Radiation necrosis in the brain commonly occurs in three distinct clinical scenarios, namely, radiation therapy for head and neck malignancy or intracranial extraaxial tumor, stereotactic radiation therapy (including radiosurgery) for brain metastasis, and radiation therapy for primary brain tumors. Knowledge of the radiation treatment plan, amount of brain tissue included in the radiation port, type of radiation, location of the primary malignancy, and amount of time elapsed since radiation therapy is extremely important in determining whether the imaging abnormality represents radiation necrosis or recurrent tumor. Conventional magnetic resonance (MR) imaging findings of these two entities overlap considerably, and even at histopathologic analysis, tumor mixed with radiation necrosis is a common finding. Advanced imaging modalities such as diffusion tensor imaging and perfusion MR imaging (with calculation of certain specific parameters such as apparent diffusion coefficient ratios, relative peak height, and percentage of signal recovery), MR spectroscopy, and positron emission tomography can be useful in differentiating between recurrent tumor and radiation necrosis. In everyday practice, the visual assessment of diffusion-weighted and perfusion images may also be helpful by favoring one diagnosis over the other, with restricted diffusion and an elevated relative cerebral blood volume being seen much more frequently in recurrent tumor than in radiation necrosis.
Drug-resistant epilepsy is a chronic debilitating disorder, but many cases are potentially curable by surgery. The key to the successful epilepsy surgery with complete postoperative seizure-free status is precise localization of the epileptic zone that must be resected and the adjacent eloquent areas of gray and white matter that must be preserved to avoid neurological defects. This article reviews the current state of the art epilepsy imaging techniques facilitating successful epilepsy surgery. The overview of the imaging appearances of the most common epileptogenic etiologies that are amenable to surgical resection is also included in this review.
F-FDG uptake in enlarged lymph nodes is always suspicious, especially in cancer patients. We report a case of hypermetabolic internal mammary lymphadenopathy in a breast cancer patient who was previously treated with bilateral mastectomy and implants. The abnormal nodal uptake turned out to be due to foreign body-induced inflammation, as confirmed histopathologically. Vigilant PET interpretation is required in breast cancer patients who have evidence of breast implant rupture.
In cases of nonhereditary osteomalacia associated with hypophosphatemia and inadequate response to vitamin D supplementation, one should consider the possibility of tumor-induced osteomalacia, a paraneoplastic syndrome caused by small mesenchymal tumors often found in obscure locations. We present a case of tumor-induced osteomalacia in which 111 In-pentetreotide scintigraphy aided in accurate localization of the culprit brachial plexus tumor and cure after resection. Tumor-i nduced osteomalacia or oncogenic osteomalacia is an uncommon disorder presenting with bone pain and fractures. It is characterized by renal phosphate wasting, hypophosphatemia, and osteomalacia and is usually caused by benign mesenchymal tumors (1). We present a case of tumor-induced osteomalacia in which 111 In-pentetreotide scintigraphy (OctreoScan; Mallinckrodt) aided in accurate localization of the culprit brachial plexus tumor and cure after resection. 111 In-pentetreotide imaging is useful for evaluating not only neuroendocrine tumors but also other tumors expressing somatostatin receptors, such as those causing tumor-induced osteomalacia, which are often small and found in obscure locations. CASE REPORTA 43-y-old man presented with bone pain and nontraumatic fractures of the right calcaneus and lumbar spine. Radiographs and dual-energy x-ray absorptiometry revealed osteopenia. The laboratory work-up showed a normal level of serum calcium (9.2 mg/dL; reference range, 8.4-10.2 mg/dL), an increased level of alkaline phosphatase (244 units/L; reference range, 39-117 units/L), undetectable 1,25-dihydroxyvitamin D (,8 pg/mL; reference range, 18-92 pg/mL), and a decreased level of serum phosphorus (1.3 mg/dL; reference range, 2.4-5 mg/dL). Fibroblast growth factor 23, key to pathogenesis of tumor-induced osteomalacia, was also elevated (320 relative units/mL; reference range, #180 relative units/mL). A planar 4-h whole-body 99m Tcmethylene diphosphonate (22 mCi) bone scan suggested osteomalacia (Fig. 1). Because tumors causing tumor-induced osteomalacia may express somatostatin receptors, 111 Inpentetreotide (223.5 MBq [6.04 mCi]) scintigraphy was done 24 h after radiotracer administration. Planar and SPECT images (Fig. 2) revealed focal uptake in the right axilla, which correlated with a well-circumscribed lesion within the coracobrachialis muscle on CT (Fig. 3) and MR imaging (Fig. 4). During surgery, the tumor was confirmed to arise from the musculocutaneous nerve of the right brachial plexus and was successfully resected. Pathologic findings were consistent with a benign spindle cell tumor. After resection, the patient reported improvement in symptoms, and biomarkers were also improved (serum phosphorus, 4.7 mg/dL; fibroblast growth factor 23, 92 relative units/mL). DISCUSSIONOsteomalacia is a bone disorder characterized by decreased mineralization of newly formed osteoid at bone turnover sites. Disorders causing osteomalacia include those associated with abnormal vitamin D metabolism, osteoid mineralization defects, and hypophosphate...
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