Survival in patients with paraaortic lymph node metastases from endometrial adenocarcinoma clinically limited to the uterus.

PURPOSE: The purpose of this study was (a) to evaluate the incidence of paraaortic lymph node metastasis from adenocarcinoma of the endometrium clinically limited to the uterus (1971 FIGO Stages I and II) and (b) to report the 5 year disease-free survival of patients with histologically documented paraaortic lymph node metastasis from endometrial adenocarcinoma clinically limited to the uterus treated on two separate protocols. METHODS AND MATERIALS: From June 1979 to June 1990, 109 patients underwent staging paraaortic lymphadenectomy or paraaortic lymph node biopsy at the time of total abdominal hysterectomy and bilateral salpingo-oophorectomy for adenocarcinoma of the endometrium clinically limited to the uterus. Patients with histologically documented paraaortic lymph node metastasis were treated on two protocols: (a) pelvic radiation (5,040 cGy) plus progestins or (b) pelvic radiation therapy (5,040 cGy) plus paraaortic radiation (4,500 cGy). RESULTS: Paraaortic lymph node metastases was primarily associated with grade 3 tumors (34.4%) and deep myometrial invasion (42%) and was present in 17.4% (19) of 109 patients. None of the women treated with pelvic radiation therapy and progestins survived five years disease-free. In contrast, the 5 year disease-free survival was 27% for patients treated by pelvic and paraaortic radiation. CONCLUSIONS: Since all patients with macroscopic metastases to the paraaortic lymph nodes developed recurrent cancer and only a small percentage of those with microscopic metastases to the paraaortic lymph nodes survived disease-free at 5 years, improved survival for patients with paraaortic lymph node metastases will necessitate the addition of effective cytotoxic chemotherapy to pelvic and paraaortic radiation.

Illusory continuity of tonal and infratonal periodic sounds.

Temporal induction can restore masked or obliterated portions of signals so that tones may seem continuous when alternated with sounds having appropriate spectral composition and intensity. The upper intensity limits for the induction of tones (pulsation thresholds) are related to masking functions and have been used to define the characteristics of frequency domain (place) analysis of tones. The present study has found that induction also occurs for infratonal periodic sounds that require a time domain analysis for perception of acoustic repetition. Limits for temporal induction were determined for iterated frozen noise segments from 10-2000 Hz alternated with a louder on-line noise. Masked thresholds were also obtained for the pulsed signals presented along with continuous noise, and it was found that the relation between induction limits and masking changed with frequency. The results obtained for induction and masking are discussed in terms of general principles governing restoration of obliterated sounds.

Effects of serial lesions of somatosensory cortex and further neodecortication on tactile retention in rats.

Four groups of rats with bilateral lesions of somatosensory cortex and one of animals sustaining only sham operations were tested for retention of a difficult tactile discrimination. Two of the lesion groups had serial ablations, in one case with interoperative testing, and two had one-stage lesions. Bilateral ablations of somatosensory cortex severely retarded retention in all lesion groups relative to the control group and serial and one-stage groups did not differ from each other. The sham operated rats then experienced lesions of cortex anterior and posterior to the somatosensory areas. These lesions only marginally affected retention. Somatosensory cortex then was ablated and severe performance decrements were seen. Removal of additional neocortex in animals that previously had relearned the discrimination after somatosensory cortex lesions also resulted in very poor retention. These data demonstrate the importance of the somatosensory cortex in mediating tactile discriminations and suggest that non-somatosensory cortex may play a role in recovery after somatosensory cortical lesions.