We report on a 64-year-old woman who initially presented to the emergency department with complaints of chest pain following a motor vehicle crash. A CT incidentally found renal abnormalities, and a postnephrectomy biopsy confirmed renal cell carcinoma. The patient was asymptomatic at that time and remained so for ten months, after which she visited her primary care physician with complaints of mild intermittent headaches and difficulty with balance. An MRI revealed five cerebellar lesions measuring 1.4 × 1.5 × 1.6 cm, 2.0 × 1.5 × 1.7 cm, 0.7 × 0.7 × 0.7 cm, 0.2 × 0.2 × 0.2 cm, and 0.1 × 0.1 × 0.1 cm, as well as extensive vasogenic edema.\nHer treatment team recommended against resection due to the sensitive location of her tumors. GKRS was recommended over WBRT due to concern that avoiding previous radiation fields from treatment for oropharyngeal carcinoma 14 years earlier would not adequately address her relatively caudal metastatic tumors. The patient then underwent her first GKRS treatment at a dose of 22 Gy at the 50% isodose line (Figures and ). On the day of treatment, her Karnofsky Performance Status score was 100. Following GKRS, she was placed on dexamethasone 2 mg daily. Within several weeks she had experienced significant resolution of symptoms.\nOver the next 51 months, she underwent a subsequent six GKRS treatments, all of which treated between one and four metastases. Many of these metastases were in new locations within the cerebellum, while several appeared in the brainstem itself. 49 months after her initial treatment, she underwent a craniotomy to relieve obstructive hydrocephalus with a ventricular shunt placement. An 8.0 mm cerebellar lesion was successfully resected in the same procedure. Around the same time, she underwent SBRT for liver metastases, which was tolerated well.\nThe patient's most recent GKRS treatment occurred 60 months after the first and was suggested when the patient presented with complaints of consistent falls. A CT demonstrated five lesions, four of which were localized to the cerebellum and one limited to the pons. Three of the lesions had increased in size since her previous CT several months earlier. Three lesions were treated with a dose of 20 Gy at the 50% isodose line, one lesion was treated with 18 Gy at the 75% isodose line, and one was treated with 18 Gy at the 55% isodose line. A posttreatment CT demonstrated reduced dimensions of all lesions. Her most recent CT was taken 5 months later and demonstrated reduced or stable sizes of all lesions. 65 months after her initial diagnosis of brain metastasis, the patient began treatment with Votrient 800 mg for her liver metastases, which was tapered down to 400 mg and eventually held completely for after severe GI side effects and elevated liver enzymes.\nOne month prior to this paper, a PET scan was obtained, showing no new evidence of systemic or metastatic disease. At that time, she remained symptom-free with a high quality of life a total of 72 months after her brain metastases were diagnosed.
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.[]