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A Perspective on Schizophrenia

Schizophrenia Risk Factors
Schizophrenia Risk Factors
Schizophrenia Risk Factors

A Perspective on Schizophrenia

I have a fascination in schizophrenia.  I work with people who have been diagnosed with schizophrenia and I see their struggles and difficulties.  This paper is an attempt to create a more cohesive framework in my understandings of the illness; my interactions with those I know and work with who deal with schizophrenia; and my practice as a clinician in helping those of my clients who suffer from it.  Because schizophrenia has a range of possible causes or contributing factors, as well as an historical context in terms of its diagnosis, I believe it is important to discuss some of the issues of diagnosis in an historical as well as a current day context; to consider aspects of epidemiology, aetiology and causal correlates in the onset of schizophrenia; and to discuss the long term prognosis of most of those who experience schizophrenia in their lives.  The opening section of this paper will deal with these aspects and be followed by a critical discussion of the various approaches involved in the treatment of schizophrenia, including aspects of and issues associated with evidence based treatment practices. 


1.  Diagnostic description, aetiology and prognosis of schizophrenia

Schizophrenia plays no favourites.  It is found in all cultures, all classes and all races.  It affects approximately one per cent of the world population.  It is a serious mental illness presenting with a range of symptoms and numerous levels of severity (Jones, Hacker, Cormac, Meaden, & Irving, 2012). 

Whilst its onset has been diagnosed across all age groups, early onset schizophrenia (or childhood onset before age 12) is considered extremely rare and a cause at times for diagnostic debate (Hollis & Rapoport, 2011).  Reviews of the literature would indicate onset as peaking over two separated “normal distributions, one with a mean and standard deviation at 19.91+/-3.56 years, and another with a mean and standard deviation at 33.48+/-8.2 years” (Jablensky, Kirkbride, & Jones, 2011, p. 199).  Generally speaking the onsets in men is greatest during the 20-24 year old period.  With women there is a lesser onset peak at this period but they experience a further moderate increase in ages over 35 years (Jablensky, Kirkbride, & Jones, 2011). 


1.1  Brief historical overview of the development of schizophrenia as a diagnosis


Schizophrenia has not always been known as “schizophrenia”.  Whilst “drawings in Sanskrit on cave walls suggest psychotic behaviors may date to 4,000 years ago” (Lake, 2012, p. 33); and whilst Hippocrates referred to “melancholia”, which was thought to be a consequence of an imbalance of the four humours (Miller, 2008) (see Figure 1), the use of the term “schizophrenia” as a definition of the illness we now know as such, was not used until 1911 when it was first introduced by Swiss psychiatrist, Eugene Bleuler (Miller, 2008).  Bleuler had coined the term in an effort to address and redefine earlier attempts to find a diagnostic terminology for the condition. 


Figure 1 - The four humors of Hippocrates


For some time many of what are currently considered the recognizable symptoms and subtypes of schizophrenia were variously seen as aspects of dementia, manic-depressive disorder, neurosis and psychosis.  Prior to Bleuler, in 1852, Bénédict Morel (1809-1873) had used the term “Démence Précoce” (premature dementia) to describe some of his younger patients with dementia like psychosis (Miller, 2008).  In addition, other subtypes of today’s schizophrenia were recognized and termed as the unique conditions – “hebephrenia” (disorganized schizophrenia) and “catatonia” (stupor and neurogenic lack of movement) by Ewald Hecker (1843-1909) and Karl Kahlbaum (1828-1899), respectively (Miller, 2008). 

Emil Kraepelin (1856-1926) used the latin form “dementia praecox” when he applied it to the understanding of a condition which sought to synthesize and unify the varying presentations of démence précoce; hebephrenia; and catatonia.  To this “umbrella” term for these three presentations, Eugene Bleuler, had also added a fourth subtype known as “simple schizophrenia” (Miller, 2008). 

It is to be noted that in the process of seeking a clear and specific definition and terminology for what we now refer to as schizophrenia a dichotomy arose between dementia praecox and manic-depressive illnesses.  Toward the end of his career, Kraepelin came to the conclusion that the dichotomy between the two, in terms of symptoms was not as great as he had initially proposed (Miller, 2008).  This still gives rise to some controversy concerning the diagnosis of schizophrenia as a separate and unique condition (Lake, 2012; Miller, 2008) and is worth keeping in mind when considering the overlaps and shifting nature of comorbid symptoms in presentation that may occur in clients. 


1.2  Schizophrenia in DSM-V

The fifth edition of the Diagnostic and statistical manual of mental disorders (DSM-5) (American Psychiatric Association, 2013a) has increased the symptomatic requirements from one in the previous DSM-IV TR (American Psychiatric Association, 2000), to at least two of the following Criterion A symptoms: delusions; hallucinations; disorganized speech; grossly disorganized or catatonic behavior; and negative symptoms (American Psychiatric Association, 2013b).  The DSM-5 also stipulates that at least one of the presenting issues must be delusions; hallucinations; or disorganized speech (American Psychiatric Association, 2013a).  There are no longer subtypes specified (such as paranoid type; disorganized type; or catatonic type (American Psychiatric Association, 2000)), but rather, some of these are now listed as “specifiers to help provide further detail in diagnosis” (American Psychiatric Association, 2013b, para. 3).  Persistence of disruption to major life areas (work, relationships, self-care, etc.  ) needs to occur for at least 6 months, including at least 1 month of Criterion A symptoms for a diagnosis to be arrived at (American Psychiatric Association, 2013a). 

Symptoms of schizophrenia are often defined in terms of those which “reflect an excess or distortion of normal functions” (American Psychiatric Association, 2000, p. 299) – the positive symptoms; and those which “appear to reflect a diminution or loss of normal functions” (American Psychiatric Association, 2000, p. 299) – the negative symptoms. 

All in all, schizophrenia is an incredibly complex illness, presenting in and often moving across a range of symptomatic manifestations with varying degrees of intensity. 

A diagnosis of schizophrenia tends to carry with it a level of social stigma, particularly in the association of violent behavior, contributed to greatly by misrepresentation and sensationalism in the media (Harper, 2005).  This stigma can often exacerbate the patient’s own concept of self and ability to deal with associated illness issues – the stigma and fear of others’ attitudes becomes an additional barrier to the client’s ability to engage in treatment process (W. Brownell, personal communication, 2013). 

When working with clients who have been diagnosed with schizophrenia, it becomes crucial to look beyond the stigma of the diagnosis and bracket out any preconceptions one may bring to the therapeutic relationship.  I have found it useful to keep in mind alternative arguments or diagnostic models to those encountered in the DSM-5, such as those presented by Lake in Schizophrenia is a misdiagnosis: Implications for the DSM-5 and the ICD-11 (2012), as well as the concepts of Neurodynamics and salience syndrome, introduced respectively by Miller and van Os in their works A neurodynamic theory of schizophrenia and related disorders (Miller, 2008), and “'Salience syndrome' replaces 'schizophrenia' in DSM-V and ICD-11: Psychiatry's evidence-based entry into the 21st century?” (van Os, 2009; see also Holt et al., 2006; Nishida et al., 2013; Pu et al., 2012). 


1.3  Schizophrenia and some correlates of its onset as an illness within the individual

There is no single organic causal factor currently known for schizophrenia.  The non-profit group,, states in their online article (, 2010) that “schizophrenia develops as a result of interplay between biological predisposition… and the kind of environment a person is exposed to” (para. 1). 

Whilst there are some recognized genetic and chromosomal correlates, and incidence of occurrence in a one’s family history is seen as increasing the possibility of onset, these cannot be determined as purely causal.  There is also a range of other biological, psychological and social correlates also present (, 2010; Sullivan, 2005; Weinberger & Harrison, eds., 2011).  This gives rise to the need to have knowledge of an individual’s past, present and potential future biopsychosocial factors in understanding and developing treatment methods when dealing with each specific client. 

Figure 2, below, gives an indication of some well-established risk factors for schizophrenia, with an odds ratio indication.  It is to be noted that most of these factors are to be understood as risk factors and not necessarily prodromal of onset of illness (an der Heiden & Häfner, 2011). 


Figure 2 - Comparison of a selected set of relatively well-established risk factors for schizophrenia, focusing mainly on pre- and antenatal factors (abbreviations: CNS=central nervous system; depr=depression; Rh=Rhesus) (Sullivan, 2005)


1.4  The long term prognosis for schizophrenia

Because of the varying nature of risk factors and influences in the onset and ongoing potential for relapse in those with schizophrenia, the prognostic outlook may vary greatly from one client to another.  For example, “long-lasting poor premorbid social and occupational functioning prior to first contact… have been shown to be a powerful predictor of an unfavorable course of schizophrenia” (an der Heiden & Häfner, 2011, p. 120).  Alcohol abuse and the use of illicit drugs, such as cannabis, are likely to increase the risk of relapse and frequency of hospital admissions (an der Heiden & Häfner, 2011).  There is also found to be a higher association with the incidence of both natural and unnatural causes of death amongst those diagnosed with schizophrenia, with suicide accounting for the majority of unnatural deaths (an der Heiden & Häfner, 2011). 

It would, however, be negligent to take a fatalistic attitude in the treatment of and prognostic determination for those with schizophrenia.  There are many available and developing effective treatments for schizophrenia covering a range of models, addressing various aspects of the biopsychosocial framework, with the result that “in contrast with the traditional view, schizophrenia now has a lifelong perspective” (an der Heiden & Häfner, 2011, p. 126). 

Some of these treatment and intervention methods are addressed in the following section. 


2.  Approaches for the treatment of schizophrenia

The various treatments of schizophrenia can be seen to fall into two major categories – physical and psychosocial – with the physical domain encompassing two sub-domains of non-pharmaceutical and pharmaceutical (or pharmacological) (Schizophrenia Research Institute, 2013).  The following sections introduce and discuss various aspects of this range of treatment options, with reference to evidence based practice and critical commentary of the application of some specific treatment methods. 


2.1  Physical treatments

Physical treatments for schizophrenia are either pharmacological or non-pharmacological in nature.  Non-pharmaceutical treatments include such interventions as acupuncture; electroconvulsive therapy (ECT); exercise therapy; repetitive trans-cranial magnetic stimulation (rTCM); and trans-cranial direct current stimulation.  On the other hand, pharmacological treatments encompass various types of medications and anti-psychotic drugs ranging in potency and side effects from placebo and vitamins for mild and short term cases through to 1st (‘typical’) and 2nd (‘atypical’) generation anti-psychotic medications (Schizophrenia Research Institute, 2013).  Whilst some people respond well to non-pharmaceutical treatments as well as pharmaceutical treatments not involving anti-psychotics (e.g. exercise therapy), particularly when intervention is early, others are treatment resistant.  There are also those respond in alarmingly negative ways to anti-psychotics and require constant refining of dosages or combinations of 2nd generation anti-psychotics with adjunct medications to control side effects and responses (Schizophrenia Research Institute, 2013). 

It is to be noted that whilst most 1st generation anti-psychotics have debilitating side effects such as dyskinesias and parkinsonism, the 2nd generation anti-psychotics are not without their issues, often having long term impact on weight, blood conditions, drowsiness and hypersalivation (Schizophrenia Research Institute, 2013). 

Most people today experiencing ongoing issues with psychosis associated with schizophrenia will be treated using 2nd generation anti-psychotics. 

In developing and designing research trials to determine the efficacy and effectiveness of one particular drug over another, a range of issues, both practical and ethical arise.  Because of the fluctuating nature of the illness of schizophrenia, compliance in trials can be difficult to obtain, as well as baseline consistency in the sample population.  In fact, the undetermined nature concerning the onset causes of schizophrenia is also a confounding factor in trying to maintain trial efficacy.  There are also ethical issues associated with research involving treatment versus non-treatment, so it becomes ethically imperative to design trials which compare one anti-psychotic treatment against another or others (Schizophrenia Research Institute, 2013). 

As a result, evidence may suggest that a particular pharmaceutical treatment is better (or worse) than another, but it cannot be easily determined whether either are better than none or combinations of treatments (physical and psychosocial).  This is particularly true in terms of long term outcomes or morbidities associated with side effects (Schizophrenia Research Institute, 2013; Weinberger & Harrison, eds., 2011). 

With this in mind, it is interesting to note that the evidence arising concerning effectiveness for various 2nd generation anti-psychotics has differing implications dependent on the specific outcome parameters.  This gives rise to the need to be mindful of the specific needs and desired outcomes of the client.  For example, there is high quality evidence that aripiprazole retains more patients in treatment compared to 1st generation anti-psychotics, but may be less effective compared to olanzapine in dealing with mental state.  At the same time there is more high quality evidence that olanzapine creates a greater likelihood of weight gain and associated co-morbidities (Schizophrenia Research Institute, 2013; Weinberger & Harrison, eds., 2011). 

Another specific example which occurs is the interaction between clozapine and nicotine, caffeine and alcohol.  Whilst alcohol can drastically increase levels of sleepiness in a person on clozapine, sudden changes in intakes of caffeine and cigarette smoking can change the effective amounts of clozapine in one’s bloodstream, which can result in over- or under- dosage.  Outcomes of this could be relapse and/or changes in white blood cell count - agranulocytosis and neutropenia (Clozaril clozapine patient monitoring service, 2010). 

It can soon be seen that because of some of the associated side effects and co-morbidities associated with various medications, but also, because of the effectiveness of anti-psychotics to control symptoms of schizophrenia, inclusion of a variety of complimentary physical forms of treatment would be a wise starting point.  The Schizophrenia Research Institute (2013) on its schizophrenia library site in its “Factsheet: Non-pharmaceutical treatment – Exercise therapies” has determined that there is moderate to low quality evidence suggesting that exercise may contribute to lower anxiety levels; better quality of life; and prevention of weight gain.  These are all important aspects to consider as complimentary in addressing some of the side effects of anti-psychotic drugs. 


2.2  Psychosocial Treatments

In addition to physical forms of treatment, there are some various levels of evidence for the effectiveness of a range of psychosocial treatments.  These include art and drama therapies; cognitive behavioural therapy (CBT); social skills training; and ‘token economies’ (Schizophrenia Research Institute, 2013). 

Whilst CBT appears to present the best quality evidence, this is associated mainly with specific reduction in positive schizophrenia symptoms (Dickerson & Lehman, 2011).  Findings as to its actual overall efficacy show that “it is not possible to assert any substantial benefit for cognitive behavioural therapy over other psychological therapies” (Jones, Hacker, Cormac, Meaden, & Irving, 2012, p. 30). 

There are many confounding factors in trying to develop an unbiased and objective evidence base for such treatments as CBT, including the logistics in designing randomization within a sample population which has a huge variation in degree of symptoms criteria and presentation; the difficulty in applying double-blind evaluations to such non-empirical interventions; and the high rate of drop out or withdrawal which is not always reflected well in outcome data (Jones, Hacker, Cormac, Meaden, & Irving, 2012).  Add to this the fact that ongoing access to subjects with schizophrenia can be problematic – exacerbated by the condition itself, and compounded by aspects of paranoia and delusion experienced by the subjects.  As a result trials of psychosocial treatments such as CBT are often biased by inadequate and limited access to viable test subjects, or subjects drawn from purely compliant and/or hospitalized subjects, thereby not necessarily providing a typical sample of the overall illness population (Vine, 2013). 


Figure 3 - Clinical illustration of the ABC model (Kingdon & Trukington, 2006)


Never-the-less, CBT is a popular and argued for method of psychosocial intervention.  A typical CBT method of working with a client with schizophrenia would follow a form of the ABC model, first developed by Ellis and Harper and presented in their text A guide to rational living (Ellis & Harper, 1961).  In this model the therapist would discuss Active events (A) and Consequences (C) of those events within the framework of the client’s Beliefs (B).  By questioning and rationalizing the beliefs that give rise to the client’s perceived consequences it is expected that the client is able to reframe their emotional and behavioural responses to the activating events (Kingdon & Turkington, 2006) (see Figure 3, below, for an example of the process). 

Given the evidence for the encouraging outcomes related to the treatment of positive schizophrenia symptoms, cognitive behavioural therapy would appear to be a useful tool for targeted use in therapy.  It is not surprising, due in part to the popularity of CBT, that many newer forms of psychosocial intervention find their basis in CBT, adapting and reforming it as subtle variations, nuanced evolutions and adjunctive components arise over time.  As a result, we find that there is a certain amount of overlapping and common aspects found in CBT and other therapies such as compliance therapy; acceptance and commitment therapy (ACT); supportive psychotherapy; and metacognitive training (Dickerson & Lehman, 2011).  Most of these therapies, however, are yet to develop a strong evidence base beyond current case studies and testimonials.  In particular the inclusion and addition of mindfulness practice as a result of strong scientific evidence, has changed the face of CBT and given rise to other forms of the intervention (Brown, Marquis, & Guiffrida, 2013). 

In closing this section, I would like to refer to one other interesting form of psychosocial therapy which implements aspects of CBT, but which is yet to produce a strong evidence base – the Hearing Voices Group (HVG) (Ruddle, Mason, & Wykes, 2011).  This is a targeted form of CBT aimed specifically at the distressing aspect of auditory hallucinations in the experience of many with schizophrenia.  In keeping with the idea of adaptation and variation HVGs variously employ aspects of CBT, mindfulness, skills-training and unstructured support groups (Ruddle, Mason, & Wykes, 2011). 



Given the complex nature of schizophrenia – its varying risk and contributing onset factors; the ongoing unpredictable, volatile and undulating nature of its symptomatic presentation; and the tenuous prognostic outlook depending on a finely tuned balance between all aspects and interactions of the client’s biopsychosocial environment within a phenomenological and existential dilemma of being (Lysaker & Lysaker, 2010) – I believe that there can be no singular, “one size fits all” treatment for schizophrenia.  Rather, I believe that the evidence points to the need for a personalized approach, structured to employ a range of treatment methods.  This requires implementation of a truly individualized and homogeneous biopsychosocial collection of interventions tailored to the specific history, experience and needs of the person experiencing schizophrenia – the customization, integration and application of relevant medical, psychological, family and social network interventions. 




American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders: DSM-IV-TR. Washington, DC: American Psychiatric Association.


American Psychiatric Association. (2013a). Diagnostic and statistical manual of mental disorders: DSM-5. (5th ed.). Washington, D.C.: American Psychiatric Association.


American Psychiatric Association. (2013b). Schizophrenia fact sheet. Retrieved October 15, 2013, from


Brown, A. P., Marquis, A., & Guiffrida, D. A. (2013). Mindfulness-based interventions in counseling. Journal of Counseling and Development, 91(1), 96-104.


Clozaril clozapine patient monitoring service. (2010). The clozaril patient handbook. South Staffordshire and Shropshire Healthcare. Retrieved October 3, 2013, from


an der Heiden, W., & Häfner, H. (2011). Course and outcome. In D. R. Weinberger & P. J. Harrison (Eds.), Schizophrenia (3rd ed., pp. 104-141). Chichester, West Sussex: Wiley-Blackwell.


Dickerson, F. B., & Lehman, A. F. (2011). Evidence-based psychotherapy for schizophrenia: 2011 update. The Journal of Nervous and Mental Disease, (199), 520-526.


Ellis, A., & Harper, R. A. (1961). A guide to rational living,. Englewood Cliffs, N. J.: Prentice-Hall.


Harper, S. (2005). Media, madness and misrepresentation: Critical reflections on anti-stigma discourse. European Journal of Communication, 20(4), 460-483. doi: 10.1177/0267323105058252


Hollis, C., & Rapoport, J. (2011). Child and adolescent schizophrenia. In D. R. Weinberger & P. J. Harrison (Eds.), Schizophrenia (3rd ed., pp. 24-46). Chichester, West Sussex: Wiley-Blackwell.


Holt, D., Titone, D., Long, L., Goff, D., Cather, C., Rauch, S., ... Kuperberg, G. (2006). The misattribution of salience in delusional patients with schizophrenia☆. Schizophrenia Research, 83(2-3), 247-256. doi: 10.1016/j.schres.2005.12.858


Jablensky, A., Kirkbride, J. B., & Jones, P. B. (2011). Schizophrenia: The epidemiological horizon. In D. R. Weinberger & P. J. Harrison (Eds.), Schizophrenia (3rd ed., pp. 185-225). Chichester, West Sussex: Wiley-Blackwell.


Jones, C., Hacker, D., Cormac, I., Meaden, A., & Irving, C. B. (2012). Cognitive behaviour therapy versus other psychosocial treatments for schizophrenia (Review). Cochrane Database of Systematic Reviews, (4), 1-167. doi: 10.1002/14651858.CD008712.pub2 Article number: CD008712


Kingdon, D., & Turkington, D. (2006, June 20). The ABCs of cognitive-behavioral therapy for schizophrenia. Psychiatric Times. Retrieved October 5, 2013, from


Lake, C. R. (2012). Schizophrenia is a misdiagnosis: Implications for the DSM-5 and the ICD-11. New York: Springer.


Lysaker, P. H., & Lysaker, J. T. (2010). Schizophrenia and alterations in self-experience: A comparison of 6 perspectives. Schizophrenia Bulletin, 36(2), 331-340. doi: 10.1093/schbul/sbn077


Miller, R. (2008). A neurodynamic theory of schizophrenia and related disorders. Morrisville, NC: Lulu.


Nishida, K., Morishima, Y., Yoshimura, M., Isotani, T., Irisawa, S., Jann, K., ... Koenig, T. (2013). EEG microstates associated with salience and frontoparietal networks in frontotemporal dementia, schizophrenia and Alzheimer's disease. Clinical Neurophysiology, (124), 1106-1114. doi:


Pu, W., Li, L., Zhang, H., Ouyang, X., Liu, H., Zhao, J., ... Wang, F. (2012). Morphological and functional abnormalities of salience network in the early-stage of paranoid schizophrenia. Schizophrenia Research, (141), 15-21. doi:


Ruddle, A., Mason, O., & Wykes, T. (2011). A review of hearing voices groups: Evidence and mechanisms of change. Clinical Psychology Review, (31), 757-766. doi: 10.1016/j.cpr.2011.03.010


Schizophrenia Research Institute. (2013). Treatments. Schizophrenia Research Library. Retrieved October 3, 2013, from (2010). Schizophrenia cause and prevention. Schizophrenia Cause and Prevention. Retrieved from


Sullivan, P. F. (2005, July 26). The genetics of schizophrenia. PLOS Medicine:. Retrieved October 12, 2013, from


van Os, J. (2009). 'Salience syndrome' replaces 'schizophrenia' in DSM-V and ICD-11: Psychiatry's evidence-based entry into the 21st century? Acta Psychiatrica Scandinavica, (120), 363-372. doi: 10.1111/j.1600-0447.2009.01456.x


Vine, R. (2013, November 1). The use and abuse of 'evidence-based' in mental health. Lecture presented at Evidence week 2013 in Royal Melbourne Hospital, Melbourne.


Weinberger, D. R., & Harrison, P. J. (Eds.). (2011). Schizophrenia (3rd ed.). Chichester, West Sussex: Wiley-Blackwell.


World Health Organisation. (1973). Report of the international pilot study of schizophrenia. Geneva: World Health Organisation. doi: