ABSTRACT
BACKGROUND: Studies reporting SBRT outcomes in oligometastatic patients with adrenal gland metastases (AGM) are limited. Herein, we present a multi-institutional analysis of oligometastatic patients treated with SBRT for AGM. MATERIAL/METHODS: The Consortium for Oligometastases Research (CORE) is among the largest retrospective series of patients with oligometastases. Among CORE patients, those treated with SBRT for AGM were included. Clinical and dosimetric data were collected. Adrenal metastatic burden (AMB) was defined as the sum of all adrenal GTV if more than one oligometastases is present.Competing risk analysis was used to estimate actuarial cumulative local recurrence (LR) and widespread progression (WP). Kaplan-Meier method was used to report overall survival (OS), local recurrence-free survival (LRFS), and progression-free survival (PFS). Treatment related toxicities were also reported. RESULTS: The analysis included 47 patients with 57 adrenal lesions. Median follow-up was 18.2 months. Median LRFS, PFS, and OS were 15.3, 5.3, and 19.1 months, respectively. A minimum PTV dose BED10 > 46 Gy was associated with an improved OS and LRFS. A prescribed BED10 > 70 Gy was an independent predictor of a lower LR probability. AMB>10 cc was an independent predictor of a lower risk for WP. Only one patient developed an acute Grade 3 toxicity consisting of abdominal pain. CONCLUSION: SBRT to AGM achieved a satisfactory local control and OS in oligometastatic patients. High minimum PTV dose and BED10 prescription doses were predictive of improved LR and OS, respectively. Prospective studies are needed to determine comprehensive criteria for patients SBRT eligibility and dosimetric planning.
ABSTRACT
Pseudobulbar mutism is rarely attributed to bilateral discrete posterior limb internal capsule-medial globus pallidus infarction. Few cases of bilateral anterior choroidal (AchA) artery territory infarction have been reported. We present 8 patients with ischaemic stroke in this location and vascular distribution who have a characterizable syndrome. All had the abrupt onset of inability to speak, swallow or phonate, accompanied by varying degrees of facial diplegia, hemiparesis, hemisensory loss, lethargy, neglect and change in affect. The appearance of clinical signs depends upon the presence of a new infarct contralateral to an older lesion in mirror position. The pathogenesis and progression of neurological deficit appears to be intimately related to hypertension. The role of intrinsic intracranial vascular pathology related to diabetes mellitus, embolism of cardiac origin and atherosclerosis is currently undefined. The prognosis for recovery is poor. Half of our patients died within a year of onset of symptoms. Capsular pseudobulbar mutism is recognized by the abrupt appearance of neurological deficit consistent with internal capsular pathology and is confirmed by CT scan or MRI.
