Schizophrenia is a serious mental illness that affects the way a person thinks, feels and acts. It is part of the psychosis group. Its prevalence in the population is around 1%, lower than that of other mental disorders, but, due to its chronic and disabling nature.
Someone with schizophrenia may have difficulty distinguishing between what is real and what is imaginary and may also have difficulty expressing normal emotions in social situations. But contrary to public perception, a person with schizophrenia does not have a divided or multiple personality. The vast majority of people with schizophrenia are not violent and do not pose a danger to others. Nor is it caused by childhood experiences, lack of parents or lack of willpower, nor are the symptoms identical for each person.
Its prevalence in the population is around 1%, lower than that of other mental disorders, but, due to its chronic and disabling nature, it requires a large contribution of resources from the health and research system.
There are many questions about schizophrenia, but the numerous investigations that have been carried out have provided data that have allowed us to develop some hypotheses about the cause of this disorder.
- 1 Causes of schizophrenia
- 2 Neurochemical alterations in the brain in schizophrenia
- 3 Morphological and functional abnormalities in the schizophrenic brain
Causes of schizophrenia
The cause of schizophrenia is still unclear. Some theories about the cause of this disease include: genetics (inheritance), biology (abnormalities in the structure or chemistry of the brain) and / or possible viral infections and immune disorders.
Schizophrenia seems to be the result of the interaction of genetic, developmental and stress factors.
Apparently, brain abnormalities are already present before the onset of the first symptoms of the disorder. The subject will not develop schizophrenia if the environment where it grows is free from stress situations, but these brain abnormalities may have other manifestations. Thus, it has been possible to prove as healthy relatives of schizophrenic patients and children who have subsequently developed schizophrenia, show certain cognitive alterations in attention and psychomotor skills, and also an emotional behavior tending to irritability.
Genetic factors could cause some brain abnormalities. This disease seems to have a genetic component important. Among univiteline twins there is a 50% concordance in the presence of this disease. That this agreement is only 50%, however, should make us think that other environmental factors should have an important role in its genesis. These same anomalies could also be caused, or enhanced, by factors that interfere with normal development, such as intrauterine complications, during childbirth or in the early stages of childhood. In any case, for schizophrenia to develop, it is necessary that this vulnerable nervous substrate interact with situations of environmental stress, which will cause the system to destabilize and symptoms appear.
Neurochemical alterations in the brain in schizophrenia
It is believed that people with schizophrenia have an imbalance of the following brain neurotransmitters: dopamine, glutamate and serotonin. These neurotransmitters allow nerve cells in the brain to send messages to each other.The imbalance of these chemicals affects the way a person's brain reacts to stimuli, which explains why a person with schizophrenia can be overwhelmed by sensory information (loud music or bright lights) that other people can easily handle. This problem when processing different sounds, images, smells and flavors can also lead to hallucinations or delusions.
It is considered that schizophrenic patients have two types of symptoms, positive and negative. The positive symptomatology refers to hallucinations, delusions and agitated behavior, while the negative symptomatology It refers to affective flattening, poverty of thought and language, disconnection of the environment, and different neuropsychological deficits such as attention and memory problems. The positive symptomatology seems to be controlled quite well with dopamine antagonists, such as chlorpromazine, but not the negative one.
Finally, an important group of antipsychotic drugs, such as chlorpromazine, act by antagonizing D-2 postsynaptic dopamine receptors. Anyway it seems that Classic antipsychotics are more effective in treating positive symptoms than negative ones..
Some authors have suggested that schizophrenia may be caused by both hyperactivity and hypoactivity of dopamine.
It seems that schizophrenic patients may have dopaminergic hypoactivity in the prefrontal cortex and an increase in dopaminergic transmission in the mesolimbic pathways.
According to this point of view, positive symptomatology is the result of mesolimbic dopaminergic hyperactivity, while negative symptomatology is a consequence of dopaminergic hypoactivity in the prefrontal cortex. This prefrontal dopaminergic hypoactivity could result from a loss of glutamatergic stimulation.
Morphological and functional abnormalities in the schizophrenic brain
One of the most important morphological findings is the following:
A subgroup of schizophrenic patients show ventricular system dilation.
This ventricular dilation seems to be a consequence of some structures, especially of the limbic system, such as the hippocampus or tonsil, having a decreased volume. Patients presenting this characteristic respond worse to drug treatment.
These limbic structures already have a smaller volume before the onset of symptoms, so it is considered that it is not a result of a loss of neurons in the adult or adolescent individual, but of developmental problems.
Schizophrenic patients show a cognitive pattern of hypophrontality.
This, which is especially true for patients with a high incidence of negative symptoms, has been observed both by neuropsychological examination and by functional neuroimaging techniques.
Usually, schizophrenic patients perform worse than control subjects in many tasks that involve making use of the prefrontal cortex, such as the Wisconsin card classification test or the Stroop test. Its pattern of execution is similar to that of patients with lesions in the frontal lobe. (See the core of knowledge "Prefrontal cortex: functional aspects").
Likewise, it has been possible to verify using functional neuroimaging techniques, such as positron emission tomography (PET), that while the control subjects show hyperactivation of the prefrontal cortex when they must solve tasks of this type, schizophrenic patients show the same degree of activation as in the resting situation.
APA Clinical Guidelines. American Psychiatric Association Practice guidelines for the treatment of patients with schizophrenia. 2004
Lemos, S. (2009). CPG assessment on Schizophrenia and Early Psychotic Disorder. Infocop Online
Travé, J. and Pousa, E. (2012). Efficacy of Cognitive Behavioral Therapy in patients with recent onset psychosis: a review. Roles of the Psychologist, 33, 48-59
- Depression test
- Goldberg depression test
- Self-knowledge test
- how do others see you?
- Sensitivity test (PAS)
- Character test