Introduction

In 1975 I proposed the inferior colliculus as a possible
locus of impairment in children with autism underlying
both the language disorder and deficits in
environmental awareness [1].  This theory has not
attracted any interest, but I continue to find more
evidence in its favor than in other explanations of how
the brain might be impaired.  Perhaps most important:
Loss of function in this brainstem nucleus in infancy
may prevent production of trophic transmitters
required for normal maturation of the language areas
of the temporal and frontal lobes [2].

The inferior colliculus is a small nucleus in the
midbrain auditory pathway, but it is more than a mere
way-station in the neural circuit conducting acoustic
sensations to the cerebral cortex.  The inferior
colliculus is metabolically the most active site in the
brain [3]; and it may be the vigilance center of the
brain [4].  The auditory sense evolved as an alerting
mechanism for visual attention, and has developed
into an information-seeking system that enables
continuous awareness of the environment, even
during sleep [4, 5].  Language for the human species
is the greatest refinement of this information-seeking
instinct.

Autism is a neurological disorder; thus theories of
causation must in the end describe how brain areas
needed for language, environmental awareness, and
social instincts are affected.  The search for autism
genes has recently been the focus of much
research.  A huge lay movement believes infant
vaccinations are responsible for the increased
prevalence of autism that has become evident since
the early 1990s.  Autism has been reported in
children with fetal alcohol syndrome, prenatal
exposure to valproic acid or thalidomide, and rubella
infection during gestation.

How the brain might be affected by these various
etiological factors receives very little discussion.  I will
discuss evidence that the inferior colliculus is
vulnerable to all of the known genetic defects and
environmental insults associated with autism.

Further, perinatal problems are frequently found as
predispositions for autism.  The greatest worry when
complications of pregnancy and birth occur is the
possibility of oxygen insufficiency.  Infants are thought
to be more resistant to oxygen lack than adults, but
this may be a serious misconception.  The infant
heart is more resistant to damage, but not the brain
[6].  

Experiments with monkeys on asphyxia at birth were
begun during the 1950s in an attempt to produce an
animal model of cerebral palsy [6].  Asphyxia was
inflicted by delivering the head of the infant monkey
into a saline-filled sac and clamping the umbilical
cord.  Thus the onset of breathing was blocked, as
was continuing respiration from the placenta.  The
surprise result was that the monkeys displayed only
transient delay in developing control of motor
functions, and initially no damage in the brain could
be found.  Damage was found only after members of
the team of Landau et al (1955) suggested looking in
the inferior colliculi (plural of colliculus).  This was the
site in the brain, where, to their great surprise, they
had recently found the highest rate of blood flow [3].

The asphyxiated monkeys did not develop cerebral
palsy, and eventually outgrew their initial
developmental delays.  However, residual lack of
manual dexterity remained in monkeys that survived
for several months or years [7].  Windle (1969)
suggested the damage to the inferior colliculi and
lesser degrees of injury in other brainstem nuclei
might be the cause of what was then known as
"minimal cerebral dysfunction" (MCD).  Pervasive
developmental disorder (PDD) has now replaced the
designation MCD, and developmental language
disorder is one of the most serious aspects of PDD.

The research on asphyxia at birth appears to be long
forgotten; I will review several aspects of the
experiments with monkeys, including what caused
cerebral palsy.  These are experiments than cannot
be repeated because of regulations on use of
laboratory animals.  However, the data remain valid
and merit reconsideration, particularly the prominent
damage found in the inferior colliculi.

With the advent of magnetic resonance imaging (MRI)
in the early 1990s, selective damage of the inferior
colliculi has been reported in several case reports of
people who lost the ability to comprehend spoken
language after traumatic head injury or cancerous
growth into the midbrain [8].  Deafness and “word
deafness” was assumed to be a psychological
reaction in some of these cases, until the small
lesions in the inferior colliculi were found in MRI
scans.  If impairment of function in the inferior colliculi
can have such a catastrophic effect on people without
previous language problems, what should we expect
when a child sustains damage to the inferior colliculi
by asphyxia at birth?

I am therefore returning to the view I put forth in 1975,
that impairment of function within the inferior colliculi
may underlie the language disorder of children with
autism.  Evidence for this view is the focus of the
chapters that follow.

My research on autism dates back to 1967 when my
three-year-old son, Conrad was diagnosed as
autistic.  I began graduate studies in 1969 at the
Boston University School of Medicine, and in October
came across the article by William Windle on asphyxia
at birth in the Scientific American.  When I saw the big
holes in the inferior colliculi caused by asphyxia, I
knew this must be the cause of Conrad's problems
learning to speak.  He had to be resuscitated after a
traumatic "face presentation" birth.  Research on
asphyxia became the focus of my graduate studies.

I began writing this book around 1997 - thirty years
later, and two years after Conrad's death in a group
home from a prescribed overdose of Thorazine.  At
the suggestion of a friend I posted a website in
Conrad's memory in April 2000.

Many people who came across my website have
contacted me.  One of these was Dr. George Morley,
a retired obstetrician, who asked me if I knew how
soon after birth Conrad's umbilical cord had been
clamped.  Clearly, it was before he was breathing,
and I still re-experience the sense of panic I felt, that
my baby was on the other side of the room, pale and
lifeless, surrounded by a team of people working to
get him breathing.

My grief is great.  I do believe now that he could have
been resuscitated sooner with the umbilical cord left
intact and functioning, and been saved from brain
damage and autism.  Over the past four years I have
become more and more involved, with many others,
trying to change the "written standard of care"
mandated by the American College of Obstetrics and
Gynecology, to clamp the umbilical cord within
seconds after birth [9].  Silence is the only response
we have received from the obstetric professionals.

Evidence seems abundant that clamping the umbilical
cord is a medical error, and it goes against a long
tradition of waiting at least for the first breath and  
preferably until pulsations in the cord cease.  It is no
doubt instinctive for most obstetricians and midwives
to wait for the infant to be breathing before clamping
the cord, but this is no longer explicitly stated in the
written protocols.  Impairment, if not gross damage, of
the inferior colliculi may occur with only the briefest
lapse in respiration at birth, and this could well
underlie  developmental language disorders in
increasing numbers of children.
References
(Note: full citations are in the
alphabetic bibliography)

1.  Locus of impaired
language and
environmental awareness

2.  Trophic transmitters
guide maturation of the
cerebral cortex

3.  Highest rates of blood
flow and aerobic
metabolism

4.  The inferior colliculus
may be the vigilance
center of the brain

5.  The auditory sense is
an information-seeking
system, language its
highest evolutionary stage

6.  Asphyxia at birth

7. Development of the
cerebral cortex did not
proceed normally following
asphyxia at birth

8. Impaired speech
comprehension following
injury of the inferior
colliculi

9. Umbilical cord clamping