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Pars Interarticularis Injury Clinical Presentation

  • Author: Gerard A Malanga, MD; Chief Editor: Craig C Young, MD  more...
 
Updated: Oct 20, 2015
 

History

The clinical presentation and reported findings of the historical examination of patients with spondylolysis may include the following:

  • Although most patients with spondylolysis are asymptomatic, those who do develop symptoms typically present during the preadolescent growth spurt. [23]
  • Patients predominantly complain of focal LBP brought on by certain performance activities. Pain may be sharp and lancinating in the acute period or may become chronic, dull, and aching over time. The pain is usually of mild to moderate intensity. Pain may be located unilaterally or bilaterally, usually along the belt line. On occasion, the pain may radiate into the buttock or proximal lower extremity.
  • The onset of symptoms may be either insidious or acute. Often, mild symptoms may be present for a time period, but then the symptoms may become exacerbated by a specific incident.
  • Movements, particularly those involving spinal extension and, to a lesser extent, rotation, are typically described as exacerbating events. Pain is often improved with rest. One study showed up to 98% of adolescent patients with spondylolysis have pain with extension and rotation movements of the spine. [24]
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Physical

Common findings during the physical examination of a patient with spondylolysis may include the following:

  • Upon inspection of the lumbar spine: A patient with LBP resulting from spondylolysis often exhibits a reduced lordotic posture with excessive hamstring tightness.
  • The classically described Phalen-Dickson sign (ie, a knee-flexed, hip-flexed gait) may be demonstrated in patients with spondylolysis. Although this sign is more often seen in those with concomitant spondylolisthesis, it may be present regardless of the degree of vertebral slippage. [25]
  • A gait pattern described as the pelvic waddle has also been described in association with spondylolysis. The hallmark of this gait abnormality includes a stiff-legged gait with a short stride length due to hamstring tightness.
  • The clinician should also note the presence or absence of skin dimpling in the lumbosacral region that may signify the presence of spina bifida occulta, thereby raising the clinical suspicion of spondylolysis.
  • Palpation of the overlying paraspinal region often produces tenderness, and there may be spasm of the paraspinal musculature that causes splinting in acute cases. [3] Take care to identify a possible "step-off" when palpating over the spinous process. This step-off is indicative of concomitant spondylolisthesis, particularly over the L5-S1 level.
  • In assessing lumbar range of motion (ROM), forward flexion is commonly diminished secondary to hamstring tightness. Flexion typically does not increase symptoms, and in many cases, it provides relief. However, extension and rotation commonly cause discomfort for the patient.
  • The preeminent physical examination maneuver thought to most reliably reproduce pain from spondylolysis is the one-legged, hyperextension maneuver, also known as the stork test.
    • The patient is asked to stand on one leg and is brought backward into lumbar extension. Pain due to spondylolysis is thought to be elicited in unilateral lesions by standing on the ipsilateral leg.
    • Although this maneuver is most often described in association with spondylolysis, it stresses other structures besides the pars interarticularis and can therefore be considered to be only suggestive of a pars interarticularis lesion within the context of the clinical picture.
  • The neurologic examination should include assessment of motor strength, sensation, and reflexes. The findings of the neurologic examination should be within normal limits. Typically, radicular findings are absent in patients with isolated spondylolysis.
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Causes

Spondylolysis is considered by most to represent a fatigue fracture that results from repeated mechanical stress with microtrauma and eventual overload to the pars interarticularis rather than as a result of a single traumatic event.[26] However, a traumatic event may result in the completion of a developing fracture.[26] Studies have shown a remarkably low or absent rate of occurrence in newborns and very young children, as well as in those patients who have never been ambulatory.

Rosenberg et al studied 143 patients who had never walked, with an average age of 27 years, and found no cases of spondylolysis.[27] This finding appears to support the theory that loading of the pars interarticularis during upright, weight-bearing activities plays a role in the pathogenesis of these lesions.

Another study investigating the mechanical loading of the spine tested cadaveric lumbar vertebrae that were cyclically loaded at the inferior articular processes to simulate shear force.[26] The authors found 55 of 74 vertebrae to sustain pars fractures. They concluded that the pars interarticularis was particularly vulnerable to this type of repetitive loading. Further analysis of the vertebrae of those subjects without a fracture revealed a larger cross-sectional area of cortical bone in the pars compared with the control group.[26] This led Wiltse et al to hypothesize that a genetic predisposition may be related to the cortical bone density of the pars. This study also suggested that the strength of the neural arch may increase up to the 4th or 5th decade of life.[26]

In an experimental model, Dietrich and Kurowski found that the greatest mechanical loads occur at L5 and S1 with flexion and extension movements.[28] Furthermore, the greatest mechanical stress was found to occur at the region of the pars interarticularis. The investigators also noted that the loads and stresses across this region are related to the physical dimensions of the vertebrae, which may offer a partial explanation regarding the varying incidence among different races and the sexes. Repeated flexion and extension maneuvers, and to a lesser degree rotation, typically have been thought to be the movements that are responsible for generating the forces across the pars interarticularis that result in spondylolysis.[28, 29]

In a retrospective analysis of 213 young athletes, Gregory et al found left-sided lower lumbar pain was more common than the right side, and a marked increase in scintigraphic uptake was noted on the left side of the neural arch more often than the right side.[30] Unilateral spondylolysis was identified by reverse gantry computed tomography (CT) scanning on the left pars 36 times and on the right pars 16 times. These findings support the hypothesis that asymmetric repetitive movements associated with certain sports may be responsible for the development of unilateral spondylolysis.[30]

Green et al concluded from their cadaveric study on pars interarticularis stress, which investigated mechanical loading, that activities involving alternating flexion and extension movements cause large stress reversals in the pars interarticularis, thereby creating the highest risk for developing a pars defect.[31] The authors found compressive or axial loading to have little effect in generating these stresses likely responsible for spondylolysis.[31] Other anatomic studies have suggested that shear stresses on the isthmic pars are the greatest with lumbar spine extension.[32]

The specific cause of LBP associated with spondylolysis and spondylolytic spondylolisthesis has not been definitively established. Theories include nerve root compression by floating laminae, intervertebral disc pain, lumbar facet joint pain resulting from spinal instability, or a combination of these pathologies.[33] . A fibrocartilage mass of scar tissue forms at the site of lumbar spondylolysis and eventually develops into a structure frequently indistinguishable from a normal ligament by adulthood.

Eisenstein et al identified nerve fibers in the fibrocartilage masses histologically,[34] and Nordstrom et al detected the existence of the slow-conducting type C pain fibers and substance P in spondylolytic tissue obtained from patients who underwent resection.[35] Mechanoreceptors were later identified in these masses as well.

Hasegawa et al concluded that these fibrocartilage masses appear to be one source of pain, as LBP was induced by injecting hypertonic saline and was blocked by injecting lidocaine into these masses in all patients in their study before resection of the lesion.[36] The authors hypothesized that the fibrocartilage mass plays a protective role by sensing instability through the mechanoreceptor and then conveying this information through nociceptive fibers as pain, while at the same time, stabilizing this area of instability by acting as a ligamentlike structure across the defect.[36]

Given the high number of asymptomatic spondylolytic lesions, an important issue that is lacking in the literature and warrants further investigation is determining the factors that are responsible for producing pain in one patient but not another.

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Contributor Information and Disclosures
Author

Gerard A Malanga, MD Founder and Partner, New Jersey Sports Medicine, LLC and New Jersey Regenerative Institute; Director of Research, Atlantic Health; Clinical Professor, Department of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey-New Jersey Medical School; Fellow, American College of Sports Medicine

Gerard A Malanga, MD is a member of the following medical societies: Alpha Omega Alpha, American Institute of Ultrasound in Medicine, North American Spine Society, International Spine Intervention Society, American Academy of Physical Medicine and Rehabilitation, American College of Sports Medicine

Disclosure: Received honoraria from Cephalon for speaking and teaching; Received honoraria from Endo for speaking and teaching; Received honoraria from Genzyme for speaking and teaching; Received honoraria from Prostakan for speaking and teaching; Received consulting fee from Pfizer for speaking and teaching.

Coauthor(s)

Nancy Kim, MD Staff Physician, Department of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey

Nancy Kim, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, Association of Academic Physiatrists

Disclosure: Nothing to disclose.

Chris Perez, MD Staff Physician, Department of Physical Medicine and Rehabilitation, University of Medicine and Dentistry of New Jersey

Chris Perez, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Medical Association

Disclosure: Nothing to disclose.

David L Tung, MD, MPH Medical Director, PainCare Ambulatory Surgical Center

David L Tung, MD, MPH is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, North American Spine Society, International Spine Intervention Society, North American Neuromodulation Society

Disclosure: Received honoraria from Purdue Pharmaceutical for speaking and teaching; Received honoraria from Endo Pharmaceutical for speaking and teaching.

Michael Goldin, MD Department of Physical Medicine and Rehabilitation, Washington Township Medical Foundation

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Henry T Goitz, MD Academic Chair and Associate Director, Detroit Medical Center Sports Medicine Institute; Director, Education, Research, and Injury Prevention Center; Co-Director, Orthopaedic Sports Medicine Fellowship

Henry T Goitz, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Orthopaedic Society for Sports Medicine

Disclosure: Nothing to disclose.

Chief Editor

Craig C Young, MD Professor, Departments of Orthopedic Surgery and Community and Family Medicine, Medical Director of Sports Medicine, Medical College of Wisconsin

Craig C Young, MD is a member of the following medical societies: American Academy of Family Physicians, American College of Sports Medicine, American Medical Society for Sports Medicine, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

Andrew L Sherman, MD, MS Associate Professor of Clinical Rehabilitation Medicine, Vice Chairman, Chief of Spine and Musculoskeletal Services, Program Director, SCI Fellowship and PMR Residency Programs, Department of Rehabilitation Medicine, University of Miami, Leonard A Miller School of Medicine

Andrew L Sherman, MD, MS is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Medical Association, Association of Academic Physiatrists

Disclosure: Nothing to disclose.

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Table 1. Outline of the Treatment Strategy Based on Results of Plain Radiographs and SPECT Scanning in the Evaluation of Defects of the Pars Interarticularis in Patients Clinically Suspected of Having Symptomatic Pars Interarticularis Lesions
Plain Radiograph SPECT Scan Interpretation Management
Negative Negative Pathology other than pars defect should be suspected Further investigation of cause of back pain should be performed (eg, MRI)
Negative Positive Early pars interarticularis fracture Conservative management in form of rest, +/– bracing
Positive Healing Spondylolysis Conservative management in the form of rest and bracing
Positive Negative Pseudoarthrosis or old unhealed fracture Consider surgical intervention for stabilization to prevent spondylolisthesis and to relieve pain. Consider further investigation to rule out alternative pathology.
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