No abstract

Fetal magnetic resonance imaging (FMRI) has gained considerable interest during the last decade, especially in its intracranial applications. Due to its high soft-tissue contrast and presumed safety, FMRI should be accepted as a complementary technique in prenatal diagnosis, useful either to elucidate equivocal findings on routine US studies or to further delineate some pathological entities. Normal patterns of fetal brain maturation, as shown by FMRI, are described because they are of paramount importance to accurately evaluate intracranial diseases. To date, however, FMRI requires specialised facilities and should be considered as an evolving clinical research modality and performed within precise guidelines in a multidisciplinary approach to prenatal pathology.

DGS MRI allows early detection of epiphyseal ischaemia and accurate analysis of the different revascularisation patterns. These changes are directly related to the prognosis of LCP disease and can aid therapeutic decision making.

Magnetic resonance imaging (MRI) has revealed isolated pituitary stalk (PS) thickening (PST) in certain cases of idiopathic or secondary central diabetes insipidus (DI) due to infiltrative processes. Twenty-six children with DI and PST underwent cerebral MRI at the age of 8 +/- 4 yr and were followed (n = 24) by clinical and MRI evaluation, respectively, for 5.5 +/- 3.6 and 3.0 +/- 2 yr in the absence of any treatment other than hormonal substitutive therapy. Patients were subdivided into groups according to the etiology of the DI: germinoma (n = 4), Langerhans' histiocytosis (n = 5), or idiopathic DI with PST (n = 17). Complete anterior pituitary evaluation for 24 of the 26 patients revealed those suffering from associated GH deficiency (n = 14; with germinoma, n = 1; histiocytosis, n = 3; idiopathic, n = 10) and from multiple hormone deficiencies (n = 7; with germinoma, n = 3; histiocytosis, n = 1; idiopathic, n = 3). At the first MRI evaluation, PS enlargement varied from 2.2-9.0 mm at a proximal (n = 10), distal (n = 2), or middle (n = 6) PS level or along the entire PS (n = 8). The intrasellar content, which usually reflects the anterior pituitary gland, was normal (n = 12), small (n = 8), or enlarged (n = 6). At the last evaluation, a change in MRI features was found in 16 patients; morphological and/or signal changes in the PST (n = 16, of whom 6 showed an increase in PST) and changes in anterior pituitary gland size (n = 8; increased, n = 3; decreased, n = 5) were noted. The presence of a growing suprasellar mass with progressively enlarging PS was demonstrated in the 6 patients who had shown increased PS enlargement 1.8 +/- 1.6 yr after the first MRI. For 4 of them, a diagnosis of germinoma was made 1.3 +/- 0.6 yr after PST identification by MRI performed after the onset of DI, but the other 2 patients showing a suprasellar mass were still categorized as idiopathic at the final clinical evaluation performed 7.8 and 12.3 yr, respectively, after DI onset. In 10 patients (all but 1 with Langerhans histiocytosis, showing idiopathic DI), the PS enlargement was diminished after 2.0 +/- 1.9 yr of MRI follow-up, with a complete reversal of PS enlargement for 5 of them. Suprasellar mass invasion of the PS was related to multiple hormone deficiency. Although intrasellar content enlargement was observed in most patients with germinoma, a normal or small anterior pituitary gland showed no clear relationship to either clinical histories or laboratory values. In conclusion, the natural history of idiopathic isolated central DI with PST is unpredictable. Although germinoma should always be considered during the first 3 yr of follow-up in patients showing isolated DI with PST requiring repeated investigations every 3-6 months, it remains a less frequent etiology for 15% of the cases.

No abstract

In GH-deficient children showing ectopic posterior pituitary hyperintense signal (EPP), the anatomical details of the pituitary-hypothalamic region and the relationship between the visibility of the pituitary stalk and anterior pituitary function were studied by magnetic resonance imaging (MRI). The absence or presence of the pituitary stalk was recorded by MRI before and after the injection of gadolinium in 25 children with GH deficiency and EPP at the age of 8.7+/-5.0 yr (16 males and 9 females). Patients were classified into 2 groups according to the presence (group 1; n = 14), or the absence (group 2; n = 11) of pituitary stalk visibility after gadolinium injection. Most patients in group 1 (12 of 14) demonstrated isolated GH deficiency, whereas all but 1 patient in group 2 showed multiple anterior pituitary hormone deficiency. The prevalence of a normally sized adenohypophysis was higher in group 1 than in group 2 (50% vs. 9%; P<0.05). Although the EPP was found at the median eminence in all group 2 patients, it was visualized in group 1 at different levels of the pituitary stalk in 60% of cases (8 of 14; at the proximal end of the pituitary stalk, n = 4; in the middle of the pituitary stalk, n = 2; at the distal end of the pituitary stalk, n = 2). This demonstrates that the ectopic posterior pituitary migration abnormality may be complete or partial. In conclusion, although the pathogenesis of GH deficiency with EPP remains unclear, these results suggest that in cases of GH deficiency associated with ectopic posterior pituitary hyperintense signal, patients with no visible pituitary stalk on MRI after gadolinium injection present a more severe form of the disease in childhood associated with multiple anterior pituitary hormone deficiency, whereas visibility of the pituitary stalk is related to isolated GH deficiency. Nevertheless, careful follow-up of these latter patients is necessary, as the natural history of the disease is not established until adulthood.

We identified a group of children at risk for intramuscular insulin injections and that may deserve specific injection technique and advice.

Our preliminary results indicate that dynamic gadolinium-enhanced subtraction MRI is a simple and promising means of early recognition of ischemia in LCP.