Comparing 3T T1-weighted sequences in identifying hyperintense punctate lesions in preterm neonates.

BACKGROUND AND PURPOSE: The loss of contrast on T1-weighted MR images at 3T may affect the detection of hyperintense punctate lesions indicative of periventricular leukomalacia in preterm neonates. The aim of the present study was to determine which 3T T1-weighted sequence identified the highest number of hyperintense punctate lesions and to explore the relationship between the number of hyperintense punctate lesions and clinical outcome. MATERIALS AND METHODS: The presence of hyperintense punctate lesions was retrospectively evaluated in 200 consecutive preterm neonates on 4 axial T1-weighted sequences: 3-mm inversion recovery and spin-echo and 1- and 3-mm reformatted 3D-fast-field echo. Statistically significant differences in the number of hyperintense punctate lesions were evaluated by using a linear mixed-model analysis. Logistic regression analysis was used to assess the relation between the number of hyperintense punctate lesions and neuromotor outcome at 3 months. RESULTS: Thirty-one neonates had at least 1 hyperintense punctate lesion indicative of periventricular leukomalacia in at least 1 of the 4 sequences. The 1-mm axial reformatted 3D-fast-field echo sequence identified the greatest number of hyperintense punctate lesions (P < .001). No statistically significant differences were found among the 3-mm T1-weighted sequences. The greater number of hyperintense punctate lesions detected by the 1-mm reformatted T1 3D-fast-field echo sequence in the central region of the brain was associated with a worse clinical outcome. CONCLUSIONS: At 3T, the 1-mm axial reformatted T1 3D-fast-field echo sequence identified the greatest number of hyperintense punctate lesions in the central region of preterm neonate brains, and this number was associated with neuromotor outcome.

Melanosis of the bladder: a rare endoscopic and histopathological finding.

Melanosis of the bladder represents a rare condition characterized by anomalous deposits of melanin-containing pigment. To our knowledge, so far, just 5 cases have been reported in the literature. We describe a case of a simply melanosis of the bladder confirmed by histochemical stains and immunohistochemistry analysis.

Prevalence of silent prostatic adenocarcinoma in 165 patients undergone cystoprostatectomy: a retrospective study.

The reported prevalence of prostatic adenocarcinoma (PCa) in adults represents only the . The present retrospective study was carried out to estimate the prevalence of the silent PCa in 165 subjects (median age: 69 years; range: 40-82) undergone radical cystoprostatectomy for bladder cancer. To this aim, 38 subjects had routinely prostatic sampling by histology (group A), whereas 127 had systematic pathological sampling of the gland (group B). Silent PCa was diagnosed in 17 subjects (9.7%): 1 subject was in the group A (0.7%) and 16 were in the group B (9%). The data suggest that systematic examination of the prostatic specimens should be performed in order to approach the real prevalence of silent PCa in adult population.

Prenatal pseudocysts of the germinal matrix in preterm infants.

Sonographic characteristics of germinal-matrix (PGM) pseudocysts of prenatal origin detected on cranial ultrasound in preterm newborns were correlated with their outcomes. PGM cysts were classified as typical or atypical, according to their location. Typical PGM cysts were present at the head of the caudate nucleus or slightly medially, adjacent to the foramen of Monro. Cysts were defined as atypical when they were located subependymally elsewhere. Only one infant of 16 with a typical PGM cyst presented with psychomotor retardation. His cerebral scan also showed subependymal calcifications due to cytomegalovirus infection. Three babies had cysts in the frontal periventricular zones (atypical PGM cyst). They had negative cranial MRI (12-15 months of age) and normal neurological follow-up (24 months). In conclusion, isolated prenatal PGM cysts in preterm infants correlate with a normal outcome.

Neonatal diagnosis of tuberous sclerosis.

Intracranial tumors are rare in the neonatal period, and generally the most common histological types are astrocytoma, medulloblastoma, choroid plexus papilloma and neuroectodermal tumors. The early diagnosis of these tumors is often very difficult. The authors report a case of a full-term newborn who presented with opisthotonus. A subependymal mass was detected by cerebral ultrasonography, and when the child was 1 month of age depigmentations appeared on the trunk and on the right leg, confirming the suspicion of tuberous sclerosis. At 3 months of age the child suffered infantile spasm with hypsarrhythmia. The developmental delay, the marked progressive neurological deterioration and the daily seizures suggested surgical resection. Histologic studies showed a subependymal giant cell astrocytoma such as typically occurs in tuberous sclerosis.

Fetal encephalopathy with cerebral calcifications: a case report.

The authors report a case of a newborn with severe encephalopathy and cerebral calcifications. The newborn was admitted to Neonatal Intensive Care Unit in Chieti at 2 days of age suffering from continuous generalized seizures. He was the child of healthy first-degree cousins. Cerebral ultrasonography showed bilateral ventricular dilatation and an intrathlamic hyperechoic image. Computed tomography and magnetic resonance imaging showed ventricular and corpus callosus hypoplasia, pachygyria, widespread delayed myelination areas, and basal nuclei and periventricular calcifications. All serum and urine analyses showed normal results. In particular, all demyelinizing metabolic diseases were excluded. Based upon these findings, we speculate that this infant may be suffering from fetal encephalopathy with cerebral calcifications.

Enamel defects in a case of Menkes' syndrome.

A patient affected by Menkes' syndrome presents some dental abnormalities, such as enamel defects, delayed eruption and a biconically shaped incisor. The deficient action of a cuproenzyme in this syndrome leads us to hypothesize an explanation of defective enamel formation.