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.
A 67-year-old previously healthy male presented in September 2011 with a 3-week history of fatigue, dizziness, balance impairment, left-sided motor/sensory deficits, and transient mainly right-sided headache. Brain CT and MRI demonstrated a 25-mm large metastasis in the superior left cerebellar hemisphere (M1) with slight compression of the brainstem in addition to three smaller metastases in the right frontal lobe and one in the left occipital lobe. Further investigations revealed a small pulmonary lesion which was deemed unlikely to be the primary tumor. A stereotactic biopsy was, therefore, performed on one of the frontal lesions to establish a definitive diagnosis; the microscopic evaluation demonstrated a metastasis from malignant melanoma with underlying BRAF-mutation.\nThree weeks after the biopsy, the patient underwent GKRS for all metastases. At the time of treatment, his neurological condition had deteriorated with increasing paresis of the left leg requiring assisted mobilization by wheelchair (KPS 60–70; RPA 2–3). The stereotactic MRI at GKRS 1 revealed a short-interval significant size increase of M1 to 37 mm (approximately 15 cm3) with central necrosis and slight surrounding edema despite ongoing corticosteroid therapy. V4 proved now deformed and partially compressed though without radiological evidence of hydrocephalus. The lesion was assessed as inaccessible for microsurgical decompression. Due to the size of the lesion and high risk for ARE in the brainstem, M1 was adaptively treated by means of 3R []; the remaining four lesions were treated with SF-GKRS. During the three-part treatment time M1 experienced a tumor reduction of almost 10% (from 15.1 at GKRS 1 to 13.8 cm3 at GKRS 3); V4 volume increased slightly (from 0.83 cm3 at GKRS 1 to 0.93 cm3 at GKRS 3). The dose fractionation schedule is described in . The first follow-up MRI was planned 4 weeks after the third GKRS; because of increased headache/dizziness and to assess the need for post-GKRS systemic treatment the examination was performed 10 days earlier than planned (MRI at 3 weeks).\nAlthough volume assessments by LGP were technically not possible on this particular MRI due to image artefacts, M1 had higher signal on T2 with a more necrotic appearance whereas V4 remained almost unchanged. However, with supportive/ongoing corticosteroid therapy, the patient recovered some balance and strength in his left leg shortly after his examination; systemic antitumoral treatment (BRAF inhibitor dabrafenib) was started at this stage. A new follow-up MRI at 8 weeks revealed decreased volume of M1 (41% compared to MRI at GKRS 1) and diminished compression of V4 (volume of V4 increased from 0.83 cm3 at GKRS 1 to 1.43 cm3 at 8 weeks) []. Local edema had diminished. The remaining treated lesions were under control. However, a CT scan at 10 weeks was performed due to general deterioration over the previous few weeks; the examination demonstrated new areas of hemorrhage and surrounding edema adjacent to two frontal metastases which were treated with SF-GKRS, and slightly increased edema surrounding M1 although with stable V4 conditions. He died 2 weeks later (10 weeks after GKRS) in palliative care. No autopsy was performed. According to the available medical data, the patient might have died of extracranial tumor activity and possible intracranial complications.