The psychotic disorder (severe mental illness). It’s lifetime prevalence


The world shuns those who are labelled abnormal. Once a person is diagnosed with any kind of psychological state, their life and their loved one’s lives are forever changed. As much as any medical illness, Schizophrenia presents suffers with an enormous array of social, biological and economic conundrums. It also confronts us with profound human suffering, for it involves alternations in the core of a person’s subjectivity.

Somebody that has schizophrenic disorder suffers in several areas of their life; but, the medical and psychological communities are fighting for the understanding and freedom for all that are concerned. This subsequent essay is a brief over read of the Psychotic disorder schizophrenic disorder, the way the disorder affects people who suffer, and therefore the research that continues to fight for a cure.  Schizophrenia is a very common form of psychotic disorder (severe mental illness). It’s lifetime prevalence is almost 1% it’s annual incidence is about 10-15 per 100,000, and in the UK the average general practitioner cares for 10-20 schizophrenia patients depending on the location and social surroundings of the practice (Davies, T., & Craig, T. K. (2009).

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Schizophrenia is one of the most controversial psychiatric diagnoses. Over time, there has been debates whether a distinct state of schizophrenia exists, whether it results from genetic or environmental causes and whether it should be treated by using drug therapy, electroconvulsive therapy, or more social and psychological approaches.

The condition now labelled as schizophrenia was first described by Kraepelin (1883,1981) using the term dementia praecox. This label was chosen to show that it was a progressive and deteriorating illness with no return to pre-morbid levels of functioning. After some time, Bleuler (1908) identified four fundamental symptoms of what he termed the group of schizophrenias ‘split mind’ ambivalence, disturbance of association, disturbance of mood and fantasy over reality.

The exact cause of schizophrenia remains hotly disputed. However, the consensus view is that it comprises many related disorders characterized by fundamental distortions of thinking and perception. Disturbance in thought process is one of the most obvious symptoms of schizophrenia.

Symptoms are termed ‘positive’ or ‘negative’ depending on whether they are psychological add-ons e.g. delusions or deficits e.g. anhedonia.  Such that it is a syndrome with various presentations and variable, often relapsing, long term course. Although schizophrenia is sometimes misconceived as ‘split personality’, the diagnosis has great reliability over all even across any ages or cultures.

Symptoms of schizophrenia are characterised most usually only as positive or negative, although the traditional diagnostic subcategories as hebephrenic, paranoid, catatonic and simple have mixtures of both.

Positive symptoms and signs


These are perceptions that occur without an appropriate sensory input. Although hallucinations can occur in any sensory form – auditory (sound), visual (sight), tactile (touch), gustatory (taste), and olfactory (smell) – hearing voices that other people do not hear is the most common type of hallucination. The hallmark of schizophrenia is that patients experience voices talking about them as ‘he’ or ‘she’ (third person auditory hallucinations). But second person ‘command’ voices also occur, as do olfactory, tactile both somatic and visceral and visual hallucinations.


Delusions are abnormal beliefs held with absolute certainty, dominating the patient’s mind, and untenable in terms of the sociocultural background. Delusions are often deriving from attempts to make sense of other symptoms such as experience of passivity (sensing that someone or something is controlling one’s body, emotions or thoughts). For example, individuals experiencing paranoid type symptoms roughly about one – third of people diagnosed with schizophrenia – often have delusions of persecution or false and irrational beliefs that they are being cheated, harassed, poisoned or conspired against. These people may believe that they, or a member of their family or someone close to them, are the focus of this persecution. In addition, delusion of grandeur, in which a person may believe he or she is famous or important figure, may occur. However, such false beliefs are often very difficult to challenge. Sufferers are frequently able to defend their deluded beliefs in a coherent way and unable to understand that other people find their delusional beliefs implausible (McGuire, Junginger, Adams, Burright et al.. 2001).

Disorganised speech and thought behaviour

Psychotic symptoms frequently exhibit a range of attributes that show disordered thinking and disordered speech.

World Salad: language of person experiencing a psychotic episode appears so disorganised that there seems to be no link between one phrase and the next. This is known as word salad. Some word salads simply do not seem to be attempts to communicate anything structured and appear to drift without substance from one unconnected sentence to the next.

Neologisms: Making up words and use them in their attempts to communicate. These are constructed by condensing or combining several words.

Clanging: trying to communicate by using words that rhyme.

Negative Symptoms

A negative symptom is the absence of some ability or attribute a normal person would possess. These include loss of personal abilities such as initiative, interest in others and the sense of enjoyment (anhedonia). Blunted or fatuous emotions (flat affect), limited speech and much time spent doing nothing are typical behaviours. Subtle cognitive deficits often persist or even worsen despite continuing treatment.

However, the signs and symptoms depend on person to person, both in severity and form. Not every person will show all the symptoms and possibly the symptoms could also change over time. The effects can be extremely hard on both the person with the disorder and for those people who are around them when the signs and symptoms of schizophrenia are ignored or not treated well.

Schizophrenia is usually treated with an individually tailored combination of therapy and medication.  Early treatment with ‘antipsychotic drugs’ , minimising the duration of untreated psychosis is the central to resolving unpleasant symptoms and social impairment. National Institute for health and clinical excellence guidelines recommend ‘atypical’ antipsychotics as first line of treatment ( i.e. Olanzapine (Zyperexa), Risperidone (Risperdal) and Quetiapine), although they are probably no more effective than the traditional dopamine blockers (e.g. Haloperidol, Chlorpromazine (Largactil or Thorazine)). Only Risperidone is available as a depot preparation and they vary in their sedating properties, weight gain and hyperglycaemia.

 These are examples of newer versions which are often referred as second-generation antipsychotics which can work quickly in comparison to other medication. You may only need antipsychotics until your acute schizophrenic episode has passed. Furthermore, besides the medication, psychological interventions are also important in treating schizophrenia. Psychological interventions are based on cognitive behavioural therapy (CBT), which for many patients can reduce the impact of hallucinations and delusional beliefs, the use of insight orientated psychoeducation for patients and carers and family work.

Relapse in schizophrenia seems closely associated with the level of the family’s emotional expression as measured by formal assessments of critical comments or expressed hostility in family interviews. Fashionable theories of causation in the 1960s which designated the ‘schizophrenogenic’ parent, have now been discarded. However, a close association between high arousal in the family and early relapse: this can be lowered by structured family education, reducing face to face contact via attendance at a day centre and formal family therapy.

In the past and still currently one of the most important idea was that the dopamine system expressively accounted for schizophrenic symptoms present in patients, by activation of the dopamine receptors. Also, the biological approach to treatment of schizophrenia consists of drug therapy by giving patients antipsychotic drug such as clozapine or haloperidol which will then target to block dopamine receptors. Using antipsychotics is only seen as effective in treating the positive symptoms (behaviour or thoughts, such as hallucinations or delusions), while having a limited effect on the negative symptoms (a withdrawal or lack of function that you would not usually expect to see in a healthy person; for example, people with schizophrenia often appear emotionless and flat) (Chavez et a..2009).

Some of the typical antipsychotic drugs causes side effects, such as tardive dyskinesia, and symptoms which includes unusual facial and body movements, these occur as a result of the blockage of D2 receptors (Remington, 2003; Horacek et al., 2006). Atypical antipsychotic drugs given in clinically effective dosages don’t give these side effects (Leucht et al., 1999; Seeman, 2002) because they don’t act directly on the dopamine receptors. Some studies have shown that atypical are effective on negative symptoms, cognitive dysfunction and aggression (Remington, 2003). Researchers have also said the real cause for this is that atypical antipsychotics such as clozapine have lower affinities for D2 receptors and bind loosely to the receptors when released (Horacek et al., 2006; Seeman, 2002), than antipsychotics such as haloperidol.

60-80% of D2 receptors are occupied by antipsychotic drugs in the brain of the patient. Whereas Clozapine and Quetiapine take about 0-50% (Seeman, 2002). Clozapine acts as partial agonists at glycine modulating site of NMDA, lower concentration increases depolarisation and higher concentration inhabits depolarisation which is why clozapine works better than others.

Antipsychotics affect glutamatergic activity in a lot go ways, such as improving the release of glutamate in the striatum, changing the density of glutamate and directly linking with BMDA receptors. New clinical trials show NMDA receptors activity improved by drugs affecting the glycine modulatory site of NMDA receptor which have shown decreased negative symptoms and improved cognitive function (Goff and Coyle, 2001).

Glutamatergic neuron is linked with limbic system, cortex and thalamus. These are implicated in schizophrenia. Therefore, some researchers proposed the idea pf glutamate system in treating schizophrenia. Diminished activation of NMDA receptors is because of schizophrenia. Psychosis models were induced in the cognitive deficits and negative symptoms are much better than the dopamine (Krystal et al., 1994; Hashimoto et al., 2003).

Haloperidol, synaptic plasticity is great to document the striatum with highest concentration of D2 receptors (Horacek et al,2006). It has also been shown in few studies that blockage of D2 receptors doesn’t reduce the symptoms of memory impairments, therefore, it has been advised that direct modulation of hyperactive NMDA by drugs may allow us to target microcircuits within the mesocratic, which cannot be accessed by D2 based treatments (Paz et al..,2008).

Acamprosate acts like a antagonist when the NMDA receptors are stimulated but acts as a agonist when the NMDA receptors stimulation is minimal. It has been predicted that this can enhance the functions of NMDA receptors in schizophrenia and improve cognition


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