schizophrenia, like many other neural disorders, is nothing but a term. It describes a group of specific functionally debilitating abnormalities that often manifest themselves together.
Although there may be other causes for some of the symptoms found in highly effected schizophrenics, this proposed model has been found to explain many of the grouped symptoms that are known to be the basis for a proper diagnosis of clinical schizophrenia.
this type of evidence has been around for years, it's not a wacky correlation: there's a very rational cause and effect happening here.
During the neuroblast stage of embryonic development (when all our cells are nothing but a fluid filled ball) our neurons begin developing on the inner surface of that ball structure relative to the functional mapping they will eventually have in the brain. This is only two dimensional though: like putting billions of dots on a piece of paper, it will fill up pretty quick. In order to help disperse the newly formed neurons through the thickness of the shell (outwards) there are helper cells called "radial glia" that move neurons to their correct three dimensional orientations in an orderly fashion.
When the mother gets the flu (@ Morgan: not a sinus infection, that's usually not anything but a localized immune response, I wouldn't worry) and it transfers to the unborn fetus, the enzyme (organic catalyst: in this case a solvent) - that is meant to break the connection between the neuron and the radial glia cell when it reaches the right position in the newly formed brain - is rendered inoperative. The radial glia keep pulling the neurons past where they're supposed to go, so instead of a neat and orderly distribution of neurons: they end up bunched up and all topsy-turvy; yet still a functionally complete model. What causes schizophrenia after this point is mostly speculation, but I've heard offhand that the brain may form new more-efficient pathways between neurons to compensate for the (now) inefficient destined pathways, and they end up competing for the same functions.
The brain's formation and function is a beautiful process that is barely understood, I hope I've helped to shed light on this situation instead of making it even more confusing.
schizophrenia, like many other neural disorders, is nothing but a term. It describes a group of specific functionally debilitating abnormalities that often manifest themselves together.
Although there may be other causes for some of the symptoms found in highly effected schizophrenics, this proposed model has been found to explain many of the grouped symptoms that are known to be the basis for a proper diagnosis of clinical schizophrenia.
this type of evidence has been around for years, it's not a wacky correlation: there's a very rational cause and effect happening here.
During the neuroblast stage of embryonic development (when all our cells are nothing but a fluid filled ball) our neurons begin developing on the inner surface of that ball structure relative to the functional mapping they will eventually have in the brain. This is only two dimensional though: like putting billions of dots on a piece of paper, it will fill up pretty quick. In order to help disperse the newly formed neurons through the thickness of the shell (outwards) there are helper cells called "radial glia" that move neurons to their correct three dimensional orientations in an orderly fashion.
When the mother gets the flu (@ Morgan: not a sinus infection, that's usually not anything but a localized immune response, I wouldn't worry) and it transfers to the unborn fetus, the enzyme (organic catalyst: in this case a solvent) - that is meant to break the connection between the neuron and the radial glia cell when it reaches the right position in the newly formed brain - is rendered inoperative. The radial glia keep pulling the neurons past where they're supposed to go, so instead of a neat and orderly distribution of neurons: they end up bunched up and all topsy-turvy; yet still a functionally complete model. What causes schizophrenia after this point is mostly speculation, but I've heard offhand that the brain may form new more-efficient pathways between neurons to compensate for the (now) inefficient destined pathways, and they end up competing for the same functions.
The brain's formation and function is a beautiful process that is barely understood, I hope I've helped to shed light on this situation instead of making it even more confusing.