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0361-803X/94/1621-0123
© American Roentgen Ray Society
Abnormality of Cerebellar Vermian
Lobules VI and VII in Patients with
Infantile Autism: Identification of
Hypoplastic and Hyperplastic Subgroups
with MR Imaging
Eric ,2
Osamu Saitoh 1-3
Rachel Yeung-Courchesne2
GaryA. Press4
Alan J. Lincoln2
Richard H. Haas1
Laura Schreibman5
Received June 1 4, 1 993; accepted after revision
September 2, 1993.
This work was supported by National institute of
Neurological Diseases and Stroke grant 5-AOl -NS
19855 and National Institute of Mental Health 1-
R01-MH-36840.
1 Neurosciences Department, School of Mcdi-
cine, University of California at San Diego, La Jolla,
CA 92093.
2Neunopsychology Research Laboratory, Chil-
dren’s Hospital, 3020 Children’s Way, San Diego,
CA 92123. Address correspondence to E.
Courchesne.
3National Center Hospital for Mental, Nervous
and Muscular Disorders, National Center of Neurol-
ogy and Psychiatry, 4-1 -1 Ogawa Higashi-Cho, Ko-
daira, Tokyo, 187 Japan.
4Department of Radiology, Kaiser Penmanente
Hospital, 4647 Zion Ave., San Diego, CA 92120.
5Department of Psychology, University of Cali-
fornia at San Diego, La Jolla, CA 92093.
OBJECTIVE. Infantile autism is a neurobehavioral disorder that is widely believed
to have etiologically distinct subtypes, including subtypes with a genetic basis, but
no neuroanatomic evidence firmly supports this belief. To date, only one type of cere-
bellar abnormality has been Identified In patients with autism: hypoplasia of the ver-
mis and hemispheres. By using a large sample of autistic patients and healthy
volunteers along with precise MR Imaging and quantitative procedures, we sought to
replicate previous reports of cerebellar vermian hypoplasla In autism and to identify
additional subtypes of cerebeilar abnormality.
MATERIALS AND METHODS. Using MR technology, we imaged and measured pos-
tenor and anterior vermian regions in 50 autistic patients (2-40 years old) and 53
healthy control subjects (3-37 years old). The autistic patients had social, language,
cognitive, behavioral, and medical history characteristics that were typical of the gen-
eral autistic population. By using precise procedures for positioning and aligning MR
slices, we obtained comparable MR Images within and across subject groups.
RESULTS. Statistical analyses showed two subgroups of autistic patients, one (86% of
the patients) with findings consistent with vermian hypoplasia and another (i2% of the
patients) with evidence of vermian hyperplasia. The hypoplasia subgroup included 43
patients whose mean midsagittal area for vermian lobules VI and VII was 237 ± 38 mm2,
and the hyperplasia subgroup included six patients whose mean area was 377 ± 12 mm2.
Thus, the area of lobules VI and VII in the hypoplasia subgroup was 16% smaller than the
mean area in the control subjects (282 ± 42 mm2) (p < .0001), whereas that in the hyper-
plasia subgroup was 34% larger (p < .0001). Analyses showed that these two subtypes of
vermian abnormalities were present across all ages of autistic patients studied.
CONCLUSION. Two different subtypes of autistic patients can be identified on the
basis of the presence of vermian hypoplasia or hyperplasia as seen on MR images.
Possible origins for vermian hypoplasia include environmental trauma and genetic
factors.
AJR 1994;162:123-i30
Infantile autism is a neunologic disorder of unknown cause that severely dis-
mupts social, cognitive, and language development [1]. Qualitative MR studies
have shown decreased volume of the panietal lobe in 43% of autistic patients
examined, and electrophysiological and behavioral studies show abnormalities in
these patients that are consistent with MR findings [2-4]; whether other autistic
patients have pamietal abnormalities remains unknown. Quantitative MA studies
have shown hypoplasia of cerebellar vemmian lobules VI and VII and cerebellar
hemispheres in the majority, but not all, of autistic patients examined [5-10];
whether other autistic patients have some other type of cemebellar abnormality is
unknown. To date, the only neurobiological abnormality known to precede the
onset of autistic signs and symptoms is loss of cerebellar neurons, which is most
severe in lobules Vl-Vll and VIll-X in the posterior part of the vemmis (50-60%
Purkinje cell loss) and hemispheres (42-56% Purkinje cell loss) [ii-14; E. Ann,
personal communication, February 1993], and undoubtedly leads to the cerebellar
hypoplasia quantified by MR imaging [5-10].
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