thirties2txt

Zimmerman and Yannet (1933) described the brain damage resulting
from neonatal jaundice. Jaundice is caused by high levels of circulating
bilirubin, from the breakdown of hemoglobin. In the past, one of the
conditions that invariably lead to severe jaundice, with subsequent
cerebral palsy and mental retardation, was hemolytic disease in
newborns of Rh-negative mothers (erythroblastosis fetalis). Antibody
production is triggered during separation of the placenta at the birth of
an infant with Rh-positive blood. During subsequent pregnancies, the
maternal antibodies can then affect the fetus, causing breakdown of
hemoglobin, which the immature biliary system of the infant is unable to
eliminate.

When the cause of hemolytic disease was first recognized, it was treated
by replacement transfusion of affected infants at birth (Pearson 1998).
Now giving Rh-negative mothers injections of the gamma globulin
RhoGAM at the time they give birth to their first child can prevent this
problem (Mittendorf & Willliams 1991). RhoGAM prevents formation of
antibodies, which protects the fetus in subsequent pregnancies.
Rh-negative blood is an example of a genetic disorder not related to
brain dysfunction that can nevertheless lead to congenital brain damage.
Many more such circumstances are likely to be found as genetic
predisposing factors for infantile autism, which is why the gene-hunt for
autism is currently so unproductive.

The paper by Zimmerman and Yannet (1933) identified the brain
damage caused by high levels of bilirubin to be in the brainstem. Their
data was from infants who died at birth, and they noted involvement of
the basal ganglia, the subcortical centers of motor control. Later
investigations of the effects of bilirubin in experimental animals would
reveal involvement of the inferior colliculi as part of the subcortical
pattern of brain damage (Rozdilsky & Olszewski 1961, Lucey et al 1964,
Chen et al 1964-1971).