Altered Brain Structure in Schizophrenia
Many scientists have reported research findings that suggest schizophrenia is related to changes in the structure of the brain. This insight follows the development of advanced neuroimaging technologies that allow neuroscientists to study pictures of living, functioning brains without compromising the health of research volunteers or patients.
Fluid-filled spaces called cerebral ventricles in the center of the brain are a normal feature of everyone's central nervous system. These chambers, filled with cerebrospinal fluid, appear to be enlarged in some people affected by schizophrenia.
Having larger spaces in the center of the brain implies less area is available for the brain's other structures. Indeed, there are reports that associate smaller brain mass with schizophrenia.
Because these studies are time-consuming and expensive, research reports must frequently concentrate on changes in one brain region at a time. It is important to remember, however, that the brain is an intricately interconnected structure in which different regions are linked by extensive nerve cell projections. It is therefore unlikely that there is one place in the brain that is responsible for schizophrenia.
Rather, it is likely that flaws in brain structure and chemistry make functioning in several parts of the brain defective. Chemical messenger systems such as dopamine, serotonin, glutamate, and perhaps others may be impaired in the many different brain regions such as the limbic structures (involved closely with emotions), basal ganglia, prefrontal cortex, temporal lobes, and even the cerebellum, a part of the brain neuroscientists once believed did nothing more than control fine muscle movements. Its involvement might explain changes in coordination, reflexes, body postures, and other functions detected in some people with schizophrenia.
The frontal lobe is reported to be smaller in some patients with schizophrenia. This part of the brain plays a unique and important role in determining personality, social interactions, and planning for the future. Smaller temporal lobes have also been observed in some people diagnosed with schizophrenia.
Other studies indicate that there is a lower level of activity in certain parts of the brain in some patients with schizophrenia. Compared to those of people who don't have schizophrenia, these brain regions receive less blood flow when the brain is thinking, feeling, reasoning, and telling the body what to do.
The differences in structure found in the brains of people with schizophrenia are not necessarily very big differences. In fact, some are very subtle, and similar variations can be seen in the brains of some people who are unaffected by mental illness.
Structural abnormalities detected on the microscopic level are also very subtle. Some of these differences involve small changes in numbers of neurons and the way they are positioned in certain regions of the brain.
Pierce J. Howard, PhD, explains in his book The Owner's Manual for the Brain how this may happen. Some scientists suggest that in schizophrenia something goes wrong with the natural process that normally does away with unneeded connections between nerve cells — synapses — in young people. This “synaptic pruning” phase begins before puberty and extends to around the age of twenty-five. Unused, unneeded synapses shrivel and disappear, while synapses that get a lot of use become stronger. It is estimated that around 15 percent of an adolescent's cerebral gray matter is pruned in the healthy brain.
In a brain affected by schizophrenia, however, as many as 25 percent of the synapses may be eliminated. Microscopic examination of brains affected by schizophrenia reveal further anomalies, such as out-of-place neurons in the cerebral cortex and in the hippocampus, which deals with memory formation and learning.
Even though brain imaging and other studies have demonstrated several differences between brains of patients with schizophrenia and those unaffected by the disease, none of these differences are big enough or consistent enough to be used to diagnose the condition. The diagnosis of schizophrenia continues to be made by clinical interviews and examinations. Research studies continue to provide clues and improve our understanding of the brain malfunctions associated with this disease.
Due to structural and chemical flaws, communication pathways between many parts of the brain are compromised in schizophrenia. Thus, neurotransmitter systems such as dopamine, serotonin, nor-epinephrine, glutamate, and perhaps others appear to be impaired. Such chemical malfunctions could affect the brain regions critical in schizophrenia. One scenario suggests that brain abnormalities seen in schizophrenia — if they contribute to disease symptoms — may be the result of problems that begin before birth, while the brain of a genetically susceptible individual is developing. These developmental problems may be the result of — or may combine with — input or damage caused by something present or absent in the environment, such as a virus or some missing essential nutrients.
Neuroscientists at the Harvard Brain Tissue Resource Center may have found an anatomical basis for several symptoms of schizophrenia, including the unusually intense perception of sights and sounds experienced by some people with the disease. Tissue from the brains of individuals with schizophrenia had more excitatory neurons compared to tissue from the brains of people who did not have the disease. Perhaps too many excitatory neurons contribute to excess stimulation and hallucinations in schizophrenia.
Another potential contributing factor in schizophrenia described by J. Pierce Howard, PhD, in The Owner's Manual for the Brain is the increase in the establishment of neuronal pathways that occurs during the adolescent years. While the number of brain synapses or points of contacts between neurons is pruned at this stage of life, the “wiring” or communication pathways between neurons is strengthened. The nerve fibers that convey these connections, called axons, are insulated by non-neuronal brain cells called glial cells. Glial cells wrap around axons, insulate them, and allow electrical signals to travel faster.
Are the brains of people with schizophrenia wired differently from those of other people?
During the late teen years and early twenties, the brain experiences a burst of nerve cell insulation, a process called myelination. Some scientists speculate that the sudden, improved connections resulting from this new myelination might help explain the onset of the disease. The connections may cause malfunction in a brain already weakened by genetic susceptibility and environmental factors.
Perhaps a brain in the process of developing schizophrenia could not handle the power of the new brain wiring. This might explain some early warning signs of the disease, such as heightened senses. This can result in an unusual — and not necessarily unpleasant — feeling of amazement and wonder associated with familiar objects and sights. Later, this pleasant aspect of heightened sensations can be replaced by hallucinations and delusions.