Lecture: Introduction and suicide

Introduction

CP is a new course with the following goals: to have knowledge on psychopathology/disorders; to know how science and practice of CP interact; and to be able to make a theoretical argument out of scientific literature.

There are 8 non-obligatory lectures (which will be streamed) and 8 obligatory workgroups (you may miss 1 workgroup with a good reason and do some compensatory work), in which you are expected to give a presentation (about 30 minutes total) and write a paper (shorter than 2500 words, see instructions on Blackboard). The exam contains 8 to 10 open questions.

There is a document on Blackboard which shows some chapters you should read before a lecture. However, all the chapters from the books are relevant for the exam (but the chapters used could be a hint on what they think is most important). Watch out for scientific papers, for tables can be quite specific – don’t learn them by heart, these are not very relevant. Percentages are sometimes relevant, but never precise numbers.

Your grade consists of an exam grade (40%, should be at least 5.5), workgroup participation grade (20%, can be any grade) and a paper grade (40%, should be at least 5.5).

Suicide

Suicide and contagion

About 1 million people a year commit suicide worldwide. For example, Dutch writer Joost Zwagerman commited suicide one day before this lecture. He had showed numerous risk factors, such as being severly depressed several times and almost losing his father to suicide (perhaps genetic factors?).

A few examples of risk factors for suicide are prior suicide attempt(s), depression, schizophrenia, economic hardship etc.

About 5 people a day commit suicide in Holland, this number is increasing.

Because of this recent celebrity suicide of Zwagerman, there will probably be a lot of attention for this suicide. This is worrysome, because suicide is contagious: hearing about suicide will make some people (mostly people who are already suicidal) commit suicide.

The number of remissions (fallbacks) after two years is higher amongst people with anxiety and people with both anxiety and depression than people with ‘only’ depression.

Antidepressants and losing personality

Kramer, a clinical practitioner, wrote about Prozac: he wrote about patients coming back to their psychiatrist after a depression, not because they have remissions, but because they feel like they lost their personality. ‘I am no longer my self’. This could be a main effect of Prozac.

Typically, depression comes with a lot of anxiety too, which is important to know because anxiety is more chronic. In a treatment, depression reduces first, then neuroticism and extraversion improve a bit later. But the first stage of treatment is a placebo-effect: the effect of just receiving help.

Knutson and colleagues showed that healthy volunteers showed more cooperative behaviour when on SSRI’s (for one week). Surprisingly, the danger of antidepressants (such as fluoxetine) is the side effect of stimulating suicide (!): there were people who weren’t suicidal before, that started committing or thinking about suicide after being on anitdepressants.

The faces of depressive episodes

When people have multiple symptoms (e.g. depressed, sleeping problems and concentration problems) in one episode, it doesn’t necessarily need to be exactly like that in the next episode. The face of the problem can change. Of all the symptoms that can come up in an episode, suicidal ideation has the highest number of comebacks. This means that when you have suicidal ideation in the first episode, you are very like to have this same symptom in your next episode. However, episodes over time within the same person often have different symptoms.

The underlying mechanism behind this is the automatic thought scheme. These depressive thought schemes are not per se treated by antidepressants and can therefor return in a next episode. However, episodes over time within the same person often have different symptoms.

You can compare the activation of these schemes to a neuronal network, in which neurons are connected and stimulate each other to fire. Neurons that repeatedly fire together, wire together (the connection between them gets stronger). It’s the same in a associative network: one event may trigger a feeling, and when they ‘fire’ together a lot, the connection is highly activated. So every time the event happens, the feelings that are associated with this also return. This is how a depressive thought scheme can be activated.

DAS (Dysfunctional Attitude Scale)

The DAS is a scale for (symptoms of depression and disorders like) depression. There are two weak points, however:

• the DAS cannot detect the distinction between people who have never been depressed and people who have been depressed but are now remitted.
• even when people who have been treated with antidepressants are also not detected: in the DAS they score as ‘normal’.

Yet in real life, people who have been depressed are at higher risk to get another depressive episode, and this should be visible in their scores. This distinction is not visible in the DAS, but they are visible in a mood induction test (a test in which people are made sad, comparing people who had been depressed at some time with people who had never been depressed): people who have a history of depression, are more sensitive to think negatively about themselves.

Lecture: Somatoform disorders

Chronic fatigue syndrome is one of the somatoform disorders: you are tired, are in a lot of pain, cannot get out of bed, and can be caused by a virus, as in the case of the example in the lecture.

DSM-IV-TR focuses on physical symptoms: you cannot explain these with medical states, there is no actual medical condition that can explain the symptoms (e.g. headache after drinking too much alcohol; the hangover is the explanation for the headache). The symptoms may not be explained by other mental disorders such as panic disorders. The symptoms must also hinder you in your daily life, cause stress and impair you.

Grouping the somatoform disorders in the DSM-IV:

• Pain disorder

• Undifferentiated somatoform disorder

• Somatisation disorder

Together these three disorders form one group that is characterized by chronic physical symptoms, impairment in daily functioning and have many different causes (drinking too little can cause a headache, sleeping too little can cause tiredness).

• Hypochondriasis

• Body Dysmorphic Disorder

Hypochondriasis and body dysmorphic disorder are the second group: dissatisfaction/anxiety about (aspects of) the body, such as appearance (BDD) or sensations (hypochondriasis). There is an emotional reaction to the body as well (e.g. seeking for help because they think they’re dying). The causes are unknown, they are not physical symptoms, however traumatic experiences/being bullied may play a role. There may also be a genetic aspect: it is very close to OCD, and we know that OCD has a genetic component.

• Conversion disorder

This is the third group. This disorder is one that you can see best in patients (from the outside). Something that can happen among patients with conversion disorder is having non-epileptic seizures (which is probably re-experiencing certain traumatic events such as being abused etc.). In the DSM-IV the criteria is even related to trauma. It is best to help the patients overcome the traumas first instead of treating the symptoms.

DSM-V

Body Dysmporphic Disorder (BDD) is no longer a somatoform disorder and is now an obsessive compulsive disorder.

Hypochondriasis = illness anxiety disorder, but it’s not exactly the same. IAD is when there is no physical symptom of any importance. Hypochondriasis could be diagnosed when there was a physical symptom present – in the DSM-V they would call that somatic symptom disorder (e.g. coughing and thinking you have lung cancer is now a somatic symptom disorder).

Conversion disorder: the key feature of it being trauma-related has disappeared. So there is no longer a difference between it being caused by exhaustion of by a trauma.

Somatic symptom disorders are now all together - but MUPS-feature is now gone. They are now (un)explained distressing somatic symptoms plús abnormal thoughts, feelings and behaviors.

Is it better this way?

Yes, because you are not classifying because of absence of explanation but the absence of abnormal thoughts, feelings and behaviour.

No, because treatment is pointed at this key feature: the abnormal thoughts, feelings and behaviour will disappear (because the treatment is based on the key feature of a disorder) but the somatic symptoms will not be treated and therefore stay.

MUPS:

• 80-90 % have had MUPS of short duration in the last week (like coughing).

• These MUPS can become chronic (lasting 2-3 weeks for example). If this is hindering you, you probably go to a doctor.

• These chronic MUPS can really affect your daily life or even be disabling (making the patients dependent on others or even bed-ridden). This last group has a somatoform disorder. This is 16% of the general population, which is quite a lot! In a clinical population this percentage is even higher: 20-40% have somatoform disorder!

How can we understand these MUPS?

• Look at the person for the answer to “what are MUPS?”
  MUPs might be some characteristic of a personality disorder or a characteristic of a person. The keyword here is somatisation: having distress experiences and instead of just feeling sad, you feel some pain in your throat. Instead of communicating emotional states, you communicate the physical symptoms and seek help for those.
  We don’t like to know that we are somatising, because telling me this is simply telling me I’m wrong. This can activate resistance in patients. However, there is no research proving this.

• Look at the physical symptoms: but there is a lot of overlap between syndroms. For example: Chronic Fatigue Syndrom and Fybromyalga both have “pain, poor sleep quality and fatigue and the prevalences are both 1-2%. How come these two disorder exist separately? One is “invented” by rumatologists, the other by physicians. MUPs are found in every disorder!

• Look at the process: 80% accepted treatment for their symptoms. 20% already had therapy or their symptoms were not that bad. So treatments are well accepted when they are especially pointed at their own symptoms. When you say “oh it’s all the same, so all symptoms get the same treatment!” it is not very well accepted.

Evidence-based treatments:

Cognitive Behavior Therapy is effective for group 1 (somatic symptom disorder) and 2 (illness anxiety disorder (previously: hypochondriasis) but not for group 3 (conversion disorder). SSRI’s can be of help for people with pain symptoms and depression because of their symptoms.

Cognitive Behavioral Therapy has a lot of factors and subtherapies. CBT exists of a lot of different interventions. How to select the most effective interventions for one patient? The maintenance model is a diagnostic tool to select the right intervention for the MUPS that the patient has and what the consequences are. How does this model work? Firstly, you collect information about the MUPS. Secondly, you select one consequence follows its symptom most directly. Thirdly, set up a vicious circle with the other consequences of the symptoms so that you can then select the most effective intervention.

When you talk to your patient, you need to make sure to prepare and gather information.

You have to know the frequence, type, gravity, duration, path and consequences of the symptom(s).

Patients have their own ideas about their symptoms: some think it is caused by physical diseases, or psychological diseases, or moral punishment by God for example, or because of social problems, so it can be very different. There are also certain cognitions that are present when the symptom comes or gets worse (e.g. “I’m angry, I don’t want this!”). These can make the symptoms even worse.

They also have certain ideas about the meaning of the symptom, which they base on the context of their learning history: do you know anyone with the same symptoms? You might worsen your ideas about the symptoms.

A physical symptom can also make your positive self-image negative, or confirm your negative self-image.

Emotional consequences can differ from anger to sadness to shame or even guilt.

These emotions can increase or maintain the symptoms and start a vicious circle!

Behavioral consequences can also worsen or maintain the symptom (e.g. scratching when you have itch may irritate the skin which gives you more itch!). When you pay more attention to your symptoms your behaviour is directly stimulated but the intensity or frequency of the symptoms is not directly increased.

Physical consequences can be tension of your muscles, breathing heavily, sleeping in a dysregulated rhythm etc. They can be direct or indirect, but they do not help decrease the symptoms.

Social consequences can be social isolation, interaction with doctors and therapist, or even loss of job or income. Social consequences do not maintain the symptoms directly but they determine how much the patient suffers from the symptom(s).

Some people follow a thought pattern which catastrophizes everything. Fear is increased, they avoid symptom-related factors (like tension of the muscles) and eventually loss of shape. This is, again, a vicious circle. Exposure is effective for this group of people.

Another kind of pattern is denial. These people do not accept the fact that they are experiencing pain of their symptom. This leads to overload and forcing your body and persevering, which also leads to a vicious circle. For this group of people it can be helpful to schedule each day: learn them when to take a break and switch between physical and mental activities, or sometimes it helps to start with a low intensity of activities and slowly build up.

The third kind of pattern is mostly found in people with depressed moods and thoughts. They are inactive and prefer to be alone. They are prone to recognize their failure in every little thing and their thoughts are based on this bias for failure. This bias can lead to depression, which has physical consequences (which increases the symptoms) as well as inactivity (loss of shape) and withdrawal from the world (if you have no distraction, you pay extra attention to your illness and symptoms). For this group of people interventions can help when they create hope (that things can change or they are liveable), create structure in their daily lives and increase activities to break the vicious circle. To help with the depression as well as the physical symptoms, you can gradually increase physical activity.

Conclusion:

Where the DSM-IV focussed on the MUPS, the DSM-V looks more at the presence of abnormal thoughts, behaviour and emotions. The symptoms itself are no longer the key feature in the DSM-V!

To understand the problem, one must:

• Look at the person

• Look at the problem

• Look at the process

To treat the problem, one must:

• Break the vicious circle (you can do so by not treating the symptoms, but the direct reactions to this symptom which can eventually maintain or even worsen that symptom!)

• Make sure the circumstances are adequate for the recovery of the patient

Lecture: Anxiety disorders

Introduction

People with panic attacks can often hyperventilate. Years ago, these people were given paper bags to breath in. This is based on the idea that, while hyperventilating, you’re inhaling too much oxygen and a paper bag will help you produce CO2, which you will then breathe in again. However, it is shown that after breathing in air with extra oxygen, you are more likely to panic after about 15 minutes (in a laboratory setting). Still, the paper bag seems to be effective against panic attacks: this is probably thanks to the placebo-effect and the fact that breathing air with extra CO2 does not immediately trigger panic attacks.

Anxiety disorders are really well-treatable (among the most treatable disorders in de DSM). This does not mean that it’s easy to treat and it can also differ between patients and kinds of anxiety disorders. You need to understand the nature of anxiety disorders before you can really set up good evidence-based practices and be effective.

We keep looking for new treatments. There are many kinds of treatments and variances. This is because many people don’t recover completely or relapse and there are many problems with the acceptability of treatments (e.g. not wanting the therapy because it involves exposure to mice). When a new treatment is introduced, it is usually used to fast! There is few experience with side effects etc. This is also the case with new medication, but medication has very strict rules about registration processes and research. Psychotherapy does not have these rules. It also costs a lot of money to research and there might be a bit of corruption . The last critical note is the publication bias, which is the effect that you are more likely to publice your research when you find your wanted effect. Luckily, many people try to replicate studies.

Mowrer’s theory of fear and avoidance

1. Classical conditioning leads to learning to have fear.

If you can learn fear by the principles of classical conditioning, you can also un-learn it by the same principles.

2. When you avoid the stimuli related to your fear, your anxiety disappears.

3. When you are afraid, you search for safety.

You need to habituate to these fear-related stimuli (you have to endure looking at the stimuli until you are completely calmed down).

There is a vicious thought pattern that often occurs in these patients. When they experience anxiety and its physical expression, they interpret this as something bad or dramatic. They then start to feel anxious, which leads to more or more extreme bodily sensations and an attentional bias: the patient pays attention to the bodily sensations, which will worsen the sensations even more.

When interviewing someone about their anxiety, try to ask “so what?” consequently. Keep asking until you get to an misinterpretation!

It is kind of strange to think that these patients are afraid of dying, fainting, etc. while having survived many panic attacks without dying.

An important feature of anxiety is safety signals:

Playing with keys, smoking a cigarette, having someone you know with you while being exposed, compulsions, holding on to a shopping cart, etc. can all be examples of safety signals and safety behaviour. Sometimes it helps to overcome your fear and feel confident while being exposed. However, a safety signal during treatment can make the treatment less effective on the long term.

Experiment

All people were asked how far they dared to walk alone (which is a measure of how scared they are). In the first session they were interviewed about their catastrophic cognitions and safety behaviours and were asked to do the walk again. After 60 minutes, they were asked to do the walk again, however this time one group was asked to drop all their safety behaviours and the other group was encouraged to use safety behaviour. There is not much difference in anxiety between both groups. Two days after, both groups are asked to perform the walk again. People who dropped the safety behaviours were now less anxious, while people who had used safety behaviours had learned nothing.

Wolitzky and Telch showed that “fear-antagonistic actions”, which are like the opposite of safety behaviours (e.g. rushing to the edge of a balcony when being afraid of height), make therapy work much faster and more effective.

Video

In the lecture we watch a clip of a therapist helping a woman with a fear of birds.

It is quite dangerous to specifically look for traumas, because with hypnosis you cannot only recover memories, but also fabricate memories, which could have serious consequences.

He should have tested the catastrophic cognitions. In Salkovskis et al.’s study they did test that. The goal would be to control the level of anxiety, or to identify the catastrophic cognitions, in which case the level of anxiety can go up as high as it can because it’s a test of the catastrophic cognitions (“Wait, I’m having a high level of panic, but I’m still not dying??”). They showed that CBT is more effective than Habituation Based Behaviour Therapy.

EMDR

The first publication on EMDR was in 1989 by Shapiro. In ten years, so much research on EMDR was done that a meta-analysis could be performed. This is very fast! The meta-analysis showed that it was just as effective as CBT! It is now in the official guidelines.

Shapiro’s theory wasn’t right, but her therapy did seem to be effective in a single session! The effects were maintained for at least three months and really worked on real traumas. Nowadays, EMDR is more like the CBT: it is no longer just one session.

A critical note on research on EMDR: to research EMDR, it has to be performed by a therapist with an EMDR-certificate – is it still unbiased?

Also, we still don’t know how EMDR is effective. There was a pseudo-neurological theory that appeared to be nonsense. Could it be that we are looking at a placebo effect? Maybe. Maybe not, because the effect doesn’t go down.

Another theory is that EMDR makes the traumatic memories less vivid so it makes the experience less intense. How does this work? Your working memory has limited capacity, when you present the memory as well as something to distract the patient (eye movements for example), the capacity is full and the memory is placed back into the long term memory less vividly.

Lecture: Eating disorders

Part 1: Various eating disorders

Introduction: DSM-V

Feeding disorders (pica, ruminating and restrictive food intake disorder) are more common among children, eating disorders (Anorexia Nervisa (AN), Bulimia Nervosa (BN) and Binge Eating Disorder (BED)) are more common among teenagers and adolescents. There is also a “rest-category” (subclinical forms of eating disorders, purging disorder and night eating syndrome) and also unspecified eating or feeding disorders.

Anorexia Nervosa

Key features are low body weight, persistent behaviour of hindering gain weight and body image disturbance. In the DSM-IV there was a cutoff of BMI (body mass index) of <17.5, in DSM-V it’s <18.5. Also based on BMI is a severity scale: <15 is very severe, <16 is severe, <17 is medium and >17 is mild. When a child or teenagers is still growing, don’t use BMI but use percentiles of data of people their age to determine their severity.

Bulimia Nervosa

Key features are eating and not being able to stop, compensatory behaviour and basing the evaluation of the self on their body shape and weight. In the DSM-IV the compensational behaviour had to be twice a week, now it’s once a week.

Severity of BN is based on the frequency of purging (compensatory behaviour).

>13 episodes a week is very severe, = or > 8 is severe, = or > 4 is medium and = or > 1 is mild.

BED

Is similar to BN, only BED-patients don’t purge or compensate for their binging. But they do binge which leads to loss of control over eating. Binging needs to happen once per week during three months. The severity scale is not based on the purging but on the frequency of binging: >13 episodes a week is very severe, = or > 8 is severe, = or > 4 is medium and = or > 1 is mild.

Among all eating disorders, there are both shared characteristics and differences.

Epidemiology and prevalence

AN and BN is more common among women (95% of the AN- and BN-patients is female) in both clinical and general populations – but is it really? Maybe AN and BN aren’t recognized as much in men, because it’s seen as a female disorder. BED is evenly distributed among men and women.

The prevalence of AN is 0,37% of all women between 15-29 years. The prevalence of BN is 1,5% of all women between 15-29 years. The prevalence of BED is 1% of all people between 18 and 65 years (!, so BED is most common!)

AN is by far the smallest group of these three, but gets the most attention. This is probably because it’s visible. There can be an overlap between AN en BN: AN-patients who binge and purge.

Not all eating disorder patients will be diagnosed, because a general practicioner does not recognize it, or doesn’t get enough information (because the patient is ashamed or in denial).

Prognosis

Of all patients of AN and BN, 50% recovers completely, 30% recovers partially and 20% doesn’t recover. About 5-10% of this last group even dies because of this disease.

Binge disorder has a more positive prognosis: 77% is better and binge-free after 5 years, only 10 % still has the diagnosis.

The average duration of an eating disorders is 6 to 7 years.

The sooner someone with an eating disorder is detected, the sooner they get better.

Consequences of eating disorders

The most of physical consequences can be reversed when you start eating healthily again. There are various psychological and social consequences.

Goldberg and Huxley filter model

Different levels of care exist. When you base your research on one level, it’s not representable for the whole population of that disease!

Etiology and comorbidity

We don’t know the cause of eating disorders, so we assume it’s multi-factorial:

Genetics, biology, physical disposition, culture, environment, psychological factors, etc.

ED show a great overlap with anxiety and mood disorders. Could one say that eating disorders are an extreme phenotype of a combination of traits within the anxiety/depression-community?

In general, people with psychiatric disorders have more than one disorder.

Theories on the causes of eating disorders become more and more complicated and complex.

Treatment

For AN family-based treatments are the first choice for children and adolescents. You try to help the parents to take control of the eating behaviour and help their child. For adults there is no evidence-based treatment for AN.

BN is one of the best studied eating disorders: CBT is very effective, interpersonal therapy is also effective. Pharmacotherapy is effective, but mostly in short term.

Binge eating disorder: CBT, pharmacotherapy and weight management are helpful.

Generally you focus on normalising the eating pattern and restoring the body weight of the patient and at the same time you focus on determining the psychological and social aspects behind the disease.

There is a wide range of therapies you can offer patients. Not only for eating disorders, but also for their comorbid disorders.

Proud2Bme is a Dutch healthy online alternative for pro-ana sites (which sometimes stimulate purging). Proud2Bme provides support, interaction and understanding and has more visitors than there are people with eating disorders in this country.

Featback is also an e-health intervention and has a fully automated feedback system. Every week people have to fill in 8 questions and based on these answers the program evaluates changes within time and provides a feedback message. This is actually quite a long e-mail.

There was a research on Featback and the added value of individual therapist support. The respondents were given the choice to receive therapy via either e-mail, Skype or chat. They were then asked what their experience was, whether it was effective or not and if there was an added value of therapist support.

Anyone with at least mild symptoms and 16 years of age could join the trial. Participants were divided over 4 groups:

1. Featback

2. Featback + low intensity therapist support (once a week, 20 minutes)

3. Featback + high intensity therapist support (three times a week, 20 minutes)

4. Waiting list

This trial lasted 8 weeks. After 8 weeks there was a post-intervention test. There was a 3 month and 6 month follow-up – there were lots of dropouts though. The participants were mostly female (99%), half of them had an eating disorder diagnosis.

The groups differed in satisfaction: group 1 gave Featback a 5.0 on average. Featback users who also had therapist support were far more satisfied: 7,1 for the low intensity group and 7,4 for the high intensity group.

Featback users also reported a much lower effectiveness!

Although the Featback + therapist support were more satisfied than the computer condition, the therapist support does not seem to have an added value over just the computer program. Which is interesting: subjectively, therapist support is better, but objectively it’s not.

Part 2: Binge eating

Binge Eating Disorder (BED)

About 1-3% of the general population has BED. It is commonly confused with obesity. But BED-patients have a more serious problem than just obesity: they eat more, feel disgusted and guilty, etc. Many BED-patients are obese, but it’s not a criterion for BED. In general, BED-patients with a normal BMI don’t seek help as fast or as much as obese BED-patients. They also tend to be younger than obese BED-patients. BED-patients compared to just obese people have more psychopathology, lower self-esteem, earlier onset/development, more failed attempts to diet and they worry more about their weight and body shape. Depression is one of the most comorbid disorders with BED.

Treatment

People seek help for their weight, not their eating problems. Most treatments for eating disorders focusses on both the disorder as well as weight loss.

Randomnized control trial tested the difference between CBT and a waiting list. 70% was abstinent after the treatment, 80% remained abstinent from binge-eating after a year. There was a decrease of eating disorder psychopathology as well as depressive symptoms. The question is: what came first? Does depression cause binge eating or does binge eating cause depressive symptoms?

There are different kinds of models on this relationship:

BN: dieting -> BN.

BED: binge eating -> dieting

Binge eating: emotional disturbances + coping deficits -> binge eating

There is an association between depressive mood, acute negative emotions and binge eating. Poor mood precedes binging, and binging decreased negative mood (not permanently).

The “escape from self-awareness model” by Heatherton and Baumeister states that binge eating leads to wanting to escape the negative mood. Binge eating seems to lighten emotional stress: it distracts the patient from their emotions and worries.

A negative emotional state -> less control over eating -> more binging.

Acute negative mood -> binging more than it leads to a more permanent negative state.

How can you research this?

They induce a specific mood by showing a short clip. After that they test binge eating behaviours.

Hypothesis 1: attempt to regulate negative emotions -> overeating

Actively suppressing or controlling negative emotions does not lead to overeating.

The more depressive symptoms, the more calories you consume. Among severely depressed more changes in a negative mood -> more calories consumed.

Among non-depressed participants there was no effect.

In a replication of the first study, again non-depressed BED patients reacted differently than depressed BED patients. Is this because their coping strategies are healthier?

Non-depressed and depressed BED-patients consume the same amount after seeing a positive clip.

Control

Negative mood -> less control over eating.

Negative mood -> binging.

Control is an executive function of the brain.

Set-shifting (multitasking by switching fast) is a part of these executive functions and requires mental flexibility. Eating disorder patients seem to have less mental flexibility and depression worsens set-shifting.

Another experiment was started to find out if baseline set-shifting abilities influence mood changes or experiencing loss of control.

BED-patients were tested on their depression, mood and eating behaviour. The first group was induced with a negative mood, the second group was induced with a neutral mood. After this, the same tests were executed again.

When you’re bad in set-shifting, you are more sensitive to the negative mood induction. In the neutral group there were no effects. There was no significant interaction between being able to set-shift and experiencing loss of control. Depressive symptoms also seem to worsen the mood after negative mood induction.

Lecture: Mood disorders

Depression

Jung had a very romantic view on depression, he thought depression had something to say and depression had a meaning.

Swaab had a very biological view on depression; depression is a deficit in the brain. A consequence of this view is that depression can only be treated with medicine.

Beck preferred the cognitive model, where dysfunctional attitudes are central, which are caused by stressful experiences, but remain latent until they are activated by stress. These activated dysfunctional schemes can lead to a negative cognitive bias (being prone to negative signals and factors), which can then lead to depression. He believed correcting faulty beliefs can decrease depressed reactions: the base for cognitive therapy. 40 years ago, Beck had some worries about depression, which he expressed in three questions. Today, we can only answer the second question: no, it probably is not a clear clinical entity. We cannot answer the first and third question.

There was an experiment with animals: rats were put in the water and it was measures how long it took for the rat to stop swimming and start floating. The scientists that performed the experiment saw the moment the rat stopped swimming as a sign the rat is hopeless: depressed.

Molendijk and Ron de Kloet don’t believe this: it’s not depression, despair or exhaustion, but a memory effect: if you start floating soon, you will survive longer. So floating sooner is smarter.

Luckily, when it comes to people, we don’t base depression on the ability to swim or float. There are comprehensive criteria for Major Depressive Disorder. You can also find the exclusion criteria: you cannot be diagnosed for depression when you have one of these symptoms or disorders.

Why do we observe and count behavioural symptoms?

The underlying networks are unknown and hard to measure, this is the closest we can get today! By using a high amount of symptom criteria, you reach a higher reliability (many people would give the same diagnosis to the same patient).

What do we diagnose?

A mental disorder or illness is a behavioural and/or psychological illness that leads to stress and functioning less.

Diagnosis is a cluster of symptoms, forming one syndrome all together.

There are many kinds of mental disorders. It is important to remember that these disorders are not perfectly defined categories! There is a lot of overlap and it will never be perfect. This is why they make new DSM-versions every time and a diagnosis is never permanent.

About 1% of the general population has bipolar disorder. The lifetime prevalence (=how many has had it once or more times ever in his or her life?) for unipolar is around 16%.

There is a lot of diversity within the depressions population: because you need 5 out of 9 symptoms and there are many combinations of 5 of these symptoms so you get a lot of different illnesses and a diverse population. Also because they are comorbid with other illnesses so this also gives lots of different images of this disorder. There are several consequences and causes.

Consequences

Relative risk is measured with the following formula: the chance of dying having a depression / the chance of dying when you do not have a depression. On average, of course.

The World Health Organisation determined DALY’s (a measure that expressed the amount of years lost due to a certain disease) for each physical and psychological condition. Depressive disorder are the main contributors worldwide to losing years.

Interestingly, the conditions with the most DALY’s get less research and attention than some other conditions that are lower on this scale. This is partially because medical disorders are a more clear cut entity and also because of the stigma’s hanging around mental disorders.

Causes

There are many factors associated with depressive disorder. But are they really causal relations? You can call something a cause when the cause is both sufficient and necessary to lead to depression. It might be so that some of these causes are not really causes but mediators, moderators or shared-risk-consequences instead!

Mediators are present when a causal relationship is not direct, but goes via another factor. Moderators decide the strength of a relationship between two factors.

Lecture: Addictions

Substances can be classified in various ways. It is important to remember the following: the pharmalogical action of any drug is inseparably linked to both the person (background, genes) and the context in which drugs are used.

DSM

The DSM criteria for addictions were different in the DSm-IV compared to the DSM-V. In the DSM-IV, Abuse is characterized by the harmful effects, where dependence is characterized by physical dependence (tolerance), withdrawal symptoms (symptoms shown when one does not use the substance anymore) and psychological dependence.

In the DSM abuse was considered as a mild form of/preliminary state of dependence. However, this distinction did not hold: many people who are dependent do not meet the abuse criteria and abuse does not often preceed dependence and the abuse and dependence criteria combined seem to form one unidimensional scale. In general populations, people often received the abuse diagnosis on basis of one criterion (mostly drunk driving). The DSM-V omitted the distinction between abuse and dependence (it’s one scale now). Another change was that behavioural addiction (gambling addiction) is also added. Craving was added as a criterion. Also a severity dimension was added (mild/moderate/severe). You now need at least 2 out of 11 criteria.

Epidemiology

Prevalences are not to be learned for the exam.

Mortality due to alcohol: worldwide nearly 4% of deaths are caused by alcohol, in Europe it’s even 6.5%. Of all men (15-60 years of age) alcohol is even the most important risk factor for deaths: 11% of deaths are related to alcohol! This can be direct or via injuries, cancer, liver/heart problems and even violence.

De Bruijn et al. researched the course of alcohol use in the Netherlands. Nearly 5% of this population had the alcohol abuse disorder. Remission rates (amount of people who had the diagnose but didn’t have it one or three years later) was quite high – does this mean alcohol abuse is not that chronic?

Those who apply for treatment generally do this after 8-9 years, so you could say these people are in a more chronic phase and therefore have a poorer prognosis.

Heroine, however, is much more chronic. During a period of 30 years about one fifth was abstinent – nearly half of them had died after these 30 years (not only due to the use but also the lifestyle).

So the epidemiology differs by person, setting and problems. Opiate users have most relaps.

Regarding the prevalence of most psychiatric disorders in the Netherlands, anxiety is most common here. Patients who have other disorders or are in mental health care have higher prevalences – as are other disorders comorbid with substance use.

Factors that contribute to chronicity

Genetic vulnerability: about 30 to even 70% can be attributed to genetic factors when looking at twin studies. Molecular genetic research, however, finds <2% of genetic variance accounted for by genes.

Neurobiological factors: the incentive-sensitization theory of addiction states that addictive substances all cause persistent neuro-adaptations in the brain, which take place in brain systems that normally motivate and reward. All psychoactive substances cause an acute direct increase of dopamine, in particular in the nucleus accumbens (part of the mesolimbic dopamine system). Dopamine causes the euphoria-feeling that you get from substances. However the reward system becomes less sensitive to natural or taken-in stimuli for reward, which has no effect on the liking of drugs, but more on the wanting of drugs.

“The dark side of addiction”-model by Koob states that there is a shift from reward-motivation (positive motivation) to relief-motivation (negative motivation). This anti-reward system serves to limit the activity of the reward system in the brain, which can gradually sensitize the stress system. So this model focusses on use motivated by relief rather than reward.

Siegel et al. formed a model about expectations. Cue reactivity (the way someone reacts to stimuli), which leads to anticipation or compensation. We try to minimize drug-effect to maintain homeostasis, so we already compensate for the drug before even taking the drug! This is anticipation. This is how tolerance develops. Siegel designed the body count experiment: they made rats tolerant for heroin. After this, the rats were divided in two groups: one group stayed in the same setting and received a potentially lethal dose. The other group received the same dose, but in a different setting. Surprisingly, about 32% died when they stayed in the same setting, and 64% died in the new setting.

The I-RISA model (Impaired Response Inhibition and Salience Attribution model) by Volkow states that our control functions play a role, not only reward and stress. Drug use leads to a decreaseof dopamine in the control areas of the brain, so the prefrontal cortex can’t function properly anymore.

You have genotype, phenotype (what can be seen) and endophenotype (something inbetween). Addicts clearly have an attention bias for drug-related stimuli. They also focus on short-term reward rather than long-term negative consequences. Different therapies focus on different factors.

Social factors were researched in monkeys. The monkeys were placed alone and fed cocaine. After a few months, they were placed together and were given the chance to feed themselves either salted water or cocaine. As hierarchy started to form, dominant monkeys did not have a preference for cocaine, but the subordinate monkeys did!

Powerful learning processes

Both the classical conditioning model and the operant conditioning model play a big role in drug use. Operant conditioning states the intake of drugs has a positive consequence (feeling good) and is therefore reinforced. Classical conditioning states a neutral stimulus such as a mood or setting can be linked to another stimulus (such as beer or drugs) (also the other way around!), which leads to a conditioned response (wanting beer) when seeing the other stimulus (such as a specific mood).

Cue Exposure Therapy (CET) is based on the classical conditioning model. It focusses on confronting the patient with drugs or drug-related stimuli while eventuallu preventing the conditioned reaction by extincting it. CET is often used for OCD and phobias, but the effectiveness in addiction is limited.

Contingency Management (CM) is based on the principles of operant conditioning: the context determines the reinforcing effect drugs can have. An experiment was conducted by Higgins et al. Dependent upon how high the financial reward was was the amount of cocaine participants administered to themselves. So the reinforcing effect of cocaine was determined by the reward the participants were given anyway.

Silvermann et al. studied the effect voucher value on cocaine abstinence. Participants were divided into three groups: one group did not receive any reward when they got a negative drugtest (which means they were abstinent of drugs), one group got a small reward with negative results (€300,-) and the third group got a big reward (€3000,-) when they remained abstinent. The group that received the big reward had the biggest percentage of drugnegative tests! But does this effect hold up after the reward? In a follow-up studie it was shown that this effect remains but slowly fades and after 15 months the difference is not significant.

Social cognitive learning (learning from others by seeing, associating and evaluating) is another way of social learning (like conditioning). Bandura states that the ability to deal with high risk situations depends on certain factors:

• cognitive appraisal (the extent to which a person is able to recognize the risk content of a certain situation)
• adequate coping skills
• self-efficacy: whether the person feels like he or she can handle the situation
• outcome expectations

Abstinence violation effect: abstinence can be violated in three ways: a slip (a sip of a drink, for example), a lapse (heavy drinking) and a relapse (heavy drinking for more than one day). When a person with low self-efficacy and an internal locus of control has a slip, he has a higher chance to have a complete relapse than people with an external locus of control. This is the abstinence violation effect.

Treatment

Treatment of addiction focusses on intoxication, decrease harm related to the intake of the drug, preventing the patient to have a relapse, treating comorbid disorders and encourage recovery of social contacts etc. These components of treatment have a certain order: acute situations need to be solved first. After this is handled or this first step is not necessary, cure the disease and taking steps to prevent relapse. But what do you do when it’s not possible to get someone to remain abstinent? Go a step lower: control the use, improve social situations or physical condition. This is harm reduction.

Is treatment for addiction effective? Approximately 40-60% worldwide relapse after a year! One single treatment less than 25%is able to remain abstinent.

There is also pharmacological treatment. This differs between the different kinds of addictions. The middle column presents the strength of evidence. Overall you could state that these medications are effective and work and are evidence-based, but in statistical terms the effects are small (e.g. low Cohen’s d) and we do not know how to pick the best one for each individual. For cocaine and cannabis there is no real evidence-based medical intervention yet.

Methadone is the first choice for treatment of heroin addicts. But you can even treat heroin addicts with heroin! Abstinence is not per se required for a treatment to improve the situation. Patients in a study improved more when they received both methadone and heroin compared to just heroin. Treatment costs a lot though.

Topiramata, modafinil and dexamfetamine can be used as treatment. In a double-blind study dexamfetamine and placebos were given to different groups. Dexafetamine probably has a clinical value. At the end participants were asked what they thought they had received. Their estimate of what they received was not better than chance: they could not guess what they had gotten!

There are also psychosocial interventions. Certain interventions are used the most, but of course the effectiveness differs per individual.

Prevention is extremely important for addiction is such a chronic disease. Overall it is shown that it is needed to intervene in an earlier phase. But this is hard, because patients do not seek help earlier and it is hard to recognize them earlier. There is an increasing focus on the role of parents in prevention. Universal prevention does not seem to work so overall they tend to shift towards selective prevention (focussing on risk groups, groups of people who have many risk factors such as poverty or high levels of impulsivity). One example of selective prevention is the study of Conrod et al. She administered a questionnaire among teens of 14 years old. Hopelessness, anxiety sensitiveness, impulsiveness and sensation seeking. The teens received to short interventions based on these personality traits. On the average she found a 30% to even 80% lower risk fir drug use for these children than children who did not receive these interventions.

Hendriks himself and colleagues performed a study among adolescents with a cannabis disorder. One group got weekly sessions of CBT for 5 to 6 months. The other group got MDFT (Multidimensional family therapy: a new, quite intense family-oriented treatment) twice a week for 5 to 6 months. The two groups did not differ in improvement (measured in number of joints smoked in the last three months) between each other when looking at the whole group. When splitting the groups in age, you see young adolescent benefitted more from MDFT and adolescents of 17 to 18 years benefitted more from CBT.

Lecture: Personality disorders

Personality disorder (PD): diagnosis

Personality is how we think, feel, act, respond to things and people. Personality is consistent: stable over time and across situations. It can be used to predict future behaviour. Traits of personality are limited and dimensional. Personality disorders often have extreme scores on certain traits.

The DSM-V lists criteria for any personality disorder. People really have to suffer from their personality or at least functional limitations. Personality disorders have a long duration. Exclusion criteria are: symptoms are not a consequence of axis-I disorder or be due to substances.

There is not one cause of personality disorder: it’s both environment (like no safety or support)and genetics (heritability index for personality are 0.34 to even 0.61! Genetic factors probably have to do with serotonin and dopamine.

Consequences of personality disorders can be poor social contacts (including being ego syntonic (it’s the fault of all other people around me)), high rates of comorbidity with axis-I disorders and these disorders being harder to treat because of the personality disorder.

ICD-10 and DSM-IV are most used systems to classify disorders. In de the ICD-10 you have to have both distress ánd impairment, whereas the DSM requires only one of the two. DSM-V has now combined axis-I and II. In the DSM you have different subtypes. It is assumed that they are different discrete entities. But can you really assume that? DSM divides the subtypes in three clusters.

Classifying has its advantages (clarity, consistency in research and choice of treatment)and disadvantages (no individual differences within the diagnosis, not taking the ill person, causes, prognosis, personal traits, environment or social contacts into account (only the illness), and the borders/cut-offs are a little bit artificial: are they really discrete entities? Personality disorders are comorbid with other personality disorders: PD-patients have 2.8 to even 4.6 personality disorders on average! This kind of refutes the idea of personality disorders being clear-cut entities.

Models of personality

The big five model is the most known model of personality traits. It’s universal, easy to understand, stable over time, the traits are based on descriptions, and it’s valid. The traits seem to be heritable (around .5).

The 5 scales are: Openness to experience (active in imagination, creative, this is the most vague scale), Conscientiousness (orderly, discipline, responsible), Extraversion/introversion (easy in interaction and social situation), Agreeableness/antagonism (antagonism= being sceptical, PD-patients score low on agreeableness) and Neuroticism (tension, being easily upset, avoid negative emotions).

The general hierarchical structure model of PD states that a supertrait has certain subtraits, which each have their own subtraits.

Average traits of some examples

Antisocial PD-patients score high on antagonism, impulsiveness, excitement seeking and hostility and low on deliberation, dutifulness, self-discipline, anxiety and self-consciousness.

Borderline PD-patients score high on anxiousness, impulsiveness, depressiveness, vulnerability, openness to feelings and hostility and low on deliberation.

Personality disorder types

There are three clusters, along with subtypes and their characteristics:

• Paranoid disorder patients are suspicious and hostile. They don’t have hallucinations but have very specific ideas about being disadvantages.

• The odd/eccentric cluster is characterized by being socially isolated, they like to be alone and have a low sexual desire.

• Schizotypical PD involves magical thinking, illusions, seeing hidden important messages and they present themselves quite eccentric.

• Borderline patients are impulsive, instable, afraid to be abandoned and have no stable or long-lasting social relationship. They switch from idealizing a person and devaluating this same person the next moment. Identity disturbance, being impulsive, affective instability, feelings of emptiness, extreme anger, sometimes even suicidal ideation (8% of PD-patients died because of suicide) or paranoid ideation. Out of those 9 criteria, one needs 5 in order to be a borderline patient: there are many manifestations of this disorder! There are more females with Borderline and are comorbid with major depression.

Social environmental causes could be parental separation, abuse, etc. Linehan’s Diathesis-Stress Theory states that there is a vicious circle: emotional dysregulation as a child demands much of a family -> the family ignores the wishes of a child -> the child bursts out of emotions, which leads to more emotional dysregulation.

Borderline has a high herability of .60! The frontal lobe can be less active (impulsivity), the serotonin can be dysregulated and the amygdala can be more active (intense emotions)

• Histrionic PD patients are self-centred, dramatic, emotionally shallow and seek attention.

• Narcissistic PD patients think they are most important and don’t really think about/feel for others.

• Antisocial PD patients have a history of Conduct Disorder which developed in the adolescence.

• An Avoidant PD patient has a more dimensional overlap with anxiety disorders. They are fearful, do not like social situations, are sensitive for rejection and this fear impairs them.

• Dependent PD patients lack confidence, have no autonomy and think of themselves as weak: they need others.

• Obsessive compulsive disorder patients are orderly and perfectionistic.

Treatment of PD

Personality disorder are a challenge to treat: they require more work, take more time, put a greater therapist. PD patients often seek help for something else than a personality problem.

Medication could be mood stabilizers and antidepressants, for PD can be comorbid with mood disorders (like major depression). But treatment specially for PD’s are not medical: metallization-based therapy focusses on their lack of empathy. Dialectical behavioural therapy by Linehan is quite popular and focusses on lack of impulse control and auto mutilation (suicidal behaviour), tolerance for their negative feelings and handling them, empathy and social skills.

Transference-focused psychotherapy: focusses on projecting things from your past on your therapist and in case of split parts of yourself it focusses on fusing these parts.

It is more complicated to research PD.

Schema-therapy(by Young) focusses on

• Stable maladaptive assumptions that form the base of their cognitions (patterns of feeling and thinking, in your early life, the way you perceive yourself and others). The origin of schemes can be biological, psychological, social or traumatic. Your basic core needs are: secure attachment, autonomy, freedom, spontaneity and self-control.

• Coping styles: how do you cope with your scheme? You could surrender to the scheme: behaving in that way. You could avoid the scheme: avoiding scheme-triggering situations or shut out your emotions by de-attaching yourself. You could overcompensate your schema: behaving in the exact other way (e.g. feeling insecure -> behaving very confident)

• Concept of a schema mode. A schema does not have to be pervasive, a patient can switch to one way of functioning to another. There are four modes: a child mode (easily exploited, dependent, vulnerable or this mode can be angry and impulsive), a dysfunctional coping mode (feeling empty, not attached to your feeling) (as protection against your feelings such as impulsivity), dysfunctional parent modes (self-critisizing, devaluating) and health adult mode (the goal of PD-therapy).

• Basic emotional needs.

Schema therapy is an integrative therapy with an emphasis on doing things (behavioural), feeling (experiential) and thinking (cognitive), so it’s taking the best of different techniques. It focusses on the relationship with the therapist, how the patient experiences things in the outside world and memories from childhood (e.g. processing abuse from the past).

In treatment:

• The Detached Protector should be replaced,

• the Vulnerable Child should be protected and nurtured,

• the Punitive Parent should be expelled,

• you need to teach the Angry Child to express their emotions appropriately

• and get to the Healthy Adult!

• You try to bond with the patient,

• help the patient to understand what’s going on and where it’s coming from,

• and then change to autonomy (which is the hardest part).

In the following experiment borderline patients received either transference-focused psychotherapy or schema-focussed therapy. TFP had more dropouts, maybe STP is more supporting? TFP had a higher recovery percentages.

In this experiment borderline patients received treatment twice a week for three years. In another experiment they compared that with twice a week in the first year and once week in the second year. It proved to be at least as effective!

Another study found that the reliance rated by patients was higher in SFT than in TFP! This of course has something to do with the cause of the dropouts.

Another study stated that condition (SFT or TFP), baseline medication and burden of dissociation (how much you were dissociated): high level of dissociation led to worse outcomes.

Is the treatment really worth the costs? Yes, it is profitable to treat these patients when you look at the costs you do not make because of this treatment (e.g. no or less hospitalisation when the patient is treated)!

Lecture: Psychosis

Diseases are hard to compare. Salomon tried to compare the global burdens of different diseases. Schizophrenia is in the top 5 of this scale.

Some very rare disorders:

• Synaesthesia is experiencing something with one sense and hallucinating with another.
• Incubus phenomenon is sleep paralysis: waking up and not being able to move. Often they think a creature is sitting on them. This is different from psychosis and is actually quite common among the general population!
• Prosopometamorphopsia is distortion of visual perception (e.g. seeing normal faces change into dragon’s faces).

Psychotic symptoms

Psychosis is being disturbed in thinking, perceiving and behaving. People like Einstein, Jeanne d’Arc, Swedenborg (had visions during epileptic attacks) and Professor Schucman (heard the voice of Jesus who told her to write down some poems). Psychotic symptoms do not necessarily need to lead to psychotic disorders!

Positive psychotic symptoms can be either positive or negative. Jackson, a neurologist, came up with the distinction between positive and negative symptoms because some parts of the brain are older than other parts.

Positive symptoms are

• Delusions (for example thinking you are way smaller than you actually are. Some special types of delusions are: capgras syndrome (recognizing faces but not believing it’s the same person); clinical lycantrophy (believing your body has changed to that of an animal –very rare); and folie à famille: a shared illusion between people. It can be hard to decide whether something is a delusion, especially when it’s based on religious or cultural beliefs: who am I to say otherwise?

• Hallucinations: do we really only have 5 senses? Or 6? Or even 15? We have different kinds of hallucinations: Olfactory (smelling something that’s not there), gustatory (tasting something that’s not is not there), auditory (hearing something that’s not is not there), visual (seeing something that’s not is not there), tactile (feeling something that’s not is not there), somatic (sensations from inside the body that are not there), proprioceptive (thinking that you have another posture than the one that you actually have), kinaesthetic (sensation of flying), cenesthetic (changed sensation of bodily identity – e.g. thinking you have the body of an animal); sexual (orgastic feelings or feelings of being touched, not often discussed by patients); vestibular (feeling dizzy); pain (feeling painful sensations without pain-triggering stimuli); sensed presence (sensing something or someone present who is not there); temperature; time (experiencing distorted psychological time, e.g. losing the sense that time passes, not being able to tell the difference between 5 minutes or 5 hours); extracampine: hearing sounds but not hearing it where your ears are placed (like you have an ear on another place on your body); and synaesthesia (see begin of the lecture). The following does not count as a real hallucination: dreams, hypnagogia, hypnopompic hallucinations, misperceptions, imaginary companions in children, illusions (misperceptions in vision)

• Thought disorders: you have many kinds: increase or decrease of pressure of speech (or tempo); poverty of speech (short answers, e.g. “yes”); poverty of content of speech (can be of more words, but still not really saying anything); thought blocking (sudden silences in speech), illogicality (understand the sentence but the content does not make sense); derailment (starting on-topic but going off-topic really fast, never getting to the point. A question is clearly understood though.) and tangentiality (extreme derailment, not wanting to talk about the question and starting to talk about something else); circumstantiality (circling around your question); perseveration (repeating of sentences or ideas); clanging (answering in the form of rhyme words); echolalia (repeating what the other is saying); incoherence (no grammatical structure in a sentence); neologism (made up words).

• Catatonic symptoms: a typical cataleptic state lie in a posture that one cannot hold very long, though they can hold it for days. This makes their body just break down. The DSM-IV-TR listst catatonic criteria. Echolalia (copying speech) and echopraxia (copying movements) are also catatonic.

Also Negative symptoms exist.

Psychotic disorders

Some psychotic disorders are new in the DSM-V. There’s a time criterion for psychotic disorders: brief is a duration of less than one month; after one month you call it schizophreniform disorder and after 6 months you call it schizophrenia. For schizophrenia, you need two of the symptoms of criterion A, it must affect one’s life significantly, and during this half year you need at least one month of active/positive symptoms. Exclusion criteria are: no mood disorders, no somatic condition, and no autism spectrum disorder.

Catatonia is in the DSM-V an independent phenomenon (in three different types), so one can have catatonic symptoms without psychosis. Schizophrenia could be a cognitive disorder. But Blom believes the cognitive is just one part of the problem. Dopamine has a big role in this: things become meaningful. Overactive dopamine reception could lead to everything meaningless being perceived as meaningful! One believes the frontal cortex is responsible for negative symptoms and the mesolimbic system is responsible for mediating the positive symptoms. Side effects of too much medication can be movement disorders. It could even induce psychosis. The genetic factors appear to play a bigger role than previously thought. But it’s not just genes. Environmental factors could be drugs, medication (such as antidepressants), urbanisation (living in urban areas increases the risk of becoming psychotic, compared to living in rural areas), the mother being undernourished during pregnancy, psychosocial stresses, the double bind theory (it’s never good enough), migration, social defeat and social deprivation.

The network theory designed a network model of psychotic symptoms, which shows you can describe these symptoms from the micro scale level (neuronal networks) to the social macro network.

Diagnosis

First, you ask about the history (how long have you had this), you try to speak to other people around the patient (they might say something else), this is called heteroanamnesis. In psychiatric examinations you try to look if it’s hallucinations or delusions or something else. Auxiliary investigations is physical, e.g. scans etc. Then, you try to diagnose. But before you do so, consider other options as well. Maybe it’s bipolar disorder, delirium (has a somatic cause, seeing animals that are not there), substance abuse that causes the psychosis.

One could consider to prescribe clozapine, an atypical antipsychotic, which acts on more receptors than traditional medication. This could work for patients that are resistant for other medication, but clozapine has severe side-effects.

Depot medication is the safest way that people use their medication regularly, so prescribe this to people who refuse or are not able to take their medication every day. Psychotherapy is also suitable for psychosis! Psychoeducation (explaining to the patient and their family or caregiver what they have and how to deal with it and that it is important to take their medication). Grieving is also used, many patients lose some special social contacts so they need to be counselled. Genetic counselling is also important: will my children also get schizophrenia? (the chance of passing it through is 10%, usually it’s 1%). Dealing with illicit substance dependence: can they cope with their use of substances? Housing: many people are so psychotic that they have no home anymore, you should take care of them so they don’t end up on the streets. Social skills training helps to develop social skills. Relapse prevention: what preceded or triggered your first psychotic episode? Wat should you do if this happens again? When all else fails: electroconvulsive treatment is an option. It’s very effective in catatonia and psychotic depression, not as much in schizophrenia, but it might work.

Future

Maybe we’ll have new antipsychotics that are developed recently. Transcranial magnetic stimulation (for medication-resistant voice hearers). Direct current stimulation could be used more (deep brain stimulation). Take home message is: live life to the fullest!

Source

These notes are based on lectures of 2015/2016.