1. Courchesne E (1995) New evidence of cerebellar and brainstem hypoplasia in autistic infants,
    children and adolescents: the MR imaging study by Hashimoto and colleagues. Journal of
    Autism and Developmental Disorders25:19-22.
  2. Hashimoto T, Tayama M, Murakawa K, Yoshimoto T, Miyazaki M, Harada M, Kuroda Y (1995)
    Development of the brainstem and cerebellum in autistic patients.  Journal of Autism and
    Developmental Disorders 25:1-18.
  3. Roebuck TM, Mattson SN, Riley EP (1998) A review of the neuroanatomical findings in children
    with fetal alcohol syndrome or prenatal exposure to alcohol. Alcoholism, Clinical and
    Experimental Research 22:339-44
  4. Schaefer GB, Thompson JN, Bodensteiner JB, McConnell JM, Kimberling WJ, Gay CT, Dutton
    WD, Hutchings DC, Gray SB (1996) Hypoplasia of the cerebellar vermis in neurogenetic
    syndromes.Annals of Neurology 39:382-5
  5. Cavanagh JB, Holton JL, Nolan CC (1997) Selective damage to the cerebellar vermis in
    chronic alcoholism: a contribution from neurotoxicology to an old problem of selective
    vulnerability. Neuropathology and Applied Neurobiology 23:355-363.
  6. Gaffney GR, Kuperman S, Tsai LY, Minchin S (1988) Morphological evidence for brainstem
    involvement in infantile autism. Biological Psychiatry 24:578-586.
  7. Jacobson R, LeCouteur A, Howlin P, Rutter M (1988) Selective subcortical abnormalities in
    autism.  Psychological Medicine 18:39-48.
  8. Hashimoto T, Tayama M, Miyazaki M, Murakawa K, Shimakawa S, Yoneda Y, Kuroda Y (1993)
    Brainstem involvement in high functioning autistic children. Acta Neurologica Scandinavica 88:
    123-128.
6 -  Magnetic Resonance Imaging (MRI)
Courchesne (1995) and coworkers used magnetic
resonance imaging (MRI) to look for signs of
neurological damage in autism [1].  They found
abnormalities in the vermis of the cerebellum.  
Hashimoto et al. (1995) measured areas of the brain
on MRI scans and found both the cerebellar vermis
and brainstem to be smaller in autistic compared with
control subjects [2].  Hypoplasia of the cerebellar
vermis is another abnormality encountered in fetal
alcohol syndrome, as are malformations attributable to
faulty neuron migration [3].  This does not implicate
prenatal alcohol exposure in the brains that have
been examined in individuals with autism; other
perinatal factors may well lead to development of the
same  abnormalities.

Schaefer et al. (1996) compared MRI images from 125
normal and 13 autistic subjects with those from 89
patients with a variety of neurogenetic disorders [4].  
In this study, no differences were found in the
cerebellar vermis of autistic compared with normal
subjects, but hypoplasia was found in patients with
other disorders, some with autistic features and some
without.  Schaefer et al. concluded that cerebellar
involvement is a common factor in many neurological
conditions and not a specific marker for autism.  
Cavanagh et al. (1997) discussed the vulnerability of
the cerebellar vermis as part of the neuropathology
caused by chronic alcoholism [5].  In every case of
autism, it would appear to be important to rule out
prenatal exposure to alcohol or other drugs, or
medical conditions, that might be the cause of
cerebellar vermis and cell migration abnormalities or
reduced brainstem size observed in cases of autism.

Gaffney et al. (1988) and Jacobson et al. (1988)
detected abnormalities of brainstem sites on MRI
scans of autistic subjects [6, 7].  Hashimoto et al.
(1993) measured brainstem areas on MRI scans and
found reduced brainstem volume in high functioning
individuals with autism [8].  The MRI data further
supports the idea that brainstem anomalies found on
autopsy may be relevant to the core syndrome of
autism; reduced brainstem volume could represent
involvement of the entire array of brainstem nuclei of
high metabolic rate, including the inferior olives and
mammillary bodies.  There are no visible signs of
brainstem damage in the MRI scans, but minimal
decrements within the group of metabolically active
brainstem nuclei could collectively produce the overall
measurable reduction in size.  However, reduced
brainstem mass cannot be viewed as characteristic of
idiopathic autism unless prenatal exposure to alcohol
is excluded as the cause.
References
  1. Courchesne E (1995) New
    evidence of cerebellar and
    brainstem hypoplasia in
    autistic infants, children and
    adolescents: the MR imaging
    study by Hashimoto and
    colleagues.
  2. Hashimoto T et al. (1995)
    Development of the
    brainstem and cerebellum in
    autistic patients
  3. Roebuck TM et al. (1998) A
    review of the
    neuroanatomical findings in
    children with fetal alcohol
    syndrome or prenatal
    exposure to alcohol.
  4. Schaefer GB et al. (1996)
    Hypoplasia of the cerebellar
    vermis in neurogenetic
    syndromes.
  5. Cavanagh JB et al. (1997)
    Selective damage to the
    cerebellar vermis in chronic
    alcoholism: a contribution
    from neurotoxicology to an
    old problem of selective
    vulnerability.
  6. Gaffney GR et al. (1988)
    Morphological evidence for
    brainstem involvement in
    infantile autism.
  7. Jacobson R et al. (1988)
    Selective subcortical
    abnormalities in autism.  
  8. Hashimoto T, et al. (1993)
    Brainstem involvement in
    high functioning autistic
    children.
Full References
top