Experimentally induced Chiari-like malformation with myeloschisis in chick embryos

Though several pathogenetic theories concerning the frequent association of Chiari malformation and hydrocephalus with myeloschisis have been suggested, none of them explains all the aspects of the disorder. To investigate whether myeloschisis is the direct cause of Chiari malformation and hydrocephalus or these conditions are the results of another basic event, we observed the morphological changes of the posterior cranial fossa and its components in the chick embryos with surgically induced myeloschisis. To make myeloschistic lesions, we opened the neural tube for a length of 9-11 somites in Hamburger and Hamilton stage 16-19 chick embryos. They were divided into cervicothoracic (C-T) and lumbosacral(L-S) groups according to the area of incision. The embryos were re-incubated until postoperative day 11. In the control group, embryos were incubated with the eggshell window open as their experimental counterparts. The survival rates of each group were as follows; 11% (9 survivors/85 operated embryos), 8% (7/83), and 17% (10/60) in the C-T, L-S and control groups, respectively. Myeloschisis positive rates were 100% in the operated groups and 0% in the control group. The heads of embryos were sectioned along the sagittal plane to observe the morphological changes in the posterior cranial fossa and its components. Of the survivors, five in the C-T group, two in the L-S group and six in the control group were available for light microscopic inspection. In the majority of embryos with myeloschisis, without difference between the C-T and L-S groups, the fourth ventricles were smaller than those of the control group and the subarachnoid spaces in the posterior cranial fossa were also narrower. In embryos with severe changes, the cerebellum displaced downward comparing with that of the control embryos. No evidence of hydrocephalus was present Though not always typical, morphological changes similar to Chiari malformation were observed in chick embryos with surgically induced myeloschisis. It suggests a strong direct causal relationship between the two conditions and supports the theories of derangements in cerebrospinal fluid dynamics rather than those of primary mesenchymal or neural origin as a pathogenetic mechanism of Chiari malformation.

Experimentally induced Chiari-like malformation with myeloschisis in chick embryos

Though several pathogenetic theories concerning the frequent association of Chiari malformation and hydrocephalus with myeloschisis have been suggested, none of them explains all the aspects of the disorder. To investigate whether myeloschisis is the direct cause of Chiari malformation and hydrocephalus or these conditions are the results of another basic event, we observed the morphological changes of the posterior cranial fossa and its components in the chick embryos with surgically induced myeloschisis. To make myeloschistic lesions, we opened the neural tube for a length of 9-11 somites in Hamburger and Hamilton stage 16-19 chick embryos. They were divided into cervicothoracic (C-T) and lumbosacral(L-S) groups according to the area of incision. The embryos were re-incubated until postoperative day 11. In the control group, embryos were incubated with the eggshell window open as their experimental counterparts. The survival rates of each group were as follows; 11% (9 survivors/85 operated embryos), 8% (7/83), and 17% (10/60) in the C-T, L-S and control groups, respectively. Myeloschisis positive rates were 100% in the operated groups and 0% in the control group. The heads of embryos were sectioned along the sagittal plane to observe the morphological changes in the posterior cranial fossa and its components. Of the survivors, five in the C-T group, two in the L-S group and six in the control group were available for light microscopic inspection. In the majority of embryos with myeloschisis, without difference between the C-T and L-S groups, the fourth ventricles were smaller than those of the control group and the subarachnoid spaces in the posterior cranial fossa were also narrower. In embryos with severe changes, the cerebellum displaced downward comparing with that of the control embryos. No evidence of hydrocephalus was present Though not always typical, morphological changes similar to Chiari malformation were observed in chick embryos with surgically induced myeloschisis. It suggests a strong direct causal relationship between the two conditions and supports the theories of derangements in cerebrospinal fluid dynamics rather than those of primary mesenchymal or neural origin as a pathogenetic mechanism of Chiari malformation.

Experimental exencephaly and myeloschisis in rats

To elucidate the early sequential morphogenetic progress of exencephaly and myeloschisis, rat embryos whose mothers had been treated with hypervitaminosis A were studied at 1-day interval from gestation day 10.5 to 15.5. In exposed animals sequential change was found in both exencephaly and myeloschisis as the embryos grew up. The 10.5-day old exencephalic embryos had still widely open cephalic neural tubes. Exencephalic embryos older than 13.5 days of gestation showed strikingly severe eversion and overgrowth of the cephalic neuroepithelium, thus failed in forming normal primitive brain. The convex dorsal surface of the exencephaly was covered with ependyma, which was connected directly with surrounding surface eqithelium at the periphery. The earliest morphologically recognized myeloschisis was in the 13.5-day old embryos. In myeloschisis, divergence at the roof plate and eversion of the spinal neural tube, disorganized overgrowth of the neuroepithelium, malformed and misplaced spinal ganglia and nerve roots, and absence of the neural arch and dermal covering were characteristic. It is suggested that exencephaly results from failure of the cephalic neural tube closure which is followed by eversion and overgrowth of the neuroepithelium. And failure in closure of the posterior neuropore and disturbance in the development of the tail bud probably play major role in the morphogenesis of myeloschisis.