Positive Symptoms

Symptoms or experienves that ADD to normal functioning. (Things normal people do not experience)

Positive Symptoms

1) Hallucinations 

Auditory: voices in the head that talk or comment on things that happen. More common than visual hallucinations
Visual: Seeing things that are not there, such as people, animals or distorted facial expressions

Haptic: Touch sensations

Maybe even catatonia?

Positive Symptoms

2) Delusions/False beliefs

- Delusions of grandeur: belief that you are an important historical or religious figure

- Delusions of Persecution: Beleif that there are people out to get you, that you are targeted (FBI/CIA aliens)

- Delusions of control: the belief that your thoughts or actions have been taken over by an external force, manipulating you to do certain things

- Thought broadcasting: the belief that your thoughts are being heard

- Referential delusions: Belief that the gestures and words of others are directed at you 

Negative Symptoms

Abilities or functions that are missing (and present in the non-schizophrenic population)

1) Avolition/apathy

The inability to maintain goal-directed activities/ lack of motivation. Being unable to keep good hygiene, lack of energy, lack of persistence in work or education

2) Speech poverty

Incoherent or random speech. Reduction of quality and amount of speech.

DSM considers'speech disorganisation' as a positive symptom as it adds incoherent and non-sensical speech

Reliability and Validity in the Classification of Schizphrenia

Reliability

How much two proffesionals can reach the same diagnosis for the same patient using the same diagnostic tool

If the diagnosis is objective, there should be consistency between the two diagnoses.

A lack of consistency indicates that the diagnosis was subjective, and that symptoms have been interpreted differently. UNSCIENTIFIC

Reliability

Evidence for poor reliability

Cheniaux found poor inter-rater reliability between two psychiatrists diagnosing the same patient using the DSM.

One diagnosed 26 while the other diagnosed 13

This shows inconsistency

Validity

The extent to which psychologists can make a correct diagnosis. The classification of schizo should be true to what it really is.

SHould also be concurrent calidity between classification systems. Same diagnosis should be reached whether the ICD or DSM is used.

Genetics

Schizophrenia is inherited, and seen to run among families.

Candidate Genes- Schizophrenia is believed to be polygenic, and controlled by several genes rather than ust one. There are different possible genes and combinations, suggesting the genetic basis of schizophrenia is very comple

Genetics

There is supporting evidence for genetic explanations

GOTTESMAN

He conducted a meta-analysis of concordance rate studies in schizophrenia.

Found that concordance increased the more closer related you were to a schizophrenic individual.

Genetics

Does not suggest that the illness is due to genes alone

even with 100% shared DNA, when twins were identical, concordance was only 48%. This shows that the environment does have an effect in the development of the illness. Therefore the explanation is not comprehensive.

Its also very complex. RIPKE found that 108 seperate genetic variations were associated with the increased risk of schizo. This is a weakness as it means the genetic theory is not a standalone theory. We must consider what the genes code for, how that can effect things like neurotransission too.

Genetics

ADOPTION STUDY Tienari

coparing groups of children born to schizophrenic mothers given up for adoption vs normal kids with non-schizo mothers.

The adoptees that had schizo mothers were more likely to develop schizophrenia and other psychotic disorders than the control group.

Adoption studies are effected by the envirnment too.

Those with schizo mothers were more likely to develop the illness if their environment was disturbed. This meant increased risk was not due to just their genes.

This means we must look at genetics and the enviroment

Dopamine Hypothesis

Originally, too much dopamine was thought to lead to the positive symptoms of schizophrenia.

Chlorpromazine was initially developed as a sedative to relax patients before surgery, but found to reduce the positive symptoms of patients with schizophrenia.

Chlorpromazine works by blocking dopamine receptors, so it can be inferred that dopamine plays a causal role in the positive symptoms of schizophrenia.

OR they just have over-active, or too many dopamine receptors

Evaluation

Drug investigations

It has been found that Chlorpromaine is successful in reducing positive symptoms in 60% of cases. Supports the idea that dopamine activity and sz symptoms are related.

-Evidence from post-mortem studies.

Low levels of DBH (the enzyme that breaks down dopamine) were found in the brains of schizophrenics. This means the patients would have had abnormally high levels of dopamine. Supports this shit

Evaluation

Amphetamines

(adderall) When given to clinically 'normal' people, induced symptoms of schizophrenia. Supports the hypothesis because it shows that increasing levels of dopamine in normal people can cause schizo so there must be a causal relationship between the two things.

L-DOPA, WHEN GIVEN TO SCHZS, make their symptoms worse. Increased dopamine makes it worse, who couldve guessed.

Evaluation

Too simplistic though.

The idea that a single neurotransmitter can lead to a wide range of symptoms is unlikely. THe DA hypotheis is reductionist in complaining a very complex illness. The origincal hpothesis does not explain the negative symptoms of sz. Thats why chlorpromazine only works for 60% of patients. Wemust consider other crap then too.

NEW RESEARCH

HYPERDOPAMINERGIA (too much) in the subcortex, has been linked to speech things cause brocas area. 

HYPODOPAMINERGIA in the cortex, has been linked to negative symptoms

Neural Correlates

How physical brain structures relate to behaviour and disfunction

• They use brain scanning techniques to image theb rin and record which areas of the brain have a high or low level of activity.
• Enlarged brain ventricles were once thought to be associated with sz. This brain structure correlate was seen in post-mortem examinations of dead sz patients.

We can now use fMRI scans and PET scans to image the brain, which gives us more evidence for activity in different parts of the brain being correlated with the positive and negative symptoms of SZ. 

ONE AREA IS THE VENTRAL STRIATUM

Neural Correlates

JUCKEL

Juckel foud a relationsip betwen avolition (lack of motivation) and activity in the ventral striatum, a reward centre in the brain. MOtivation involves the anticipation of a reward, so the relationship has face validity.

He found that compared to normal people, SZ patients had overall less activity in this brain ara. 

A negative correlaton between the amount of activity and the severity of overall negative symptoms.

(as activity decreased, severity of negative symptoms increased)

AVOLITION= low activity in ventral striatum

Neural Correlates

ALLEN

Allen performed fMRI scans on 10 sz patients with a history of auditory hallucinations, 10 with none, and 11 controls. All were male.

They lisented to normal and distorted recordings of their own voice and other's voices, and were asked to identify which were theirs and which were someone else's.

They heard 80 adjectives, 40 their own and 40 not,

The hallucinatory group made more external missattributions than the other two conditiions.

This group also had lower neural activity levels in the left superior temporal gyrus. This area was more active in the other groups when listening to their own voice

Evaluation

Allen is supporting evidence for positive symptoms

One weakness is that the corelations do not infer causation. Just because a part of the brain shows certain activity levels, this does not mean that that causes the symptoms.

The symptoms could be causing less information to pass through certain areas, which leads to the patterns seen by researchers. E.g avolition may cause less info to reach the ventral striatum rather then the other side

WE must be careful therefore in the conclusions we draw.

~INTERACTIONIST APPROACH COMES IN TOO~

Family Dysfunction

Schizophrenia could be linked to childhood experiences and family environment

Schizophrenogenic Mother

Literally 'schizophrenia-causing mother'

Proposed by Fromm-Reichmann, this kind of mother is cold, rejeting, controlling, and creates a family environment of tension and secrecy. This kind of environment can lead to symptoms such as delusions and paranoia.

Double-bind Theory

Double-bind statements send mix messages to children.

Bateson emphasised the role of communication in the family environment. Double-bind statements makes the child feel as though no matter what they do, it would be the wrong thing. They then get punished by the withdrawal of love.

This makes children become withdrawn to escape the double-bind, and this can lead to negative symptoms such as avolition. 

It also leaves them with a view that the world is confusing and dangerous.
Bateson suggested this theory not as a sole cause of SZ, but as a risk factor

High Expressed Emotion

High level of negative emotion expressed towards a SZ patient by their family. 

Involves hostility, verbal criticism from family members. Anger, rejection. Emotional over-involvement such as needless self-sacrifice. 

This expressed emotion is a source of stress that could trigger someone who is genetically disposed to being SZ, or cause relapse in someone diagnosed

Evaluation

Schizophrenogenic mother lacks empirical evidence.

THeory was based on the researchers own obbservations from partients, or from his own assesment of the mothers. This is a weakenss because blaming mothers can have a negative effect on families already dealing with the mental illness.

Supporting evidence for Double-bind

BErger foud that SZ patients had a higher recll of dobule-bind statements by their mothers than non. This supports family dysfunction as t shows a relationship between communication style and the presecne of SZ. This is however not a causal relationship, nor does it really hold validity because SZ patients are deluded

Evaluation

Family dysfunction as an explanation is that it is generally well supported by  A SHIT TON of evidence

in a meta-analysis of 46 studies into child abuse and SZ, found that 69% of women and 58% of men had a hsitroy of sexual abuse or physical abuse. That shows there is a relationship between poor childhood experiences and the development of SZ

EE has supporting evidence

Some studies have found that relapse is more than 4x as likely if a SZ patient returns to a high EE family. This is a strength because it s upports the idea that a hostile family climate can prevent recovery from SZ, even if it doesn't cause it,

This is a strength because this can be applied to family therapy to help family members reduce their level of EE.

Evaluation

Stirling found that 30 patients with SZ performed worse on a range of cognitive tasks, inclooding the Stroop test compared to a control group. Supports Frith's theory cause it demonstrates how SZ participants struggled to suppress the impulse to read the words in order to complete the task.

Evaluation

Research support

Sarin ad Walin found, in  a review of evidence, that SZ patients showed various biases in informational processing. Delusional patients tended to jump to conclusions and patients with hallucinations tended to experience their own thoughts as voices. THis supports the theory of cognitive biases and faulty thinking processes

Still doesn't reveal the cause of SZ though. Faulty cognition only helps us understand the symptoms, doesn't tell us the origin of those faulty conditions. What has cause the dysfunction? Its not a full explanation 

Evaluation

Success of cognitive Therapies

NICE  review of treatments for SZ in 2014 found that cognitive therapy was more effective than anti-psychotic medication in reducing symptom severity and improving social fucntioing.

REinforces the idea that faulty cognition is the underlying cause of the symptoms in the first place

typical antipsychotics

DOPAMINE ANTAGONISTS. STOP THE FUNCTION OF DOPAMINE. BLOCK RECEPTORS.

Normalises dopamine activity in the brain, reduces positive symptoms.

typical antipsychotics

THEY WORK

There is evidience they work compared to a placebo.

THORNLEY found that, across 13 trials, patients taking Clorpromazine had reduced symptom severity and lower relapse rates than matched patients taking a placebo. This provides support for the use of medication!

But they have many side effects.

Parkinson's-like synptoms can be caused by the interference of dopamine pathways. Involuntary of the mouth and jaw can also start to occur. This medication can therefore be distressing for the patient to take , and they may have to take more medicine to counter the side effects. May put patients off the idea of medicine 

typical antipsychotics

Leucht found in a meta-analyis that 64% of patients that were given a placebo relapsed in 12 months compared to 27% who carried on with real medication. This demonstrates the effectiveness of the actual medication , and that interfering with dopamine is a viable solution. Useful medicine

But doesnt work for everyone

Rsearchers found their only effective for 60% of patients

Other treatments are required to help al SZ patients function adequaylu and improve quality of life.

atypical antipsychotics

Evaluation

Evaluation of Drug Therapy

Evaluation of Drug Therapy

Cognitive Therapies

CBTp

Based on the assumption that delusions arise from faulty interpretations of events. Works to identify and correct those misinterpretations. Doesn't cure anything, but helps patients cope.

• Encourages evaluation delusions
• Ways to test beliefs
• Homework
• Alternative explanations for their beliefs.

Cognitive Therapies

Evaluation

Evidence, what NICE said in 2014

COSTLY

TRained therapist and at least 16 trials are recomended. While useful, there are econoic implivations, NHS  budget cannot allow this to be given to all patients  when othher treatments , meds, are cheaper

Cognitive Therapies

Evaluation

Effectiveness depends. Works best when they are not detached from reality and are stabilised with medication. wouldnt help duroing initial acute stage. Issue because therapists must onsider whethere, for each patient, CBTp is the best option. IT may help patients normalise their experience by engaging with others in group sessions, but one-on-one sessions are the most effective for those who have had it for longer

Cognitive Therapies

FAMILY THERAPY

Based on the assumption of family dysfunction and hostile family atmospheres. Aims to improve communication and interaction. 

Should be recommended to all SZ patients who are in contact with or live with family. Should be a priority to those with high risk of relapse.

• Goes for 3-12 months
• Provides fam members with information on SZ
• Involves patient where possible
• Provides practical solutions for the family members
• Encourages them to listen to each other
• Identifies expressed emotion

Cognitive Therapies

FAMILY THERAPY

Evidenc eto show it reduces relapse rates. Pharoah's meta-analysis found that compared to meds, fam therapy reduced relapse more. Strength because idk helps!

May only be effective because it increases the amount of medicine compliance, less of an impact on actual mental state or social functioning. Effectiveness could be overestimated

Cognitive Therapies

FAMILY THERAPY

Economic benefits

AKthiugh expensive, the cost is offset by the reduction of costs of hospitalisation. Relapse rates are much lower due to family therapy and so yeah. Shows how it has a better impact on society as a whole and NHS nd shit 

Garety found that individuals who simply had carers showed relapse rates as low as those who had family therapy

Could indicate its just the family thats the problem

Cognitive Therapies

TOKEN ECONOMY

Behaviour can be unlearnt

BEhaviour modification. USually used for those who have been institutionalised from being in a hospital

HELPS WITH MANAGING THEM, NOT CURING THEM

U KNOW HOW IT GOES

Cognitive Therapies

TOKEN ECONOMY

UNETHICAL

THOSE WITH LESS SEVERE SYMPTOMS RECEIVE LESS TOKENS which they cant help cause of their symptoms. This is discrimination and can be considered a human rights abuse since they do not receive the same privileges as others.

Interactionist Approach

DIATHESIS-STRESS MODEL

Originally it was thought that a patient had a genetic disposition, and an environmental factor would trigger.

Stress on its own couldn't.

Interactionist Approach

BUT NOW

Many candidate genes are seen to increase vulnerability to SZ. No single 'schizogene'.

Trma could actually be the diasthesis that makes the patient vulnerable to stressors later in life. And e.g. complications at birth can affect the brain and could cause a vulnerability for SZ

Stress could be anything that triggers SZ. Cannabis could be a potential stressor or trigger for someone who has a genetic vulnerability.

Interactionist Approach

Evaluation

Useful practical applications in therapy. Most patients in england are now treated with both medication and CBTp. This means that clinicians are recognising that a combination of factors can lead to the development of SZ, and are putting this to practice when treating patients. SZ benefit from each treatment and have a better chance of improving quality of life

One strength of the interactionist approach is Tienari, who conducted an adoption study and fond that those with schizophrenic mothers could be triggered by a diturbed environs. Provides evidence for noth genes and environment having an effect on development. Both the genetic vulnerability and environment were important and demonstrate the diathesis stress 

Interactionist Approach

Evaluation

Research to support environmental triggers

Varese found that children who experienced severe trauma before the age of 16 were three times more likely to develope SZ than the general population. This supports the link between environmental triggers and SZ. If these factors were the sole cause, SZ would be far more common. The must have the genetic vulnerability, and when that combines with a triggering environment SZ  can occur.

Focuses too much on stress close to the onset. A patient could have had a traumatic event in early life that lead to them having bad coping skills. This could make them more supseptible to stress later in life and therefore more likely to develop SZ. Stress might not be a causal factor then, the relationship is far more complex.