T1 signal hyperintensity is a common finding at magnetic resonance imaging of the sellar region. However, this signal intensity pattern has different sources, and its significance depends on the clinical context. Normal variations in sellar T1 signal hyperintensity are related to vasopressin storage in the neurohypophysis, the presence of bone marrow in normal and variant anatomic structures, hyperactive hormone secretion in the anterior pituitary lobe (eg, in newborns and pregnant or lactating women), and flow artifacts and magnetic susceptibility effects. Pathologic variations in T1 signal hyperintensity may be related to clotting of blood (in hemorrhagic pituitary adenoma, pituitary apoplexy, Sheehan syndrome, or thrombosed aneurysm) or the presence of a high concentration of protein (Rathke cleft cyst, craniopharyngioma, or mucocele), fat (lipoma, dermoid cyst, lipomatous meningioma), calcification (craniopharyngioma, chondroma, chordoma), or a paramagnetic substance (manganese, melanin). After treatment, T1 signal hyperintensity may result from the presence of materials used for surgical packing (gelatin sponge, fat); from compression of the cavernous sinus and reduction of the venous flow, caused by overpacking of the operative bed; or from hormone hypersecretion by a remnant of normal tissue in the anterior lobe of the pituitary gland.

During the first hours after acute ischemic stroke, the CT usually shows no abnormalities. Therapeutic trials of ischemia in the middle cerebral artery (MCA) territory involves decision-making when the CT may not show obvious ischemic changes. We reviewed 100 consecutive patients, admitted within 14 hours after a first stroke. Selective criteria were clinical presentation with MCA ischemia and at least two CTs (1 initial and 1 control). All CTs were retrospectively analyzed by at least two physicians blinded to the patient's status. On the first CT, early signs were hyperdense MCA sign (HMCAS), early parenchymatous signs (attenuation of the lentiform nucleus [ALN], loss of the insular ribbon [LIR], and hemispheric sulcus effacement [HSE]), midline shift, and early infarction. Subsequent infarct locations were classified according to total, partial superficial (superior or inferior), deep, or multiple MCA territories. Clinical features, etiology, and Rankin scale were collected. There were 52 women (mean age 70.8). The CTs were performed at mean 6.4 hours (1 to 14 hours) and before the sixth hour in 62% of the patients. Early CT was abnormal in 94% of the cases, and the abnormalities found were an HMCAS in 22 patients, ALN in 48, LIR in 59, HSE in 69, midline shift in 5, and early infarct in 7. CT was normal in six patients where it was performed earliest (mean 4.5 hours) and in the oldest patients (mean age 80.1). Early parenchymatous CT signs were significantly associated with subsequent MCA infarct location and extension: ALN and deep infarct, HSE and superficial infarct, LIR and large infarct. HMCAS was never found in isolation and was always associated with the three other signs in extended MCA infarct. The presence of two or three signs (ALN, LIR, or HSE) was associated with extended MCA infarct (p < 0.001) and poor outcome (p < 0.001). Our findings suggest that CT frequently discloses parenchymal abnormalities during the first hours of ischemic stroke. Early signs allow the prediction of subsequent infarct locations; CT may provide a simple tool in evaluating the early prognosis of MCA infarction and thus may be useful in selecting better treatments.

Today, MR is the only method needed for the morphological investigation of endocrine-active pituitary adenomas. In acromegaly and Cushing's syndrome, the therapeutic attitude is directly dictated by MR data. We present the MR aspect of pituitary adenomas according to size, sex, age, endocrine activity and a few particular conditions such as hemorrhagic pituitary adenomas, pituitary adenomas during pregnancy, cavernous sinus invasion and postsurgical changes. When an intrasellar mass extending out of the sella turcica is detected, the goal of the MR examination is to indicate precisely the origin of the tumor, its extension in relation to the various surrounding structures, its structure and its enhancement in order to help in the differential diagnosis. Demonstration of very small pituitary adenomas remains a challenge. When SE T1- and Turbo SE T2-weighted sequences are non-diagnostic, enhanced imaging becomes mandatory; half-dose gadolinium injection, delayed sequence, dynamic imaging can be of some help.

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There are two species of the genus Echinococcus, Echinococcus multilocularis (also called alveolar hydatid) and Echinococcus granulosus, characterized by distinct growth features in humans. The main endemic regions for human alveolar echinococcosis (AE) caused by E. multilocularis are Central Europe, Russia, Turkey, Japan, China, eastern France and North America. Human echinococcosis is usually caused by an intrahepatic growth of parasitic larvae. Cerebral occurrence of E. multilocularis disease is rare, accounting for only 1% of cases, and is generally considered to be fatal. This report presents two cases of intracerebral E. multilocularis disease which occurred in two infected patients with AE pulmonary metastases. The anatomical and clinical features are discussed. Our retrospective survey would indicate that surgical treatment should be envisaged whenever possible.