lissencephaly/hypoxia

A case report on a 4 year old boy with physical and mental retardation noted since the age of 7 months is presented. In the 10th month a hydrocephalus internus was diagnosed. The autopsy showed a cerebral dystrophy with diffuse pachygyria presumably caused by a disturbance in the neuroblast

The architectonic features of abnormal cerebral cortex in a brain with lissencephaly and pachygyria suggest that neuronal migration was interrupted by cortical and subcortical laminar necrosis in the fourth fetal month. The severest cortical abnormality lies in the distal perfusion fields of the

A 4-month-old infant with lissencephaly syndrome who was diagnosed on the basis of clinical symptoms and computed tomography experienced four apnea attacks during three polysomnographies. Apnea attacks were of two types. Type I apnea attacks were thought to be sleep apnea. The cause is unknown.

In a recent case of monochorionic diamniotic twinning we observed one twin with acardia, cyclopia, and aprosencephaly, an association not reported previously. In most cases of acardia, the development of tissues in superior regions of the body is disrupted severely, while inferior structures develop

Sleep EEG patterns in 23 mentally retarded children with cerebral palsy (CP) (from 4 months to 5 years of age) and 39 reference mentally retarded children of no abnormality with the exception of psychomotor retardation (from 4 months to 12 years of age) were studied throughout nocturnal sleep, and

Platelet-activating factor (PAF) is a phospholipid mediator whose synthesis and degradation depend on specific sets of enzymes. PAF-acetylhydrolase (PAF-AH) hydrolyzes the acetyl moiety of PAF at its sn-2 position and thereby inactivates it. PAF-AH Ib, originally identified in brain, exists in the

Oxygen deprivation can cause severe defects in human brain development, yet the precise cellular and molecular consequences of varying oxygen levels on nervous system development are unknown. We found that hypoxia caused specific axon pathfinding and neuronal migration defects in C. elegans that