Development of Behavior Patterns and Myelinization of Tracts in the Nervous System

Apparent Diffusion Coefficient Assessment of Brain Development in Normal Fetuses and Ventriculomegaly

“…Analogously to other works in normal fetuses [13-15, 21, 23], we found that during brain development, ADC linearly decreased in CSO, TH, CH and pons, as well as in VM cases, reflecting the morphological changes of brain maturation that involves increasing cellularity, histogenesis and myelination [24]. The latter starts in the spinal cord (12 GA), followed by pons, cerebellar peduncles, and thalamic axons (14-20 GA), in the frontal, parietal and occipital lobes (30 GA) and finally in the cortex (35 GA), lasting for decades in the human brain [25][26][27][28].…”

Apparent Diffusion Coefficient Assessment of Brain Development in Normal Fetuses and Ventriculomegaly

“…Analogously to other works in normal fetuses [13-15, 21, 23], we found that during brain development, ADC linearly decreased in CSO, TH, CH and pons, as well as in VM cases, reflecting the morphological changes of brain maturation that involves increasing cellularity, histogenesis and myelination [24]. The latter starts in the spinal cord (12 GA), followed by pons, cerebellar peduncles, and thalamic axons (14-20 GA), in the frontal, parietal and occipital lobes (30 GA) and finally in the cortex (35 GA), lasting for decades in the human brain [25][26][27][28].…”

Myelin Basic Protein and Glial Fibrillary Acidic Protein in Human Fetal Brain*

“…Our results generally conform to results of earlier workers regarding the basic chronology of human developmental myelination: phylogenetically older regions myelinated earlier (Langworthy, 1933;Yakovlev & Lecours, 1967). Therefore a timetable of developmental myelination revealed by the MBP immunostain, utilizing larger numbers of gestational ages and sections, would result in some improvement in the precision of those older studies.…”

Infantile spongy degeneration of the central nervous system associated with glycogen storage and markedly fatty liver

“…However, in the present case the presence of oedema alone can not explain the whole pathological picture of the brain, especially the systematic preservation of certain fibre tracts. The fibre tracts preserved in our case-that is, medial lemniscus, medial longitudinal tracts in the brain-stem, superior cerebellar peduncle, dorsal column and spinocerebellar tracts in the spinal cord, etc.-are those known to be myelinated in the earlier stages of development, approximately from the end of foetal life through early postnatal life (Langworthy, 1933;Yakovlev and Lecours, 1967;Rorke and Riggs, 1969). In other words, the spongy change and associated myelin defect were much more severe in those tracts which are normally myelinated later in development.…”

Apparent Diffusion Coefficient Assessment of Brain Development in Normal Fetuses and Ventriculomegaly

“…Analogously to other works in normal fetuses [13-15, 21, 23], we found that during brain development, ADC linearly decreased in CSO, TH, CH and pons, as well as in VM cases, reflecting the morphological changes of brain maturation that involves increasing cellularity, histogenesis and myelination [24]. The latter starts in the spinal cord (12 GA), followed by pons, cerebellar peduncles, and thalamic axons (14-20 GA), in the frontal, parietal and occipital lobes (30 GA) and finally in the cortex (35 GA), lasting for decades in the human brain [25][26][27][28].…”

Myelin Basic Protein and Glial Fibrillary Acidic Protein in Human Fetal Brain*

“…Our results generally conform to results of earlier workers regarding the basic chronology of human developmental myelination: phylogenetically older regions myelinated earlier (Langworthy, 1933;Yakovlev & Lecours, 1967). Therefore a timetable of developmental myelination revealed by the MBP immunostain, utilizing larger numbers of gestational ages and sections, would result in some improvement in the precision of those older studies.…”

Infantile spongy degeneration of the central nervous system associated with glycogen storage and markedly fatty liver

“…However, in the present case the presence of oedema alone can not explain the whole pathological picture of the brain, especially the systematic preservation of certain fibre tracts. The fibre tracts preserved in our case-that is, medial lemniscus, medial longitudinal tracts in the brain-stem, superior cerebellar peduncle, dorsal column and spinocerebellar tracts in the spinal cord, etc.-are those known to be myelinated in the earlier stages of development, approximately from the end of foetal life through early postnatal life (Langworthy, 1933;Yakovlev and Lecours, 1967;Rorke and Riggs, 1969). In other words, the spongy change and associated myelin defect were much more severe in those tracts which are normally myelinated later in development.…”

Apparent Diffusion Coefficient Assessment of Brain Development in Normal Fetuses and Ventriculomegaly

“…Analogously to other works in normal fetuses [13-15, 21, 23], we found that during brain development, ADC linearly decreased in CSO, TH, CH and pons, as well as in VM cases, reflecting the morphological changes of brain maturation that involves increasing cellularity, histogenesis and myelination [24]. The latter starts in the spinal cord (12 GA), followed by pons, cerebellar peduncles, and thalamic axons (14-20 GA), in the frontal, parietal and occipital lobes (30 GA) and finally in the cortex (35 GA), lasting for decades in the human brain [25][26][27][28].…”

Myelin Basic Protein and Glial Fibrillary Acidic Protein in Human Fetal Brain*

“…Our results generally conform to results of earlier workers regarding the basic chronology of human developmental myelination: phylogenetically older regions myelinated earlier (Langworthy, 1933;Yakovlev & Lecours, 1967). Therefore a timetable of developmental myelination revealed by the MBP immunostain, utilizing larger numbers of gestational ages and sections, would result in some improvement in the precision of those older studies.…”

Infantile spongy degeneration of the central nervous system associated with glycogen storage and markedly fatty liver

“…However, in the present case the presence of oedema alone can not explain the whole pathological picture of the brain, especially the systematic preservation of certain fibre tracts. The fibre tracts preserved in our case-that is, medial lemniscus, medial longitudinal tracts in the brain-stem, superior cerebellar peduncle, dorsal column and spinocerebellar tracts in the spinal cord, etc.-are those known to be myelinated in the earlier stages of development, approximately from the end of foetal life through early postnatal life (Langworthy, 1933;Yakovlev and Lecours, 1967;Rorke and Riggs, 1969). In other words, the spongy change and associated myelin defect were much more severe in those tracts which are normally myelinated later in development.…”