Topographical and cytological evolution of the glial phase during prenatal development of the human brain: histochemical and electron microscopic study.

An ultrastructural analysis of prenatal gliogenesis and neuronal-glial relationships in the developing fetal brain was carried out using reduced osmium and periodic acid-thiocarbohydrazide-silver proteinate to stain selectively the glycogen content of the glial population. Gliophilic neuronal migration was confirmed in the human fetus, with radial glial fibers (RGF) acting as obligatory corridors for neuronal migration in the prospective neocortex and underlying intermediate zone (IZ). With this method, the entire glial phase was differentiated from neuronal elements; this permitted a description of the evolutionary distribution pattern of RGF: in the cortical plate, glial fascicles fully dissociate by 18 weeks gestation, whereas in the IZ, they remain grouped in fascicles until their transformation into astrocytes. The most conspicuous and constant developmental feature observed in the maturing glial cytoplasm between 21 and 30 weeks gestation was a radical enhancement in the abundance and activity of the lysosomal apparatus and autophagic vacuoles observed in the RGF, a cytological basis for the transformation of radial glial cells into astrocytes. These data have implications for the understanding of the ontogenesis of the neocortical vertical modules in the human brain and for the phylogenetic analysis of the vertical cortical units in terms of comparative mammalian anatomy

The Human Transient Subpial Granular Layer - An Optical, Immunohistochemical, and Ultrastructural Analysis

The cytological features, origin, migration, and fate of the subpial granular layer cells of the human embryonic cerebral cortex are studied with light and electron microscopy, Golgi impregnations, and immunocytochemical staining with the microtubule associated protein 2 and glial fibrillary acidic protein antibodies. Subpial granular layer (SGL) cells form a distinct neuronal population in the molecular layer, characterized by a small dark nucleus with abundant chomatin clumps and prominent nucleoli, and a lightly stained cytoplasm containing few organelles. Somata and processes of SGL cells are intensively stained with microtubule-associated protein 2 antibody but do not express glial fibrillary acidic protein antibody. These cells apparently originate from the olfactory germinative zone. They follow two major strands from the olfactory subventricular zone to the subpial region. Subsequently, they migrate tangentially at the subpial level to all cortical regions, as is observed on Golgi and ultrastructural preparations. They constitute a transient population that penetrates the deep molecular layer and subsequently disappear from it. Several cytological features of these cells suggest an inward migration with growth of a radial process toward the cortical plate and subsequent nuclear translocation. The fate and the role of this new phylogenetic neuronal population has yet to be determined although the abundance of degenerating SGL cells in the deep molecular layer suggests at least partial degeneration

Early diagnosis of Sheehan's syndrome.

Early diagnosis of Sheehan's syndrome

Early diagnosis of Sheehan's syndrome

Early diagnosis of Sheehan's syndrome

Prolonged dysphagia caused by congenital pharyngeal dysfunction.

We describe two patients with severe, isolated, congenital dysphagia caused by paralysis of the pharyngeal muscles, who recovered at the ages of 40 months and 20 months, respectively. No other evidence of neurologic or muscular dysfunction was present except for a transient paralysis of the adductors of the vocal cords in one child. Radiocinematographic studies showed paralysis of the pharyngeal stage of swallowing, with minimal involvement of the oral stage. One child refused oral feeding for several months after apparent radiologic recovery. Two other patients with a similar disorder died of tracheal aspiration at the ages of 8 months and 4 months, respectively. Autopsies showed no abnormality of the central nervous system, and the cranial nerves involved in swallowing were normal. Only five other well-studied cases of this syndrome have been reported. These observations demonstrate the existence of a type of severe, idiopathic, congenital dysphagia related to paralysis of the constrictor muscles of the pharynx, with a propensity to recover after several months or years if properly managed. The cause of the disorder is obscure, but it is probably related to a dysfunction of the central nervous system

The germinative zone produces the most cortical astrocytes after neuronal migration in the developing mammalian brain.

The origin of astrocytes of the mouse neocortex during the fetal and early postnatal periods as determined by immunocytological, autoradiographic, electron microscopic and antimitotic methods is described. Most astrocytes destined for the white matter and the infragranular cortical layers are derived from the transformation of radial glial cells between P0 and P10 with an inside-out pattern. This cell metamorphosis is not directly preceded by mitosis and involves the activation of the radial glial lysosomal apparatus. In opposition to recent hypotheses, our findings suggest that most astrocytes destined for the supragranular cortical layers are produced in the germinative zone after the migration of the infragranular neurons and themselves migrate afterwards to the upper cortex between E16 and the first postnatal days. These astrocytes do not display an intermediate stage of the radial glial cell and do not participate in the pattern of appearance of the deeper astrocytes. This second step of astrocytogenesis is a condition for normal cytoarchitectonic development and the maintenance of the supragranular layers, since the deprivation of the astrocytic equipment of the supragranular layers by an antimitotic drug drastically reduces the number of supragranular neurons

Brain defects in infants with Potter syndrome (oligohydramnios sequence)

Defects of neuronal migration were detected in the brains of five unrelated infants with Potter syndrome (oligohydramnios sequence). These consisted of abnormal lamination of cerebral cortex, white matter heterotopias, and meningeal and molecular zone neuronal-glial ectopias. Besides, various other brain anomalies were sometimes found. They comprised one or more of the followings: abnormal gyration patterns (gyral fusion, cerebellar microgyria), cerebellar granule and Purkinje cell heterotopias, brain stem heterotopias, adysplasia of basal ganglia, gliosis, mineralization, and hydrocephalus. Detailed investigations, using standard neuropathologic stains, immunohistochemical and Golgi methods, and a new electron microscopic histochemical technique that we applied to study the developing human brain, suggest that migration defects of neurons are caused by an abnormality in their glial guides, the radial glial fibers, during the period of cortical histogenesis. We hypothesize that abnormally and precociously induced radial glial transformation into astrocytes is the pathogenic mechanism for the defects in neuronal migration. The etiological factor(s) that precipitates such abnormal glial transformation seems to be heterogeneous. Its relation to the Potter anomaly is discussed

Multiple aggressive vertebral haemangiomas in an adolescent: a case report.

We describe a neurologically symptom-free adolescent with aggressive vertebral body haemangiomas at two sites