Neurosurgery
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We reviewed the data of children with high-stage primitive neuroectodermal tumors (medulloblastomas) who were treated on Children's Cancer Group-921 protocol to evaluate the correlation between tumor resection and prognosis. Patients enrolled in the study had either tumors that were operatively categorized to be Chang tumor stage 3b or 4, postoperative residual tumors > 1.5 cm2, or evidence of tumor dissemination (Chang metastasis Stages [M Stages] 1-4) at diagnosis. Resections were analyzed in two ways, as follows: 1) by the extent of resection (percent of the tumor that was removed), as estimated by the treating neurosurgeon; and 2) by the extent of residual tumor (how much of the tumor was left), as estimated from postoperative scans. ⋯ However, adjusting for other factors, extent of residual tumor was important; PFS was 20% (standard error, 14%) better at 5 years in children with no dissemination (M Stage 0) who had < 1.5 cm2 of residual tumor (P = 0.065) and was 24% (standard error, 14%) better at 5 years in children > 3 years old with no tumor dissemination (M Stage 0) and with < 1.5 cm2 residual tumor (P = 0.033). On the basis of our observations, we conclude that extent of tumor resection, as estimated by the neurosurgeon, does not correlate with outcome but that extent of residual tumor does correlate with prognosis in certain children (those who are > 3 years old, with no tumor dissemination). In contrast to age and M stage, the major factors associated with outcome, residual tumor is an important variable in outcome, one that neurosurgeons can control.
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Case Reports Randomized Controlled Trial Clinical Trial
Intrathecal octreotide for relief of intractable nonmalignant pain: 5-year experience with two cases.
Somatostatin is distributed in the substantia gelatinosa in the dorsal horn of the spinal cord, and its application has been found to produce an inhibitory effect on nociceptive neurons. Although intraspinal administration of somatostatin-14 produces pain relief in patients with cancer and in postoperative patients, its short half-life limits its clinical usefulness. ⋯ This article describes the 5-year clinical course of two patients receiving intrathecal octreotide for severe, intractable nonmalignant pain. Included in this description are the results of blinded, randomized "N of 1" trials conducted in each of these patients.
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Ischemia is one of the major factors causing secondary brain damage after severe head injury. We have investigated the value of continuous partial pressure of brain tissue oxygen (PbrO2) monitoring as a parameter for cerebral oxygenation in 22 patients with severe head injury (Glasgow Coma Scale score, < or = 8). Jugular bulb oxygenation, intracranial pressure, and cerebral perfusion pressure were simultaneously recorded. ⋯ The early occurrence of ischemia after head injury can be monitored on a continuous basis. Deficiency of oxygen autoregulatory mechanisms can be demonstrated, and their occurrence is inversely related to outcome. For practical clinical use, the method seemed to be superior to jugular oximetry.
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We described a new ventricular catheter that is the combination of a "classic" ventricular catheter with a piezo-resistive transducer at its tip. The device allows parallel recordings of intraventricular fluid pressure via a chip and a fluid-filled external transducer, drainage of cerebrospinal fluid from the ventricle or injection of fluid into the ventricle with simultaneous monitoring of intracranial pressure, and recording of brain tissue pressure in cases of misplacement or dislocation of the ventricular catheter or in cases of progressively narrowing ventricles caused by brain edema. Clinical tests in various situations at different pressure ranges (total recording time, 1356 h in 13 patients) gave excellent correlations of both pressures. Application of the device is especially indicated in clinical situations in which pressure-controlled drainage is desirable, occlusion of ventricular bolts is likely, or pressure-volume tests are needed.
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Hyponatremia is frequently seen in neurosurgical patients and is often attributed to inappropriate secretion of antidiuretic hormone. A number of studies in recent years have shown that hyponatremia in many patients with intracranial disease may actually be caused by cerebral salt wasting, in which a renal loss of sodium leads to hyponatremia and a decrease in extracellular fluid volume. The appropriate treatment of cerebral salt wasting fluid and salt replacement, is opposite from the usual treatment of hyponatremia caused by inappropriate secretion of antidiuretic hormone. This review summarizes the evidence in favor of cerebral salt wasting in patients with intracranial disease, examines the possible mechanisms responsible for this phenomenon, and discusses methods for diagnosis and treatment.