International Meeting for Autism Research: Dystrophy with Calcification within Brains of Autistic and Control Subjects

Dystrophy with Calcification within Brains of Autistic and Control Subjects

Friday, May 21, 2010
Franklin Hall B Level 4 (Philadelphia Marriott Downtown)
3:00 PM
I. Kuchna , Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
K. Nowicki , Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
H. Imaki , Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
J. Wegiel , Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
S. Y. Ma , Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
E. Marchi , Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
I. Cohen , Psychology, NYS Institute for Basic Research in Developmental Disabilities, Staten Island, NY
E. London , Psychology, NYS Institute for Basic Research in Developmental Disabilities, Staten Island, NY
W. T. Brown , Human Genetics, NYS Institute for Basic Research, Staten Island, NY
T. Wisniewski , Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
J. Wegiel , Developmental Neurobiology, New York State Institute for Basic Research in Developmental Disabilities, Staten Island, NY
Background: Intracranial calcifications are observed in many diseases including those with viral and bacterial infections, vascular pathology, toxic injury, brain tumors, teratomas, lissencephaly, in children with Fahr’s disease, and very often in parasitic infections (Rabbitt et al 1969).

Objectives: Our neuropathological studies of autistic subjects brains have revealed the presence of dystrophic changes with calcification. The aim of this study was to determine the prevalence of this type of encephalopathy in autistic and control cohorts.

Methods: The brain hemispheres of 13 autistic and 14 control subjects 4 to 64 years of age were fixed in 10% formalin, dehydrated and embedded in celloidin and cut into 200 μm- or 50 μm-thick coronal serial sections

Results: Dystrophy with calcification was found in all of the 13 autistic and 14 control brains examined. Dystrophic changes disrupt the continuity of the cortical ribbon and white matter in the frontal, temporal and occipital lobes but only on the lateral side of the brain. The pathology spreads from the leptomeningeal vessels to the cortex and white matter and was detectable by postmortem MRI and histopathological examination. Microscopic examination revealed linear dystrophic lesions free of neurons but with signs of neuronal degeneration at the border between the dystrophic and normal cortex. There was no sign of activation of astrocytes or macrophages within the dystrophic and adjacent brain tissue. The dominant component of the dystrophic lesions was calcium deposits.

Conclusions: Similar morphology of lesions in control and autistic subjects 4 to 64 years of age suggests that dystrophic calcifications undergo relatively limited modifications with age. However, the presence of degenerated neurons and vessels with degenerated smooth muscle cells in the border zone between the lesion and cortex suggests the process of brain tissue damage continues to progress decades after the original causative events. Multifocal dystrophy with calcification in all the examined brains of autistic and control subjects reflects a common pathological mechanism with yet undetermined subclinical or clinical manifestations.

See more of: Neuropathology
See more of: Brain Structure & Function