Object The purpose of this study was to validate a new prognostic index for patients with brain metastases. This index, the Graded Prognostic Assessment (GPA), is based on an analysis of 1960 patients whose data were extracted from the Radiation Therapy Oncology Group (RTOG) database. The GPA is based on 4 criteria: age, Karnofsky Performance Scale score, number of brain metastases, and the presence/absence of extracranial metastases. Each of the 4 criteria is given a score of 0, 0.5, or 1.0, so the patient with best prognosis would have a GPA score of 4.0. Methods Between April 2005 and December 2006, 140 eligible patients with brain metastases were treated at the Gamma Knife Center at the University of Minnesota. The GPA score was calculated for each patient, and the score was then correlated with survival. Survival duration was calculated from the date treatment began for the brain metastases. Eligibility criteria included patients treated with whole-brain radiation therapy, stereotactic radiosurgery, or both. Results The median survival time in months observed in the RTOG and Minnesota data by GPA score was as follows: GPA 3.5–4.0, 11.0 and 21.7; GPA 3.0, 8.9 and 17.5; GPA 1.5–2.5, 3.8 and 5.9; and GPA 0–1.0, 2.6 and 3.0, respectively. Conclusions The University of Minnesota data correlate well with the RTOG data and validate the use of the GPA as an effective prognostic index for patients with brain metastases. Clearly, not all patients with brain metastases have the same prognosis, and treatment decisions should be individualized accordingly. The GPA score does appear to be as prognostic as the RPA and is less subjective (because the RPA requires assessment of whether the primary disease is controlled), more quantitative, and easier to use and remember. A multiinstitutional validation study of the GPA is ongoing.
We examined binding to excitatory amino acid and inhibitory amino acid receptors in frozen hippocampal sections prepared from surgical specimens resected from 8 individuals with medically refractory temporal lobe epilepsy. The excitatory receptors studied included N-methyl-D-aspartate (NMDA), strychnine-insensitive glycine, phencyclidine, and quisqualate. The inhibitory receptors studied were gamma-aminobutyric acid type A (GABAA) and benzodiazepine. Excitatory and inhibitory amino acid receptor binding were differentially altered in the patients with temporal lobe epilepsy in comparison to 8 age-comparable autopsy control subjects, and changes in receptor binding were regionally selective in four areas. Binding to phencyclidine receptors associated with the NMDA channel was reduced by 35 to 70% in all regions in the hippocampi of the patients. In contrast, binding to the NMDA recognition site and its associated glycine modulatory site was elevated by 20 to 110% in the cornu ammonis (CA) 1 area and dentate gyrus of the hippocampus of the patients. Binding to these sites was unaffected in area CA4. Binding to the quisqualate-type excitatory amino acid receptor was unchanged in all regions except the stratum lacunosum moleculare CA1, where it was increased by 63%. GABAA and benzodiazepine receptor binding was reduced by 20 to 60% in CA1 and CA4, but unchanged in dentate gyrus. The data indicate that excitatory and inhibitory amino acid receptors are altered in the hippocampus of patients with temporal lobe epilepsy.
We performed interictal [18F]-2-fluoro-2-deoxy-D-glucose positron emission tomography in 17 patients with well-defined unilateral anterior mesial temporal epileptogenic foci as determined by EEG procedures. Sixteen of these patients subsequently underwent surgical resection of the epileptogenic focus. We measured local cerebral metabolic rates for glucose in mesial and lateral temporal structures and compared them with metabolic rates for analogous regions in 16 healthy normal volunteers and the contralateral hemisphere of the epileptic patients. We found relative hypometabolism ipsilateral to the seizure focus more frequently and to a greater degree in the lateral than in the mesial temporal cortex. Since the physiologic abnormalities involved mesial temporal structures, this observation suggests that functional pathways exist between mesial and lateral temporal cortex normally and that these pathways are altered in epilepsy of mesial temporal origin. Hypometabolism did not correlate well with histologic abnormalities in the surgical specimens.
Despite improved brain-stem imaging by magnetic resonance and high-resolution x-ray computerized tomography, definitive diagnosis and therapy of intrinsic lesions of the brain stem require histological verification. A stereotaxic approach to brain-stem lesions provides a high yield of positive histological diagnosis with a low incidence of morbidity. A series of 14 stereotaxic procedures performed on 12 patients with intrinsic lesions of the mesencephalon, pons, and medulla is reviewed. A detailed description of the transfrontal approach used by the authors is presented. Definitive pathological diagnosis was obtained in all patients. There was no operative mortality and only one case of permanent neurological deficit. The significance of accurate histological diagnosis in the therapy of brain-stem lesions is discussed.
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