TYPES, SYMPTOMS AND CHARACTERISTICS OF SCHIZOPHRENIA
Schizophrenia literally means “a splitting of the mind”, derived from the German word schizophrenie which was coined in 1910 by Eugen Bleuler, a Swiss psychiatrist. Schizophrenie comes from the Greek words skhizein (meaning “to split”) and phren (meaning “heart, mind or diaphragm”).
Although schizophrenia is often mistaken as a personality disorder wherein a person takes on a ‘Doctor Jekyll and Mr Hyde’ persona, the reality is something else. Schizophrenia affects a person’s cognitive functioning; it is a mental disorder.
The DSM-V (Diagnostic and Statistical Manual, 5th edition, 2013) states that a person can only be diagnosed as schizophrenic if their major symptoms are persistent for at least six months – but the symptoms cannot be the result of substance use/abuse or due to a general medical condition. The person’s social or occupational performance must also be affected.
The symptoms are grouped into two categories: type 1 (positive) symptoms and type 2 (negative) symptoms. Positive symptoms are related to abnormalities while negative symptoms are related to deficits (a lack of something).
Positive symptoms of schizophrenia:
- Thought disorder
- Disorganised speech
- Catatonic behaviour
Negative symptoms of schizophrenia:
- Affective flattening/Blunted affect (lack of emotional expression)
- Alogia (lack of speech)
- Avolition (lack of motivation)
- Anhedonia (inability to feel pleasure)
- Asociality (lacking in social interactions)
Schizophrenia has been divided into five sub-types. However, in 2013, the DSM-V actually removed the sub-types because they were seen to have little importance in diagnosing patients. But because your syllabus is outdated, we’re going to learn about them anyway!
Paranoid schizophrenia is characterised by hallucinations and delusions which usually revolve around one theme, such as a government-related conspiracy threat. The person’s temperament and general behaviour is likely to be related to their thoughts. For example: a man who believes he is being persecuted unfairly may get angry or hostile quickly. Since there are not a lot of observable characteristics of this sub-type, patients being diagnosed would need to be completely open with their thoughts… which is hard if they are experiencing paranoia and suspicion. Paranoid schizophrenics are usually formal and intense but do not suffer from disorganised behaviour, thought disorder or affective flattening. They generally experience jealousy, radical religiosity (I swear I don’t even make these words up), delusions of grandeur (e.g. I am in a relationship with a famous celebrity/I am a famous celebrity), delusions of persecution (e.g. Everyone around me wants to harm me), auditory hallucinations (e.g. hearing voices) or somatisation (physical pain or discomfort caused by purely psychological distress).
Known as “hebephrenic schizophrenia” in the ICD (International Classification of Diseases), this sub-type is characterised primarily by thought disorder and affective flattening. Hallucinations and delusions are much less distinct but thought processes are significantly affected to the point where a person may become incapable of simple routines like bathing and changing clothes. The emotions of a disorganised schizophrenic may be flattened and unexpressed, or they may be inappropriate. A common occurrence in this sub-type is an unintentional social insensitivity. For example: the patient may giggle at a funeral. Speech may also become incomprehensible and muddled.
Catatonic schizophrenics have disturbed movements; they may become totally immobile or purposelessly agitated. “Catatonic stupor” is the term used to describe a patient who reduces their activity and “catatonic excitement” is the term used to describe a dramatic increase in activity. Patients may stand in a strange position for hours on end, or they may constantly repeat a seemingly pointless action. These are known respectively as “waxy flexibility” and “stereotypic behaviour”. If someone tries to force a patient in a catatonic stupor to move positions, the patient is likely to resist attempts with significant physical strength. Because catatonic schizophrenics may have abnormal bodily positions, facial contortions or limb movements, their disorder is often confused with something called “tardive dyskinesia”. Other common symptoms associated with this sub-type are echolalia (repeating someone’s speech) and echopraxia (mimicking someone’s actions).
Undifferentiated schizophrenics are diagnosed with symptoms of schizophrenia but their symptoms are not sufficiently formed or specific enough to classify them as paranoid, disorganised or catatonic. In a way, this is like the “extra” category. Undifferentiated schizophrenics can have fluctuations in their symptoms at any time or simply show a set of stable symptoms that just cannot be classified properly.
Residual schizophrenia is diagnosed when a schizophrenic patient no longer displays prominent symptoms of their illness; the symptoms are much less severe and things like hallucinations and delusions become very mild. Residual schizophrenics are seen to be in a transitional stage of their disorder. The clinical history of a residual schizophrenic will show at least one significant episode of schizophrenia which has been classified as either paranoid, disorganised, catatonic or undifferentiated.
EXPLANATIONS OF SCHIZOPHRENIA
The cause of schizophrenia has never been identified as a single factor; it is more likely – based on current evidence – that biology, behaviour and society all interlink to play a part in this mental illness.
The genetic model states schizophrenia as a result of genetic phenomena, such as inheritance. Researchers have tested this possibility with studies on twins, families and adoption.
Irving Isadore Gottesman and James Shields (1972):
Gottesman and Shields examined the records of 57 schizophrenics who all had twins. Monozygotic (MZ) twins are born from one zygote (one egg is fertilised by sperm) and are known as identical twins. Dizygotic (DZ) twins are born from two separate zygotes (two eggs are fertilised by sperm) and are known as fraternal twins.
Their zygocity was determined by three methods: fingerprint testing, blood testing and resemblance assessments. They wanted to examine “concordance rates”, which basically means they wanted to know how often both twins (rather than just one twin alone) were diagnosed with schizophrenia or a related psychosis. Their results showed:
- There was always a significant difference between MZ and DZ twins.
- MZ twins had more similar diagnoses than the DZ twins.
- In both MZ and DZ twins, female twins (MZ: 91%, DZ: 62%) had a greater similarity than male twins (MZ: 69%, DZ: 29%).
- Concordance rates were higher for severe schizophrenia than for mild schizophrenia.
All in all, Gottesman and Shields showed that the closer the genetic relationship between two people, the higher the chance that if one of them is diagnosed with a psychosis like schizophrenia, the higher the chance that the other will also be diagnosed. Their results also imply that this is more common in females. However, the concordance rates were not at 100% and this led the researchers to assume that although genes do play a big role by predisposing a person to schizophrenia, the environment may also play a part in triggering this. The role of an environment is also questioned because even MZ twins that grow up separately still share the same womb for nine months.
A different study conducted by Leonard L. Henson in 1970 found that if one MZ twin has a mental illness, there is a 90% chance that the other twin will also be diagnosed with a mental illness.
Seymour S. Kety and his colleagues also carried out a study to test the influence of genetics in schizophrenia. In 1962, they began a longitudinal (long-term) study in Denmark. They identified 207 adopted children whose mothers were schizophrenics (the high-risk group) and found a control group of 104 adopted children with “healthy” mothers (the low-risk group). All the children were between 10-18 years old when the study began. The results showed the following:
- Schizophrenia diagnoses were at 16.2% in the high-risk group but only 1.9% in the low-risk group
- Schizotypal personality disorder was diagnosed at 18.8% in the high-risk group but only 5% in the low-risk group
- In conclusion: the high-risk group had a 35% rate and the low-risk group had a 6.9% rate.
Kety et. al.’s results showed a strong link between genes and schizophrenia because the even though all the children were adopted, the ones whose biological mothers were schizophrenic had a higher chance of developing schizophrenia than the children whose biological mothers were “healthy”.
Based on this evidence and much more, genetics does have a link to schizophrenia. However, no specific chromosome that could be responsible for this mental illness has been identified, although the tips of chromosomes 5 and 22 as well as an area on chromosome 15 have all been considered at some point.
The biochemical explanation of schizophrenia revolves around the brain and neurotransmitters.
The dopamine hypothesis:
Dopamine is a neutrotransmitter – a chemical that acts like a “messenger” by sending impulses from one nerve cell to another across a ‘synapse’. Some hallucinogenic drugs (drugs that cause hallucinations), like LSD and cocaine, produce effects in people that are almost identical to the symptoms of schizophrenia. Since hallucinogenic drugs are chemically similar to dopamine, researchers wondered if dopamine could cause schizophrenia. They studied its effects and concluded that schizophrenics’ brains are more sensitive to dopamine than non-schizophrenic brains.
Some evidence to support the dopamine hypothesis is as follows:
- Amphetamines and cocaine both increase dopamine activity in the brain and result in schizophrenic symptoms, like hallucinations.
- L-Dopa (a chemical that increases dopamine levels) has produced schizophrenic symptoms in non-psychotic patients.
- Chlorpromazine (an anti-psychotic drug used to treat schizophrenia) blocks dopamine receptor sites to make the brain less sensitive to dopamine. To make it simple: this treatment for schizophrenia targets dopamine in the brain.
However, Chlorpromazine is only used to reduce positive symptoms (e.g. delusions) because it does not have any effect on negative symptoms. Also, 30% of schizophrenic patients are unaffected by this drug.
- When Falkai et al. examined the brains of dead schizophrenics in 1998, they found an excess of dopamine.
Another neurotransmitter called serotonin is also studied in relation to schizophrenia. John Kane and other researchers conducted research on the drug Clozapine and its effects on schizophrenics. They found it successfully reduced negative symptoms by seemingly blocking serotonin sites in the brain.
David Barlow and Vincent Durand acknowledged that while dopamine and serotonin are most likely involved in the treatment of schizophrenia, their specific roles are still unclear. The evidence so far is all correlational and does not specify a separate cause and effect. In fact, it is possible that abnormal chemical levels are a result of schizophrenia, rather than vice versa.
The cognitive model basically states that schizophrenia is a result of defective processing mechanisms, a selective attention deficiency, a lack of a brain filter for relevant information and an inability to interpret external stimuli.
Christopher Donald Frith (1992):
Frith studied faulty cognitive processes and the schizophrenic theory of mind. He hypothesised that schizophrenics cannot differentiate between actions that take place externally and actions that are generated internally. He believed that positive symptoms of schizophrenia could be explained by three faulty cognitive processes:
- Inability to generate voluntary action
- Inability to monitor voluntary action
- Inability to monitor the beliefs and attention of other people
Frith said that these processes may be part of a “meta-representation”, which is a mechanism that allows us to have a theory of mind. This theory of mind makes us aware of our own intentions and helps us to understand the intentions of others. The faulty operation of this meta-representation is caused by a disconnection between the frontal areas of the brain (concerned with action) and the rear areas of the brain (concerned with perception). Frith conducted some experiments and concluded that blood flow changed in the brains of schizophrenics who were asked to perform specific tasks related to cognition. However, Frith is criticised for his reductive approach (he ignores all other potential factors) and his unclear research.
In 1993, David Hemsley also gave a cognitive explanation for schizophrenia after testing animals. He claimed that schizophrenics have a breakdown in the relationship between their old existing information and their new incoming information. Their schemas are not activated “normally” so they experience a sensory overload and their brain fails to filter all the information. This means that they may see trivial incidents as something important. Also, he explains auditory hallucinations as the result of internal thoughts being unrecognised by the person. The person does not realise it is their own prior information and attributes it to some external source (i.e. voices in their head). However, this doesn’t actually give an explanation for schizophrenia. Hemsley only explains why certain symptoms may occur.
TREATMENTS FOR SCHIZOPHRENIA
The biochemical treatment of schizophrenia primarily involves medication.
Antipsychotics and atypical antipsychotics:
Antipsychotics help to make biochemical imbalances stable. There are two types: traditional and new. Traditional antipsychotics, such as Chlorpromazine and Haloperidol, control positive symptoms of schizophrenia. They have been available since the mid-1950s. They mainly block the dopamine receptors.
- Drugs which block dopamine sites are called phenothiazines.
Some of their side effects may include blurred vision, constipation, drowsiness and a dry mouth. More serious side effects are loss of muscle control, muscle spasms, head and neck cramps, tremors, fidgeting and shuffling. Some side effects have been observed to develop after a prolonged use of traditional antipsychotics, namely: facial tics, tongue rolling, lip licking, panting and grimacing.
Since the 1990s, new antipsychotics like Risperdal and Seroquel have become available. Some of these newer drugs work on serotonin receptors as well as dopamine receptors, thus allowing them to simultaneously treat positive and negative symptoms.
Other even newer antipsychotics are called “atypical antipsychotics” because of the different way they affect the brain’s dopamine receptors. They are known to have mood-stabilising properties, thus reducing chances of hallucinations and delusions. Their side effects primarily include weight gain and drowsiness.The major downside to drug therapy is relapse. As Malgorzata Rzewuska observed in 2002, the symptoms of schizophrenia often reappear when the patient terminates their drug therapy. This makes is unsuitable for long-term treatment.
ECT was introduced by Ugo Cerletti and Lucio Bini in the mid-1930s. It has been used for various disorders in the past, including alcoholism and eating disorders. In modern times, it is used very rarely and is often a last resort in cases where absolutely nothing else is working. This is mostly because successful drug therapy, cognitive treatments and psychotherapies have been introduced. People believe these kinds of treatments are more humane and that ECT is more like kicking a computer to make it work normally. It is not yet clear exactly what ECT does to a person, meaning that doctors are even more reluctant to use it.
In ECT, an electrical current is passed through a patient’s brain for a few seconds, resulting in a seizure (fit). The body goes into convulsions but the patient is given a muscle relaxant which relatively soothes this. A mouth gag and other precautions are taken to prevent the patient from accidentally hurting themselves. The side effects include short-term memory loss, dizziness and confusion. The patient is also given oxygen after the procedure because the muscle relaxant can affect their breathing.
In the past, when ECT was first introduced, many patients died because of heart problems. Now all patients’ medical records are thoroughly checked before even considering this treatment.
Token economy refers to a system of behaviour modification that is based on positive reinforcement (rewarding) of target behaviour. Changing behaviour through a training programme like this is called “conditioning”. Token economy is based on the principles of a type of conditioning: operant conditioning. Operant conditioning is behaviour modification based on rewards (positive reinforcers) and punishments (negative reinforcers).
In token economy, the positive reinforcers are symbols or tokens that can be exchanged for other material reinforcers or privileges. For example: an alcoholic in rehab meets his goal of cutting down his alcohol intake by a certain amount so he will be rewarded for meeting his target behaviour. In this treatment, the token is the secondary reinforcer and is exchanged for a proper reward, which is the primary reinforcer (e.g. a person who collects five tokens can exchange them for a big reward).
The first token economies were designed for chronic psychotic patients who were resistant to other forms of treatment. This method is always used in combination with other treatments. Research has shown that patients find a token economy to be a very positive experience and many recent reviews of schizophrenic treatment have mentioned this to be a very effective and credible method.
Gordon Paul and Robert Lentz (1977):
Paul and Lentz directed this method in the 1970s at a mental health centre in Illinois. They designed an environment that encouraged socialisation, participation in group sessions, and self-care without violence. Their method meant that patients could gain access to fancy meals and small luxuries whenever they behaved properly. A patient could gain tokens and swap them for a box of cigarettes as a reward for good behaviour, while others would lose their tokens for any disruptive behaviour.
Paul and Lentz created a daily schedule of activities for the patients and found that the schizophrenics who were given this treatment became more cooperative and needed less medication. Their abnormal motor behaviours were also reduced. The patients who followed this programme progressed better with their social, self-care and vocational skills. Many of them also reached a stage of health which allowed them to be discharged from the hospital.
CBT for schizphrenia was originally developed as a way to provide extra treatment for residual symptoms. It stemmed from the principles and intervention methods used on patients with anxiety and depression.
Tom Sensky (2000):
Sensky and other researchers conducted a study on schizophrenia and CBT. They recruited 90 patients from five clinical services: two in West London and three in North England. Patients were between 16 to 60 years of age, were diagnosed with schizophrenia, and had experienced distressing symptoms that lasted for at least six months – even though they had taken antipsychotics. The patients received CBT for nine months and were then checked up on again after nine months.
Sensky et. al.’s experiment showed that if a schizophrenic patient is treated with CBT, their positive and negative symptoms will be reduced and the effects of the therapy will still remain even after nine months. This shows that this method of treatment can be very effective even in patients who do not respond positively to antipsychotic drugs.