Thoracolumbar and lumbar trauma account for the majority of traumatic spinal injuries. The mainstay of current treatments is still nonoperative therapy with bracing. Classic treatment algorithms reserved absolute surgical intervention for spinal trauma patients with neurological compromise or instability. Relative indications included incapacitating pain and obesity/body habitus making brace therapy ineffective. In the past decade, minimally invasive surgical (MIS) techniques for spine surgery have been increasingly used for degenerative conditions. These same minimally invasive techniques have seen increased use in trauma patients. The goal of minimally invasive surgery is to decrease surgical morbidity through decreased soft-tissue dissection while providing the same structural stability afforded by classic open techniques. These minimally invasive techniques involve percutaneous posterior pedicle fixation, vertebral body augmentation, and utilization of endoscopic and thoracoscopic techniques. While MIS techniques are somewhat in their infancy, an increasing number of studies are reporting good clinical and radiographic outcomes with these MIS techniques. However, the literature is still lacking high-quality evidence comparing these newer techniques to classic open treatments. This article reviews the relevant literature regarding minimally invasive spine surgery in the treatment of thoracolumbar and lumbar trauma.
Theodore Koreckij, Daniel K. Park and Jeffrey Fischgrund
Ho-Yeon Won, Jong-Beom Park, Eun-Young Park and K. Daniel Riew
Diabetes mellitus is thought to be an important etiologic factor in intervertebral disc degeneration. It is known that notochordal cells gradually disappear from the nucleus pulposus (NP) of the intervertebral disc with age by undergoing apoptosis. What is not known is whether diabetes has an effect on apoptotic rates of notochordal cells. The purpose of this study was to investigate the effect of hyperglycemia on apoptosis of notochordal cells and intervertebral disc degeneration in age-matched OLETF (diabetic) and LETO (control) rats.
Lumbar disc tissue (L1–2 through L5–6), including cranial and caudal cartilaginous endplates, was obtained from 6- and 12-month-old OLETF and LETO rats (40 rats, 10 in each of the 4 groups). The authors examined the NP using TUNEL, histological analysis, and Western blot for expression of matrix metalloproteinase (MMP)–1, -2, -3, and -13, tissue inhibitor of metalloproteinase (TIMP)–1 and -2, and Fas (apoptosis-related protein). The apoptosis index of notochordal cells was calculated. The degree of transition of notochordal NP to fibrocartilaginous NP was classified on a scale ranging from Grade 0 (no transition) to Grade 4 (transition > 75%). The degree of expression of MMP-1, -2, -3, and -13, TIMP-1 and -2, and Fas was evaluated by densitometry.
At 6 and 12 months of age, OLETF rats showed increased body weight and abnormal 2-hour glucose tolerance tests compared with LETO rats. The apoptosis index of notochordal cells was significantly higher in the OLETF rats than in the LETO rats at both 6 and 12 months of age. The degree of transition of notochordal NP to fibrocartilaginous NP was significantly higher in the OLETF rats than in the LETO rats at 6 and 12 months of age. The expression of MMP-1, -2, -3, and -13, TIMP-1, and Fas was higher in the OLETF rats at 6 and 12 months of age. The expression of TIMP-2 was significantly higher in the OLETF rats than in the LETO rats at 6 months of age, but not at 12.
The findings suggest that diabetes is associated with premature, excessive apoptosis of NP notochordal cells. This results in an accelerated transition of a notochordal NP to a fibrocartilaginous NP, which leads to early intervertebral disc degeneration. It remains to be determined if these premature changes are due to hyperglycemia or some other factors associated with diabetes. Understanding the mechanism by which diabetes affects disc degeneration is the first step in designing therapeutic modalities to delay or prevent disc degeneration caused by diabetes mellitus.
Anton V. Zaryanov, Daniel K. Park, Jad G. Khalil, Kevin C. Baker and Jeffrey S. Fischgrund
As a result of axial compression, traumatic vertebral burst fractures disrupt the anterior column, leading to segmental instability and cord compression. In situations with diminished anterior column support, pedicle screw fixation alone may lead to delayed kyphosis, nonunion, and hardware failure. Vertebroplasty and kyphoplasty (balloon-assisted vertebroplasty) have been used in an effort to provide anterior column support in traumatic burst fractures. Cited advantages are providing immediate stability, improving pain, and reducing hardware malfunction. When used in isolation or in combination with posterior instrumentation, these techniques theoretically allow for improved fracture reduction and maintenance of spinal alignment while avoiding the complications and morbidity of anterior approaches. Complications associated with cement use (leakage, systemic effects) are similar to those seen in the treatment of osteoporotic compression fractures; however, extreme caution must be used in fractures with a disrupted posterior wall.
Sharad Rajpal, Tiffany A. Gerovac, Nicholas A. Turner, Jessica I. Tilghman, Bradley K. Allcock, Shannon L. McChesney, Gurwattan S. Miranpuri, Seung W. Park and Daniel K. Resnick
The authors previously discovered that genes for the bradykinin-1 (B1) receptor and the transient receptor potential vanilloid subtype 1 (TRPV1) were overexpressed in animals exhibiting thermal hyperalgesia (TH) following spinal cord injury (SCI). They now report the effect of TRPV1 (AMG9810) and B1 (Lys-[Des-Arg9, Leu8]-bradykinin) antagonists on TH in animals following SCI.
The rats were subjected to contusion SCI and then divided into groups in which TH did or did not develop. The animals from both groups were given either AMG9810, Lys-(Des-Arg9, Leu8)-bradykinin, or the drug-specific vehicle (control groups). Animals were tested for TH preinjury and at regular intervals after SCI by using the hindlimb withdrawal latency test.
The administration of AMG9810 likely improves TH as a result of a generalized analgesic effect, whereas the effect of Lys-(Des-Arg9, Leu8)-bradykinin appears more specific to the reversal of TH. This information has potential usefulness in the development of treatment strategies for post-SCI neuropathic pain.