Re: How does a human body form without a brain, ie Anencephaly?

   The main reason that in anencephaly ("without a brain") 
the rest of the body can function is that lots of the 
development and physiological body controls develop 
independently of the brain.


WHAT IS ANENCEPHALY AND WHEN DOES IT BEGIN?

      Anencephaly is a developmental defect in which part or 
most of the brain  is absent at birth.  Only some 24% of 
humans with anencephaly are born alive.  Most,  some 54% 
abort spontaneously and 22% are stillborn (dead at birth).   
The timing of the defect is probably as early as the first 18-20 
days of human pregnancy.  This is the time at which mesenchymal 
defects can result in failure of the neural tube (precursor 
of the brain) to close.   Analysis of the development of the 
affected tissues localizes the impaired development as 
occuring near  the fifth to tenth week of gestation;  probably 
closer to the fifth week.   The reduced size of the brain is 
accompanied by a change in the remodeling pattern of the internal 
as well as the external surface of the head. Compared to normal 
newborns, there is a flattening of the cranial base.


WHAT OTHER BIRTH DEFECTS OCCUR WITH ANENCEPHALY?

          The ears internally and externally are most often 
underdeveloped.  Brain tissue may be prone to undergo 
cancerous changes (becoming a neuroblastoma).  Often the 
spinal column is deformed.   Cardiovascular and renal 
defects are common. Adrenal glands (on the kidneys) are 
smaller and thinner than are those in normal fetuses.   
Cleft palates, underdeveloped digestive systems are also 
seen in anencephaly infants.  About 5 to 10% of them also 
have underdeveloped limbs.

    Interestingly, development of the reproductive systems 
in male and female is not so severely affected. This 
believed to be because hormones from placenta which stimulate the 
development of embryonic cells that form testis and ovaries are 
normally produced in anencephaly embryos. 


ARE GENETIC OR ENVIRONMENTAL FACTORS RESPONSIBLE FOR 
ANENCEPHALY?


         Genetics -

       There is still a  debate among geneticists as to the 
origin of  anencephaly.   The condition has not been 
associated with the chromosomal anomaly of trisomy 18 (a 
chromosome commonly associated in humans with birth 
defects). So far it has been assumed that anencephaly 
results from secondary destruction of the neural tube 
during early development.

       Anencephaly in the xn strain of mouse is a 
condition determined by a single autosomal recessive gene. 
Detection of the cerebral malformation at this early stage 
of gestation suggests that inherited anencephaly is due to 
primary failure of the neural tube to close. 


         Environmental factors

      Injecting pregnant golden hamsters with arsenic salts 
early in gestation results in high embryonic-fetal 
mortality (approximately 50%).   Among the surviving 
fetuses, nearly 90% of them develop 3neural tube defects."  
More specifically, injecting  golden hamsters with sodium 
arsenate (20 mg/kg) on the 8th day of their 16 day 
gestation period induced in the embryos failure of the 
neural tube to close.  This resulted in fetal anencephaly. 

    Similarly, injecting large doses of vitamin A into 
experimental rats during the 8th to 10th day of gestation 
produces anencephaly.  Gestation to term in rats is 22 days.
 
     These animal experiments further demonstrate 
that anencephaly  results from the neural tube failing to 
close during embryonic development, and that the condition 
can be produced environmentally.