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I. J. Radiation Oncology
● Biology ● Physics
Volume 60, Number 1, Supplement, 2004
mean reduction 0.28mm, CI 0.5 to 0.05mm, p ⫽ 0.02. In both univariate and multivariate analysis, the only statistically significant risk factor, apart from radiotherapy, was smoking pack years (p ⫽ 0.02). Conclusions: Therapeutic doses of ionizing radiation result in increased carotid artery stenosis and vessel wall abnormalities. The use of a matched-pair study design of irradiated and unirradiated carotids in the same patient has avoided the selection bias inherent in previous studies, which compared irradiated patients with unirradiated controls. We demonstrated an increase in ICA wall disease with dose levels ⬎35.5Gy. Six of forty irradiated carotids had an ICA/ Bulb stenosis ⱖ60%, which is often considered the threshold for further assessment and intervention. Only one such stenosis was found in an unirradiated vessel. Larger studies are planned to evaluate the absolute risk of stenosis caused by radiotherapy, meanwhile the risk of carotid stenosis should be borne in mind when planning treatment for head and neck tumours.
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Preventing Radiation Retinopathy with Hyperfractionation
A. T. Monroe, N. Bhandare, C. G. Morris, W. M. Mendenhall Radiation Oncology, University of Florida, Gainesville, FL Purpose/Objective: The purpose of this study was to determine factors associated with the development of radiation retinopathy in a large series of patients with head and neck cancer. In particular, we addressed whether the use of hyperfractionated radiation therapy was effective in reducing the risk of retinopathy. Materials/Methods: One hundred eighty-six patients received a significant dose to the retina as part of curative radiotherapy. Primary sites were: nasopharyngeal, 46; paranasal sinus tumors, 64; nasal cavity, 69; and palate, 7. Prescription doses varied depending on primary site and histology. Hyperfractionated (twice-daily) radiation was delivered to 42% of the patients in this study, typically at 110 to 120 cGy per fraction. The remainder were treated once-daily. Retinal doses were determined from computerized dosimetry plans when available. For all other patients, retinal doses were retrospectively calculated using reconstructed off-axis dosimetry taken from contours through the center of the globes. Retinal dose was defined as the minimum dose received by at least 25% of the globe. The median retinal dose was 5685 cGy (range). Patients were followed for a median of 7.6 years. Results: Thirty-one eyes in 30 patients developed radiation retinopathy, resulting in monocular blindness in 25, bilateral blindness in one, and decreased visual acuity in four. The median time to the diagnosis of retinopathy was 2.6 years (range, 10 months to 5.3 years). The actuarial incidence of developing radiation retinopathy was 20% at both 5 and 10 years. The incidence of developing ipsilateral blindness due to retinopathy was 16% at 5 years and 17% at 10 years. Site-specific incidences varied significantly with ethmoid sinus (9 of 25, 36%), nasal cavity (13 of 69, 19%), and maxillary sinus (6 of 35, 17%) being the most common sites associated with radiation retinopathy. Three of seventy-two patients (4%) receiving retinal doses less than 5000 cGy developed retinopathy. Higher retinal doses resulted in a steady increase in the incidence of retinopathy, with twenty-five of the thirty cases occurring after 6000 cGy or more. Of the patients receiving more than 5000 cGy to the retina, hyperfractionation was associated with a significantly lower incidence of radiation retinopathy (55% vs. 15%; p ⫽ 0.0020). On multivariate analysis, retinal dose (p ⬍ 0.0001), fractionation schedule (p ⫽ 0.0005), age (p ⫽ 0.027), and overall treatment time (p ⫽ 0.028) were significant predictors of radiation retinopathy. Conclusions: The incidence of radiation retinopathy following treatment of nasal cavity paranasal tumors is 20% at five and ten years. Retinal dose and fractionation schedule are the strongest predictors of retinopathy. Hyperfractionated radiotherapy is associated with a significant reduction in the incidence of radiation retinopathy, especially when the retina receives more than 5000 cGy.
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Masticatory Muscle Function and Cross-Sectional Area After Unilateral Head and Neck Radiotherapy
T. Roques,1 A. Nichol,1 C. Peck,5 Y. D’Yachkova,2 J. Robar,3 M. Williams,4 K. Jeffery,1 L. Barrett,1 J. Hay1 1 Radiation Oncology, Vancouver Cancer Centre, Vancouver, BC, Canada, 2Population and Preventative Oncology, Vancouver Cancer Centre, Vancouver, BC, Canada, 3Medical Physics , Vancouver Cancer Centre, Vancouver, BC, Canada, 4Oral Oncology / Dentistry, Vancouver Cancer Centre, Vancouver, BC, Canada, 5Faculty of Dentistry, University of British Columbia, Vancouver, BC, Canada Purpose/Objective: 1) To quantify the rate of atrophy of the masseter and medial pterygoid muscles after unilateral head and neck radiotherapy using CT imaging. 2) To correlate atrophy with changes in bite force and masticatory muscle function. Materials/Methods: Patients who had undergone unilateral radiotherapy to tonsil, parotid or unknown primary malignancies with no recurrent disease were identified from the departmental cancer database and invited to participate. Twenty-five patients who underwent radiotherapy between 8 and 110 months previously consented to the study. Each underwent a diagnostic CT scan in the same position as their original pre-radiotherapy (diagnostic or planning) CT. Corresponding matched CT slices were bisected and stored under randomly assigned names. Two observers contoured the masseter and medial pterygoid muscles on each slice. Subjects underwent a formal assessment of mandibular function and oral health. This included maximum bite force measurement using a thin (0.1 mm) pressure sensitive film inserted between the maxillary and mandibular teeth, dental examination and a mandibular function impairment questionnaire that assesses the impairment of normal activities and functions of the masticatory system. Results: Muscles on the treated (high dose) side received a median dose of 57.4Gy (range 50 – 61.2). Median follow up was 4 years (range 8 months to 9 years). On the high dose side, masseter muscle area decreased by 0.09cm2 (95% CI ⫽ -0.19, 0.2) per year and medial pterygoid area by 0.06cm2 (95% CI ⫽ 0, 0.12) per year. When the contralateral muscle was used as a control, to account for the effects of ageing and for changes in the CT scanning equipment over time, the treated masseter muscle area decreased by 2.3% per year relative to baseline (p ⬍ 0.001) whilst medial pterygoid area decreased by 1.1% per year (p ⫽ 0.10).