To: cvnet@lawton.ewind.com
From: Stephen Grossberg <steve@cns.bu.edu>
Subject: The imbalanced brain: From normal behavior to schizophrenia
Cc: steve@cns.bu.edu
Dear Dr. Chan, Please post the following abstract on CVnet.
Many thanks, Steve Grossberg
The following article is available at
http://www.cns.bu.edu/Profiles/Grossberg in HTML, PDF, and Gzipped
postscript:
Grossberg, S. (2000). The imbalanced brain: From normal behavior to
schizophrenia. Biological Psychiatry, in press. Preliminary version
appears as Boston University Technical Report CAS/CNS TR-99-018.
ABSTRACT: An outstanding problem in psychiatry concerns how to link
discoveries about the pharmacological, neurophysiological, and
neuroanatomical substrates of mental disorders to the abnormal behaviors
that they control. A related problem concerns how to understand abnormal
behaviors on a continuum with normal behaviors. During the past few
decades, neural models have been developed of how normal cognitive and
emotional processes learn from the environment, focus attention and act
upon motivationally important events, and cope with unexpected events. When
arousal or volitional signals in these models are suitably altered, they
give rise to symptoms that strikingly resemble negative and positive
symptoms of schizophrenia, including flat affect, impoverishment of will,
attentional problems, loss of a theory of mind, thought derailment,
hallucinations, and delusions. The
present article models how emotional centers of the brain, such as the
amygdala, interact with sensory and prefrontal cortices (notably ventral,
or orbital, prefrontal cortex) to generate affective states,
attend to motivationally salient sensory events, and elicit motivated
behaviors. Closing this feedback loop between cognitive and emotional
centers is predicted to generate a cognitive-emotional resonance that can
support conscious awareness. When such emotional centers become depressed,
negative symptoms of schizophrenia emerge in the model. Such emotional
centers are modeled as opponent affective processes, such as fear and
relief, whose response amplitude and sensitivity are calibrated by an
arousal level and chemical transmitters that slowly inactivate, or
habituate, in an activity-dependent way. These opponent processes exhibit
an Inverted-U whereby behavior become depressed if the arousal level is
chosen too large or too small. The negative symptoms are due to the way in
which the depressed opponent process interacts with other circuits
throughout the brain.
Keywords: schizophrenia, arousal, prefrontal cortex, amygdala, opponent
process, neural networks
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