1405 
effect in this fish, by cultivating the larvae in a solution of sulfas 
magnesiae and Speman caused eyclopian larvae of triton through 
putting a ligature around their “Urmund”. 
This interpretation however has the same difficulty as the former. 
It does not account for the internal hydrocephalus. Moreover STOCKARD 
declares that the brains of these eyclopian buildings were normal. 
Therefore the experimental cyclopia cannot be compared, without 
restriction, with that made by nature. 
This interpretation points to a certain period in the development, 
to the so-called period of termination, of eyelopia. Its development 
commenced, at a time in which the eye-vesicles were differentiated, 
the telephalon is not vet divided and perhaps even in an earlier stage. 
In this interpretation the sagittal separation of the telencephalon is 
not formed because its ventro-medial end is ruined by the defect. 
The totally missing sagittal fissure in the telencephalon would be in 
direct opposition to the facts. It is only missing in the frontal pole. 
In all the eyclopian brains of men and calves, examined by me, 
the hemispheres are distinctly divided at the distal end, only at the 
frontal pole they are united. 
Another interpretation, suggested long ago by Kunprat, also appeals 
to pathologic influences. It may be supposed that a primary lesion 
in a loealised spot in the brain can account as well for the medio- 
ventral defect at the embryonal frontal pole, as for the origin of 
the sac. 
I want to insist upon the possibility of this interpretation, because 
| think it agrees better with some facts than the two other above- 
mentioned ways of interpretation do. 
Suppose a pathologie process altering the proximal part of the 
thin roof of the IIId ventricle at an early period of the embryonal 
life, but not so early that the termination-period falls before the 
sagittal division of the telencephalon. On the contrary, the termination- 
period now asks, that the medial fissure, dividing the telencephalon 
into hemispheres, has already begun its formation. 
The great amount of fluid, result of the pathologic process, dilates 
in dorsal direction the roof of the IIId ventricle. It prominates in 
the fissure between the two hemispheres, pushing the occipital poles 
of the hemispheres far aside, and pressing on the other hand the 
frontal poles against each other. As soon as the pressure in the 
ventricle becomes too intense, the brain vesicle will burst and 
probably the burst will take place there, where its resistence is 
small, i.e. through the lamina terminalis, in the direction of the 
prechordal part of the base of the ventricle. 
