Exploring schizophrenia

December 8, 2010 at 7:58 pm 2 comments

Schizophrenia (commonly abbreviated to SZ) is very often portrayed in the media as something it is most certainly not. One only needs to watch films like Hide and Seek to see exactly what schizophrenia isn’t. There are common misconceptions that:

  • Schizophrenics have split personalities
  • All schizophrenics are violent or dangerous
  • Schizophrenia is untreatable (note: I’m not saying there’s a cure, but it can be treated)

In fact, most schizophrenics couldn’t be distinguished from a crowd of ‘normal’ people. They are often not violent or dangerous, and certainly do not have more than one personality (that’s called Multiple Personality Disorder). Many psychologists/psychiatrists argue that split personalities aren’t even possible, but that’s another kettle of fish.

With a lifetime prevalence of less than 1%, one can begin to question whether schizophrenia is even a useful diagnosis. The main ‘clinical handbook’, known as the Diagnostic and Statistical Manual (currently DSM IV-TR) suggests that for a patient to be diagnosed as schizophrenic, they must demonstrate two or more symptoms for a “significant portion of time” over at least one month. Regardless of this, let’s explore this psychopathology in more detail.


These are split into positive and negative. Some people find it hard to come to terms with “positive” symptoms – besides, how can any symptom of a disorder be positive? Well, it doesn’t mean that they’re good. Positive symptoms refer to the fact that the symptom has added to the behaviour, whereas negative symptoms describe absence/withdrawal of behaviour. Let’s look at the symptoms to get a clearer picture:

Positive symptoms

  • Hallucinations – perceiving stimuli which is actually not present. These can be olfactory (smelling), visual (seeing), gustatory (tasting), tactile (touch) or, the most common, auditory (hearing).
  • Delusions – holding a firm belief even when faced with strong contradictory evidence. Examples include thought insertion (the delusion that people have put thoughts in your head), thought broadcasting (the delusion that everyone can ‘tune in’ to your thoughts like mind-readers), delusion of reference (the delusion that everyone is talking about you all the time) and delusions of persecution (the delusion that you’re being conspired against, spied on, followed or harassed)
  • Disorganised speech/behaviour
  • Catatonic state (excessive motor movement)

Negative symptoms

  • Lack of affect (emotion)
  • Catatonic state (no/little motor movement) – sometimes schizophrenics can sit for hours and hours on end without moving a muscle; they just sit there completely motionless.
  • Low motivation/energy
  • Alogia – trouble speaking properly

Theoretical explanations for schizophrenia
I have a case study due in for the 17th December 2010 which is all about schizophrenia. Therefore, I’m going to leave out a lot of the other research and studies I have found until after this date; I don’t want people copying all the work I spent hours researching! I’ll therefore only be including studies that were mentioned in the lecture I had on this, rather than ones I have found. Check back after this date for a much more detailed, research rich section on theoretical explanations.

There is much research that leads to many suggestions as to the cause of schizophrenia. The main ones are brain structure, pharmacology and genetics.

Brain structure
Examples of abnormalities in schizophrenic brains include reduced brain size/weight (van Haren et al., 2004), structural variation in the prefrontal cortex and limbic system (Andreasen, 1994; Lawrie et al., 2003), and enlarged lateral ventricles (Rao and Moller, 1994).

Ventricle differences in unaffected (left) and affected (right) brains.

As can be seen above, the brain on the right – with schizophrenia – has a much larger ventricle area (look in the centre of the brain at the two ‘holes’). This difference in ventricular area has been suggested as one contributor to the onset of schizophrenia. With regards to the limbic system, it has been found that the size of key structures of this system are much smaller in schizophrenics than non-schizophrenics (in particular the  hippocampus and amygdala). Not only this, but the pyramidal cells in the hippocampus are disorganised in schizophrenic brains. I’m afraid I couldn’t find a picture for this anywhere so I apologise for that.

It has been suggested that there is a genetic predisposition for developing SZ in later life. Studies have shown that monozygotic twins (that share 100% of genetics) have around a 50% chance of developing SZ if the other twin also has it. Criticism aimed at these studies suggested that it may be an environmental factor; the likelihood is that twins will be raise in an identical manner. Therefore, it could be down to their upbringing and environment, not genetics. To solve this, adoption studies were conducted. These showed the same level of concordance (around 50%) regardless of where they were raised. This suggests there is a genetic link with SZ. The following table sums up the chance of schizophrenia development with different relations. It can be seen that having a close relative with SZ brings a much higher chance of developing it than less close relatives.

It can be seen that the more genetic material shared between relatives, the higher the chance is of developing SZ.

The dopamine hypothesis (part of the monoamine hypothesis) is perhaps the most important pharmacological explanation for schizophrenia. It is suggested that an imbalance of the neurotransmitter dopamine leads to the occurrence of  positive symptoms of schizophrenia. Domaine is widely known as the “pleasure” neurotransmitter, and is normally associated with feelings of happiness, ecstasy and stimulation. In the brain, dopamine helps with regulating the flow of information and controlling of movement. Drugs such as cocaine mimic the effects of dopamine – so it’s no surprise that cocaine users experience hallucinations, paranoia and delusions also. Support for this hypothesis comes from the breakthrough drug “chlorpromazine”, which is a dopamine receptor blocker. This alleviates most of the positive symptoms, which suggests that the blocking of dopamine reception (and therefore their effect on post-synaptic neurones) is a major treatment for positive psychotic symptoms. These aptly named antipsychotic drugs have since been a major contributory treatment for SZ (see the next section). However, there are issues with the dopamine hypothesis. Firstly, approx. 25% schizophrenics do not respond to dopamine blocking drugs; this lack in consistency for treatment highlights the varied nature of human brains. It has also been shown that the alleviation of positive symptoms occurs weeks after initial drug taking schedules – whereas the actual dopamine blocking occurs almost straight away. So, with all the problems of antipsychotics, let’s look at treatment of SZ.


Before the 1950’s, there was a very poor level of treatment for schizophrenia; doctors simply didn’t understand enough about the disorder to treat it effectively. Most patients suffered through lifetime hospitalisation, life in straitjackets and electroconvulsive therapy (or ECT, which is sending electrical pulses/shocks through the brain). Thanks to Paul Charpentier, a french surgeon, Chlorpromazine was synthesised in December, 1950 (although many, many other French scientists need to be credited in the run up to the discovery). Now, the prognosis is much better for schizophrenic patients. We’ll start by looking deeper into Charpentier’s discovery.

Antipsychotic drugs

As described in the pharmacological explanation of SZ, antipsychotics are now a widely used treatment for schizophrenia. Charpentier, a French surgeon, was initially looking for new antihistamines, but accidentally synthesised a drug now known as chlorpromazine. He noticed the calming effects of the drug, and suggested it may be useful for psychotic patients. He was correct, and this lead to a breakthrough in schizophrenia treatment. His drug is now classed as first generation antipsychotics (which are also known as neuroleptics). There are now second generation drugs, known as ” atypical antipsychotics”. The table below summarises their effects:

First generation antipsychotics (aka neuroleptics/typical) Second generation antipsychotics (aka atypical)
Block dopamine D2 receptor Block dopamine D2 and D4 reception
Reduce positive symptoms Reduce both positive and negative symptoms
Many side effects: drowsiness, dry mouth, movement abnormalities (similar to Parkinson’s disease), weight gain

Less side effects: drowsiness, weight gain, reduced white blood cell count

As atypical drugs block two receptors rather than one, have less side effects and alleviate both positive AND negative symptoms, it may seem common sense to always use this drug. This isn’t always the case though; some schizophrenics respond better to one drug than the other. Some may not have any negative symptoms, so why use the drug that does? In some cases, those with an already poor immune system would be dangerously affected by the 2nd gen drugs, as they reduce white blood cells. It would be too dangerous to use that in this case. As you can see, it’s not clear cut which drug to use; it’s usually a case of trial and error. If one works, great – if it doesn’t, it may be advisable to switch to a different course of antipsychotics.

Cognitive Behavioural Therapy (CBT)

Possibly psychology’s best friend with regards to therapy, CBT is once again a suggested treatment. The aim of this in SZ is to reduce the intensity of positive symptoms, prevent relapse and to reduce the level of social impairment. Very often, a therapist will help the schizophrenic undergo “reality checks”, whereby they assess the evidence for delusions and convince the patient that they are not true. By rewiring faulty cognitions, some of the underlying symptoms can be countered and usually help patients to stop having delusions at the high intensity they normally do.

Other treatment

Social skills training (SST) is sometimes used to help schizophrenics form bonds with other people. By gaining friends and social networks, it can help to stop the isolation and social exclusion some schizophrenics experience. It can also help them acquire jobs and fit into their community, creating a sense of belonging. Labelling and stigma can very often negatively affect suffers of mental disorders, and SST may help schizophrenics prepare for the fact they may be stigmatised for their condition. Of course, as mentioned before, schizophrenics are not maniacs with split personalities who murder people because “the strange man told me to” – they’re very often calm, non-violent and passive. Unfortunately, ignorance to such conditions is very high, and stigmatisation and labelling do occur. Case managers are often appointed to patients, who aid them with finding jobs, fitting in, forming friends and recovering. They will stay with the schizophrenic and schedule meetings to ensure things are running as smoothly as they can, and the assess the progression of a patients recovery. In some cases family therapy is also required, which aims to educate the family on the symptoms, treatments and causes of SZ. Often families will struggle to cope with the stress of such a change in lifestyle, and family therapy can help there as well. It is suggested that there is a link between family and relapse to SZ, so they are told what they need to do to prevent such a thing happening.

So which treatment to use?

As always, it is never a case of “this treatment will work for every patient”. Very often, there needs to be a mixture of different treatments depending on the individuals needs. Whereas drugs might work on their own for one patient, another might show no response to this, and will therefore need to seek other modes of treatment.

As a rule of thumb, the appropriate antipsychotic (either neuroleptic or atypical) will be issued, along with complimentary CBT. It appears that this method is the most effective. Again, depending on the situation, SST, family therapy or a case manager might also be required, either in place of drugs/CBT, or as a further compliment to the treatment.


That concludes the basic exploration of a very often misconceived mental psychopathology. I hope you received all the information you needed, and that maybe you’ll be interested in looking further into this disorder. As mentioned before, not many people are properly educated about this, and with the media often blowing SZ out of context and making inaccurate portrayals of the disorder, now is definitely the time to educate people about this delicate issue.

Thanks for reading
Please rate, comment and/or subscribe!

Sam Eddy.

Entry filed under: Psychopathology. Tags: , .

Guest post: The counselling relationship Evaluating and comparing two theories of cognitive development.

2 Comments Add your own

  • […] an essay on schizophrenia, for example, you might begin by explaining what schizophrenia is. Then you might have a paragraph […]

  • 2. Jennifer  |  April 9, 2012 at 11:22 pm

    Thank you found very informational, my dad has been diagnosed paranoid schizophrenia, about 4 yrs ago, it has been very stressful..


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