A fetal MRI study obtained at 21 weeks’ gestation revealed a suboccipital meningocele without hydrocephalus. One day after term birth, MRI demonstrated an acquired cerebellar encephalocele, and MRI obtained 5 months later showed progressive enlargement of the encephalocele, still without obvious hydrocephalus. The patient underwent an operation in which an external ventricular drain was placed, the grossly normal cerebellum was reduced into the posterior fossa without resection, and the dural defect was closed. The drain was weaned out over 5 days, and no ventriculoperitoneal shunt was placed. Postoperative MR images revealed normal cerebellum and no hydrocephalus. The patient is developmentally normal. Meningocele and encephalocele are embryologically distinct. An acquired encephalocele could develop from hydrocephalus (which was not present in this case), or secondary to the lower resistance to expansion into the dural defect of the meningocele relative to the resistance to expansion of the fetal skull. The cerebellar tissue was normal in this case, and was thus preserved. The developmental prognosis is excellent. To the authors’ knowledge, this is the first reported case of this occurrence. It is important to differentiate between congenital and acquired encephalocele etiologies, because resection of the cerebellar tissue in an acquired encephalocele (as is routinely done in cases of congenital encephalocele) would be expected to result in neurological deficits.
Gurpreet S. Gandhoke, Ezequiel Goldschmidt, Robert Kellogg and Stephanie Greene
Hazem Mashaly, Erin E. Paschel, Nicolas K. Khattar, Ezequiel Goldschmidt and Peter C. Gerszten
The development of symptomatic adjacent-segment disease (ASD) is a well-recognized consequence of lumbar fusion surgery. Extension of a fusion to a diseased segment may only lead to subsequent adjacent-segment degeneration. The authors report the use of a novel technique that uses dynamic stabilization instead of arthrodesis for the surgical treatment of symptomatic ASD following a prior lumbar instrumented fusion.
A cohort of 28 consecutive patients was evaluated who developed symptomatic stenosis immediately adjacent to a previous lumbar instrumented fusion. All patients had symptoms of neurogenic claudication refractory to nonsurgical treatment and were surgically treated with decompression and dynamic stabilization instead of extending the fusion construct using a posterior lumbar dynamic stabilization system. Preoperative symptoms, visual analog scale (VAS) pain scores, and perioperative complications were recorded. Clinical outcome was gauged by comparing VAS scores prior to surgery and at the time of last follow-up.
The mean follow-up duration was 52 months (range 17–94 months). The mean interval from the time of primary fusion surgery to the dynamic stabilization surgery was 40 months (range 10–96 months). The mean patient age was 51 years (range 29–76 years). There were 19 (68%) men and 9 (32%) women. Twenty-three patients (82%) presented with low-back pain at time of surgery, whereas 24 patients (86%) presented with lower-extremity symptoms only. Twenty-four patients (86%) underwent operations that were performed using single-level dynamic stabilization, 3 patients (11%) were treated at 2 levels, and 1 patient underwent 3-level decompression and dynamic stabilization. The most commonly affected and treated level (46%) was L3–4. The mean preoperative VAS pain score was 8, whereas the mean postoperative score was 3. No patient required surgery for symptomatic degeneration rostral to the level of dynamic stabilization during the follow-up period.
The use of posterior lumbar dynamic stabilization may offer a valid and safe option for the management of patients who develop ASD rostral to a previously instrumented arthrodesis. The technique may serve as an alternative to multilevel arthrodesis in this patient population. By implanting a dynamic stabilization device instead of an extension of a rigid construct, this might translate into a reduction in the development of yet another level of ASD.
The effect of vancomycin powder on human dural fibroblast culture and its implications for dural repair during spine surgery
Presented at the 2016 AANS/CNS Joint Section on Disorders of the Spine and Peripheral Nerves
Ezequiel Goldschmidt, Jorge Rasmussen, Joseph D. Chabot, Gurpreet Gandhoke, Emilia Luzzi, Lina Merlotti, Romina Proni, Mónica Loresi, D. Kojo Hamilton, David O. Okonkwo, Adam S. Kanter and Peter C. Gerszten
Surgical site infections (SSIs) are a major source of morbidity after spinal surgery. Several recent studies have described the finding that applying vancomycin powder to the surgical bed may reduce the incidence of SSI. However, applying vancomycin in high concentrations has been shown in vitro to inhibit osteoblast proliferation and to induce cell death. Vancomycin may have a deleterious effect on dural healing after repair of an intentional or unintentional durotomy. This study was therefore undertaken to assess the effect of different concentrations of vancomycin on a human dura mater cell culture.
Human dura intended for disposal after decompressive craniectomy was harvested. Explant primary cultures and subcultures were subsequently performed. Cells were characterized through common staining and immunohistochemistry. A growth curve was performed to assess the effect of different concentrations of vancomycin (40, 400, and 4000 μg/ml) on cell count. The effect of vancomycin on cellular shape, intercellular arrangement, and viability was also evaluated.
All dural tissue samples successfully developed into fusiform cells, demonstrating pseudopod projections and spindle formation. The cells demonstrated vimentin positivity and also had typical features of fibroblasts. When applied to the cultures, the highest dose of vancomycin induced generalized cell death within 24 hours. The mean (± SD) cell counts for control, 40, 400, and 4000 μg/ml were 38.72 ± 15.93, 36.28 ± 22.87, 19.48 ± 6.53, and 4.07 ± 9.66, respectively (p < 0.0001, ANOVA). Compared with controls, vancomycin-exposed cells histologically demonstrated a smaller cytoplasm and decreased pseudopodia formation resulting in the inhibition of normal spindle intercellular arrangement.
When vancomycin powder is applied locally, dural cells are exposed to a concentration several times greater than when delivered systemically. In this in vitro model, vancomycin induced dural cell death, inhibited growth, and altered cellular morphology in a concentration-dependent fashion. Defining a safe vancomycin concentration that is both bactericidal and also does not inhibit normal dural healing is necessary.