Diabetes insipidus (DI) after endoscopic transsphenoidal surgery (ETSS) can lead to increased morbidity, longer hospital stays, and increased medication requirements. Predicting which patients are at high risk for developing DI can help direct services to ensure adequate care and follow-up. The objective of this study was to review our institution's experience with ETSS and determine which clinical/laboratory variables are associated with DI in this patient population. The authors wanted to see if there was an easily determined single value that would help predict which patients develop DI. This represents the largest North American series of this type. We retrospectively reviewed the charts of patients who had undergone ETSS for resection of sellar and parasellar pathology between 2006 and 2011. We examined patient and tumor characteristics and their relationship to postoperative DI. Out of 172 endoscopic transsphenoidal surgeries, there were 15 cases of transient DI (8.7%) and 14 cases of permanent DI (8.1%). Statistically significant predictors of postoperative DI (p < 0.05) included tumor volume and histopathology (Rathke's cleft cyst and craniopharyngioma). Significant indicators of development of DI were postoperative serum sodium, preoperative to postoperative change in sodium level, and urine output prior to administration of 1-deamino-8-D-arginine vasopressin. An increase in serum sodium of ≥2.5 mmol/L is a positive marker of development of DI with 80% specificity, and a postoperative serum sodium of ≥145 mmol/L is a positive indicator with 98% specificity. Identifying perioperative risk factors and objective indicators of DI after ETSS will help physicians care for patients postoperatively. In this large series, we demonstrated that there were multiple perioperative risk factors for the development of DI. These findings, which are consistent with other reports from microscopic surgical series, will help identify patients at risk for diabetes insipidus, aid in planning treatment algorithms, and increase vigilance in high risk patients.

HOD should be recognized as a possible complication of surgery within the brainstem and must be diagnosed promptly so that patients can be appropriately counseled and symptoms can be treated.

N 1958, Nelson et al. 72 first described the appearance of an ACTH-producing tumor after bilateral adrenalectomy for Cushing disease. Dr. Don H. Nelson (Fig. 1) was a fellow in endocrinology and had already done considerable basic research in adrenal physiology when he initially reported the syndrome that now bears his name. In the original paper, the authors indicated that the syndrome was characterized by hyperpigmentation, sellar mass demonstrated by an enlarged sella turcica on skull radiographs, and increased plasma ACTH levels. 72 Two years later, Nelson and colleagues 73 had compiled the information obtained in nine additional patients with the same characteristics and findings as the patient in the initial case description. This clinical syndrome was initially known as postadrenalectomy syndrome but by 1962 became known as Nelson syndrome. 56 Although the early definitions of this syndrome are paramount in the history of Nelson syndrome, the complete story involves the history of the treatment and diagnosis of Cushing disease and Dr. Nelson's contributions to the fields of endocrinology and neurosurgery.

Radical resection of giant-cell tumors is generally agreed to be the best treatment option. However, complete resection is often not a feasible option for tumors in the cervical spine because of involvement of critical neurovascular structures. In these cases, the benefits of radiotherapy to reduce the risk of local recurrence may well outweigh concerns about the treatment's theoretical risks.