frequently asked questions
 
 
 
 
 
 
 
 
Brain Anatomy or Brain Chemistry?
 
 
Q: How are the brains of people with schizophrenia different from normal brains (the brains of unaffected people)?
 
A: The differ both in terms of structure and function.
 
 
Introduction
 
People who are diagnosed with this disease exhibit changes in their brains that involve both structure and function.  Both anatomy and chemistry are abnormal. New imaging techniques have allowed scientists and clinicians to explore and understand changes in the composition of schizophrenics’ brains and also reveal performance abnormalities.
 
 
Structure
 
Structural brain imaging techniques 1 include conventional X-rays, CAT (Computerized Axial Tomography) scans, and MRI (Magnetic Resonance Imaging) scans.
 
Those who suffer from schizophrenia may demonstrate changes in the overall size of their brains.  Total brain volume is reduced, particularly in the prefrontal regions of the frontal lobes.  These regions seem to have atrophied (they have wasted) or they may not have developed normally in the first place.
 
The ventricles (fluid filled spaces within the brain) are larger.  Since the area inside of our cranium (skull) is fixed and constant after the fissures between the plates of our skills fuse in childhood, enlarged ventricles means that some other material within our skulls must be reduced.
 
At the microscopic level, there are abnormalities in the wiring 2 (the connections between neurons).  Chemically, neurotransmitters or their receptors may be abnormal.
 
 
Function
 
Several functional brain imaging methods 3 are currently available that shed light on the neurobiology of schizophrenia.  They include:
 
  1. The Xenon technique for measuring CBF (cerebral blood flow).
  2.  
  3. Positron Emission Tomography (PET) scanning, which assesses metabolism,
  4. CBF and neuroreceptor functioning.
  5.  
  6. Single Photon Emission Computerized Tomography (SPECT) for studying CBF and neuroreceptors.
  7.  
  8. Functional Magnetic Resonance Imaging (MRI) for measuring changes linked to CBF.
 
The prefrontal cortex, the area of the brain that controls thinking and higher mental functions (those things other than the basic control of the body) show increased activity in the brains of healthy people when they are asked to perform an analytical task.  This area remains quiet in the brains of schizophrenics what they are required to accomplish these same activities.
 
Because certain chemicals (antipsychotic medications) that interfere with the activity of dopamine reduce some of the typical symptoms of schizophrenia, we have concluded that one or both of two things are happening.  Either areas in the brains of people with schizophrenia are quite sensitive to dopamine, and/or brain tissue in these areas produces excessive amounts of dopamine.
 
This conclusion is supported by what we have learned about schizophrenia and Parkinson’s Disease; how deficiencies of this same neurotransmitter (dopamine) cause the symptoms of this illness and certain medications (antiparkinson drugs) that alter the levels of dopamine improve those symptoms.
 
In some ways, schizophrenia resembles autoimmune diseases like MS (multiple sclerosis) and ALS (amyotrophic lateral sclerosis, or Lou Gherigs’s disease).  These diseases appear to be caused by confused cells that are part of our body’s immune system.  These cells are not able to properly recognize normal tissue and instead of ignoring those cells, they are seen as foreign and are attacked and destroyed.
 
As is the case with those autoimmune diseases, Schizophrenia does not appear to be present at the time of birth.  It appears to develop sometime later, almost invariably during adolescence or our early adult years.  The timing may be related to the changes in hormone levels that begin in puberty.
 
Other similarities between Schizophrenia and autoimmune disease are the observations that they both may periodically intensify and remit (wane) and both seem to be genetically mediated (they are heritable).
 
 
1 Lewis. SC,  Structural Brain Imaging in Biological Psychiatry. British Medical Bulletin.  1996; 52930:465-473.
2 Gorazd Rosoklija, MD, PhD; Glen Toomayan, BS; Steven P. Ellis, PhD; John Keilp, PhD; J. John Mann, MD; Norman Latov, MD, PhD; Arthur P. Hays, MD; Andrew J. Dwork, MD. Structural Abnormalities of Subicular Dendrites in Subjects With Schizophrenia and Mood Disorders, Arch Gen Psychiatry. 2000;57:349-356.
3 Gur, RE, Introduction Functional Brain Imaging Studies in Schizophrenia, Psychopharmacology-The Fourth Generation of Progress, American College of Neuropsychopharmacology (2000);  Gur RE, Resnick SM, Gur RC, Alavi A, Caroff S, Kushner M, Reivich M. Regional brain function in schizophrenia. II. Repeated evaluation with positron emission tomography. Arch Gen Psychiatry. 1987 Feb;44(2):126–129; and Gur RE, Chin S. Laterality in functional brain imaging studies of schizophrenia. Schizophr Bull. 1999; 25(1):141-56.
 
 
(Sources: The author’s knowledge base,unless otherwise noted.)
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