A novel technique for image-guided local heart irradiation in the rat.

In radiotherapy treatment of thoracic, breast and chest wall tumors, the heart may be included (partially or fully) in the radiation field. As a result, patients may develop radiation-induced heart disease (RIHD) several years after exposure to radiation. There are few methods available to prevent or reverse RIHD and the biological mechanisms remain poorly understood. In order to further study the effects of radiation on the heart, we developed a model of local heart irradiation in rats using an image-guided small animal conformal radiation therapy device (SACRTD) developed at our institution. First, Monte Carlo based simulations were used to design an appropriate collimator. EBT-2 films were used to measure relative dosimetry, and the absolute dose rate at the isocenter was measured using the AAPM protocol TG-61. The hearts of adult male Sprague-Dawley rats were irradiated with a total dose of 21 Gy. For this purpose, rats were anesthetized with isoflurane and placed in a custom-made vertical rat holder. Each heart was irradiated with a 3-beam technique (one AP field and 2 lateral fields), with each beam delivering 7 Gy. For each field, the heart was visualized with a digital flat panel X-ray imager and placed at the isocenter of the 1.8 cm diameter beam. In biological analysis of radiation exposure, immunohistochemistry showed γH2Ax foci and nitrotyrosine throughout the irradiated hearts but not in the lungs. Long-term follow-up of animals revealed histopathological manifestations of RIHD, including myocardial degeneration and fibrosis. The results demonstrate that the rat heart irradiation technique using the SACRTD was successful and that surrounding untargeted tissues were spared, making this approach a powerful tool for in vivo radiobiological studies of RIHD. Functional and structural changes in the rat heart after local irradiation are ongoing.

Cervical branch of the facial nerve in leprosy

This study demonstrates that the platysma is occasionally palsied in leprosy and that this only occurs when the facial nerve already has some other palsy. That there needs to be a facial palsy before there can be a platysma palsy is strongly suggested, in that there was no case of an isolated platysma palsy. Patients, regardless of age or other factors, could mimic a platysma contraction. This obviates the need for electrical testing to examine for a platysma palsy. It also means that a nonfunctioning platysma on clinical examination is, in fact, a palsied platysma. While lagophthalmos is regularly examined for, and any obvious facial paresis would be noticed, less severe forms of facial muscle paresis will only be found if formally examined for. The mechanism whereby the facial nerve is involved in leprosy is not clarified, but our findings suggest that proximal spread of a lesion that began in the zygomatico-temporal branches and reaches to the facial nerve trunk is more likely than new lesions developing de novo in other peripheral facial nerve branches. That the primary lesion is within the facial nerve trunk in all cases but we only see the frequent zygomatic sequelae due to secondary factors is not excluded.