Physical changes in the brain have been identified in some people with schizophrenia. The analysis of brain tissue after death has revealed a number of structural abnormalities, and new brain-imaging techniques have revealed changes in both the structure and function of the brain during life. Techniques such as magnetic resonance imaging (MRI) reveal changes in the size of different parts of the brain, especially in the temporal lobes. The fluid-filled spaces (the ventricles) in the interior of the temporal lobes are often enlarged and the temporal lobe tissue diminished. The greater the observed changes the greater the severity of the person’s thought disorder and his or her auditory hallucinations.
Some imaging techniques, such as positron emission tomography (PET), measure the actual functioning of the brain and provide a similar picture of abnormality. PET scanning reveals hyperactivity in the temporal lobes, particularly in the hippocampus, a part of the temporal lobe concerned with orientation and very short-term memory. Another type of functional imaging, electrophysiological brain recording using EEG tracings, shows that most people with schizophrenia seem to be excessively responsive to repeated environmental stimuli and more limited in their ability to blot out irrelevant information. In line with this finding, those parts of the brain that are supposed to screen out irrelevant stimuli, such as the frontal lobe, show decreased activity on PET scan.
Tying in with this sensory screening difficulty, post-mortem brain tissue examination has revealed problems in a certain type of brain cell? the inhibitory interneuron. These neurons damp down the action of the principal nerve cells, preventing them from responding to too many inputs. Thus, they prevent the brain from being overwhelmed by too much sensory information from the environment. The chemical messengers or neurotransmitters (primarily gamma-amino butyric acid or GABA) released by these interneurons are diminished in the brains of people with schizophrenia, suggesting that there is less inhibition of brain overload.
Abnormality in the functioning of these interneurons appears to produce changes in the brain cells which release the neurotransmitter dopamine. The role of dopamine has long been of interest to schizophrenia researchers, because drugs such as amphetamines that increase dopamine’s effects can cause psychoses that resemble schizophrenia, and drugs that block or decrease dopamine’s effect are useful for the treatment of psychoses. Dopamine increases the sensitivity of brain cells to stimuli. Ordinarily, this heightened awareness is useful in increasing a person’s awareness during times of stress or danger, but, for a person with schizophrenia, the addition the effect of dopamine to an already hyperactive brain state may tip the person into psychosis.
These findings suggest that in schizophrenia there is a deficit in the regulation of brain activity by interneurons, so that the brain over-responds to the many signals in the environment and lacks the ability to screen out unwanted stimuli. This problem is made worse by a decrease in the size of the temporal lobes, which ordinarily process sensory inputs, making it more difficult for the person to respond appropriately to new stimuli.