In and out of schizophrenia: activation and deactivation of the negative and positive schemas – Article 1

Schizophrenia has positive and negative symptoms that are both analysed using a traditional cognitive model. The model exists of the cognitive triad: schemas about self, world and the future. When interventions are made, they should target the meaning behind both positive and negative symptoms. However, in the current system, the content for both symptoms is similar. The view of the self is weak, vulnerable, ineffective and worthless. The view of others as controlling, dangerous and rejecting.

What are cognitive schemas?

Cognitive schemas are responsible for cognitive organization. The content originates from the cognitive triad. If schemas interfere with accommodation in life situations, they are called dysfunctional. If schemas are extreme of fantastic, they are called delusional.

How do cognitive schemas affect symptoms of schizophrenia?

Schizophrenia can develop due to a genetic predisposition in combination with the development of negative thoughts and stressful life-events. These negative thoughts become embedded into cognitive schemas and a person can develop negative symptoms, such as withdrawal, violence and isolation. On the other hand, positive symptoms can come from dysfunctional symptoms and get transformed into delusions. These symptoms start with an overstimulation of the HPA axis which leads to an excessive output of cortisol. That leads to an overflow of dopamine and the development of hallucinations.

Motivation is one of the main factors in developing negative symptoms. There are two ways that motivation affects the symptoms, in belief and expression.

1. Factor 1 of negative symptoms: amotivation factor. This symptom comes from a dysfunctional belief about the self. The self-image is focused on weakness, worthless and helplessness. To avoid pain and frustration, symptoms like avoidance and distancing arise. It is possible to get above these thoughts, for example when a positive expectation overrides the negative attitude.
2. Factor 2 of negative symptoms: expressive factor.  These symptoms evolve because of inhibition of behavioural responses. It includes inhibition of speech or general motor activity.

What is the empirical basis for the cognitive model of negative symptoms?

Evaluation of the self has an influence on negative symptoms. Positive evaluations lead to less negative symptoms. On the other hand, dysfunctional beliefs correlate to the severity of negative symptoms. It was found that a lower self-efficacy leads to more severe negative symptoms. The three components of the cognitive triad (self, others and future) express themselves in specific situations in the context of task orientation, pleasure, interpersonal relations and energy.

Negative symptoms are related to beliefs about the future, negative thoughts about task performance or future success corelate with severe negative symptoms. Individuals that have the deficit syndrome (more severe negative symptoms) have more defeatist beliefs then those that do not experience severe negative symptoms. Furthermore, a decrease in the expectation of pleasure can contribute to more negative symptoms. Asocial beliefs also play a role and correlate with asociality in schizophrenia.

How are positive symptoms developed?

Development of positive systems is labelled the transformational or imaginal system. It is isolated from other cognitive functions. The connection with the cognitive triad is the same. It is based on an exaggeration of fears or fantasy. However, negative symptoms represent expectancy of failure whereas positive symptoms embody the basic universal needs such as acceptance. Symptoms can become less prevalent after a series of positive experiences or by becoming part of an active social network. By helping other people both negative and positive symptoms can be reduced. Automatic thoughts can be positive, critical or about other people and events. These command hallucinations are often ascribed to a powerful individual such as god. They also reflect an exaggerated fear.

What is the empirical basis for the cognitive model and positive symptoms?

Delusions

Research has shown that negative cognitive schemas about the self, predict positive symptoms. It is suggested that negative symptoms occur before positive symptoms. A lower self-esteem and more negative evaluations result in delusions and greater suicidal ideation. Beliefs about the self being powerful lead to decreased distress. Beliefs about other correspond to more severe hallucinations. People with schizophrenia tend to believe they are inferior to others. Consequently, negative beliefs about the future result in the expectation of criticism and rejection. Negative self-esteem and expectations showed a high correlation with paranoid delusions.

Voices

Low self-esteem correlates with automatic thoughts (voices). Negative beliefs about these voices corresponded to negative self-evaluations. For example, malevolence, omnipotence, metaphysical beliefs and loss of control. These evaluations also reflect on thoughts about others. Interpersonal relationships are an important predictor in hearing voices. Individuals that feel inferior to others in life, also tend to feel inferior to the voices they experience.  

What is the concept of mode?

A mode is a situation-specific cognitive system including affect, motivation and behaviour. There are two modes:

1. The adaptive mode is active when someone is playing a game or listening to music
2. The “patient” mode is more active in schizophrenia patients and consists of negative attitudes. The motivation is to avoid and escape and resulting behaviour is withdrawal.

The goal of therapy is to diminish the expectation of failure when starting a task. Therefore, the individual should experience something as a success, rather than a failure. At times people can shift between modes, when delusions are happening people can show personalities that contrast to when they are in patient mode of inactivity. When patients are engaged in something meaningful, the patent mode is not longer present. Then the adaptive mode is activated. When this mode is activated for longer periods, this leads to cognitive restructuring and positive beliefs about experiences.  

What do the researchers conclude?

Both positive and negative symptoms of schizophrenia are related to the cognitive triad and more specific: the negative cognitive triad. Most literature focused on the negative symptoms. However according to this article, positive symptoms arise from the same nature. Therefore, it is important to use the cognitive model for delusions as well. Using the cognitive model for delusions and hallucinations can contribute to treatment. The observation that activation of positive beliefs lead to replacement of the patient mode with the adaptive mode can be used in cognitive therapy. More research should be done to stress the importance of activation of positive adaptive beliefs, rather than deactivating negative and dysfunctional beliefs.

Summary: In and out of schizophrenia: activation and deactivation of the negative and positive schemas. - Article 1

• Cognitive schemas are responsible for cognitive organization. The content originates from the cognitive triad. If schemas interfere with accommodation in life situations, they are called dysfunctional. If schemas are extreme of fantastic, they are called delusional.
• A mode is a situation-specific cognitive system including affect, motivation and behaviour. There are two modes:
  
  1. The adaptive mode is active when someone is playing a game or listening to music
  2. The “patient” mode is more active in schizophrenia patients and consists of negative attitudes. The motivation is to avoid and escape and resulting behaviour is withdrawal.

Tentamenticket: In and out of schizophrenia: activation and deactivation of the negative and positive schemas. – Article 1

• Make sure you can explain the (negative) cognitive triad and the relationship between this and the existence of negative and positive symptoms of schizophrenia.
• You should be able to explain how treatment of schizophrenia can benefit from the distinction between adaptive and patient mode.

Management of somatic symptom disorder – Article 2

Many patients of somatic symptom disorder complain about pain on different places of the body or fatigue, weakness or cardiovascular disturbances. In most patients, suffering entails psychological and behavioural aspects like anxiety and checking behaviour. The spectrum is wide and bodily complaints are often attributed to organic disease. Somatoform disorders are single functional somatic syndrome diagnoses (such as fibromyalgia syndrome, FMS). After suffering unsuccessful treatment, patients often feel frustrated. Overall severity is explained by the total number of bodily symptoms and the health anxiety. Depression and anxiety, together with the bodily distress of the well-defined pathology characterize patients.

How is the somatic symptom disorder classified in the DSM-V?

The criteria that must be met according to the DSM-V are the following:

• One or more somatic symptoms that cause distress and disruption of daily life.
• One or more excessive thoughts, feelings and behaviours that are associated with concern about health. Thoughts about the seriousness of the symptoms, anxiety about symptoms and time and energy devoted to the symptoms or concern about health.
• The symptoms must last for more than 6 months.

When one of the symptoms is present the disorder is moderate, when two or more symptoms are present and there are multiple somatic complaints the classification is severe.  Illness anxiety disorder is when people experience hypochondriasis without bodily complaint. Because many patients have been mislabelled in the past, the classification of “medically unexplained” is not present in the DSM-V. The term bodily distress may describe the suffer from bodily symptoms but can be just psychological distress.

What is already known about somatic symptom disorder?

Genetics can contribute to the predisposition and chronic pain in general. However, the extend is limited. Epigenetic mechanisms are relevant as they are shaped by prenatal experiences. Childhood adversities seem to be a predictor of development of bodily distress. Attachment patterns formed in childhood can contribute, attachment anxiety can lead to health anxiety. Cultural influences can also contribute to the development of bodily distress, stressful work conditions and adverse life events can cause organic illness, but also bodily distress.

How is somatic symptom disorder diagnosed?

When individuals are referred with SSD in mind, it is not difficult to define the presence or absence of criteria. Measurement instruments include the Patient Health Questionnaire-15 (PHQ-15) for somatic symptom burden and the Whiteley index for health anxiety. There are some recommendations for adequately diagnosing SSD:

• Consider the possibility of SSD as early as possible.
• Avoid risky and repetitive investigations that serve to calm the patient
• Mind clues from the patient that indicate emotional distress beyond the scope of the main symptom.
• Assess experiences, expectations and illness behaviour. For example, body checking and avoidance.
• If SSD is diagnosed, decide if the condition is mild, moderate or severe.

How is somatic symptom disorder treated?

Treatment currently has moderate effect because bodily distress in general is covered by categories (such as SSD) that are used in mental health settings. However, research of the bodily patterns and psychobehavioural features of SSD should include a broader perspective. Currently there is no evidence for the efficacy of training and enhanced care of physicians. Not much evidence has been found for the effectiveness of antidepressants or hypnotherapy either.

Treatment exists of good management of this group of patients, the bodily complaints must be taken seriously even without a well-defined pathology. Encouraging the patient to take on a healthy lifestyle, hobbies and regular exercise can be helpful. In mild cases, these principles combined with waiting is enough but when the case is more severe, other approaches may help:

• Introducing contextual factors, providing of a blame-free narrative that is linked to both psychological and physical mechanisms.
• Encourage and monitor functional behaviour and attitudes. Stimulate relaxation, positive thinking, self-help guides and set realistic goals together with the patient.
• Provide pain relief medication or digestives. Allow medicine according to the patients wishes, they are temporarily helpful, but less effective than self-management.
• Consider antidepressants if pain is predominant or the patient gets depressed.
• Set appointments for intervals rather than waiting for initiation of the patient.
• Ensure that traumatic stressors are assessed.
• Consider multidisciplinary treatment including psychotherapy, occupational therapy and physiological therapy.

Psychotherapy is an established treatment but challenging in the beginning when patients often have difficulty accepting talking can help their cure. Some things could be helpful in such a situation:

• Clarify the motivation for psychotherapy consultation.
• Use the measures above in an appropriate manner.
• Listen to bodily complaints and experiences with doctors and health professionals. Also give feedback on the emotional aspects of these experiences.
• Give support in organisation of the history of complaints.
• Encourage the patient to see additional influence of psychosocial or biological context factors.
• Negotiate realistic and modest treatment goals.
• Resist concentration on bodily symptoms.
• Liaise with others involved in the care about relevant information.

Summary: Management of somatic symptom disorder – Article 2

• Many patients of somatic symptom disorder complain about pain on different places of the body or fatigue, weakness or cardiovascular disturbances. In most patients, suffering entails psychological and behavioural aspects like anxiety and checking behaviour.
• Treatment exists of good management of this group of patients, the bodily complaints must be taken seriously even without a well-defined pathology.
• Psychotherapy is an established treatment but challenging in the beginning when patients often have difficulty accepting talking can help their cure.

Tentamenticket: Management of somatic symptom disorder – Article 2

• You should be able to explain why diagnosing SSD is difficult.
• Make sure you can explain what kind of treatment is being used in patients suffering from SSD and why psychotherapy, although being used a lot, can be quite challenging at the beginning.
• You should be able to list some approaches on how to deal with patients with severe SSD. For example: providing a blame-free narrative that is linked to both psychological and physiological symptoms.

Psychotic Disorders – Article 3

A psychotic disorder refers to a condition where psychotic symptoms meet the criteria for a disease. Psychoses can be characterized in three groups:

1. Idiopathic psychoses. Causes a rapid decline in functional capacity. It is an abrupt onset of symptoms.
2. Psychoses due to medical condition. For example, neurodegenerative disorders.
3. Toxic psychoses. Due to substance abuse.

These three classifications are not fixed, they reflect the current lack of knowledge on psychotic disorders and their causes.

What are the differences between type I and type II psychosis?

The most frequent period in life where psychotic symptoms appear is in the third phase of life. However, this varies depending on the underlying disorder. Delusions often appear in middle ages, psychosis caused by drug abuse or medicine can occur at any age. Type II psychoses include toxic and psychoses due to a medical condition.  Idiopathic disorders, and more specifically schizophrenia or depression have an unpredictable course of their illness. The number of psychosis differs from one patient to another. In general, psychotic persons are at high risk for suicide attempts, substance abuse, homelessness and violence.

What are causes of the development of psychoses?

Many disorders are caused by an alteration of neurotransmission in the pathways of glutamate and dopamine in the brain. These are situated in the hippocampus, midbrain, corpus striatum and prefrontal cortex. Excess synaptic levels of glutamate and dopamine cause increased stimulation which can result in psychotic symptoms. In molecules, the disruption is a deficiency of the y-aminobutyric acid (GABA) inhibition neurons and N-methyl-D-aspartate (NMDA) glutamate receptors (NMDARs). The neural balance of dopamine cannot be regulated and results in an increased level of glutamate.  

Research is done by examining the neural consequences of taking cannabinoids (especially cannabinoid-I receptors). They guide the traffic of glutamate and dopamine. Synthetic drugs work in a similar manner releasing dopamine and serotonin in the brain. These drugs can induce psychotic symptoms. Psychedelic drugs stimulate the 5-HT_2A which implicates that 5-HT_2A  and serotonin are in the pathophysiology of psychosis. However, psychological drugs induce qualitatively different psychosis than idiopathic disorders.

What are genetic factors in psychosis?

Idiopathic psychotic disorders are heritable. The specific genes responsible for this heritability is not clear. Two hypotheses are defined:

1. The common disease-common allele hypothesis where prevalent genes with low penetrance act through other genes to confer a risk of developing a psychotic disease. However common genetic variants with low penetrance are not biologically plausible. However, there is some evidence the major histocompatibility complex (MHC) can de-regulate the development of neural connections in presynaptic terminals. This way is can influence the form and function of neural circuits.
2. The common disease-rare allele hypothesis where rare mutations of (novo mutations) that occur in a small proportion but are highly penetrant cause the psychotic disease. Rare genetic variants with high penetrance are mostly associated with psychotic disorder. The 22q11.2 deletion syndrome (also known as DiGeorge syndrome) is associated with schizophrenia. Similar copy-variations are associated with psychotic disorders.

What are neurodevelopmental factors in psychosis?

Maternal infections of nutritional deficiencies in the prenatal period are associated with the development of psychoses. Autoimmune and inflammatory disease can stimulate or block the glutamate system because of antibody regulation. Systemic autoimmune disorders are related to autoimmune diseases with nerve system manifestations such as SLE. Paraneoplastic and nonparaneoplastic autoimmune syndromes cause antibodies to be directed against the glutamate NR1 unit of NMDAR.

How is the diagnosis of a psychosic disorder?

Psychotic disorders are diagnosed clinically, based on observed behaviour, subjective reports and the history of the patient. Also, diagnostic tests such as EEG, genotype and toxicology are examined. Some of these tests reveal differences between psychotic and non-psychotic patients none have proved to be reliable in diagnosing individual cases of psychosis. There are three important diagnostic tests to expose the biological basis of psychosis.

1. Neuroimaging (MRI or PET) is used to reveal abnormalities in the brain that cause schizoaffective disorder, schizophrenia or bipolar disorder. The temporal, frontal and parietal lobes are reduced in size as well as cortical thickness. Magnetic resonance spectroscopy shows increased glutamate levels in the prefrontal and temporal lobes.
2. Neurophysiological tests (EEG) are conducted when a neurodegenerative or causative medical condition is assumed. Event-related potentials are abnormal in patients is psychotic disorders.
3. Serologic test for syphilis is recommended in psychosis. The immunologic conditions should be considered when the onset of psychotic symptoms is very sudden.

How is psychosis treated?

Psychoses can be treated with medicine. These work on dopamine and D2 receptors. Their effectiveness depends on the safety profile of the patient which varies with the underlying cause and previous pharmacology. Most patients are treated with short-acting medicine that requires daily administration. Long-acting medicine (haloperidol, olanzapine) are available and can facilitate adherence to the treatment. Effects of antipsychotics are moderate, and efficacy limited. Other medicines work on the 5-HT_2A receptor. These are useful for psychotic symptoms that are caused by dopamine, such as with Parkinson. However, they are less effective in treatment of schizophrenia and mood disorders. A careful review of the patients’ condition and medical history is needed before antipsychotic drugs are considered.

Another way of treatment is brain-stimulation such as ECT, TMS, DBS or tDCS. For example, ECT is affective for catatonia but also for mood disorders (depression) and schizoaffective disorders unresponsive to anti-psychotics. A promising effect is that auditory or verbal hallucinations can be controlled. When tDCS is applied over the auditory cortex this can result in less hallucinations and decrease of negative symptoms such as apathy and social withdrawal. Then, DBS is the most invasive and used when all other treatments fail.

Psychosocial approaches, such as behavioural rehabilitation consists of social skills training in which patients receive instructions about appropriate ways of behaviour and communication. Another psychosocial treatment is family psychology education. Cognitive behavioural therapy (CBT) may also be useful because it includes cognitive restructuring. CBT in patients with schizophrenia can reduce distress caused by hallucinations of delusional beliefs.

Summary: Psychotic Disorders – Article 3

• A psychotic disorder refers to a condition where psychotic symptoms meet the criteria for a disease. Psychoses can be characterized in three groups:

1. Idiopathic psychoses. Causes a rapid decline in functional capacity. It is an abrupt onset of symptoms.
2. Psychoses due to medical condition. For example, neurodegenerative disorders.
3. Toxic psychoses. Due to substance abuse.

• Psychotic disorders are diagnosed clinically, based on observed behaviour, subjective reports and the history of the patient. Also, diagnostic tests such as EEG, genotype and toxicology are examined. Some of these tests reveal differences between psychotic and non-psychotic patients none have proved to be reliable in diagnosing individual cases of psychosis.

Tentamenticket: Psychotic Disorders – Article 3

• Make sure you can explain the difference between type I and type II psychoses.
• What are heritable (genetic factors) of psychoses and what two hypotheses exist about the genetics?
• There are three ways in which psychoses are treated currently. One of them is psychosocial (social skills training). You should be able to name and explain the other two and list some of the sub-categories of these approaches.