Solitary fibrous tumors tend to be well-defined, ovoid, heterogeneously enhancing lesions. MRI characteristically depicts areas of low signal intensity that correspond to dense collagen. The findings of lesion multiplicity and hypermetabolism on PET images should raise the suspicion of malignancy.
Various substances, including methemoglobin, melanin, lipid, protein, calcium, iron, copper, and manganese, are responsible for the intrinsically high signal intensity observed in intracranial lesions at T1-weighted magnetic resonance (MR) imaging. Many of these substances have physical properties that lead to other specific imaging features as well. For example, lipid-containing lesions frequently produce chemical shift artifact, and some melanin-containing lesions exhibit a combination of high signal intensity on T1-weighted images and low signal intensity on T2-weighted images. The location and extent of a region of abnormal signal hyperintensity may be helpful for identifying rare diseases such as an ectopic posterior pituitary gland near the floor of the third ventricle, bilateral involvement of the dentate and lentiform nuclei in Cockayne syndrome, and involvement of the anterior temporal lobe and cerebellum in neurocutaneous melanosis. In cases in which diagnostically specific T1-weighted imaging features are lacking, findings obtained with other MR pulse sequences and other modalities can help narrow the differential diagnosis: An elevated glutamine or glutamate level at MR spectroscopy is suggestive of hepatic encephalopathy; a popcorn ball-like appearance at T2-weighted imaging, of cavernous malformations; and hyperattenuation at computed tomography, of mineral deposition disease. In many cases, a comparison of imaging features with clinical measures enables a specific diagnosis.
Background: Patients with HPVþ oropharyngeal squamous cell carcinoma were assigned to dose and volume de-escalated radiotherapy (RT) or chemoradiotherapy (CRT) based on response to induction chemotherapy in an effort to limit treatmentrelated toxicity while preserving efficacy. Patients and methods: Patients were classified as low-risk (T3, N2B, 10 pack-year history) or high-risk (T4 or N2C or >10 PYH). After three cycles of carboplatin/nab-paclitaxel, response was assessed using Response Evaluation Criteria in Solid Tumors 1.1. Low-risk patients with 50% response received 50 Gray (Gy) RT (RT50) while low-risk patients with 30%-50% response or high-risk patients with 50% response received 45 Gy CRT (CRT45). Patients with lesser response received standardof-care 75 Gy CRT (CRT75). RT/CRT was limited to the first echelon of uninvolved nodes. The primary end point was 2-year progression-free survival compared with a historic control of 85%. Secondary end points included overall survival and toxicity. Results: Sixty-two patients (28 low risk/34 high risk) were enrolled. Of low-risk patients, 71% received RT50 while 21% received CRT45. Of high-risk patients, 71% received CRT45. With a median follow-up of 29 months, 2-year PFS and OS were 95% and 100% for low-risk patients and 94% and 97% for high-risk patients, respectively. The overall 2-year PFS was 94.5% and within the 11% noninferiority margin for the historic control. Grade 3þ mucositis occurred in 30%, 63%, and 91% of the RT50, CRT45, and CRT75 groups, respectively (P ¼ 0.004). Rates of any PEG-tube use were 0%, 31%, and 82% for RT50, CRT45, and CRT75 groups, respectively (P < 0.0001). Conclusions: Induction chemotherapy with response and risk-stratified dose and volume de-escalated RT/CRT for HPVþ OPSCC is associated with favorable oncologic outcomes and reduced acute and chronic toxicity. Further evaluation of induction-based de-escalation in large multicenter studies is justified. Clinical trial registration: Clinical trials.gov identifier: NCT02258659.
From a clinical-radiologic standpoint, there are a limited number of structures and disease entities in the temporal bone with which one must be familiar in order to proficiently interpret a computed tomographic or magnetic resonance imaging study of the temporal bone. It is helpful to examine the region in an organized and systematic fashion, going through the same checklist of key structures each time. This is the first of a two-part review that provides a practical approach to understanding temporal bone anatomy, localizing a pathologic process with a focus on inflammatory and neoplastic processes, identifying pertinent positives and negatives, and formulating a differential diagnosis.
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