar lordosis, a truncal shift, and pelvic tilt. Watch the gait: a shortened stride with more hip and knee flexion is described in advanced slips in children, because the tight hamstrings and the sagittal alignment distort the normal walk. ^[6]

Palpation localises tenderness over the pars at the affected level and may reveal a step-off, a palpable ledge where the vertebra has moved. The step is felt below the affected level in isthmic disease and above it in degenerative disease. ^[5] A prominent sacrum may be obvious in advanced disease. ^[5]

Range of motion is usually reduced into extension, and sometimes into flexion. Muscle spasm in the paraspinal muscles is common. ^[5]

Two signs are often taught, and both need qualification.

• The one-legged (stork) hyperextension test is positive when the patient, standing on one leg, extends the spine and reproduces ipsilateral back pain. Jackson described it as pathognomonic, but more recent work gives a sensitivity of about 81% and a specificity of only about 39%; a positive test is more likely than a negative one to be misleading. The test is therefore a prompt for imaging, not a diagnosis. ^[1][4]
• Popliteal angle on full knee extension is a useful way of quantifying hamstring tightness: angles greater than 30 to 45 degrees are considered abnormal. ^[1]

Red flags that change management:

• neurological deficit (weakness, reflex change, sensory loss), especially L5 function such as ankle dorsiflexion and great toe extension;
• symptoms of central stenosis or cauda equina (saddle anaesthesia, bowel or bladder disturbance, bilateral leg pain);
• night pain, unexplained weight loss or fever;
• a rapidly progressive slip on follow-up films;
• a slip greater than 50% (high grade) at any age.

These patients need imaging, urgent neurosurgical or spinal review, and no return to sport until assessed.

The task is to distinguish spondylolysis and spondylolisthesis from other causes of back pain in the young and from other causes of low back and leg pain in the older patient.

In adult patients, the main differentials for the degenerative slip are pure spinal stenosis without spondylolisthesis, degenerative disc disease, facet arthropathy, osteoporotic compression fracture and metastatic disease. Imaging settles the distinction in almost every case.

Imaging starts with plain radiographs, because a simple film is cheap, quick, and often diagnostic. ^[1][4][6]

• Lateral radiograph of the lumbar spine is the screening film and the one on which the Meyerding grade is measured. The collimated (spot) lateral view is the single most sensitive plane at about 84%. ^[1] Ask the radiographer to centre on L5/S1.
• Oblique views bring out the "Scotty dog": the pars interarticularis is the neck of the dog, and a defect is its collar. Oblique films are reported with about 97% accuracy for chronic spondylolysis, but they add little when the lateral view is clear. They can be hard to read at L5 because the iliac wing overlaps. ^[1][4]
• Anteroposterior view shows callus in healing lesions and rules out other pathology. ^[4]
• Dynamic (flexion and extension) lateral views look for instability: slippage that increases by more than 4 mm or an angular change greater than 10 degrees between adjacent endplates counts as significant instability. ^[4][5]
• CT is the gold standard for bony detail. It shows the defect, its chronicity (sclerotic margins mean chronic disease), and is the test used for preoperative planning and for follow-up of union. ^[1][4] It still cannot diagnose an early stress reaction, before a crack has formed.
• MRI is the earliest detector. It shows bone marrow oedema and a fracture line on T1- and T2-weighted images, before the CT is abnormal. It is radiation-free, which is why most paediatric algorithms prefer it as the first advanced study. The sensitivity of MRI is about 80 to 83% against the reference of CT or SPECT, but it is the best way to watch a healing lesion. ^[2][4]
• SPECT / bone scintigraphy shows osteoblastic activity in acute lesions and can separate acute from chronic disease when combined with plain films; it is poor at showing morphology. It is usually reserved for professional athletes or for cases where the diagnosis remains uncertain. ^[1][4]

On cost, plain two-view and four-view films are estimated at about 350 and 500 US dollars, with bone scan near 1650, CT near 2000 and MRI near 2900 US dollars, in the studies cited. ^[2] In most health systems the principle is therefore the same regardless of cost: plain film first, then MRI for children and active athletes, with CT for surgical planning or to confirm union.

Meyerding grading. The Meyerding system, first described by Henry Meyerding in 1932, grades the slip by the percentage of the superior vertebral body that has moved relative to the inferior one. ^[3][5] The grade is measured on a standing (not supine) neutral lateral radiograph by drawing lines through the posterior walls of the two vertebral bodies and expressing the translation as a fraction of the length of the vertebra below. ^[5]

Grades I and II are generally low grade; grades III to V are high grade. ^[3][5] About 70 to 90% of all cases are grade I and II. ^[6] High grade slips (more than 50%) are unusual and usually belong to the isthmic rather than the degenerative type, because only a fractured pars permits that much translation. ^[6]

Two points about Meyerding are commonly misunderstood. First, the grade is not a strong predictor of symptoms: many grade I patients are badly symptomatic and many grade IV patients are not. ^[5] Second, although the grade alone is a poor predictor of progression, higher grades correlate with a higher risk of progression in children and adolescents, and so the grade still matters. ^[5]

A practical point on imaging technique: supine radiographs should be avoided when grading a slip, because the vertebra can temporarily reduce into an anatomical position on the couch and understate the disease. ^[6]

MRI classification of the pars injury. The early stages of spondylolysis are well described on MRI before a line appears on CT: normal pars (stage 0), stress reaction with marrow oedema but intact cortex (stage 1), incomplete fracture (stage 2), acute complete fracture (stage 3), and established chronic defect without oedema (stage 4). ^[4] This matters clinically because stage 1 and 2 lesions heal with activity restriction while stage 4 does not.

Management is conservative first, for almost every patient, for at least six months. Between 70 and 90% of athletes with spondylolisthesis return to their sport within three to six months on conservative treatment alone. ^[6] One meta-analysis found an 84% overall success rate in children with spondylolisthesis treated without surgery. ^[5] Surgery exists for the minority who do not respond and for those whose slip is already high grade.

1. Activity restriction. The core intervention, and the one with the clearest evidence. The athlete stops the provoking sport for at least three months, and many paediatric protocols recommend four. ^[2][3] Walking and cycling are allowed throughout; stationary cycling and swimming remain good conditioning. In one large cohort of 436 young patients, three months off sport plus a thoracolumbar brace and structured physiotherapy produced excellent results in 95% and no patient needed surgery. ^[2] Crucially, rest can be combined with early physiotherapy: patients whose physiotherapy started earlier returned to sport sooner than those whose physiotherapy waited until after three months of rest. ^[2]
2. Core and pelvic-floor strengthening. The evidence supports activating the deep stabilisers: transversus abdominis, internal oblique and multifidus. A graded programme runs from basic isometric holds (for example 10 repetitions of 10-second holds) through dynamic limb work to sport-specific multiplanar control. Adjacent hip flexor and hamstring stretching is added as symptoms allow. ^[2][6]
3. Pain control. NSAIDs are the mainstay in the acute phase, with short courses of oral or injected analgesia and, where appropriate, pars or epidural steroid injections. ^[6]
4. Electrical stimulation is a second-line conservative option in some protocols. ^[1]
5. Bracing is the controversial ingredient. Several sources support an antilordotic thoracolumbosacral (TLSO) brace for 6 to 12 weeks, especially in unilateral disease, combined with and not instead of physiotherapy. ^[1][5] Others have shown that rigid thoracolumbar bracing does not improve union rates compared with placebo and that bracing itself (along with duration of symptoms and type of lesion) did not predict long-term sport participation, symptom recurrence or perceived outcome. ^[2][3] Some sports medicine authors argue against routine bracing altogether, because a brace can cause trunk muscle atrophy, does not immobilise across the hip, and can interfere with rehabilitation. ^[2][4] A reasonable, evidence-based position is therefore: do not brace routinely; consider a time-limited brace (6 to 12 weeks) when symptoms persist or when a specific protocol is followed, and always keep the rehabilitation programme running. ^[1][2][4]
6. Follow-up and re-imaging. Healed or nearly healed lesions are checked with CT; pain that is not improving invites earlier imaging. Young patients with residual growth are followed with plain films and examination yearly through the growth spurt. ^[3][4]

Outcomes of conservative care. About 92% of adolescent athletes return to sport within six months, whether treated with rest, bracing or physiotherapy or a combination of them. ^[2] Most low grade slips in children have a good prognosis: in one 13-year follow-up, only 3 of 72 children had progression of 10% or more. ^[3] Even after non-union, many patients are symptom-free for years. ^[3]

Persistent symptoms, bilateral disease, and a long-standing symptomatic pars defect can be managed in steps:

• A diagnostic pars or facet injection helps to confirm that the defect is the pain source. ^[4]
• Direct repair (Buck's screw across the defect, Scott wiring, pedicle or hook constructs) preserves motion and is attractive in athletes under about 20 to 25 years with a healthy disc and no segmental motion on flexion and extension films. It is not shown to produce better long-term results than fusion in head-to-head comparisons. ^[3][4]
• Posterolateral fusion (usually L5 on S1) gives lower back pain rates at mid- and long-term follow-up than direct repair. ^[3]
• Instrumented reduction with fusion has a higher union rate than in situ fusion in high grade slips, but opinions differ and it carries a risk of transient or permanent L5 nerve root injury. ^[3]

Surgery is considered when any of these is present. ^[1][3][5][6]

• Failure of at least six months of well-conducted conservative management, with ongoing pain or functional limitation.
• A high grade slip (Meyerding grade III or greater, more than 50%).
• Progression of slip greater than one grade on follow-up.
• High instability on flexion and extension radiographs (more than 4 mm translation or more than 10 degrees angular change).
• Neurological impairment, including radiculopathy refractory to injection, and any sign of cauda equina or progressive focal deficit.
• Symptoms that are disabling in a patient who is otherwise fit for surgery.

Grade by grade: low grade (I and II) slips are managed conservatively or, after failure, with decompression and fusion. High grade (III to V) slips, and all symptomatic slips with neurological involvement, are managed with decompression and fusion, with or without reduction. ^[5][6]

In degenerative disease, the surgical target is the stenosis. Decompression alone is reasonable in older patients without dynamic instability; decompression with fusion is preferred where there is dynamic slip, segmental lordosis to correct, or progressive deformity. ^[6]

Adolescent athletes. Return to sport timelines are long because bone heals slowly. Conservative care expects return within 6 months. After direct repair or fusion, physiotherapy follows the surgeon's protocol and a return to high-impact activity waits until imaging confirms healing. ^[2] Two cautions from the sport medicine literature: "overtraining" (single sport, year-round, no off-season) is a recurrent precipitant and must be addressed in counselling, and growth periods during and after treatment require a return to the basic deep-abdominal routine. ^[2]

Adults with degenerative disease. The slip is usually low grade and slow. The aim is not to reverse the slip (grade I degenerative slips do not progress in the natural history series) but to relieve pain and, where present, the stenosis. ^[5] Lumbar stabilisation exercise programmes (the "core" programmes that include transversus abdominis and multifidus work) have the best evidence for symptom control in chronic spondylolysis and spondylolisthesis; low impact exercise (cycling, swimming, elliptical) is preferred to running. ^[5][6] The classical randomised comparison suggests that patients with definite instability gain more from fusion than from decompression alone. ^[6]

Pregnancy. The increased ligamentous laxity of pregnancy, on a susceptible isthmic defect, can make a latent slip symptomatic. Management is conservative: analgesia, activity modification and bracing where appropriate. ^[6]

Children with dysplastic disease. The management of high grade dysplastic slips (congenital facet deficiency at L5/S1, often with spina bifida occulta) is surgical, because these carry a real risk of progressive slip and cauda equina compression during growth. ^[3]

Low-resource settings. Plain radiographs are usually available and carry the diagnostic weight. An undiagnosed adolescent with back pain for more than two weeks and extension-provoked pain, particularly with hamstring tightness, should be steered toward rest and structured exercise even where MRI and CT are unavailable. A sclerotic pedicle on one side (the "responsive pedicle sign") or a lucent gap on the oblique film supports the diagnosis. Physiotherapy staff can deliver the core stabilisation programme. Early referral for any case of neurological impairment or a slip of 50% or more, because surgical capacity is concentrated in specialist centres.

• Progression to spondylolisthesis. About a quarter of adolescents with bilateral, non-united spondylolysis develop a low grade slip over two years. ^[3]
• Non-union. Terminal or chronic defects (sclerotic, rounded margins) do not heal with rest; these are the main source of recalcitrant symptoms. ^[3]
• Neurological deficit. Most often L5 when a disc degenerates or a slip progresses; cauda equina syndrome is possible in high grade slips or dysplastic disease. ^[3][6]
• Intersegmental instability on standing (more than 4 mm or more than 10 degrees on flexion and extension films) is both a complication and an indication for fusion. ^[4]
• Post-operative: pseudoarthrosis (reported at 17.8% in non-reduced fusions versus 5.5% where reduction was obtained), adjacent segment degeneration after fusion, and L5 root stretch injury after reduction of a high grade slip. ^[3][6]
• Sporting career and quality of life. Even when symptoms resolve, the injury marks a vulnerable segment for life, and patients should understand that activity management is a lifelong habit.

Low grade isthmic disease has an excellent prognosis. The short-term return-to-sport rate is 92% within 6 months on conservative care. Long-term follow-up studies show that most adolescents have little disability once the slip has stopped progressing. ^[2][3]

Higher grades carry proportionately more risk. In adolescents with grades III and IV slips who were not operated on, six of eleven progressed to spondyloptosis over a mean of 18 years, and five had neurological symptoms at the end of follow-up; by contrast, 20 of 21 who were fused had minimum or no symptoms at a mean of 24 years. ^[3]

For the degenerative disease, the grade I and II slips that dominate practice are usually stable and respond to a sustained programme of physiotherapy and lifestyle adaptation. ^[5][6]

Prevention is sport-specific and technique-focused rather than medical:

• coaching of neutral-spine technique for landings and tumbling, and limits on repetition of hyperextension skills;
• avoidance of year-round single-sport participation and adequate recovery weeks;
• strength and neuromuscular control training of the trunk and hip girdle in adolescent athletes, particularly at entry to intensive training;
• prompt evaluation of back pain in young athletes that lasts more than two weeks: every such episode should be treated as a stress fracture until imaging proves otherwise. ^[4]
• screening remains informal. No national programme exists, and the screening test available (the stork test) is too non-specific to be useful in asymptomatic athletes.

Same-day or urgent spinal referral is indicated for:

• any red flag on history or neurological examination;
• a slip of 50% or more;
• a progressive slip on follow-up films;
• significant instability on flexion-extension radiographs (more than 4 mm or more than 10 degrees);
• failure of six months of well-conducted conservative treatment.

Early referral to a sports medicine physician, a paediatric orthopaedist or a spinal surgeon is appropriate whenever the diagnosis is uncertain, imaging is unavailable, or the case affects a scholarship or competitive career.

• Spondylolysis is a defect of the pars interarticularis; spondylolisthesis is the slip of a vertebra on the one below. They are a continuum, and a bilateral pars defect is what allows the slip. ^[1][3]
• About 95% of spondylolysis occurs at L5, because that is where lumbar shear is greatest. ^[1]
• Prevalence runs from 4.4% of 6-year-olds to 6 to 8% of adults, yet only 23% are symptomatic before 20. ^[1][3][6]
• Spondylolysis explains around 47% of back pain in adolescent athletes. Sports with repetitive extension and rotation (gymnastics, football, baseball, tennis, rowing, cricket) dominate. ^[1][4]
• Hamstring tightness and a backache provoked by lumbar extension are the clinical hallmarks. ^[1][5]
• The one-legged hyperextension (stork) test has a sensitivity of about 81% but a specificity of only about 39%; it is a prompt to image, not a diagnosis. ^[1]
• Meyerding: less than 25% grade I; 25 to 49% grade II; 50 to 74% grade III; 75 to 99% grade IV; 100% or more (spondyloptosis) grade V. ^[3]
• Low grade slips (I and II) are managed conservatively and succeed in 84 to 92% of cases. About 25% of non-united bilateral pars defects slip into a low grade listhesis within two years. ^[2][3]
• The commonest first intervention is activity restriction for 3 to 4 months with physiotherapy running through it. Bracing is contested and should not be routine; a time-limited brace (6 to 12 weeks) is reasonable for persistent symptoms. ^[1][2][3][4]
• Surgery is indicated after 6 months of failed conservative care, or sooner for a high grade slip or neurological signs; fusion is the workhorse, and direct repair is an attractive alternative in young athletes with a healthy disc. ^[3][5][6]
• Adult degenerative disease is a different illness: women outnumber men six to one, the level is usually L4 on L5, the slip is usually grade I or II, and the symptom set is back pain plus radiculopathy or neurogenic claudication relieved by sitting. ^[5][6]

Pars stress fracture and spondylolysis in young athletes; low back pain in adolescents; spinal stenosis and neurogenic claudication; radiculopathy and disc herniation; kyphosis and Scheuermann disease; scoliosis; osteoporosis and fractures in older adults; sports medicine and resistance training. Plain text only; no internal links are included here because none of these MedGrasp topics are confirmed as written.