5 -  The broader autism phenotype
Asperger syndrome is a condition related to autism in
which minor motor impairments may be prominent.  
Children with Asperger syndrome may be delayed in
learning to speak, but appear to develop full
command of language by age three or four.  A small
percentage of children with autism develop normal
language past the age of four or five and are thus
referred to as children with "high functioning autism"
(HFA).  As they grow older, children with high
functioning autism cannot easily be distinguished from
children with Asperger syndrome [1, 2].  Cederlund
and Gillberg (2004) studied 100 males with asperger
syndrome and concluded that Asperger syndrome is
not "mild" autism, but autism with mild (or lesser)
cognitive impairment [3].

Asperger syndrome is considered to be part of a
spectrum of autistic disorders.  One difficulty with
thinking of Asperger syndrome as on a true spectrum
with autism (as defined by Kanner) is the motor
clumsiness often noted in children with Asperger
syndrome.  However, autism and Asperger syndrome
resulting from trauma and hypoxia during a difficult
birth can be viewed as on a spectrum of impairment
resulting from varying degrees of involvement of
Myers' two patterns of perinatal brain damage:

    1 - A brief episode of total oxygen cutoff would, as
    in the case of the experimental moneys, result in
    the brainstem pattern of damage with most severe
    involvement of the inferior colliculi.  A child so
    afflicted would develop, as the monkeys did, with
    some transient delay in motor development, which
    would be optimistically dismissed by pediatricians
    as totally within the normal variation of normal
    limits.  Concern might arise only when difficulties
    with speech development become noticeable.

    2 - A difficult, traumatic birth would more likely
    result in Myers' second pattern of damage,
    affecting the circulatory  "watershed" areas of the
    cortex, as well as the nuclei of the subcortical
    motor system, which are metabolically somewhat
    less active than the inferior colliculi.  A final brief
    period of total anoxia would involve the inferior
    colliculi, but if not for quite as prolonged period of
    time as the monkeys experienced, the impact on
    learning to speak might be less severe.

Late language development is a problem for children
with Asperger's sysndrome.  In their research on 100
males with Asperger's syndrome, Cederlund and
Gillberg noted, "Forty-five of 92 children (49%) for
whom fairly detailed data about early language
development were available, clearly did not have
normal language development at 2 years of age. It
cannot be concluded that the remainder had normal
language development."

Children with Asperger's syndrome are often reported
to have a superior command of language.  They may
have an unusually large repertoire of learned
expressions, which as is often noted they may use
slightly or strangely tangential to the context or topic
of a conversation.  Could this be the reason they are
also often viewed as good punners?

With severe involvement only of the inferior colliculus
(autism) on one end, and lesser involvement of the
inferior colliculus plus some impairment of motor
control (Asperger syndrome) at the other, the
spectrum could represent different degrees of the two
patterns of brain damage found by Myers.  Cerebral
palsy is on this spectrum too, but with serious motor
handicaps and perhaps no language learning
difficulties at all.  Unfortunately, brain damage most
often involves some degree of disability in every
functional sphere.

Even dyslexia should probably be investigated as a
language learning difficulty in which maturation of the
cross-modal tracts between the temporal, occipital,
parietal, and frontal lobes has not progressed
normally.  How many different problems might be
related to the "trans-neuronal" disruption of brain
development observed by Faro and Windle as long
term outcomes of asphyxia at birth in monkeys.

Preventing oxygen insufficiency at birth needs to be a
priority.  Optimism cannot overcome afflictions that
have for too long been viewed as mild or minimal in
young children.  Outcomes in adulthood need to be
investigated.  Oxygen deficiency at birth must be
taken seriously, because of the patterns of brain
damage known to result, and that these patterns
correspond to functional deficiencies of people with
autism spectrum disorders.
  1. Szatmari P et al. (1989)
    Asperger's syndrome and
    autism: comparison of early
    history and outcome.
  2. Szatmari P et al. (1990)
    Asperger's syndrome and
    autism: neurocognitive
    aspects.
  3. Cederlund M, Gillberg C
    (2004) One hundred males
    with Asperger syndrome: a
    clinical study of background
    and associated factors.  
  4. Freitag CM et al. (2006)
    Quantitative Assessment of
    Neuromotor Function in
    Adolescents with High
    Functioning Autism and
    Asperger Syndrome.
  5. Tani P et al. (2006). Clinical
    neurological abnormalities in
    young adults with Asperger
    syndrome.
  6. Rinehart NJ et al. (2006) Gait
    function in high-functioning
    autism and Asperger's
    disorder : evidence for basal-
    ganglia and cerebellar
    involvement?
  7. Gillberg C, Kadesjo B. (2003)
    Why bother about
    clumsiness? The
    implications of having
    developmental coordination
    disorder (DCD).
  8. Hippler K, Klicpera C. (2003)
    A retrospective analysis of
    the clinical case records of
    'autistic psychopaths'
    diagnosed by Hans Asperger
    and his team at the University
    Children's Hospital, Vienna.
  9. Myers RE (1972) Two
    patterns of perinatal brain
    damage and their conditions
    of occurrence.  
  10. Faro MD, Windle WF (1969)
    Transneuronal degeneration
    in brains of monkeys
    asphyxiated at birth.
References
Full References
top
  1. Szatmari P, Bartolucci G, Bremner R (1989) Asperger's syndrome and
    autism: comparison of early history and outcome. Developmental Medicine
    and Child Neurology 31:709-720.
  2. Szatmari P, Tuff L, Finlayson MA, Bartolucci G (1990) Asperger's
    syndrome and autism: neurocognitive aspects. Journal of the American
    Academy of Child and Adolescent Psychiatry 29:130-136.
  3. Cederlund M, Gillberg C (2004) One hundred males with Asperger
    syndrome: a clinical study of background and associated factors.  
    Developmental Medicine & Child Neurology 46: 652-660.
  4. Freitag CM, Kleser C, Schneider M, von Gontard A. Quantitative
    Assessment of Neuromotor Function in Adolescents with High Functioning
    Autism and Asperger Syndrome. J Autism Dev Disord. 2006 Dec 15; [Epub
    ahead of print]
  5. Tani P, Lindberg N, Appelberg B, Nieminen-von Wendt T, von Wendt L,
    Porkka-Heiskanen T. Clinical neurological abnormalities in young adults
    with Asperger syndrome. Psychiatry Clin Neurosci. 2006 Apr;60(2):253-5.
  6. Rinehart NJ, Tonge BJ, Bradshaw JL, Iansek R, Enticott PG, McGinley J.
    Gait function in high-functioning autism and Asperger's disorder : evidence
    for basal-ganglia and cerebellar involvement? Eur Child Adolesc
    Psychiatry. 2006 Aug;15(5):256-64.
  7. Gillberg C, Kadesjo B. Why bother about clumsiness? The implications of
    having developmental coordination disorder (DCD). Neural Plast. 2003;10
    (1-2):59-68.
  8. Hippler K, Klicpera C. A retrospective analysis of the clinical case records
    of 'autistic psychopaths' diagnosed by Hans Asperger and his team at the
    University Children's Hospital, Vienna. Philos Trans R Soc Lond B Biol Sci.
    2003 Feb 28;358(1430):291-301.
  9. Myers RE (1972) Two patterns of perinatal brain damage and their
    conditions of occurrence.  American Journal of Obstetrics and Gynecology
    112:246-276
  10. Faro MD & Windle WF (1969) Transneuronal degeneration in brains of
    monkeys asphyxiated at birth.  Experimental Neurology 24:38-53.