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Scott D. Wait, Adib A. Abla, Brendan D. Killory, Peter Nakaji and Harold L. Rekate

Object

Hypothalamic hamartomas (HHs) are devastating lesions causing refractory epilepsy, rage attacks, social ineptitude, and precocious puberty. Microsurgical and/or endoscopic resection offers an excellent risk/benefit profile for cure or improvement of epilepsy.

Methods

The authors reviewed a prospective database maintained during the first 7 years of the Barrow Hypothalamic Hamartoma program. They describe and illustrate their surgical methods, and they review data from several previous publications regarding surgical outcome.

Results

To date, the authors have performed surgery in 165 patients for symptomatic HHs. Patients underwent an endoscopic, transcallosal, or skull base approach, or multiple approaches. Twenty-six patients (15.8%) required more than 1 treatment for their HH.

Conclusions

Microsurgical and endoscopic resection of symptomatic HHs are technically demanding but can be performed safely with excellent results and an acceptable risk profile. Meticulous attention to the subtleties of surgical management helps optimize outcomes.

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Adib A. Abla, Scott D. Wait, Jonathan A. Forbes, Sandipan Pati, Roger E. Johnsonbaugh, John F. Kerrigan and Yu-Tze Ng

Object

In this paper, the authors' goal was to describe the occurrence of alternating hypernatremia and hyponatremia in pediatric patients who underwent resection of hypothalamic hamartomas (HHs) for epilepsy. Hypernatremia in patients after pituitary or hypothalamic surgery can be caused by diabetes insipidus (DI), whereas hyponatremia can occur due to a syndrome of inappropriate antidiuretic hormone, cerebral salt wasting, or excessive administration of desmopressin (DDAVP). The triphasic response after surgery in the pituitary region can also explain variations in sodium parameters in such cases.

Methods

One hundred fifty-three patients with HH who underwent surgery were enrolled in a prospective study to monitor outcomes. Of these, 4 patients (2.6%) were noted to experience dramatic alterations in serum sodium values. The medical records of these patients were identified and evaluated.

Results

Patients' ages at surgery ranged from 1.2 to 6.0 years. All patients were girls. Two patients had Delalande Type IV lesions (of 16 total Type IV lesions surgically treated) and 2 had Type III lesions (of 39 total Type III lesions). All patients had a history of gelastic seizures refractory to medication. Seizure frequency ranged from 3 to 300 per day. After surgery, all patients experienced hypernatremia and hyponatremia. The largest fluctuation in serum sodium concentration during hospitalization in a single patient was 53 mEq/L (range 123–176 mEq/L). The mean absolute difference in maximum and minimum sodium values was 38.2 mEq/L.

All patients exhibited an initial period of immediate DI (independent of treatment) after surgery followed by a period of hyponatremia (independent of treatment), with a minimum value occurring between postoperative Days 5 and 8. All patients then returned to a hypernatremic state of DI, and 3 patients still require DDAVP for DI management. A second occurrence of hyponatremia lasting several days without DDAVP administration occurred in 2 patients during their hospitalization between periods of hypernatremia. One patient stabilized in the normal range of sodium values prior to discharge from rehabilitation without the need for further intervention. At last follow-up, 3 patients are seizure-free.

Conclusions

Severe instability of sodium homeostasis with hypernatremia and hyponatremia is seen in up to 2.6% of children undergoing open resection of HH. This risk appears to be related to HH type, with a higher risk for Types III (2 [5.1%] of 39) and IV (2 [12.5%] of 16) lesions. Here, the authors describe alternating episodes of hypernatremia and hyponatremia in the postoperative period following HH surgery. Management of this entity requires careful serial assessment of volume status and urine concentration and will often require alternating salt replacement therapy with DDAVP administration.

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Scott D. Wait, M. Yashar S. Kalani, Andrew S. Little, Giac D. Consiglieri, Jeffrey S. Ross, Matthew R. Kucia, Volker K. H. Sonntag and Nicholas Theodore

Object

Patients who develop a lower-extremity neurological deficit after lumbar laminectomy present a diagnostic dilemma. In the setting of a neurological deficit, some surgeons use MRI to evaluate for symptomatic compression of the thecal sac. The authors conducted a prospective observational cohort study in patients undergoing open lumbar laminectomy for neurogenic claudication to document the MRI appearance of the postlaminectomy spine and to determine changes in thecal sac diameter caused by the accumulation of epidural fluid.

Methods

Eligible patients who were candidates for open lumbar laminectomy for neurogenic claudication at a single neurosurgical center between August 2007 and June 2009 were enrolled. Preoperative and postoperative MRI of the lumbar spine was performed on the same MRI scanner. Postoperative MRI studies were completed within 36 hours of surgery. Routine clinical and surgical data were collected at the preoperative visit, during surgery, and postoperatively. Images were interpreted for the signal characteristics of the epidural fluid and for thecal diameter (region of interest [ROI]) by 2 blinded neuroradiologists.

Results

Twenty-four patients (mean age 69.7 years, range 30–83 years) were enrolled, and 20 completed the study. Single-level laminectomy was performed in 6 patients, 2-level in 12, and 3-level in 2. Preoperative canal measurements (ROI) at the most stenotic level averaged 0.26 cm2 (range 0.0–0.46 cm2), and postoperative ROI at that same level averaged 0.95 cm2 (range 0.46–2.05 cm2). The increase in ROI averaged 0.69 cm2 (range 0.07–1.81 cm2). Seven patients (35%) had immediate postoperative weakness in at least 1 muscle group graded at 4+/5. The decline in examination was believed to be effort dependent and secondary to discomfort in the acute postoperative period. Those with weakness had smaller increases in ROI (0.51 cm2) than those with full strength (0.78 cm2, p = 0.1599), but none had evidence of worsened thecal compression. On the 1st postoperative day, 19 patients were at full strength and all patients were at full strength at their 15-day follow-up. The T1-weighted epidural fluid signal was isointense in 19 of the 20 patients. The T2-weighted epidural fluid signal was hyperintense in 9, isointense in 4, and hypointense in 7 patients.

Conclusions

Immediately after lumbar laminectomy, the appearance of the thecal sac on MRI can vary widely. In most patients the thecal sac diameter increases after laminectomy despite the presence of epidural blood. In this observational cohort, a reduction in thecal diameter caused by epidural fluid did not correlate with motor function. Results in the small subset of patients where the canal diameter decreased due to epidural fluid compression of the thecal sac raises the question of the utility of immediate postoperative MRI.

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Ryszard M. Pluta, Scott D. Wait, John A. Butman, Kathleen A. Leppig, Alexander O. Vortmeyer, Edward H. Oldfield and Russell R. Lonser

Hemangioblastomas are histologically benign neoplasms that occur sporadically or as part of von Hippel–Lindau disease. Hemangioblastomas may occur anywhere along the neuraxis, but sacral hemangioblastomas are extremely rare. To identify features that will help guide the operative and clinical management of these lesions, the authors describe the management of a large von Hippel–Lindau disease–associated sacral hemangioblastoma and review the literature.

The authors present the case of a 38-year-old woman with von Hippel–Lindau disease and a 10-year history of progressive back pain, as well as left lower-extremity pain and numbness. Neurological examination revealed decreased sensation in the left S-1 and S-2 dermatomes. Magnetic resonance imaging demonstrated a large enhancing lesion in the sacral region, with associated erosion of the sacrum. The patient underwent arteriography and embolization of the tumor and then resection. The histopathological diagnosis was consistent with hemangioblastoma and showed intrafascicular tumor infiltration of the S-2 nerve root. At 1-year follow-up examination, pain had resolved and numbness improved.

Sacral nerve root hemangioblastomas may be safely removed in most patients, resulting in stabilization or improvement in symptomatology. Generally, hemangioblastomas of the sacral nerve roots should be removed when they cause symptoms. Because they originate from the nerve root, the nerve root from which the hemangioblastoma originates must be sacrificed to achieve complete resection.