Stereotactic radiosurgery for cavernous malformations: Kjellberg's experience with proton beam therapy in 98 cases at the Harvard Cyclotron.

OBJECTIVE: The lack of treatment options for surgically inaccessible cavernous malformations has made radiosurgery a possible alternative to conservative management. The few previous reports of radiosurgical efficacy have been limited by small numbers, short follow-up, or lack of attention to the full spectrum of end points, including neurological disability. In an attempt to elucidate the risk-to-benefit ratio of radiosurgery for cavernous malformations, we undertook a retrospective analysis of of 95 patients with 98 lesions treated by the late Raymond N. Kjellberg. METHODS: Patients were followed for an average of 5.4 years (range, 0.3-12.3 yr), and data regarding hemorrhage, seizure, neurological disability, and incidence of radiation-induced complications were gathered. RESULTS: The analysis revealed a drop in annual hemorrhage rates from 17.3% per lesion per year before treatment to 4.5% per lesion per year after a latency period of 2 years. Improvement in seizure control was evident. However, a 16% incidence of permanent neurological deficit and a 3% mortality rate were attributable to radiographically confirmed radiation-induced complications. Neurological disability scores, measured by the modified Rankin disability scale, indicated a significant decline in neurological functioning during the follow-up interval, a result of the combined effects of radiation-related injury, hemorrhage, and clinical progression of the lesion. CONCLUSION: We conclude that although radiosurgery does seem to reduce hemorrhage, there is potential for complications and continued lesion progression after radiosurgery. These risks and benefits must be carefully balanced against the natural history of untreated lesions if the use of radiosurgery is considered.

One-year outcome after decompressive surgery for massive nondominant hemispheric infarction.

OBJECTIVE: Massive cerebral infarction is often accompanied by early death secondary to transtentorial herniation. We have tested the hypothesis that decompressive hemicraniectomy for massive nondominant cerebral infarction is lifesaving in a series of 14 patients presenting with right hemispheric infarction and clinical signs of uncal herniation and impending death. We have further analyzed, in prospective follow-up examinations, the levels of physical, psychiatric, and social disabilities in these patients. METHODS: The methods used included retrospective analysis to determine rates of immediate mortality and morbidity after surgical intervention. Prospective follow-up data were obtained to determine the level of recovery in surviving patients after 1 year. Standardized measures of outcome to assess physical, psychiatric, and social recovery included the Barthel Index, Zung Depression Scale, and Reintegration to Normal Living Index. RESULTS: With decompressive hemicraniectomy, we were able to prevent death secondary to transtentorial herniation in all cases; 11 patients experienced long-term survival after the procedure, and three deaths were related to non-neurological causes. We observed that 8 of the 11 surviving patients were at home, were functioning with minimal to moderate assistance, and had Barthel scores greater than 60. The remaining three patients were severely disabled. Seven of the 11 survivors were able to walk at 1 year after undergoing the procedure. Depression and failure to reintegrate socially were experienced by most patients. CONCLUSION: This series confirms the lifesaving nature of hemicraniectomy in patients deteriorating because of cerebral edema after infarction. In patients younger than 50 years, recovery to a state of near-independence is possible.

Effect of intravenous sodium nitroprusside on cerebral blood flow and intracranial pressure.

Local cerebral blood flow was measured with the hydrogen clearance technique during intravenous infusion of nitroprusside in monkeys. Concentrations of the drug required to reduce the mean arterial blood pressure by less than 40% resulted in no significant change or only a slight increase in regional cerebral blood flow. Larger doses, however, produced a loss of cerebral autoregulation, thereby inducing a drop in cerebral blood flow. Intracranial pressure rose proportionately to the nitroprusside dose during the infusion.