Causes of schizophrenia

2021-07-15 04:22 PM

A recent genetic study by Tienari et al compared the prevalence of schizophrenia in adopted children of mothers diagnosed with schizophrenia.

Genetic factors

Schizophrenia is at the heart of the scientific debate about the nature and role of nutrition in the development of mental health problems. Perhaps predominating is the etiological model of schizophrenia, which holds that it has a biological cause, driven by genetic factors, although there is still fierce controversy among proponents of these causes. environmental person. The evidence regarding genetic factors has been scrutinized and almost no one objected. Previous genetic studies have shown that the risk of schizophrenia among people related to the "case" is determined to be related to the level of common genes.

These studies also suggest a partial genetic link in schizophrenia. However, when evidence suggests that schizophrenia runs in families, it does not mean that there is a genetic cause (see chapter 1). For people who are closely related, it means that they also share the same environment and can be influenced by each other's behavior. Attempts to assess biological and environmental factors have led to numerous studies comparing the risk of schizophrenia among blood relatives or twins versus those who have been adopted.

A close review of these studies reveals that the evidence is not as clear-cut as one might think. For example, adoption studies in Denmark (Kety et al., 1975) studied people related by blood to 34 children who were adopted and subsequently developed schizophrenia in 34 cases. controls had “clean pedigrees” and compared the rates of schizophrenia among them. Interestingly, they found that only one person was diagnosed with chronic schizophrenia among the study and control groups. It was only when they extended their diagnosis to the disorders of the schizophrenic group, comparing a variety of diagnoses, including borderline status, mismatched personality, and suspected schizophrenia that the difference between the two groups increased. With these diagnoses, The study group had 9 cases and the control group had 2. However, some authors (eg Roberts, 2000) said that the study also did not provide evidence of heredity within schizophrenia. Roberts also points out that at least some of the diagnoses were taken from the hospital and not confirmed by the team themselves, and that at least one person was changed by the team from being unfit to personality. borderline schizophrenia. Worse still: a review of all the records of this individual revealed that the initial diagnosis was bipolar affective disorder (Rose et al., 1984). Roberts also points out that at least some of the diagnoses were taken from the hospital and not confirmed by the team themselves, and that at least one person was changed by the team from being unfit to personality. borderline schizophrenia. Worse still: a review of all the records of this individual revealed that the initial diagnosis was bipolar affective disorder (Rose et al., 1984). Roberts also points out that at least some of the diagnoses were taken from the hospital and not confirmed by the team themselves, and that at least one person was changed by the team from being unfit to personality. borderline schizophrenia. Worse still: a review of all the records of this individual revealed that the initial diagnosis was bipolar affective disorder (Rose et al., 1984).

Recent genetic research by Tienari et al. (2000) compared the rates of schizophrenia in adopted children of mothers diagnosed with schizophrenia with those adopted by mothers without schizophrenia. The risk of schizophrenia among children of mothers with schizophrenia is four times higher than that of children of mothers without schizophrenia: overall incidence was 8.1% vs. 3%. However, it is not entirely genetic. Using the results of the same study, Wahlberg et al. (2000) reported on the interaction between genetic and environmental factors. Children of women with schizophrenia living with adoptive parents without any communication disorders are not at increased risk for thinking disorders. Opposite,

Thus, the development of schizophrenia seems to depend both on genetic risk and communication aberrations in the adoptive family. It is important to note that communication deviations are analyzed before adoption, not because of the child's behavior.

Along with other findings, biologists' data support a model in which genetic factors influence the risk of developing schizophrenia but not the cause. single. They combine to be a vulnerability factor rather than a causal factor. Studies looking for genes that increase the risk of schizophrenia have also been inconclusive, although dozens of chromosomes have been suspected (Tsuang, 2000). Even genetic advocates such as Corsinco & Meguffin (2001) have stated that determining a genetic relationship in schizophrenia presents "great difficulties". When it comes to the role of genetics in schizophrenia, it should always be kept in mind that 89% of people diagnosed with schizophrenia are unaware of the relationship to the disorder. There are clearly other factors involved in development.

Biomechanics

Dopamine hypothesis

A great deal of neuroimaging research aimed at identifying the causes of schizophrenia is done on people who are thought to be schizophrenic. This can cause different feelings. However, it also raises important problems in interpreting the data. Johnstone (2000) argues that any evidence of neurological differences between people with schizophrenia and those without cannot say that it is the cause. Furthermore, these differences may also be explained by medication and/or stress due to vivid hallucinations or persistent strong delusions.

Despite these opinions, many biological models of schizophrenia have been proposed. The first is the theory of the brain's dopamine systems. Dopamine-secreting neurons have been found in the A10 area of ​​the limbic system, which has connections to the thalamus, hippocampus, and frontal cortex, and substantia nigra. The key thesis of the dopamine hypothesis is that the experience of people diagnosed with schizophrenia is the result of an excess of dopamine or of neuronal synaptic receptors that are oversensitive to normal dopamine levels. In general, the evidence seems to support the latter claim, however, in other words, the theory explains that at least some of the experiences of people with schizophrenia may be due to activation. excessive dopamine in areas of the brain controlled by dopamine.

Amphetamine use increases dopamine levels and can cause experiences such as positive symptoms and parodies of schizophrenia. Small amounts of controlled amphetamines can also cause schizophrenia-like symptoms in at least some 'naive' individuals. These experiences may persist even after discontinuation of the drug. These phenomena, however, resemble only one form of schizophrenia: the paranoid body.

Several therapeutic agents that are effective for both amphetamine-induced psychosis and schizophrenia are neuroleptic drugs known as phenothiazines (see chapter 3). These drugs block dopamine by preventing its absorption at postsynaptic receptors.

Autopsy studies have shown a significant increase in dopamine receptor sites in individuals with schizophrenia compared with "normal" subjects considered to be hypersensitive to dopamine. However, it is not possible to determine how much is due to the drug and how much is due to the disease.

Evidence against the dopamine hypothesis (Duncan et al., 1999):

There is no direct evidence of dopamine-induced neuropathological activity, such as increased levels of dopamine, its metabolism, or its receptors, which are a potential consequence of antipsychotic therapy.

One of the most effective antipsychotics, clozapine, appears to act by a mechanism that affects the serotonin system, but not the dopamine system. This leads to the assumption that there may be other neurotransmitters involved in schizophrenia.

There are some people with neuroleptic-resistant schizophrenia, so it can be argued that the dopamine systems are not always involved in the etiology of schizophrenia.

“Schizophrenia-like” experiences are rare in “normal” individuals when they take drugs that increase dopaminergic activity.

Neuroleptic drugs have only a partial effect on negative symptoms of schizophrenia.

Such conflicting evidence may speak to the difficulty of unifying the different biological processes behind a disease that may manifest itself differently in different people. However, instead of identifying specific biological bases for psychological experiences, biologists continue to try to come up with a model that can explain all experiences of people with schizophrenia. paralysis. One way they did it was by expanding the number of neurotransmitters involved in the cause. For example, Duncan et al. (1999) suggested that NMDA and serotonin dysregulation may also play a role in this disorder.

Nervous facilities

As well as errors in neurotransmitter concentrations, some studies have suggested that negative symptoms, adolescence, and some positive symptoms may be due to damage to the nervous system (Basoo et al. 1998). ). The findings on CT brain scan are mainly of dilatation of the ventricles and atrophy of the cerebral cortex, especially in the frontal and temporal lobes. Postmortem examination revealed a decrease in neuronal density and size in the limbic, temporal, and frontal regions. This also entails disordered neuronal junctions. As a result, many psychological functions are also affected, such as attention, memory, and emotion (the limbic system), planning and coordination (frontal and prefrontal lobes), memory, sound, and language (the lobes). Sun). The later the treatment, the later it ends. Liberman et al. (1990) take it as an indicator that neuronal degeneration is a progressive disintegration process, reduces the individual's ability to respond to antipsychotic medications. The later the therapy, the greater the degree of neuronal damage and the more difficult it is to make a full recovery. Biologists have proposed several causes of neuronal damage. Those hypotheses are presented in the next section.

Excess dopamine

To extend the dopamine hypothesis, Liberman et al. (1990) suggested that the initiation of the first phase of schizophrenia may be increased dopaminergic activation leading to positive symptoms. However, continued excessive dopamine activity leads to degeneration of neurons in the dopamine system and leads to excessive lowering of dopamine activity, thus producing negative symptoms.

Viral infection

There is strong evidence that children born in winter have a higher risk of developing schizophrenia than in summer (Torrey et al. 1997). It is not clear why that is the case. The widely accepted conjecture, however, is the viral neuronal damage that viral diseases are common in winter. Jones and Cannon (1998) also provide evidence to support this hypothesis. The authors found that among children infected with the virus, the rate of later development of schizophrenia was five times higher than in those who were not. Likewise, Takei et al. (1995) found that female (but not male) fetuses infected with the influenza virus during the last 5 months of pregnancy had a higher risk of developing schizophrenia in adulthood than uninfected fetuses. However, large-scale studies do not completely confirm these findings. While some studies have found a higher risk of schizophrenia in people born close to viral outbreaks than in others, others have not (Battle et al. 1999).

Pregnancy and obstetric complications

Pregnancy and obstetric complications can also cause microscopic brain damage and increase the risk of schizophrenia. Meta-analysis of 11 studies in this regard, Geddes et al. (1999) compared data on 700 children, who later developed schizophrenia, with 835 controls. Some of the obstetric complications associated with this problem are low birth weight, premature delivery, intervention or incubator, hypoxia, and premature rupture of membranes.

Mom's Stress

Several studies have also addressed the role of maternal stress in the development of schizophrenia. Van Os and Selten (1998) found that the children of women who suffered World War II bombing while they were pregnant had a higher risk of developing schizophrenia than those of women not. However, the interpretation of these data also has certain complications because the stress experienced by women is not necessarily caused by the above factors. Furthermore, the cause of any relationship between maternal stress and subsequent disorders has not been clearly demonstrated. It can be indirect, affecting hormonal changes during times of stress, changes in health behaviors such as smoking, alcohol consumption, obstetric complications or due to some other mechanism. 

Substance abuse

Thus this chapter has identified several factors that either increase the risk of developing schizophrenia or account for the chronic degenerative changes associated with the condition. However, these factors cannot be considered as direct drivers for each specific phase.

Such direct motivations may be psychological (see below). However, another factor is also possible, which is biochemistry.

Stimulants can induce a temporary psychotic state and promote remission of a psychotic state (Satel and Edell, 1991). Evidence that cannabis use increases the risk of schizophrenia was found in a 15-year study by Andreasson et al. (1987) over 45,000 Swedes. Marijuana users aged 18 and older were hospitalized with a diagnosis of schizophrenia more than non-users. Furthermore, there was an association between frequency of use and risk of schizophrenia: the more marijuana smoked, the higher the risk of schizophrenia. The biochemical channel through which cannabis has an effect has also been identified. Activation of cannabis (delta-9 tetrahydrocannabinol) increases brain dopamine levels and may induce psychosis.

Psychosocial factors

The highest rates of schizophrenia are among the lower social classes. Enton et al. (1989) calculated that individuals in the low socioeconomic class were three times more likely to develop schizophrenia than the highest group. This argument has (at least) 2 points. Either socioeconomic status is a risk factor for schizophrenia, and or schizophrenia is a risk factor for low socioeconomic status: social cause or effect (see chapter 6). first). Fox (1990) analyzed the literature gathered over the years and other published research findings and came to the conclusion that there is no evidence to support the social consequences hypothesis. Thus, it seems that low socioeconomic status is the cause of schizophrenia rather than its consequence.

Another explanation supports the above data. Low socioeconomic status is often associated with high stress, and it may be the driving force behind the emergence of schizophrenia in vulnerable individuals. That claim is supported by another study. Approximately 24% of the schizophrenic phase occurs after acute life stressors (Tsuang et al. 1986).

Prolonged stress also increases the risk of first-time onset schizophrenia. Family can also be a chronic stressor. One of the early theories suggested the mother-child relationship as one of the predisposing factors for schizophrenia. This is the theory of psychoanalyst Fromm-Reichman (1948). According to the author, schizophrenia has almost no chance to appear when a mother is a kind person, devoted to her children. In contrast, this chance appears to be higher in cold, authoritarian mothers who are called "schizophrenic mothers". Fromm-Reichman argues that the mixed signals that mothers give out further confuse children, making it difficult for them to perceive and make sense of the world, and this process easily leads to behavioral and cognitive confusion. Bateson et al. (1956) also proposed a similar theory. Their "double binding" theory suggests that some parents often treat their children in a contradictory and confusing way. For example, they may tell their children that they love them very much but in an opposite tone or ask them to do conflicting things such as: “I think you need to go out with your friends but I want you to stay here.” home with mom…”. Such often conflicting demands can confuse children, create stress, and can lead to schizophrenia. Both models have a certain logic, but there is not much evidence to confirm them. “I think you need to go out with your friends but I want you to stay home with me…”. Such often conflicting demands can confuse children, create stress and can lead to schizophrenia. Both models have a certain logic, but there is not much evidence to confirm them. “I think you need to go out with your friends but I want you to stay home with me…”. Such often conflicting demands can confuse children, create stress and can lead to schizophrenia. Both models have certain logic, but there is not much evidence to confirm them.

Another family theory offers another explanation. According to this theory, the most sensitive element in the family is how critical the family is to the individual's expressions. According to the same model, high expression of negative, hostile, or critical emotions can trigger relapse in people who have had at least one episode of schizophrenia. The classical study of this phenomenon known as high negative expressed emotion (NEE) was performed by Vauglin and Leff (1976) in patients with recurrent schizophrenia who were hospitalized. at Maudsley Hospital in the 1970s. Their results were startling: those who were discharged and returned home with low NEE had a lower relapse rate than those who went home with high NEE. This phenomenon is also related to the duration. People who stay at home for less than 35 hours/week because they still work or go to day centers have a lower rate of relapse than those who stay at home for more than 35 hours/week. Evidence for the familial processes leading to the initial onset of schizophrenia in vulnerable individuals has been shown in the study by Wahlberg et al. (2000b) and presented at the beginning of the chapter.

Psychobiological pattern

Thus, there is evidence linking dopamine, microscopic brain damage, and stress to schizophrenia. However, what has not been done is to explain the nature of each disorder or the psychological factors affecting its development. The dopamine hypothesis could extend to many of the relationships between stress and schizophrenia as there is evidence of increased dopamine levels when animals are under stress (Walker & Diforio, 1997). It was also added that rats sensitized to prolonged amphetamine administration showed increased behavior and higher stress levels of dopamine than the control group (Duncan et al. 1999). Thus, from the above data, it is possible to provide a model of the possible association between stress and vulnerability in schizophrenia. This model can include 3 phases:

Stage 1 - Neurodevelopmental disorders due to genetics, obstetric factors or fetal period. These problems predispose to early subtle damage to the cognitive, motor, and social aspects. It creates the possibility of being prone to schizophrenia.

These deficiencies can lead to stage 2 appearing in adolescence and early adulthood. During this time stressful but normal experiences lead to increased dopamine activity. As a result, it disrupts neuronal organization, the dopaminergic neuron system becomes more sensitive to current dopamine levels and reacts more strongly to them leading to positive symptoms of schizophrenia.

If prolonged or re-occurring, high dopamine levels can lead to neuronal degeneration and, subsequently, to structural neuronal disturbances, the onset of negative symptoms. Thus, at the heart of schizophrenia is coordination disorder that can be the result of both types of factors: biological factors that increase vulnerability and can contribute to chronicity and stress factors. trigger the onset of illness. Even the psycho-biological-social model in the eyes of some critics is too biological. For example, Johnstone (2000) argues that there is not yet a fundamental basis for any biological pillar for with schizophrenia or its components. They still feel that there is no need to combine biological and psychological factors and prefer a psycho-social model rather than a bio-psychosocial model.

Psychological pattern

Psychological models often offer different interpretations of schizophrenia. Instead of identifying the factors that trigger the "phases" of schizophrenia, they seek to explain the process behind each of the different forms. They choose a dimensional approach to understand the experiences of people diagnosed with schizophrenia (see chapter 1), because, according to their interpretation, these individuals' experiences are only on the opposite side of the spectrum. further from “normal” than from normal. The cognitive processes of these individuals are the same as that of everyone else, only the content is different.

One approach to psychology is to consider the cognitive processes behind the behavior to be related to schizophrenia:

Memory deficiency is caused by the inability to link separate elements and events into a block, a memorable whole.

Speech hallucinations may result from abnormalities in language perception and defense mechanisms against the reality of traumatic memories.

Disturbances represent a specific deficiency in meaning processing, arising from unusual associations in a semantic system.

Negative symptoms are related to intellectual, coordination, memory, and attention deficits.

The cognitive model of delusions

The cognitive model of delusions developed by Bentall et al. is based on a psychological approach to account for the fate of individuals diagnosed with schizophrenia. Perhaps the most understandable thing about the paranoia of people with schizophrenia is the qualitative difference from the beliefs of the “normal” people. For example, Berrios (1991) considers paranoia to be an "empty linguistic movement", referring to neither the world nor to the self: it is not a symbol of anything. In contrast, clinicians, such as Bentall (Bentall et al. 2001) argue that delusions lie only at the top end of a spectrum of thought patterns, extending from the "common person" to the extremely strange and impossible combinations, but they are all just the end products of similar cognitive processes. Cognitions, including delusions, are viewed as an interpretation of events, it can be a rational attempt to induce unusual emotion. When the content of thought can go beyond the ordinary, there is no longer the underlying psychological process.

Bentall et al. focus on explaining one of the types of delusions of abuse. Their research shows that people with this type of delusion also have cognitive disturbances common to many other disorders. As another example, Bentall et al. (2001) found that in stories—part of a memory test—people with delusions of being watched were more likely to re-enact threatening themes than depressed people and control groups. control (volunteer, no mental health problems). They take that as an indicator of the general difficulty in interpreting events.

The authors' model of victimized paranoia (Bentall et al. 2001) outlines the humanistic conception of the ideal self and the real self. They argue that many people with schizophrenia have a very poor self-concept, a very significant difference between the ideal self and the real self. It's what they see themselves as and who they want to be. Such inconsistencies may be reinforced by attentional and attribution biases, namely, that they view negative events or outcomes as due to individual limitations. Being aware of the inconsistency between the ideal self and the real self can lead to depression. Victim delusions may also arise as a result of the struggle to reduce such inconsistencies. According to Bentall et al. When some negative event disturbs the disparity between the ideal self and the actual self, the individual tries to reduce the disparity by shifting the attribution to the other - a form of mental defense. Common sense: "I think I'm fine, even if others don't." The idea that others misunderstand you is less stressful for you than accepting your own feelings of inadequacy. Next, Bentall et al. argue that the nature of schizophrenia in each family can be explained by this model because attributions can be learned from other family members and that parental criticism may increase inconsistencies between the ideal self and the real self, leading to relapses of schizophrenia. individuals try to reduce that disparity by shifting the attribution to something else—a common form of psychological defense: “I think I'm fine, even though others don't.” The idea that others misunderstand you is less stressful for you than accepting your own feelings of inadequacy. Next, Bentall et al. argue that the nature of schizophrenia in each family can be explained by this model because attributions can be learned from other family members and that parental criticism may increase inconsistencies between the ideal self and the real self, leading to relapses of schizophrenia. individuals try to reduce the disparity by shifting the attribution to something else—a common form of psychological defense: “I think I'm fine, even though others don't.” The idea that others misunderstand you makes you less stressed than accepting your own feelings of inadequacy. Next, Bentall et al. suggests that the nature of schizophrenia in each family can be explained by this model because attributions can be learned from other family members and that parental criticism may increase inconsistencies between the ideal self and the real self, leading to relapses of schizophrenia. The idea that others misunderstand you is less stressful for you than accepting your own feelings of inadequacy. Next, Bentall et al. argue that the nature of schizophrenia in each family can be explained by this model because attributions can be learned from other family members and that parental criticism may increase inconsistencies between the ideal self and the real self, leading to relapses of schizophrenia. The idea that others misunderstand you is less stressful for you than accepting your own feelings of inadequacy. Next, Bentall et al. argue that the nature of schizophrenia in each family can be explained by this model because attributions can be learned from other family members and that parental criticism may increase inconsistencies between the ideal self and the real self, leading to relapses of schizophrenia.

Traumatic model of hallucinations

Romme and Escher's (1989) model views hallucinations as a normal response to traumatic events, namely physical and sexual compulsion and abuse.

They argue that their function is to direct attention to emotional traumas that need to be addressed and offer a defense against memory-related emotional reversals by channeling those into a secondary character. 3.

Therefore, the goal of therapy is to help clients develop strategies for understanding and interpreting the voices they are hearing, not to help them eliminate them.

Coping pattern

This is the ultimate approach to the experience of people diagnosed with schizophrenia. According to this model, schizophrenia is just the end of a series of poor strategies for dealing with stress. Analysis of the "early signs" before onset, as the DSM calls the schizophrenic phase, often reveals behavioral features such as: alienation from friends and family, or being alone in the room more, Insomnia leads to fatigue, weakness, delay in scheduling tasks for the day, and possibly starting medication to relieve stress disorders or low mood. This state is no different from the sensory suppression that causes paranoia or hallucinations in most people.

Birchwood et al. (2000) asked the client to mark the ballot “early signs”. Those are the signs they feel at different times of the relapse. Others are suggested to be determined through discussion. Here are some early signs identified by people using this approach. Signs are ordered within several months before a clear “relapse”:

Outstanding pattern

The pattern that stands out from others is this: in people diagnosed with schizophrenia when faced with particular life stress, they withdraw, become very tired, and delay their day's work. and medication can be used to alleviate the insecurities. This state is not much different from sensory suppression, which, as is known, often causes paranoia and hallucinations. It can therefore be argued that the experience of people diagnosed with schizophrenia is not much different from that of others. A “relapse” appears to be the difficult outcome of a series of inappropriate coping behaviors and puts them at risk of having an unusual experience rather than the emergence of a “disorder” that is different from one another. with the experiences of others.