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Purpose The purpose of the current study was to investigate whether prophylactic cranial irradiation (PCI) reduces the incidence of symptomatic brain metastases in patients with stage III non-small-cell lung cancer (NSCLC) treated with curative intention. Patients and Methods Patients with stage III NSCLC-staged with a contrast-enhanced brain computed tomography or magnetic resonance imaging-were randomly assigned to either observation or PCI after concurrent/sequential chemoradiotherapy with or without surgery. The primary end point-development of symptomatic brain metastases at 24 months-was defined as one or a combination of key symptoms that suggest brain metastases-signs of increased intracranial pressure, headache, nausea and vomiting, cognitive or affective disturbances, seizures, and focal neurologic symptoms-and magnetic resonance imaging or computed tomography demonstrating the existence of brain metastasis. Adverse effects, survival, quality of life, quality-adjusted survival, and health care costs were secondary end points. Results Between 2009 and 2015, 175 patients were randomly assigned: 87 received PCI and 88 underwent observation only. Median follow-up was 48.5 months (95% CI, 39 to 54 months). Six (7.0%) of 86 patients in the PCI group and 24 (27.2%) of 88 patients in the control group had symptomatic brain metastases ( P = .001). PCI significantly increased the time to develop symptomatic brain metastases (hazard ratio, 0.23; [95% CI, 0.09 to 0.56]; P = .0012). Median time to develop brain metastases was not reached in either arm. Overall survival was not significantly different between both arms. Grade 1 and 2 memory impairment (26 of 86 v seven of 88 patients) and cognitive disturbance (16 of 86 v three of 88 patients) were significantly increased in the PCI arm. Quality of life was only decreased 3 months post-PCI and was similar to the observation arm thereafter. Conclusion PCI significantly decreased the proportion of patients who developed symptomatic brain metastases with an increase of low-grade toxicity.

(1) bleeding from the abnormal vessels causing haemoptysis or a haemothorax, both of which are potentially fatal; and (2) interruption of the capillary filter of the lung so that emboli, normally trapped in the pulmonary capillaries, can enter the systemic circulation via the pulmonary arteriovenous malformations.4 Thrombi arising in the malformation itself may also cause systemic emboli.5 Thus, up to 56% of patients with pulmonary arteriovenous malformations report a history of stroke or transient ischaemic attack.6`8 Brain abscess occurs in 5-14% of patients with a pulmonary arteriovenous malformation as a result of septic emboli.4910It is generally accepted that these risks justify treatment of pulmonary arteriovenous malformations, even when asymptomatic, if the diameter of the feeding vessels is more than 3 mm.'" Disadvantages of surgical treatment are loss of normal lung tissue surrounding the pulmonary arteriovenous malformations and morbidity associated with thoracotomy. Nowadays, embolisation of the feeding vessel(s) with silicone balloons or metal coils is an accepted mode of treatment'2-'4 and usually eliminates the need for thoracotomy. Whether coils or balloons are superior has not yet been studied and still depends on personal preference and experience. ' Advantages and disadvantages of both methods have been reviewed elsewhere.'5 In a recent series from a large thoracic unit the complications of balloon embolisation led the authors to conclude that "conservative surgical resection remains the treatment of choice". "Although many reports concerning embolisation of pulmonary arteriovenous malformations have been published, data on long term results are limited. We therefore present our long term results oftreatment ofpulmonary arteriovenous malformations by embolisation. MethodsThirty two patients with pulmonary arteriovenous malformations have been treated with embolisation during the last five years, 31 of whom had HHT. Fifteen patients were found during a screening programme involving family members of patients with HHT. Nineteen of the 31 patients had multiple pulmonary arteriovenous malformations. Three had undergone surgery prior to embolisation and were treated for new or enlarging pulmonary arteriovenous malformations; all three had HHT. The signs and symptoms caused by the pulmonary arteriovenous malformations are listed in table 1. Ten patients were asymptomatic.Before and after embolisation arterial oxygen tension breathing air (Pao2) and right to left shunt were measured in all patients while semirecumbent. The 100% oxygen method was used to calculate the shunt fraction,'6 values of <5% being considered normal. Every six months chest radiography, Pao2, and right to left shunt were measured for follow up.