Patients recently diagnosed with schizophrenia have abnormalities in a specific part of the brain's white matter. The study, published this month in the journal Neuropsychopharmacology, suggests that brain signals passing through the temporal lobe may get "crossed" and lead to some of the symptoms associated with schizophrenia.
The research was
done at The Zucker Hillside Hospital and The Feinstein Institute for Medical Research.
The brain consists of gray matter and white matter. The gray matter
comprises neurons; the white matter contains the long axon projections
that control messages sent throughout the brain and forms the
connections among different gray matter regions. Without adequate
insulation on these projections, akin to wiring in an electrical
outlet, brain cells fail to communicate effectively. The resulting
cross-talk may explain why patients with schizophrenia have
disturbances in emotion, social functioning, thinking and perceiving
information.
All study participants had a relatively novel scanning technique called
"diffusion tensor imaging", which enables the quantification of movement
of water molecules along white matter pathways to assess brain white
matter integrity. Abnormalities in the brain's white matter can be
identified from the scans. Philip R. Szeszko, PhD, and his colleagues
found these abnormalities when they looked at the images from the
brains of people with schizophrenia. There is growing evidence that the
mind-altering condition may be laid down at birth and that an
alteration in genes that regulate white matter development could play a
role in the neurobiology of the disorder when it arises, generally in
late adolescence or early adulthood.
White-matter abnormalities in schizophrenia have been identified by
others, but this is one of the first studies to identify abnormalities
in patients early in the course of illness when symptoms first emerge
and prior to extensive pharmacologic intervention. Moreover, Dr.
Szeszko found that these temporal lobe white matter abnormalities were
associated with more severe symptoms and neuropsychological deficits,
further supporting a role for this brain region in the neurobiology of
the disorder.