First, let's consider how the brain matures during adolescence. While significant growth occurs early on—the brain reaches 90 percent of its adult size by the age of 6—a second wave takes place in the years before puberty. During this time, gray matter—areas of the brain responsible for processing information and storing memories—increases in size, particularly in the frontal lobe of the brain, as a result of an increase in the number of synaptic connections between nerve cells. Around puberty, however, a winnowing process begins in which connections that are not used or reinforced begin to wither (hence the "use-it-or-lose-it" hypothesis). This pruning, which begins around age 11 in girls and 12 in boys, continues into the early or mid-20s, particularly in the prefrontal cortex, an area associated with "higher" functions such as planning, reasoning, judgment, and impulse control. As Dr. Jay Giedd of the National Institute of Mental Health has said, the real cognitive advances come with paring down or reducing the number of synaptic connections. During adolescence, the amount of myelin, a fatty, insulating material that coats the axons of nerve cells—similar to the way insulation coats a wire—also increases, improving the nerve cells' ability to conduct electrical signals and to function efficiently; this too continues into adulthood and occurs later in "higher" regions of the brain, such as the prefrontal cortex.
The most detailed evidence for these maturation processes comes from magnetic resonance imaging studies, which underscore the changing arrangement of gray matter and extent of myelination in adolescents and adults. Such research makes the case, for instance, that marked differences do exist between the brain of a 13-year-old and that of a 25-year-old.
Dr. Frohman asks Dr. Lee-
Why the latency for onset of MS compared to other VM disease?
Dr. Lee states that some cases of Budd Chiari are diagnosed at age 30, not all are pediatric. It depends on the level of vena cava obstruction. It is too late to repair by the time they do a liver biopsy. The venous system is not like the atrial system- extra pressure makes it very vulnerable. Acute venous hypertension is easy to find and obvious, but this is not the issue...it is the slower progress such as CCSVI...what we do not know is what we do not know.
fogdweller wrote:This is a very smart, informed and and well educated group of people. Using our creativity, and assuming CCSVI is correct and the venous malformations are congenital, any speculations as to why childhood onset is rare and some cases of MS don't even show up 'til late adulthood?
mrsilkykat wrote:What about the geographic distribution of MS? What about gender? How do these MS issues fit into congenital CCSVI.
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