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 previously healthy 56-year-old man developed gradual left- side hemiparesis, more accentuated in the lower limb (July 2016). A brain computerized tomography (CT)-scan and complementary magnetic resonance imaging (MRI) showed a solitary metastatic lesion (Met 1) in the right central sulcus (11.95 cc) with extensive perilesional edema [ and ]. The investigative tumor screening, including a CT- scan of the thorax and abdomen, revealed a suspect primary tumor in the left kidney as well as multiple, disseminated metastatic lesions in the lungs, liver, peri-aortic abdominal nodes, and left adrenal gland. A thrombotic mass positioned within the boundaries of the left renal vein was also reported. The subsequent biopsy revealed a clear cell renal cancer, Fuhrman Grade 2, as the primary. Due to the underlying extension of metastatic activity, nephrectomy was not indicated. Because of his relatively young age and previous healthy condition, the patient was accepted for upfront RRR- treatment of Met 1, structured on three separate fractions (GKRS 1–3) over a 7-day period [ and ]. This strategy aimed to sustain the patient’s performance status by avoiding further neurological deterioration while providing a window to start first-line targeted therapy (sunitinib). The rationale behind RRR can be found elsewhere in the literature.[-,]\nFollow-up MRI at 1, 3, and 6 months confirmed subsequent tumor volume reduction of Met 1 with ensuing significant improvement of the patient’s motor function []. Notably, a discrete, nonsymptomatic adverse radiation effect (ARE) around Met 1 was reported at 3 months, however, this subsequently resolved at 6 and 10 months. Despite the positive evolution of Met 1, the corresponding follow-up MRI at 10 months demonstrated a new, large metastatic lesion (17.3 cc) with extensive perilesional edema within the confinements of the left frontotemporal region, threatening the area of Broca and the insular region (Met 2). A parasagittal micrometastasis in the posterior boundaries of the left temporal lobe was also reported (Met 3). Despite further thoracic disease progression on anti-PD1 treatment (nivolumab), the patient’s clinical condition remained stable (Karnofsky Performance Scale [KPS] 90, recursive partitioning analysis [RPA] Class II); it was, therefore, decided to treat Met 2 with RRR and Met 3 with SF-GKRS [ and ] before switching systemic treatment to axitinib.\nMet 2 decreased in volume by 15% between GKRS 1 and GKRS 3. Follow-up MRI at 14 months after RRR-treatment of Met 1 (=2 months after RRR-treatment of Met 2) showed further tumor volume reduction of Met 2 while Met 1 and Met 3 remained unchanged [-]. However, edema increment around Met 2 was also reported, suggesting an additional focal (yet asymptomatic) ARE. Due to further radiological evidence of extracranial disease progression (CT-scan thorax and abdomen, October 2017), low- tolerance to axitinib and the patient’s own choice, further systemic therapy was altogether disrupted 14 months post- RRR of Met 1. Last follow-up MRI (20 months after RRR of Met 1) showed almost complete ablation of all GKRS-treated lesions and a reduction in perifocal edema surrounding Met 2, without major corticosteroid intervention [- and -]. Despite remaining free from motor-sensory deficits, epileptic seizures (Engel score of 1) or cognitive impairment, the patient promptly deteriorated at this stage due to extracranial disease progression (KPS 50, RPA 3). The patient succumbed to his disease 21 months post-RRR-treatment of Met 1.