Determining C2 Pedicle Screw Placement Feasibility in the Pediatric Population: A Computed Tomographic Safe Zone Analysis.

BACKGROUND: Due to high rates of anatomic variability of the C2 pedicle, thin-sliced pedicular-oriented computed tomography (CT) and 3-dimensional reconstructive CT technologies have been introduced to predict safe C2 pedicle screw placement. However, this technology may not be readily available in all centers. The purpose of this study was to perform a C2 pedicle safe zone analysis using standard sagittal CT scans to predict the feasibility of C2 pedicle screw placement in a pediatric population and to compare the results with our previously obtained safe zone analysis from the adult population. METHODS: A retrospective analysis was performed at a single level I trauma center of pediatric patients who completed CT scans of the cervical spine. The feasibility of C2 pedicle screw placement was analyzed using our previously described C2 pedicle safe zone analysis technique. The risk profiles were compared with our previously obtained safe zone analysis from the adult population. RESULTS: Thirty-nine consecutive patients with a mean age of 7.8±4.4 years and 78 total pedicles were included in the study. Fourteen pedicles (18%) were considered low risk, 37 (47%) were moderate risk, and 27 (35%) were high risk for vertebral artery injury. Individual patients were found to have a significant amount of side-to-side variability between pedicles with 21 patients (54%) having left and right pedicles with different risk profiles. Four patients (10%) demonstrated low risk profiles in bilateral pedicles. There was no significant difference between the risk profiles of pediatric and adult patients. CONCLUSIONS: There is a considerable amount of anatomic variability within the pediatric C2 pedicles. Using this simple and accessible technique during the review of preoperative imaging, C2 pedicle screw placement may be considered in appropriately selected pediatric patients. LEVEL OF EVIDENCE: Level III.

A novel muscle-sparing high thoracotomy for upper thoracic spine resection and reconstruction.

PURPOSE: High thoracotomy allows access to the anterior cervicothoracic and upper thoracic vertebrae; however, traditional techniques transect shoulder girdle muscles, leading to postoperative shoulder dysfunction. Muscle-sparing techniques diminish this concern, but often sacrifice the quality of exposure. We describe a novel muscle-sparing, high thoracotomy approach for the treatment of ventral cervicothoracic and upper thoracic spine lesions. METHODS: A novel muscle-sparing, high thoracotomy approach is described, utilizing a midline posterior incision with lateral extension from the lateral decubitus position. Five patients are presented to illustrate the application of this technique in thoracic tumors with intimate spinal involvement. RESULTS: The muscle-sparing, high thoracotomy approach afforded gross total resection and spinal reconstruction in five consecutive patients, including stage IV lung carcinoma with invasion of the T5 and T6 vertebral bodies, two malignant fibrous histiocytomas causing thoracic cord compression, a metastatic T6 lesion of unknown primary with associated cord compression; and a Pancoast tumor. All patients seen at 6 months had full symmetric shoulder range of motion postoperatively. CONCLUSIONS: The described muscle-sparing, high thoracotomy approach provides excellent exposure of the ventral cervicothoracic and upper thoracic spine without the morbidity associated with the transection of shoulder girdle muscle bellies. This technique is particularly useful in patients with primary malignant bone tumors requiring en bloc excision and metastatic tumors with large soft tissue components.

Efficacy of MRI for assessment of spinal trauma: correlation with intraoperative findings.

STUDY DESIGN: Observational diagnostic study on consecutive patients. OBJECTIVE: To assess the efficacy of magnetic resonance imaging (MRI) for detecting spinal soft tissue injury after acute trauma using intraoperative findings as a reference standard. SUMMARY OF BACKGROUND DATA: Recognizing injuries to spinal soft tissue structures is critical for proper decision making and management for blunt trauma victims. Although MRI is considered the gold standard for imaging of soft tissues, its ability to identify specific components of soft tissue damage in acute spine trauma patients is poorly documented and controversial. METHODS: Intraoperative findings were recorded for 21 acute spinal trauma patients (study group) and 14 nontraumatic spinal surgery patients (control group). Preoperative MRI's were evaluated randomly and blindly by 2 neuroradiologists. MRI and intraoperative findings were compared. By using the intraoperative findings as the reference standard, sensitivity, specificity, positive and negative predictive values of MRI in detecting spinal soft tissue injury were determined. RESULTS: MRI was 100% sensitive and specific in detecting injury to the anterior longitudinal ligament. MRI was moderately sensitive (80%) but highly specific (100%) for injury to the posterior longitudinal ligament. In contrast, MRI was highly sensitive but less specific in detecting injury to paraspinal muscles (100%, 77%), intervertebral disk (100%, 71%), and interspinous ligament (100%, 64%). MRI was moderately sensitive and specific in detecting ligamentum flavum injury (80% and 86.7%) but poorly sensitive for facet capsule injury (62.5%). CONCLUSIONS: MRI demonstrated high sensitivity for spinal soft tissue injuries. However, MRI showed a definite trend to overestimate interspinous ligament, intervertebral disk, and paraspinal muscle injuries. On the basis of these results, we would consider MRI to be a useful tool for spine clearance after trauma. Conversely, caution should be applied when using MRI for operative decision making due to its less predictable specificity.

Protection against late-onset AIDS in macaques prophylactically immunized with a live simian HIV vaccine was dependent on persistence of the vaccine virus.

This is a 5-year follow-up study on 12 macaques that were immunized orally with two live SHIV vaccines, six with V1 and six with V2. All 12 macaques became persistently infected after transient replication of the vaccine viruses; all were challenged vaginally 6 mo later with homologous pathogenic SHIV(KU-1). Two of the V1 group developed full-blown AIDS without evidence of vaccine virus DNA in tissues. The data on the 10 vaccinated survivors showed that all 10 became infected with SHIV(KU-1) and that DNA of both vaccine and SHIV(KU-1) viruses were present 6 mo postchallenge, with minimal replication of SHIV(KU-1). During the following 5 years, these animals remained persistently infected, but with only one of the two viruses. Six animals eliminated their vaccine virus after variable periods of time and four of these succumbed to reactivation of the challenge virus and AIDS. Five years after challenge, four latently infected animals, two with V2 and two with SHIV(KU-1), were reinoculated with SHIV(KU-1.) This resulted in transient superinfection and the animals promptly returned to their prechallenge status. Immunosuppression of the four animals 1 year later with Abs to CD8+ lymphocytes resulted in transiently productive replication of their respective latent viruses, and upon recovery of CD8+ lymphocytes, they reverted to their latent virus status. The major finding was that of eight animals that eliminated the vaccine virus, six developed AIDS. The two others harboring SHIV(KU-1) remain at risk for developing late-onset disease. The primary correlate against AIDS was persistence of the vaccine virus.

Immunization of macaques with live simian human immunodeficiency virus (SHIV) vaccines conferred protection against AIDS induced by homologous and heterologous SHIVs and simian immunodeficiency virus.

To evaluate the vaccine potential of SHIVs attenuated by deletion of viral accessory genes, seven rhesus macaques were sequentially immunized with Delta vpu Delta nefSHIV-4 (vaccine-I) followed by Delta vpuSHIV(PPC) (vaccine-II). Despite the absence of virological evidence of productive infection with the vaccine strains, based on analysis of infectivity among peripheral blood mononuclear cells (PBMC) of the vaccinated animals, all seven animals developed binding as well as neutralizing antibodies against both vaccine-I and -II. The animals also developed vaccine virus-specific CTLs that recognized homologous as well as heterologous pathogenic SHIVs and SIV, and also soluble inhibitory factors that blocked the in vitro replication of the vaccine strains and different challenge viruses. Virus-specific cellular and humoral responses were sustained throughout a 58-week prechallenge period. To model aspects of natural transmission, the animals received a mucosal (rectal) challenge, with a mixture of three challenge viruses, SHIV(KU), SHIV(89.6)P, and SIV(mac)R71/17E. Two mock-vaccinated control animals inoculated with the same mixture of challenge viruses developed large numbers of infectious PBMC, high plasma viremia, and precipitous loss of CD4(+) T cells. The control animals did not develop any immune responses and succumbed to AIDS between 6 and 7 weeks postchallenge. All seven vaccinated animals became infected with challenge viruses as indicated by the presence of infectious cells in the PBMC and/or viral RNA in plasma. However, peak plasma viremia in vaccinates was two to nearly five logs lower than in the control animals and later plasma viral RNA became undetectable in all vaccinates. Vaccinated animals maintained normal CD4(+) T cell levels throughout the study. Challenge with pathogenic viruses caused massive anamnestic responses as determined by quantitation of virus-specific CD4(+) and CD8(+) T cells by intracellular IFN-gamma staining, and these cells persisted for at least 74 weeks. The study is still in progress and at this time DNA of SIV has become undetectable in lymph nodes of six of the seven vaccinates, SHIV(89.6)P in five of the seven, and SHIV(KU) in three of the seven animals.

Presence of Intact vpu and nef genes in nonpathogenic SHIV is essential for acquisition of pathogenicity of this virus by serial passage in macaques.

Use of the macaque model of human immunodeficiency virus (HIV) pathogenesis has shown that the accessory genes nef and vpu are important in the pathogenicity of simian immunodeficiency virus (SIV) and simian-human immunodeficiency virus (SHIV). We examined the ability of two nonpathogenic SHIVs, SHIV(PPC) and DeltavpuDeltanefSHIV(PPC), to gain pathogenicity by rapid serial passage in macaques. In this study, each virus was passaged by blood intravenously four times at 4-week intervals in macaques. Animals were monitored for 40 weeks for levels of CD4 T cells and quantitative measures of virus infection. DeltavpuDeltanefSHIV(PPC) maintained a limited phase of productive replication in the four animals, with no loss of CD4(+) T cells, whereas SHIV(PPC) became more pathogenic in later passages, judging by plasma viral load and viral mRNA in lymph nodes, infectious peripheral blood mononuclear cells and CD4(+) T cell loss. The nef, LTR, and env of the SHIV(PPC) viruses underwent numerous mutations, compared to DeltavpuDeltanefSHIV(PPC). This study confirms the seminal role that nef, LTR, and vpu could play in regulation of pathogenesis of HIV infection.