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Evidence That Schizophrenia is a Brain Disease

Rashmi Nemade, Ph.D. & Mark Dombeck, Ph.D.

Evidence That Schizophrenia is a Brain Disease

Data from scientific research proves that schizophrenia is clearly a biological disease of the brain, just like Alzheimer's Disease and Bipolar Disorder. Schizophrenia is now known to be partially caused by genetics and to be inherited. Non-invasive brain imaging techniques such as Magnetic Resonance Imaging (MRI) and Computerized Tomography (CT), have documented structural differences between normal brains and those with schizophrenia. People with schizophrenia have up to 25% less volume of gray matter in their brains, especially in the temporal and frontal lobes. These areas are known to be important for coordination of thinking and judgment. People demonstrating the worst brain tissue losses also tend to show the worst symptoms.

brain scan images Functional scanning of the brain, using technologies like Positron Emission Tomography (PET) and functional MRI have made it possible to create real-time maps of regional brain blood flow and metabolism. This has provided another window into how brains with schizophrenia are distinct from those without the condition. People who tend to have more negative symptoms of schizophrenia also tend to show lower levels of brain activity in key brain areas.

Brains with schizophrenia are, on average, different in terms of total tissue volume and activity. However, there is most often no obvious single point of structural damage (a "lesion") to point at as the specific location in the brain where schizophrenia is happening.

Brains with schizophrenia also show neurochemical differences when compared with normal brains. The brain uses a number of chemicals as messengers to communicate with other parts of the brain and nervous system. These chemical messengers, known as neurotransmitters, are essential to all of the brain's functions. Since they are messengers, they typically come from one place and go to another to deliver their messages. Where one neuron or nerve cell ends, another one begins.

In between two linked neurons is a tiny space or gap called a synapse. In a simple scenario, one cell sends a neurotransmitter message across this gap and the next cell receives the signal by catching the messenger chemical as it floats across the gap. The receiving neuron's capture of the neurotransmitter chemicals alerts it that a message has been sent, and this neuron in turn sends a new message off to additional neurons that it is connected to, and so on down the line.

Neurons cannot communicate with each other except by means of this synaptic chemical message. The brain would cease to function in an instant if chemical messengers were somehow removed. By providing a way for allowing neurons to communicate with one another, neurotransmitters literally allow the brain to function. There are millions and millions of individual synapses, or gaps, in the brain. The neurotransmitter traffic and activity happening inside those gaps is constant and complicated.

At the most basic level, brains with schizophrenia appear to be sensitive to the neurotransmitter dopamine in a different way than brains without the condition. The "dopamine hypothesis" of schizophrenia believes that schizophrenia is caused by excess dopamine or extra sensitivity to dopamine. Support for this idea comes from several main sources. First, drugs known to block the effects of dopamine in the brain are also known to be useful as antipsychotic medications. These medications reduce the intensity and frequency of hallucinations, for example. Second, stimulant drugs like cocaine and methamphetamine are known to either mimic the action of dopamine, or to cause dopamine to become more active in the brain. These stimulant medications are known to be capable of causing hallucinations and delusions in people without schizophrenia if enough of those substances are taken. It is also known that too little dopamine is responsible for Parkinson's disease. Chronic use of antipsychotic medications (which block dopamine) can result in a Parkinson's-like condition called tardive dyskinesia.

The dopamine hypothesis has been dominant for a long time. However, after a lot of recent research, it is no longer so clear that dopamine alone is responsible for causing schizophrenia. It appears more likely that other chemical messengers are also involved in creating conditions for schizophrenia and psychosis. These may include serotonin, which is involved in depression and anxiety., It may also include glutamate, which is known to be involved in the hallucinatory effects of the drug PCP ("angel dust"). The details of exact neurochemical involvement in schizophrenia change as research continues. However, it is clear that the neurochemical basis of schizophrenia has been very firmly established and appears to be beyond question.

Considered as a group and compared to those without the condition, people with schizophrenia show observable functional deficits as well. Functional deficits are problems people have in performing basic mental and physical tasks and activities. This may include:

  • remembering things - compared to those without schizophrenia, they may be less able to remember things they learned 5-minutes ago, but have no problem remembering long-term memories from the past
  • being able to flexibly shift between various tasks (known as executive functioning)
  • making judgment, etc.)
  • figuring out rules from consequences
  • reduced hand grip strength
  • reduced memory attention span and reaction time
  • being more distractible
  • having a harder time engaging in problem solving and planning

Abnormalities in sensory processing are also noticeable in those with schizophrenia. It is common for them to show 'soft' neurological signs. This means that they might have difficulty telling the difference between two simultaneous touches or in being able to identify numbers drawn on the palm of their hand. They also tend to confuse the right and left sides of their bodies more frequently than those without the condition. These sensory processing problems suggest impairments or irregularities in the way that their brains are wired.

Electroencephalogram (EEG) data are tests of brain electrical activity. About one-third of people with schizophrenia show abnormal electrical brain impulses. This also suggests irregularities in the way the brains of those with schizophrenia are wired. These many results, which come from different types of studies, tools and observations, suggest very strong and believable evidence for the idea that schizophrenia is a biologically based brain disease.


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