The course of schizophrenia
The course of schizophrenia
Wide variation occurs in the course of schizophrenia. In some cases the onset of illness is gradual, extending over the course of months or years; in others it can begin suddenly, within hours or days. Some people have episodes of illness lasting weeks or months with full remission of symptoms between each episode; others have a fluctuating course in which symptoms are continuous; others again have very little variation in their symptoms of illness over the course of years. The final outcome from the illness in late life can be complete recovery, a mild level of disturbance or continued severe illness.
Figure I.2 is an illustration of the onset, course and outcome of the illness in 228 people with schizophrenia followed into old age by the Swiss psychiatrist, Luc Ciompi. He found that the onset of the illness was either acute (with less than six months from first symptoms to full-blown psychosis) or, conversely, insidious, in roughly equal numbers of cases. Similarly, the course of the condition was episodic or continuous in approximately equal numbers of patients; and the outcome was moderate to severe disability in half the cases and mild disability or full recovery in the other half. Full recovery was observed in more than a quarter of the patients. It is clear that the course of schizophrenia varies a good deal between individuals and that the outcome is often favorable.
It is also true to say that schizophrenia usually becomes less severe as the person with the illness grows older. In addition, the later the illness begins in life, the milder it proves to be. Women usually develop their first symptoms of schizophrenia later than men and the course of their illness tends to be less severe. Onset of schizophrenia before the age of 14 is rare, but when it does begin this early it is associated with a severe course of illness. Onset after the age of 40 is also rare, and is associated with a milder course.
What Causes Schizophrenia?
There is no single organic defect or infectious agent which causes schizophrenia, but a variety of factors increase the risk of getting the illness? among them, genetics and obstetric complications.
Relatives of people with schizophrenia have a greater risk of developing the illness, the risk being progressively higher among those who are more genetically similar to the person with schizophrenia (see Figure I.3). For a nephew or aunt the lifetime risk is about two percent (twice the risk for someone in the general population); for a sibling, parent, or child the risk is about ten percent, and for an identical twin (genetically identical to the person with schizophrenia) the risk is close to 50 percent.
Studies of people adopted in infancy reveal that the increased risk of schizophrenia among the relatives of people with the illness is due to inheritance rather than environment. The children of people with schizophrenia have the same increased prevalence of the illness whether they are raised by their biological parent with schizophrenia or by adoptive parents.
There is evidence implicating several genes in causing schizophrenia, and it is likely that more than one is responsible, either through an interactive effect or by producing different variants of the disorder.
Since identical twins only have a 50 percent risk of developing the illness, we know that genetics alone do not explain why someone gets the illness. Other powerful factors have to play a part; one of these is problems of pregnancy and delivery. The risk for people born with obstetric complications, such as prolonged labor, is double the risk for those born with none. A history of obstetric complications has been found in up to 40 percent of patients with schizophrenia, making it a major risk factor.
The risk of intrauterine brain damage is increased if a pregnant woman contracts a viral illness. We know that more people with schizophrenia are born in the late winter or spring than at other times of year, and that this birth bulge sometimes increases after epidemics of viral illnesses like influenza, measles and chickenpox. Maternal viral infections, however, probably account for only a small part of the increased risk for schizophrenia.
Poor parenting does not cause schizophrenia
Contrary to the beliefs of professionals prior to the 1970s and to the impression still promoted by the popular media, there is no evidence, even after decades of research, that family or parenting problems cause schizophrenia.
As early as 1948, psychoanalysts proposed that mothers fostered schizophrenia in their offspring through cold and distant parenting. Others blamed parental schisms, and confusing patterns of communication within the family. The double-bind theory, put forward by anthropologist Gregory Bateson, argued that schizophrenia is promoted by contradictory parental messages from which the child is unable to escape. While enjoying broad public recognition, such theories have seldom been adequately tested, and none of the research satisfactorily resolves the question of whether differences found in the families of people with schizophrenia are the cause or the effect of psychological abnormalities in the disturbed family member.
Millions of family members of people with schizophrenia have suffered needless shame, guilt and stigma because of this widespread misconception.
Drug abuse does not cause schizophrenia
Hallucinogenic drugs like LSD can induce short-lasting episodes of psychosis and the heavy use of marijuana and stimulant drugs like cocaine and amphetamines may precipitate brief, toxic psychoses with features similar to schizophrenia. It is also possible, though by no means certain, that drug abuse can trigger the onset of schizophrenia.
Relatives of a person with schizophrenia sometimes blame hallucinogenic drugs for causing the illness, but they are mistaken. We know this because, in the 1950s and 1960s, LSD was used as an experimental drug in psychiatry in Britain and America. The proportion of these volunteers and patients who developed a long-lasting psychosis like schizophrenia was scarcely greater than in the general population. It is true that a Swedish study found that army conscripts who used marijuana heavily were six times more likely to develop schizophrenia later in life, but this was probably because those people who were destined to develop schizophrenia were more likely to use marijuana as a way to cope with the pre-morbid symptoms of the illness.
The Brain In Schizophrenia
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.