Ethanol-induced apoptotic neurodegeneration and fetal alcohol syndrome.

The deleterious effects of ethanol on the developing human brain are poorly understood. Here it is reported that ethanol, acting by a dual mechanism [blockade of N-methyl-D-aspartate (NMDA) glutamate receptors and excessive activation of GABA(A) receptors], triggers widespread apoptotic neurodegeneration in the developing rat forebrain. Vulnerability coincides with the period of synaptogenesis, which in humans extends from the sixth month of gestation to several years after birth. During this period, transient ethanol exposure can delete millions of neurons from the developing brain. This can explain the reduced brain mass and neurobehavioral disturbances associated with human fetal alcohol syndrome.

Neurotransmitters and apoptosis in the developing brain.

In the immature mammalian brain during a period of rapid growth (brain growth spurt/synaptogenesis period), neuronal apoptosis can be triggered by the transient blockade of glutamate N-methyl-d-aspartate (NMDA) receptors, or the excessive activation of gamma-aminobutyric acid (GABA(A)) receptors. Apoptogenic agents include anesthetics (ketamine, nitrous oxide, isoflurane, propofol, halothane), anticonvulsants (benzodiazepines, barbiturates), and drugs of abuse (phencyclidine, ketamine, ethanol). In humans, the brain growth spurt period starts in the sixth month of pregnancy and extends to the third year after birth. Ethanol, which has both NMDA antagonist and GABA(A) agonist properties, is particularly effective in triggering widespread apoptotic neurodegeneration during this vulnerable period. Thus, maternal ingestion of ethanol during the third trimester of pregnancy can readily explain the dysmorphogenic changes in the fetal brain and consequent neurobehavioral disturbances that characterize the human fetal alcohol syndrome. In addition, there is basis for concern that agents used in pediatric and obstetrical medicine for purposes of sedation, anesthesia, and seizure management may cause apoptotic neuronal death in the developing human brain.

[Arterial supply of the sartorius muscle]. / Die arterielle Versorgung des Musculus sartorius.

According to dissections of 40 specimen we received an impression of the arterial supply of the sartorius muscle. The results were as following that the sartorius is supplied by 2-4 arteries, occasionally up to 9, which originate from the middle and distal third of the femoral artery. As a result of the dissections we may state that the sartorius receives an adequate supply, when only the proximal or distal artery remains intact. Because of the above, the sartorius is suitable as a proximally or distally based flap in plastic surgery of the abdominal wall and as covering of bone defects of the hip, femur and knee.

[Restoration of an infected hip joint with sartorius-plasty]. / Die Sanierung des infizierten Hüftgelenkes mit der Sartorius-Plastik.

For treatment of infected hip joints we use the proximally based sartorius muscle. After ligation of the vessels in the distal part of the muscle, the sartorius muscle is elevated and transposed to the floor of the deep joint cavity. By completely filling the space defect, reinfection of the osteomyelitic cavity is prevented. In addition, the transposed muscle flap directs optimal blood perfusion to the hypoxemic capsule tissue via its own vascular pedicle.

[MRT of epiphyseolysis capitis femoris]. / MRT der Epiphyseolysis capitis femoris (ECF).

MR imaging provides exact measurement of the epiphyseal angle by drawing a ventral tangent to the femoral neck in parasagittal images along the femoral neck. The average MR imaging angle was 49.7 degrees in SCFE. Important information is provided about the activity of the slipping process (reattachment) and the contralateral epiphysis.