The aim of this study was to investigate the capability of Gd-DTPA-enhanced MRI to differentiate between exudative and transudative pleural effusions. An MRI examination was performed on 22 patients with different types of pleural effusion (10 transudative and 12 exudative effusions). T1-weighted SE images were obtained before and 20 min after administration of Gd-DTPA (0.1 mmol/kg). The degree of enhancement of pleural effusions was evaluated both by visual assessment and by quantitative analysis of images. None of 10 transudative effusions showed significative enhancement, whereas 10 of 12 exudative effusions showed enhancement (sensitivity 83 %, specificity 100 %, positive predictive value 100 %). The postcontrast signal intensity ratios (SIRs) of exudates were significantly higher than corresponding precontrast ratios (P = 0. 0109) and the postcontrast SIRs of exudates were significantly higher than those of transudates (P = 0.0300). Exudative pleural effusions show a significant enhancement following administration of Gd-DTPA. We presume that this may be caused by increased pleural permeability and more rapid passage of a large amount of Gd-DTPA from the blood into the pleural fluid in case of exudative effusions. In our limited group of patients, signal enhancement proved the presence of an exudative effusion. Absence of signal enhancement suggests a transudate, but does not exclude an exudate.

We describe the CT and MRI patterns of cerebral venous sinus thrombosis (CVST) on the basis of the venous angioarchitecture and the underlying pathophysiological mechanism. We also investigated if any radiologic data exist to establish which patients can be followed conservatively and which warrant endovascular treatment. The clinical, CT-CTA and MRI-MRA findings of 11 patients (2 men; 9 women; 24 to 69 years-old) with CVST were reviewed. The morphological patterns of CVST were divided into two major groups: Vascular signs: spontaneous sinusal hyperdensity (9); spontaneous all-sequences hyperintensity (4); venous engorgement (9); empty delta sign (4); lack of sinusal contrast-enhancement (3); delayed sinusal transit-time (11); lack of flow-related signal (3). Parenchymal signs: mass effect and cortical sulcal effacement (8), white matter edema (7), venous ischemia (6), haemorrhagic infarct (3), breakdown of the blood-brain barrier (4), hydrocephalus (2). The clinical and radiologic pictures are related to cerebral venous angioarchitecture and underlying pathophysiologic mechanism of venous thrombosis. Reversibility of clinical symptoms and parenchymal lesions is far more frequent, because vessel damage slowly and progressively develops, whereas damage to brain tissue occurs later. Consequently, a prompt CT-MRI diagnosis may allow a good prognosis. Treatment using selective sinusal instillation of urokinase is considered only when the patient clinically and radiologically does not improve within the first two weeks after heparinization.

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Computed tomography (CT) is used increasingly as an early radiological examination in patients with suspected bowel infarction because it provides information about the intestinal wall, mesenteric circulation and peritoneal cavity [1, 2]. Other disorders that present with similar symptoms such as intraabdominal abscess, pancreatitis and ulcerative colitis can be excluded [3]. CT can demonstrate small amounts of air within the bowel wall, in the spleno-mesenteric-portal venous system and in the peritoneal cavity, making it possible to differentiate portal venous gas from pneumobilia. The authors describe a patient in whom a specific diagnosis of bowel infarction was made on the characteristic CT findings. Furthermore, air embolism was observed in the splenic parenchyma. This finding has not been previously reported in bowel infarction or in any other abdominal disorder.

Hypoglossal nerve (cranial nerve XII) palsy is uncommon. Damage to this nerve produces characteristic clinical manifestations, of which unilateral atrophy of the tongue musculature is the most important. When these features are recognized, the radiologist, armed with knowledge of the normal anatomy of the area, can focus on each segment of the nerve in search of a cause. The hypoglossal nerve is divided into five segments: the medullary, cisternal, skull base, nasopharyngeal/oropharyngeal carotid space, and sublingual segments. Because each segment is usually affected by different disorders, localizing a lesion to a particular segment allows the radiologist to narrow down the differential diagnosis to develop the most efficient imaging strategy for the evaluation of symptoms. Both computed tomography (CT) and magnetic resonance imaging (MRI) are useful in assessing dysfunction of the hypoglossal nerve; the choice depends on the status of the patient and the preference of the radiologist.