Delayed cerebral radiation necrosis after neutron beam radiation of a parotid adenocarcinoma: a case report and review of the literature

Abstract

Cerebral radiation necrosis (CRN) is a well described possible complication of radiation for treatment of intracranial pathology. However, CRN as sequelae of radiation to extracranial sites is rare. Neutron beam radiation is a highly potent form of radiotherapy that may be used to treat malignant tumors of the salivary glands. This report describes a patient who underwent neutron beam radiation for a parotid adenocarcinoma and who developed biopsy-confirmed temporal lobe radiation necrosis thirty months later. This represents the longest time interval described to date, from initial neutron radiation for extracranial pathology to development of CRN. Two other detailed case studies exist in the literature and are described in this report. These reports as well as our patient's case are reviewed, and additional recommendations are made to minimize the development of CRN after extracranial neutron beam radiation. Physicians should include the possible diagnosis of CRN in any patient with new neurologic signs or symptoms and a history of head and neck radiation that included planned fields extending to the base of the skull. Counseling of patients prior to neutron beam radiation should include potential neurologic complications associated with CRN and risks of treatment for CRN including neurosurgical intervention.

Figure 1

A representative axial slice from the patient's radiation plan is shown. The left temporal lobe of the brain is contoured in black. This area received 1678 centi-nGy and falls between 1500 centi-nGy (pink) and 1748 centi-nGy (orange) isodose lines. The treatment isocenter received a total dose of 1819 centi-nGy.

Figure 2

Axial slices of T1 postcontrast (a) and T2 FLAIR (b) MRIs are shown, corresponding to the radiation plan seen in Figure 1. Additional axial T1 postcontrast (c), axial T2 FLAIR (d), coronal T1 postcontrast (e), and sagittal T1 postcontrast (f) slices depict an irregularly enhancing mass lesion in its greatest dimensions, involving the left temporal lobe tip. The lesion measured 4.6 cm in the greatest dimension with significant surrounding edema. There was evidence of temporal bone resection, consistent with prior resection of the left parotid gland.

Figure 3

Axial T1 postcontrast (a), T2 FLAIR (b), coronal T1 postcontrast (c), and sagittal T1 postcontrast (d) MRIs obtained on postoperative day 1 demonstrated total resection of the enhancing mass seen on preoperative imaging. There were some minor blood products and enhancement, consistent with expected normal reactive change after surgery.

Figure 4

Formalin fixed, paraffin embedded tissue sections stained with hematoxylin and eosin demonstrate reactive astrogliosis, radiation-induced vasculopathy, and necrosis. (a) Reactive astrocytes show hypertrophic, eosinophilic cytoplasm with eccentrically placed nuclei. (b) Higher magnification of inset in (a). (c) Hyalinized arterioles are seen, characteristic of radiation-induced vasculopathy. (d) Higher magnification image of (c). Radiation necrosis is demonstrated at (e) interface of brain and necrotic area and (f) necrosis in the center of the lesion.