Gamma Knife Radiosurgery for Choroidal Hemangioma: A Single-Institute Series.

OBJECTIVE: Choroidal hemangioma (CH) is a benign vascular tumor that induces subretinal fluid collection or exudative retinal detachment and consequent visual symptoms. Current standard treatments for CH include cryotherapy, diathermy, photocoagulation, photodynamic therapy, transpupillary thermotherapy, and radiation therapy. Stereotactic radiosurgery has recently been applied to the treatment of CH because of its characteristic stiff dose-fall-off and accuracy. We have adopted gamma knife radiosurgery (GKRS) to treat CH and have retrospectively assessed tumor volume reductions and improvements to visual acuity achieved thereby. METHODS: Fourteen patients with CHs were treated with GKRS from November 2006 to December 2017. Eight patients had circumscribed CH, and 6 exhibited diffuse CHs and were diagnosed with Sturge-Weber syndrome. The mean age of patients was 27.1 years (range: 8-68 years) and the mean duration of clinical or radiological follow-up was 40.2 months (range: 5-105 months). The mean volume of the tumors at the time of GKRS was 533.5 mm3 (range: 124-1150 mm3), and the mean prescribed marginal dose was 11.6 Gy (range: 10-16 Gy) with 50% isodose lines. RESULTS: The tumor volume decreased by the last follow-up in all patients. The visual acuity improved in 9 patients (64%) and decreased in 1 (7%). Six patients (43%) required trans-pars plana vitrectomy before or after GKRS. There were no symptomatic complications from radiation injury during the follow-up periods. CONCLUSIONS: GKRS could be an acceptable alternative treatment for symptomatic CH when standard therapy is not feasible.

Injury in the spinal cord may produce cell death in the brain.

Functional deficits after spinal cord injury have originated not only from the direct physical damage itself, but from the secondary biochemical and pathological changes. Apoptotic cell death has been seen around the periphery of an injured site and has been known to ultimately progress to necrosis and infarction. We have initiated the present study focusing on the role of apoptosis in the secondary injury of the brain after acute spinal cord injury (SCI), and conducted a series of experiments, the study examining the morphological changes in the brain following the spinal injury. Under pentobarbital anesthesia, male Sprague-Dawley rats were subjected to SCI model. Rats were laminectomized and SCI was induced using NYU spinal impactor at T9 segment. The behavioral test was performed. Electrophysiologically, motor evoked potentials (MEPs) were recorded. The animals were subjected to morphological study at 12, 24, 48, 72 h, and 1 week, postoperatively. Locomotor deficits were observed after SCI, and changes in the amplitudes and latencies of the MEPs were observed. The morphological changes were evidenced by terminal TUNEL staining and Calbindin-D(28K) immunohistochemistry. The TUNEL-positive cells were located at the brain motor cortex after SCI. TUNEL-positive cells were seldom found 4 h after injury. In addition, Calbindin-D28K immunoreactive neurons were observed in the motor cortex after injury. These results suggest that apoptosis may play an important role in the pathophysiology of the brain motor cortex following acute spinal cord injury and functions that were deteriorated after SCI may be related to these electrophysiological and morphological changes.