[Translated article] Effects of duroplasty with bovine pericardium on fibrosis and extent of spinal cord injury: An experimental study in pigs.

INTRODUCTION: Traumatic spinal cord injury (SCI) leads to increased intraspinal pressure that can be prevented by durotomy and duroplasty. The aim of the study was to evaluate fibrosis and neural damage in a porcine model of SCI after duroplasty and application of hyaluronic acid (HA) in the tissue cavity. MATERIALS AND METHODS: Experimental study. We created a porcine SCI model by durotomy and spinal cord hemisection of a cervical segment (1cm). Six pigs (Sus scrofa domestica) were used to evaluate three surgical scenarios: (1) control injury with dural reparative microsurgery, (2) duroplasty using bovine pericardium (BPD), and (3) previous method plus HA applied at the lesion. Animals were sacrificed one-month post-injury to assess fibrotic responses and neural tissue damage using conventional histological and immunohistochemical methods. RESULTS: In the control case, dural suture prevented invasion of the lesion by extradural connective tissue, and the dura mater showed a 1-mm thickening in the perilesional area. The bovine pericardium patch blocked the entrance of extradural connective tissue, decreased dura-mater tension, and satisfactorily integrated within the receptor tissue. However, it also enhanced subdural and perilesional fibrosis, which was not inhibited by filling the lesion cavity with low- or high-molecular-weight HA. CONCLUSIONS: Duroplasty prevents collapse of the dura-mater over the spinal cord tissue, as well as invasion of the lesion by extramedullary fibrotic tissue, without creating additional neural damage. Nevertheless, it enhances the fibrotic response in the spinal cord lesion and the perilesional area. Additional antifibrotic strategies are needed to facilitate spinal cord repair.

Effects of duroplasty with bovine pericardium on fibrosis and extent of spinal cord injury: An experimental study in pigs. / Efecto de la reparación de la duramadre con pericardio bovino sobre la fibrosis y la extensión de la lesión medular: estudio experimental en cerdos.

INTRODUCTION: Traumatic spinal cord injury (SCI) leads to increased intraspinal pressure that can be prevented by durotomy and duroplasty. The aim of the study was to evaluate fibrosis and neural damage in a porcine model of SCI after duroplasty and application of hyaluronic acid (HA) in the tissue cavity. MATERIALS AND METHODS: Experimental study. We created a porcine SCI model by durotomy and spinal cord hemisection of a cervical segment (1cm). Six pigs (Sus scrofa domestica) were used to evaluate three surgical scenarios: (1)control injury with dural reparative microsurgery, (2)duroplasty using bovine pericardium (BPD), and (3)previous method plus HA applied at the lesion. Animals were sacrificed one-month post-injury to assess fibrotic responses and neural tissue damage using conventional histological and immunohistochemical methods. RESULTS: In the control case, dural suture prevented invasion of the lesion by extradural connective tissue, and the dura mater showed a 1-mm thickening in the perilesional area. The bovine pericardium patch blocked the entrance of extradural connective tissue, decreased dura-mater tension, and satisfactorily integrated within the receptor tissue. However, it also enhanced subdural and perilesional fibrosis, which was not inhibited by filling the lesion cavity with low- or high-molecular-weight HA. CONCLUSIONS: Duroplasty prevents collapse of the dura-mater over the spinal cord tissue, as well as invasion of the lesion by extramedullary fibrotic tissue, without creating additional neural damage. Nevertheless, it enhances the fibrotic response in the spinal cord lesion and the perilesional area. Additional antifibrotic strategies are needed to facilitate spinal cord repair.

Morphologic Features on MR Imaging Classify Multifocal Glioblastomas in Different Prognostic Groups.

BACKGROUND AND PURPOSE: Multifocal glioblastomas (ie, glioblastomas with multiple foci, unconnected in postcontrast pretreatment T1-weighted images) represent a challenge in clinical practice due to their poor prognosis. We wished to obtain imaging biomarkers with prognostic value that have not been found previously. MATERIALS AND METHODS: A retrospective review of 1155 patients with glioblastomas from 10 local institutions during 2006-2017 provided 97 patients satisfying the inclusion criteria of the study and classified as having multifocal glioblastomas. Tumors were segmented and morphologic features were computed using different methodologies: 1) measured on the largest focus, 2) aggregating the different foci as a whole, and 3) recording the extreme value obtained for each focus. Kaplan-Meier, Cox proportional hazards, correlations, and Harrell concordance indices (c-indices) were used for the statistical analysis. RESULTS: Age (P < .001, hazard ratio = 2.11, c-index = 0.705), surgery (P < .001, hazard ratio = 2.04, c-index = 0.712), contrast-enhancing rim width (P < .001, hazard ratio = 2.15, c-index = 0.704), and surface regularity (P = .021, hazard ratio = 1.66, c-index = 0.639) measured on the largest focus were significant independent predictors of survival. Maximum contrast-enhancing rim width (P = .002, hazard ratio = 2.05, c-index = 0.668) and minimal surface regularity (P = .036, hazard ratio = 1.64, c-index = 0.600) were also significant. A multivariate model using age, surgery, and contrast-enhancing rim width measured on the largest foci classified multifocal glioblastomas into groups with different outcomes (P < .001, hazard ratio = 3.00, c-index = 0.853, median survival difference = 10.55 months). Moreover, quartiles with the highest and lowest individual prognostic scores based on the focus with the largest volume and surgery were identified as extreme groups in terms of survival (P < .001, hazard ratio = 18.67, c-index = 0.967). CONCLUSIONS: A prognostic model incorporating imaging findings on pretreatment postcontrast T1-weighted MRI classified patients with glioblastoma into different prognostic groups.

[Treatment of central neurocytoma. Experience at a single institution]. / Tratamiento neurocitoma central. Experiencia en nuestro centro.

Central neurocytomas are classically considered as a rare, intraventricular benign tumours with neuronal differentiation derived from precursor cells of subventricular matrix. However some patients with neoplasms with histologic atypia and elevated proliferation potential may have a poor outcome. Treatment of choice is complete surgical excision. Adjuvant therapy is reserved for patients with residual or recurrent lesions including reoperation, radiotherapy or chemotherapy. We review our experience with the treatment of this neoplasm. Five patients with an intraventricular mass studied with magnetic resonance imaging underwent craniotomy for tumour resection. All cases were reviewed retrospectively. Histopathological analysis confirmed central neurocytoma in all cases. Proliferation index was assessed by Ki-67 immunohistochemistry. Complete radiological tumor resection through transcortical approach was achieved in all except one patient. In this case adjuvant therapy with radiosurgery was given with important reduction in tumor size. All the tumours had a proliferation index below 2% except one with 5%. Follow-up in four patients ranged from 12 to 36 months. There were no tumour recurrences in this period. Complete surgical excision of central neurocytoma provides better local control and survival compared with other treatments. Radiosurgery as adjuvant therapy in incomplete resections may eliminate the need of reoperation and avoid long-term side effects from conventional radiotherapy.

Granulomatous amebic encephalitis in a patient with AIDS: isolation of acanthamoeba sp. Group II from brain tissue and successful treatment with sulfadiazine and fluconazole.

A patient with AIDS, treated with highly active antiretroviral therapy and trimethoprim-sulfamethoxazole, presented with confusion, a hemifield defect, and a mass lesion in the right occipital lobe. A brain biopsy confirmed granulomatous amebic encephalitis (GAE) due to Acanthamoeba castellanii. The patient was treated with fluconazole and sulfadiazine, and the lesion was surgically excised. This is the first case of AIDS-associated GAE responding favorably to therapy. The existence of a solitary brain lesion, absence of other sites of infection, and intense cellular response in spite of a very low CD4 count conditioned the favorable outcome. We review and discuss the diagnostic microbiologic options for the laboratory diagnosis of infections due to free-living amebae.