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 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.