What causes psychoses?

A psychosis can occur as part of a number of different disorders, for instance, a psychosis can occasionally arise from medical conditions such as some kinds of epilepsy, a head injury, some brain infections, a stroke or a brain tumor. A psychotic episode can also occur after taking drugs such as amphetamines, LSD, cocaine or cannabis. Some people experience a psychosis after a traumatic or very stressful event, while other people experience a psychosis as part of a developing or established mental disorder.

In the past, some people believed that a psychotic disorder could be caused by family relationships or by certain parenting styles. However, the evidence for ‘psychotogenic’ (‘psychosis causing’) families is dubious at best, and suggesting this is the case is not constructive. Families or parents do not cause psychoses by their behaviour or styles.

Mental health professionals generally believe that a psychosis occurs when an individual has an underlying brain-related vulnerability or predisposition to experience a psychosis, and when this vulnerability is coupled with a stressor (or trigger), a psychotic episode can occur. Usually not one single factor causes a psychosis, although that can happen - e.g. with certain types of brain poisons such as hallucinogenic drugs or heavy metal intoxication. Most kinds of psychoses are very similar to other conditions such as heart disease, in the sense that these illnesses are caused by the interaction of multiple genetic and environmental factors.

What factors can predispose someone to experiencing a psychotic disorder?

Certain biological factors can predispose an individual to experiencing a psychotic disorder. Genetic factors, often revealed by having a close relative who has experienced a psychotic episode, can put a person at higher risk for developing a psychosis. If one parent has experienced a psychosis, then the chance of a child experiencing a psychosis is approximately ten to fourteen percent. However, many people who have experienced psychotic episodes have no family history of a psychotic disorder, and other people who have a family history of psychoses will never experience a psychosis. A family history of psychoses does not, by itself, mean that an individual will experience a psychosis.

Multiple genes involved in brain development have been associated with psychosis, and as our understanding of the functions of these genes develops, so will our understanding of this illness. We are in a very exciting time for expanding our knowledge of the intricacies of brain function as molecular and other gene technologies develop.

Researchers also believe that certain differences in brain structure and function are strongly associated with psychoses. Using neuroimaging techniques, researchers have found that some individuals who have experienced a psychosis show an enlargement of the fluid-filled cavities in the brain (called the ventricles) and decreased size of some other brain regions. Interestingly, in identical twins discordant for psychosis (that is one twin is psychotic, the other is healthy), only the ill twin shows these significant differences. Nevertheless, the ‘healthy’ twin shows differences intermediate between the ‘normal’ population and their ill twin, again suggesting that they may have some fundamental susceptibility to developing psychosis. Decreased metabolic activity in certain other regions of the brain, and increases in other regions, has also been documented. It should be noted that these studies have found only slight or subtle differences in brain structure and function between people who have experienced a psychosis and people who have not experienced a psychosis. Also, not all people who have experienced a psychosis show these differences and people who have never experienced a psychosis can also show these differences. Furthermore, it is not known if these differences are a cause or product of the illness. This means that these tests are, currently, of very little use in diagnosing a psychotic disorder. The problems may well exist at a chemical or molecular level which cannot yet be readily and accurately tested for in the brain. There are no definitive diagnostic tests for psychotic disorders, and therefore accurate diagnosis is left to an appropriately trained medical professional.

An association has been documented, in many studies, between psychotic disorders and complications during birth, or resulting from a viral infection or some other insult (e.g. exposure to toxic chemicals or starvation) during pregnancy. For example, in women who were infected with influenza during the 2nd trimester of pregnancy, there is a markedly elevated risk of psychosis in her offspring. This is an extremely critical period of brain development. It is believed that these factors, amongst others, can affect the structure and chemistry of the brain during early development, leading to long-lasting changes which increase a person's risk for developing a psychotic disorder later in life.

One brain chemical (neurotransmitter) that is believed to be intricately related to the expression of psychosis is dopamine. Researchers currently think that people who have experienced a psychosis may have too much of this brain chemical in certain brain regions. This was determined through observations that agents which reduce psychotic symptoms (anti-psychotics) attenuate dopamine activity, while substances which increase dopamine activity (eg, amphetamines, cocaine), can precipitate psychotic-like symptoms. However, the fact remains that dopamine is only one of the neurotransmitters that have been implicated in psychoses. Unfortunately, the complexity of the brain and our relatively poor understanding of how it functions, even in people without psychosis, significantly hamper efforts at discovering new and better treatments for this illness.

There are many theories about the factors that might predispose someone to experience a psychosis, and understanding of these factors is improving all the time. However, much more research needs to be done in this area. Most of these theories centre on neurodevelopmental abnormalities. However, these theories are hard-pressed to describe psychotic illnesses which develop in later life.

What stressors can trigger a psychotic episode?

In people who are vulnerable to experiencing a psychosis, an episode can be triggered by factors such as drug use or withdrawal from substances. Using or withdrawing from drugs such as cannabis, LSD, cocaine, amphetamines, ecstasy and alcohol can all potentially trigger or indeed cause a psychotic episode. Research has shown that people who use cannabis are more likely to experience a psychotic episode than people who do not use cannabis. However, this is not conclusive evidence that cannabis causes psychosis. There are a number of possible explanations for this association.

It is important to bear in mind that the use of substances is only one possible factor contributing to an increased risk of psychosis in individuals who are vulnerable. Sometimes high doses of certain prescription medicines can also trigger a psychotic episode e.g. steroids and amphetamines or anti-asthmatic medication.

Very often, psychosis can be triggered by stress, extreme or otherwise. Different people deal with different types of stressors in different ways. Extreme stress such as the loss of a job, a big change in living arrangements, or a great deal of stress in important relationships can trigger a psychotic episode, however, stresses and strains within relationships, alone, do not cause psychosis, though they may contribute. The amount and type of stressor that can trigger a psychotic episode varies from person to person because, as noted, people differ in the degree of their vulnerability or predisposition to experiencing a psychotic episode, and how they deal with stress.

In many cases, it can be very difficult for a medical professional to tease apart the relationship between the symptoms and the drugs: similar to the ‘chicken and the egg’ dilemma. For instance, it is conceivable that some psychotic symptoms were present before taking the drug, but were not identified as such.