A 41-year-old, nonsmoking female was initially diagnosed with metastatic TTF-1 positive lung adenocarcinoma in 2011. She underwent radiotherapy for her primary lesion as well as several lines of systemic treatments with initially positive but later mixed response. In March 2013, the patient reported symmetric sensory symptoms with numbness and tingling around her lips and limbs which eventually caused impaired balance. Brain MRI revealed more than 20 supra and infratentorial metastases including one to the left in the pons (M1) and signs of leptomeningeal carcinomatosis. The lesion in the pons (M1) had central necrosis and measured 25 × 30 × 26 mm at the time of diagnosis. The patient started high-dose systemic corticosteroid therapy and was treated the same month with whole brain radiation therapy (WBRT) with a dose fractionation of 4 Gy delivered over 5 consecutive days (4 Gy × 5). A follow-up MRI in July 2013 revealed volume reduction of all intracranial metastases including the pontine lesion (M1). The ensuing follow-up MRI in October 2013 demonstrated progression of M1 from 19 mm to 27 mm and slight V4 floor compression without hydrocephalus. A previously known small metastasis in the left lateral occipital lobe (M2) showed signs of progression as well. All other metastases were deemed under control at this point. To avoid further neurological impairment and V4 obstruction due to tumor growth and/or posttreatment ARE, M1 was treated by 3R in November 2013 [].\nAt the time of GKRS 1, M1 proved larger (9.2 cm3) with further perilesional edema and more apparent V4 floor compression, though still without signs of hydrocephalus. M2 had also grown slightly (from 10 to 12 mm in diameter) and was treated by SF-GKRS with 21 Gy to the 50% isodose prescription line. Apart from slight fatigue, left-sided facial numbness, and tingling the patient reported no other symptoms at the time of GKRS 1; at this stage, her KPS was estimated to be 90 and the RPA to be 1–2.\nDespite ongoing cortisone treatment, the perilesional edema remained nearly unchanged between GKRS 1 and GKRS 3; cortisone treatment was discontinued shortly after completion of GKRS 3. Nevertheless, V4 proved slightly wider at the time of GKRS 3 (from 0.9 cm3 at GKRS 1 to 1.2 cm3 at GKRS 3) and the tumor had decreased approximately 18% in volume (from GKRS 1 to GKRS 3). At 1-month follow-up, the patient was almost asymptomatic (KPS 90–100); the corresponding MRI revealed a significant reduction of tumor volume of approximately 67% (from 9.2 cm3 at GKRS 1 to 3.1 cm3 at the first follow-up) as well as renormalization of V4 boundaries (0.9 cm3 to 1.7 cm3) [; ].\nM1 developed a local ARE radiologically verified by MRI (follow-ups between March and November 2014) as well as 18F-FDG PET-CT (April and December 2014), which subsequently yielded without cortisone 6 months later (October 2014). Despite the above, the patient remained next to asymptomatic from her treated lesion during the follow-up. Unfortunately, systemic treatment eventually failed; the patient underwent SF-GKRS for several metastases (distant to M1 and M2 boundaries) from April to November 2014; her condition deteriorated steadily in December 2014, and she subsequently died in February 2015 (15 months after 3R) mainly due to intrathoracic tumor progression. Her quality of life was overall good from the time of 3R treatment and 12 months onwards.[]
A 62-year-old female patient was diagnosed in 2005 with ovarian carcinoma. She underwent surgery, several lines of antitumoral treatment, and regional fractionated radiotherapy prior to developing metastases to regional lymph nodes as well as peritoneal carcinomatosis (2008). In January 2016, the patient presented with 2-week history of nausea, vomiting, impaired balance and speech, severe swallowing difficulties, and sensory symptoms. The brain MRI demonstrated a large, solitary, 20-mm metastasis in the upper part of the medulla oblongata (M1) without significant perilesional edema, yet compressing the foramina of Luschka and Magendie with signs of mild hydrocephalus []. Corticosteroid therapy was initiated shortly thereafter. Microsurgical removal/debulking of the metastasis were deemed not feasible and 3R was offered after multidisciplinary in-hospital discussion. At the time of GKRS 1 in February 2016, KPS was estimated to be 60 and RPA 3. The corresponding dose fractionation schedule is described in . No tumor volume reduction or V4 decompression was noted between GKRS 1 and GKRS 3. A follow-up MRI at 4 weeks revealed a 54% decrease in the size of M1 (4.8 cm3 at GKRS 1 to 2.2 cm3 at follow-up). V4 volume increased (1.56 cm3 at GKRS 1 to 2 cm3 at follow-up), and the foramina of Luschka and Magendie were less compressed []. There was no evidence of hydrocephalus. The patient's neurological condition also improved dramatically at this time and KPS was estimated to be 70. The dysphagia, nausea, and vomiting disappeared, and she could articulate much better. Nevertheless, no considerable improvement in balance was reported. The patient continued systemic antitumoral treatment. Consecutive, initially monthly and later bimonthly radiological follow-ups until September 2016 (7 months after 3R) showed further volume decrease of M1. However, the patient developed mild radiation-induced perilesional edema (assessed as ARE) 5 months after treatment which slowly progressed until her last MRI at 7 months (September 2016) though without evidence of hydrocephalus. At this time, the patient was experiencing mild facial numbness almost solely limited to her right cheek and the right side of the jaw. The patient was also experiencing some more fatigue and balance impairment than usual although it was difficult to assess whether it was caused by the lesion itself and/or other factors such as aggressive systemic tumor progression, ongoing systemic treatment, and steroids. Nevertheless, despite the presence of perilesional edema, we assessed her neurological status and quality of life in relation to M1 as stable. She died 7 months after completion of 3R-treatment due to aggressive extracranial tumor disease progression.