Resection of an Intramedullary Glomus-type Arteriovenous Malformation of the Conus Medullaris: Technical Note and Step-by-step Surgical Video.

Arteriovenous malformations (AVMs) of the spine include a broad spectrum of lesions that vary from a simple arteriovenous fistulous connection to a more complex net of abnormal vessels involving multiple spinal levels. These entities are poorly studied and understood because of their rarity and are often either managed conservatively with observation if the lesion is complex, or treated surgically or interventionally in the presence of an accessible and distinct fistulous connection. Most surgeons avoid intervening on more intricate lesions until they become symptomatic with progressive neurological decline. We describe the case of a 38-year-old man who presented with severe sharp back pain after an appendectomy procedure. A magnetic resonance angiogram (MRA) revealed an arteriovenous malformation of the conus medullaris, with a compact glomus-type nidus and arterial feeders originating from an enlarged artery of Adamkiewicz. The malformation was resected through a posterior midline approach, and the patient was neurologically intact at his discharge on postoperative Day 2. Follow-up angiography showed complete obliteration of the lesion. Our operative video is meant to serve as a step-by-step and systematic guide to the approach and management of conus arteriovenous spinal lesions, which can be difficult to treat. We provide a pre- and postoperative radiological description of the anomaly as well as a technical guide to the resection of a spinal vascular lesion. This video could serve as an operative guide and reference to neurosurgeons-both established and in training-when confronting similar disease processes in the future.

Osteodiskitis of Lumbar Spine Due to Migrated Fractured Inferior Vena Cava Filter.

BACKGROUND: Venous thromboembolism can be a significant cause of morbidity in the trauma population. Medical and surgical specialties have been pushing the indication for prophylactic filter placement. CASE DESCRIPTION: A 36-year-old man presented with axial lower back pain with a radicular right L2 component after lifting a heavy object. He had a history of penetrating brain trauma 3 years prior, with placement of a prophylactic inferior vena cava filter. His radiograph, computed tomography, and magnetic resonance imaging of the lumbar spine showed fracture of his filter, with migration of the fractured fragment through the inferior vena cava and into the L2-L3 disk space, and surrounding bony lysis and severe osteodiskitis. He was treated medically with intravenous and then oral antibiotics and improved clinically and radiographically. CONCLUSIONS: Conservative use of filter devices and early retrieval once their indication expires are paramount to avoid unnecessary complications.

Tumor necrosis factor is critical for cytolytic T cell activity against allospecific hepatocytes and splenic targets in major histocompatibility complex class I disparate graft versus host disease.

The present studies determined the role of tumor necrosis factor (TNF)/tumor necrosis factor receptor (TNFR) interactions on cytolytic (CTL) activity of splenic and intrahepatic lymphocytes (IHL) isolated from mice undergoing graft versus host disease, induced by transfer of B6 T cells to major histocompatibility complex (MHC) class I disparate bm1 × B6 F1 mice. Allospecific killing of anti-H-2(bm1) splenic and hepatocyte targets was assessed by 4-h (51)Cr release and 16-h DNA lysis assays, respectively, utilizing spleen cells (SpC) and IHL isolated (1) from sublethally irradiated bm1 × B6 F1 who had received B6 spleen and bone marrow cells, and a control adenovirus (Adv-ßgal) or a TNF inhibitor expressing adenovirus (Adv-TNFi), or (2) from bm1 × B6 F1 recipients of B6, B6.129-Tnfrsf1a(tm1Mak)/J (TNFR1(-/-)), B6.129S2-Tnfrsf1b(tm1Mwm)/J (TNFR2(-/-)), or B6.129S-Tnfrsf1a(tm1Imx) Tnfrsf1b(tm1Imx)/J (TNFR(-/-)) SpC and bone marrow cells, or (3) from in vitro-activated SpC. Splenic and IHL from bone marrow transplant recipients who had received Adv-TNFi at the time of transplant displayed lower allospecific CTL activity than controls. Addition of TNFR-Ig or a TNF antibody before the CTL activity assay further reduced allospecific killing against bm1 SpC blast targets. Both TNF/TNFR1 and TNF/TNFR2 interactions were critical for the development of optimal CTL activity against allospecific hepatocyte targets. Further, TNFR1- and TNFR2-deficient SpC from MHC class I disparate mixed lymphocyte cultures displayed lower CTL activity and expression of effector molecules than control B6 SpC. TNF/TNFR interactions were critical for the development of optimal CTL activity of IHL and splenic cytotoxic T cells against MHC class I disparate SpC blast and hepatocyte targets in MHC class I disparate graft versus host disease.