Paragangliomas of the cauda equina are rare neuroendocrine tumors. Four cases of nonsecreting paraganglioma of the cauda equina, preoperatively misdiagnosed as neurinoma, are presented with an emphasis on the correlation between magnetic resonance imaging findings and pathological features. Although it is difficult to correctly diagnose paraganglioma preoperatively for intradural extramedullary tumors, especially in the cauda equina, paraganglioma should be included in differential diagnoses.
Radiation-induced glioblastoma multiforme (GBM) is a rare complication of radiotherapy. The authors report such a case occurring 10 years after treatment of cerebellar medulloblastoma. The patient was a 15-year-old boy who had undergone a gross-total removal of a medulloblastoma and received radiation therapy at the age of 5 years. He had experienced no tumor recurrences for 10 years until a new enhancing mass was found at the original site of the medulloblastoma. Following its resection the new lesion was found to be a GBM and there was no evidence of a medulloblastoma. The second tumor developed at the same site as the previous one after a sufficient latent period and fulfilled the criteria for a radiation-induced neoplasm. The original tumor cells expressed synaptophysin without p53 overexpression, a characteristic feature of medulloblastomas. In contrast, cells from the later tumor expressed glial fibrillary acidic protein and p53 but not synaptophysin. A sequence analysis of the p53 gene showed deletion at codon 233 and a C to G transition at codon 278 in the GBM but no mutation in the medulloblastoma. A GBM specimen revealed no amplification of the epidermal growth factor receptor compared with a normal control specimen. In conclusion, the clinical features of a radiation-induced GBM are similar to that of the primary GBM, whereas its genetic alterations render it a secondary GBM. These findings indicate that radiation-induced GBM should be considered a distinct clinical entity.
Purpose In previous studies, insulin reversed the cardiac toxicity gradually induced by a continuous infusion of bupivacaine. In this randomized controlled study, we intended to simulate a more relevant clinical situation by injecting bupivacaine rapidly as a bolus to induce suddenonset circulatory collapse in dogs. We then evaluated the insulin effect.Methods Bupivacaine (10 mgÁkg -1 iv) was rapidly administered intravenously to 12 dogs. At the onset of circulatory collapse (defined as a mean arterial pressure [MAP] of 30 mmHg), external chest compression was initiated. Insulin (2 UÁkg -1 iv) was given to the insulinglucose (IG) group (n = 6) and the same volume of 0.9% saline was given to the control (C) group (n = 6). The primary outcome was successful resuscitation defined as both MAP C 60 mmHg and sinus rhythm on an electrocardiogram that lasted C 60 sec. Hemodynamic and blood variables were measured, including cardiac output and electrocardiogram intervals. Results All IG dogs were successfully resuscitated within 15 (3) min, whereas none of the control dogs were resuscitated (P = 0.002). After circulatory collapse, the average MAP was higher in group IG than in group C (P = 0.006). Conclusion Insulin effectively reversed the sudden-onset circulatory collapse in dogs caused by an intravenous bolus injection of bupivacaine.
RésuméObjectif Dans des e´tudes pre´ce´demment publie´es, il a e´ted e´montre´que l'insuline neutralisait la toxicite´cardiaque progressivement induite par une perfusion continue de bupivacaı¨ne. Dans cette e´tude randomise´e contrôle´e, nous avons tente´de simuler une situation clinique plus pertinente en injectant rapidement de la bupivacaı¨ne en bolus afin d'induire un collapsus circulatoire subit chez les chiens. Nous avons ensuite e´value´l'effet de l'insuline. Méthode De la bupivacaı¨ne (10 mgÁkg -1 iv) intraveineuse a e´te´rapidement administre´e chez 12 chiens. Au de´but du collapsus circulatoire (de´fini tel qu'une tension arte´rielle moyenne [TAM] de 30 mmHg), un massage cardiaque a e´teÁ uthor contributions Mi-Hyun Kim, Kook-Hyun Lee, and ChongSoo Kim helped design the study.
Bupivacaine inhibits cardiac conduction and contractility. Insulin enhances cardiac repolarization and myocardial contractility. We hypothesizes that insulin therapy would be effective in resuscitating bupivacaine-induced cardiac toxicity in rabbits. Twelve rabbits were tracheally intubated and midline sternotomy was performed under general anesthesia. Cardiovascular collapse (CVC) was induced by an IV bolus injection of bupivacaine 10 mg/kg. The rabbits were treated with either saline (control) or insulin injection, administered as a 2 U/kg bolus. Internal cardiac massage was performed until the return of spontaneous circulation (ROSC) and the time to the return of sinus rhythm (ROSR) was also noted in both groups. Arterial blood pressure, and electrocardiography were continuously monitored for 30 min and plasma bupivacaine concentrations at every 5 min. The ROSC, ROSR and normalization of QRS duration were attained faster in the insulin-treated group than in the control group. At the ROSC, there was a significant difference in bupivacaine concentration between two groups. Insulin facilitates the return of myocardial contractility and conduction from bupivacaine-induced CVC in rabbits. However, recovery of cardiac conduction is dependent mainly on the change of plasma bupivacaine concentrations.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.