- Coleman PD, Romano J, Lapham L, Simon W (1985) Cell counts in cerebral cortex of an
autistic patient. Journal of Autism and Developmental Disorders 15:245-255
- Rodier PM, Ingram JL, Tisdale B, Nelson S, Romano J (1996) Embryological origin for autism:
developmental anomalies of the cranial nerve motor nuclei. Journal of Comparative Neurology
370:247-261.
- Rodier PM, Ingram JL, Tisdale B, Croog, V.J. (1997b) Linking etiologies in humans and
animal models: Studies of autism. Reproductive Toxicology 11:417-422.
2 - Rodier et al. (1996) and Coleman et al. (1985)
Coleman et al. (1985) examined the brain of a 21-
year old woman with autism for subtle signs of
damage in areas of the cerebral cortex involved in
language, the primary auditory cortex, auditory
association cortex, and Broca’s speech area [1]. The
clinical course of the subject’s language disorder and
autistic behaviors had been documented in detail from
the time she was five years old. No significant
differences could be found in comparisons of her
brain, including counts of neurons in tissue from both
left and right sides, with two brains from age-and-sex-
matched individuals who had not been mentally
disabled. Smaller glia/neuron ratios in the three brain
areas from the autistic subject were found, but the
differences were not statistically significant.
However, Rodier et al. (1996, 1997b) later
examined the brainstem in the same case and found
abnormalities from the inferior olive in the medulla to
the superior olive and facial nucleus in the pons [2,
3]. They could not discern the usually distinctive
spindle-shaped cells or the pattern of fibers that
should surround them in the superior olive. The
brainstem appeared shortened between the inferior
olive and trapezoid body, and there was a severe
reduction of facial motor neurons. The upper
brainstem was not available, and thus auditory nuclei
between the superior olive and primary auditory cortex
could not be examined: nuclei of the lateral lemniscal
tract, inferior colliculi, or medial geniculate bodies.
Except for the case described by Rodier et al.,
visible damage of the auditory system has not been
found in individuals with autism. But the impairment of
brain function in autism is widely believed to be
submicroscopic. Lack of visible signs in the brain has
prompted the efforts to uncover a genetic etiology for
autism. The case of Rodier et al. may represent
autism as result of prenatal exposure to alcohol. The
visible disruption of the auditory pathway in this one
case is of interest.
- Coleman PD et al. (1985)
Cell counts in cerebral cortex
of an autistic patient.
- Rodier PM et al. (1996)
Embryological origin for
autism: developmental
anomalies of the cranial
nerve motor nuclei.
- Rodier PM et al. (1997b)
Linking etiologies in humans
and animal models: Studies
of autism.
Notes on postmortem findings of Coleman et al. (1985) and Rodier et al.
(1996)
One Case - Female, age 21
Brain: Weight 1380 g. Normal cell counts in language areas of the cerebral cortex,
primary auditory cortex, audidtory association cortex, and Broca’s area. Decreased
motor neurons of facial nuclei. No cells in the mid or caudal levels of the facial
nucleus. Superior olive missing.
Clinical: Born two years after the birth of a normal sister. Mother became a chronic
abuser of alcohol and dexedrine during the patient’s infancy, but she could not
remember whether the addiction problems arose before or after the birth. No smiling
response. No facial expression, but made bizarre grimaces when excited.
Photographs show no nasolabial folds and a sagging lower lip and jaw. Speech
consisted of a few words and phrases often spoken in imitation; for example she often
answered a question by repeating it. Learned songs from the radio. Covered her
ears in response to some sounds. Hyperactive aggressive episodes. She was
treated for seizures.