Stresses for Trainee Counselling Psychologists | Review

Stresses for Trainee Counselling Psychologists | Review Title: A critical commentary on the following research paper: Kumary, A Martyn, B. (2008) Stresses reported by UK trainee counselling psychologists. Counselling Psychology Quarterly, March; 21:19-28 The prospect of entering any postgraduate training program can often be intimidating. Not only due to the academic commitment required, but because of the emotional demands and potential financial stranglehold placed on a student. These issues alone can leave trainees in both counselling and related psychological professions vulnerable to stress, which can not only damage the well-being of the student, but lower the overall quality of care experienced by patients when trainees are on placement (Cushway Tyler 1996; Kumary Baker 2008). Kumary Martyns make the simple argument, based loosely around Crushways (1992) study of UK clinical psychology trainees, that there are key aspects of training that impact on self-reported stress levels. These included poor supervision, financial costs, childcare, personal therapy and extra supervision. Some of these stressors identified cannot be thought of as essential or necessary aspects of training but this in itself is an area of key debate. (Kumary et al 2008). Other research has also highlighted the same key issues within counselling (Szymanska 2002), but has only looked at one issue in isolation and with this in mind, the present study was an investigation of UK counselling psychology trainees self-reports of their experiences of stress when training. One might go as far to question the rational of any study examining potential stress within such professions considering that having gone through an undergraduate degree already, students are already accustomed to a moderate l evel of stress and it simply goes with the territory (Cooper Quick 2003). On the other hand, such a study has never been conducted and may produce compelling results. Subjects were easy to identify and obtain although only UK counselling trainees who were studying for Part 1 of the BPS diploma were recruited. Are we to assume that this is when stress levels are at an optimal level? Questionnaires were sent out to all institutions. While the general characteristics of the sample are well represented, there was only a 41% return rate. This is good, but not outstanding in comparison to research conducted in similar domains, despite numerous follow-up e-mails and telephone calls (Robertson Sundstorm 1990). A financial incentive might have improved this return rate, but pre-paid return envelops were provided. However this data was collected in 2003, but not submitted for publication until 2007. Ethically, this delay in analysis and publication produces results that are already four years out of date in an education system that is constantly evolving (Hadley et al 1995). While such a simple methodology may initially seem sound, on closer inspection, the differences between the training programs of clinical and counselling are only glossed over and there is some evidence to suggest that the disparity between the two hinder a repetition of a seemingly straightforward approach last consulted in 1992 by Cushway. Aside from the time lapse, it is therefore important to consider the other issues surrounding the modification of a methodology previously used to investigate stress in clinical trainees. Firstly, counselling psychologist training tends to be less scientifically orientated than its clinical counterpart and most NHS posts are only open to Clinical Psychologists (Mayne, Norcross Sayette 2000). For example, it is generally accepted that counselling psychologists focus more on the therapeutic alliance with clients having to complete 450 hours of contact by the end of 3rd year training (Hadley et al 1995). While there are considerable similarities between the two disciplines, Norcorss (2000) documents many salient differences including professional activities, theoretical orientations, employment and training settings, graduate admissions and research areas. The question what are the differences in training clinical and counselling psychologists? -does not lend itself to an easy answer because psychology can be applied in so many ways. Traditionally, the main difference is in their training and perspective (Mayne et al 2000). It would appear to be an oversight on Kumary et als (2008) part to use a similar, modified methodology, previously applied to clinical trainees when the stress causing factors may be quite different. With these differences outlined in more detail, the old methodology would appear to require a more radical modification or adaptation from that used previously. Two main instruments were used to examine stress within the sample. The Counselling Psychology Trainee Stress Survey (CPTSS) and The General Health Questionnaire (GHQ12) (Wemeke, Goldberg Yalcin 2000). The CPTSS was developed from Cushways (1992) stress survey for clinical psychology trainees with four categories (academic stressors, placement stressors, organizational stressors and personal stressors). What is concerning is the lack of both research confirming the validity of the measure and the small brainstorm session using five trainees under those headings. Furthermore, from their discussion the CPTSS, constructed from 36 items, was only piloted on a further six trainees. This did lead to some changes being made with the authors settling on four descriptive categories slightly different from Cushways; academic demands, lack of support systems, placement stressors and personal and professional development. This displays neither convergent or discriminant validity. Finally, despi te other more valid forms of questionnaires available measuring stress (for example the Psychological Stress Measure (PMS), this study chose one which was quickly devised from a brief investigation and remains untested in the general population (Lemyre Tessier 2003; Trovato et al 2006). The General Health Questionnaire (GHQ12) on the other hand has been specifically validated for use in non-psychotic populations (Wemeke et al 2000). Because it is a shortened, 12-item version of the GHQ, it allows for quick completion, is likely to increase participant response, is quick to code and statistical mistakes also become less likely. For the purposes of this study, it appears to be the ideal choice and has been used to great effect in a large body of pervious work (Winefield, Goldney, Winefield, Tiggemann 1989; Vaglum Falkum 1999; Quek, Low, Razack, Loh 2001). A recent review by Jackson (2007) however, pointed out that the 28 item is usually used because the GHQ28 has been more widely used in other working populations, which allows for better comparisons, but the reliability coefficients have ranged from 0.78 to 0.95 in numerous studies and Jackson concludes (2007, p. 57) that: ‘In using this tool with postgraduate students conducting research in many areas of occupational health, the GHQ rarely fails to provide reliable and effective measures of well-being that usually correlate very highly with other measures of working environments or organizations Regardless of how carefully survey data is collected and analyzed, the value of the final result depends on the truthfulness of the respondents answers to the questions asked. Over the last twenty years, researchers have debated extensively about the truthfulness of peoples self-reports, and no clear cut conclusion has emerged (Zechmeister, Zechmesiter, Shaughnessy 2001). If someone is asked whether or not they enjoyed their bath, there is generally no need to question whether this accurately reflects their real feelings. However, in everyday life there are some situations in which researchers should have reason to be suspect. Survey research involves reactive measurement because respondents know that their responses are being recorded. Pressures may be strong for people to respond as they think they should rather than what they actually feel or believe (Zechmeister et al 2001). The term used to describe theses pressures is social desirability and in Kumary Martyns study (2008) the se issues are present in their entirety (Zechmeister et al 2001). For example, a trainee counselling psychologists attitudes towards their own stress and health levels, may be a far cry from their actual stressful behavioural responses. Both the questioners administered rely solely on self report and this gives rise to some further criticism. The approach is straightforward, but there is a trade-off between allowing for a simple analysis and the complex use of questionnaires in any survey based study. It is a fine balance that is difficult to maintain. Self-report questionnaires are all answered at different times and in different locations by each subject. As a result, the measures are vulnerable to inaccuracies caused by confounding variables. For example, a trainee filling in a stress based measure might have just had a particularly stressful day or experience that will effect their score. They could even have exams in a few weeks. Alternatively, reporting the issue of time-management and stress may be meaningless when the respondent evidently has time to sit down and take part in such a study anyway. The results from any self report also lack directness. While there is no ideal direct measure of stress, it is possible to get a better indication by measuring some of the physiological effects in the body. For example, stress might be better measured via heart rate, blood pressure, breathing rate, brain waves, muscle tension, skin conductance or temperature (Lemyre et al 2003). While more costly, such a study could be replicated using skin conductance monitors, worn by trainee counselling psychologists and correlate daily activities with any changes. This might produce results documenting what aspects of the course give rise to more stress and allow for re-development and changes to be applied where necessary. A more elementary approach might be to use an electronic pager device which asks every hour, how stressed are you now and what are your currently doing? In summary, researchers and clinicians must be careful when adapting clinical tools and methodologies to assess stress. They were designed for pathological disorders and validated using clinical populations and so the statistical distributions are not normal (Trovato et al 2006). As Lemyre et al (2003, p. 1159) state: The concept of stress refers to a set of affective, cognitive, somatic and behavioral manifestations within the range of functional integrity Despite this, thirteen items from the CPTSS were identified as being the most stressful issues in the sample population (none came from lack of support), which were split into two groups. The first included practical issues of finding time, funds and suitable placements. One item was also linked with negotiating these three key areas and could have a subsequent impact on their social life. A second group comprised of more general postgraduate issues: academic pressure and professional socialization. In order to determine a basis for the four groupings within the 37 single items of the CPTSS they were employed as four sub-scales (academic, placement, PPD and lack of support). These also gave acceptable levels of reliability. (Kumary et al 2008). The authors also found some good evidence for demographic variants in stress, with significantly higher stress ratings reported by younger participants and lower for those who were older. The GHQ12 results were in two scoring forms casesness and extend of distress with 54 participants identified as cases had significantly higher CPTSS scores than the 39 non-cases. Key findings from Kumary et al (2008, p. 24) included: The higher the stress rated for an aspect of counselling psychology training, the clearer the indicators of psychiatric distress became older participants had lower CPTSS ratings especially on placement issues men reported lower CPTSS ratings, most notably on academic items The support items attracted less attribution in comparison to academic, placement and PPD issues, despite pilot discussions (Kumary et al 2008), suggesting again that the methodology behind this study was flawed from the start. This does to some extent mirror Cushways (1992) data in that support was viewed by participants as a resource to ease training-induced stress, and participants viewed it as a resource to be used rather than a cause of stress because it was insufficiently provided. Again, with this knowledge available at the outset, why was the same methodology used? At this point, one might mention the issue of correlation and how this does not imply causation, but no profile of a stressed student was possible because most of the results were not significant. The authors admit themselves that the data collected is nothing to be proud of (2008, p. 25). It is difficult to believe that Krumary et al (2008) did not clearly see the unsophisticated and non-standardized status of the CPTSS as a serious issue before conducting such a study particularly when compared with more experimental research methods (Lemyre et al 2003). It is possible that the measures used were not sensitive enough to pick up on individual stress differences between participants. The fact remains however, that the fundamental assumptions were wrong and the question remains, do trainees in professions such as clinical and counselling psychology experience more stress than those within the normal population and if so are such emotional demands a critical part of training? Should t rainees be exposed to unacceptable stress levels and their apparent resilience used as an assessment criterion of professional suitability? (Hadley Mitchell 1995) The basis of this study is not sound enough to warrant any overall generalizations within the target population. The approach was oversimplified at the expense of generalized, poor-quality results. In this sense, the study has contributed little to our knowledge into how trainee counselling psychologists experience stress. The lack of an original approach is a reminder of how academic journals vary in the quality of the research they publish. It is nevertheless important that it was published to illustrate a methodology that clearly failed and thus prevents further repetition. This is the constant winding road of modern applied psychological research. References Cooper, L. C., Quick, C. J. (2003). The stress and loneliness of success. Counselling Psychology Quarterly, 16, 1-7 Cushway, D. (1992). Stress in clinical psychology trainees. British Journal of Clinical Psychology, 31, 169-179 Cushway, D., Tyler, P. (1996). Stress in clinical psychologists. British Journal of Clinical Psychologists, 31, 169-179 Goldberg DP, et al. (1978) Manual of the General Health Questionnaire (NFER Publishing, Windsor, England). Hadley Mitchell (1995). Counselling Research and Program Evaluation. London: Brooks/Cole Publishing Company Jackson, C. (2007). The General Health Questionnaire. Occupational Medicine, 57, 79 Kumary, A Martyn, B. (2008). Stresses reported by UK trainee counselling psychologists. Counselling Psychology Quarterly, 21,19-28 Lemyre, L., Tessier, R. (2003). Measuring psychological stress concept, model and measurement instrument in primary care research. Canadian Family Physician, 49, 1159-1160 Mayne, T. J., Norcross, J. C., Sayette, M. A. (2000). Insiders guide to graduate programs in clinical and counseling psychology (2000-2001 ed). New York: Guilford. Norcross C. J. (2000) Clinical Versus Counselling Psychology: Whats the Diff? Eye on Psi Chi, 5 (1), 20-22 Quek, F. K, Low, Y. W., Razack, H. A., Loh, S. C. (2001). Reliability and validity of the General Health Questionnaire (GHQ-12) among urological patents: A Malaysian study. Psychiatry and Clinical Neurosciences, 55 (5), 509-513 Robertson, M. T., Sundstrom, E. (1990). Questionnaire design, return rates, and response favorableness in an employee attitude questionnaire. Journal of Applied Psychology, 75 (3), 354-357 Szymanska, K. (2002). Trainee expectations in counselling psychology as compared to the reality of the training experience. Counselling Psychology Review, 17, 22-27 Trovato, M. G., Catalano, D., Martines, G. F., Spadaro, D., DI Corrado, D., Crispi, V., Garufi, G., Nuovo, S. (2006). Psychological stress measure in type 2 diabetes. European Review for Medical and Pharmacological Sciences, 10, 69-74 Vaglum, P., Falkum, E. (1999). Self-criticism, dependency and depressive symptoms in a nationwide sample of Norwegian physicians. Journal of Affective Disorders, 52 (1-3), 153-159 Wemeke, U., Goldberg, D., Yalcin, I. (2000). The stability of the factor structure of the General Health Questionaire. Psychological Medicine, 30, 823-829 Winefield, R. H., Goldney, D. R., Winefield, H. A., Tiggemann, M. (1989) The General Health Questionnaire: Reliability and Validity For Australian Youth. Australian and New Zealand Journal of Psychiatry, 23 (1), 53-58 Zechmeister, S. J., Zechmesiter, B. E., Shaughnessy, J. J. (2001). Essentials of Research Methods in Psychology, McGraw-Hill Higher Education Schizophrenia: the biological and psychological effect Schizophrenia: the biological and psychological effect The study of psychosis has been much published within the literature. Investigations into the biological, psychological and clinical aspects of the disorder have been greatly seen. An approach which views schizophrenia as a disturbance of information processing appears promising as a way of linking all of the aspects of the disorder. A review of the research in this area led to the suggestion that the basic disturbance in schizophrenia is a weakening of the influences of stored memories of regularities of previous input on current perception. It is argued that the link between information processing disturbances and biological abnormalities may be facilitated by the use of paradigms derived from animal learning theory (latent inhibition and Kamins blocking effect). In a number of animal model studies and indeed human subject studies, on an individuals pattern of performance in acute schizophrenics, the information gained is consistent with the cognitive model. The ways in which such an information-processing disturbance may lead to schizophrenic symptomatology will thus be outlined, with particular reference to the formation and maintenance of delusional beliefs. The core cognitive abnormality may result from a disturbance in any of the brain structures involved in the prediction of subsequent sensory input. The proposed circuit implicates in particular the hippocampus and related areas and is consistent with studies of brain pathology in schizophrenia. Thus, this paper will aim to provide an insight into the biological and psychological effects of schizophrenia and will give an insight into the current treatments available and their effects on the individual and their biological status. Introduction Understanding the varied presentation of the many types of psychotic disorders is still a major challenge within todays scientific capacity. The approaches utilized to clarify their complex nature of such disorders of the neurological system present an ongoing challenge, due to the complexity of the interaction between both biological entities (the brain) and the psychological effects. Thus, the aim of this paper is to review the evolution of our understanding of schizophrenia in terms of the biological and psychological effects of the disorder, based upon a review of the literature findings. Studies, which have been conducted regarding the life-long evolution of mental illnesses, especially schizophrenia, have been publicized for decades and this has managed to initiate the early standing of schizophrenia and of the nature of its chronic states. These experiences have further contributed to the views we hold today regarding the illness, leading in a third phase to the development of a biological-psychosocial model of its evolution which has proved useful for both theoretical and practical purposes. Finally, an understanding of therapeutic experiences and theoretical explorations based on the biological and psychological has helped to minimize the effects of the disease within the patient population. Biological basis of schizophrenia Across the findings within the literature, the question of whether schizophrenia is associated with structural or functional abnormalities of the nervous system, or both, appears to have become the principal focus in many of the biological studies of schizophrenia. A number of different methods of investigation of this system have been conducted including computed tomography studies, which have been able to reveal ventricular enlargement and cortical atrophy in a subgroup of schizophrenic patients. When such enlargement is found within the brain of the majority of patients in the early stages of the illness, they appear to be most severe in patients with negative symptoms and poor outcome. Quantitative neuropathological studies have tentatively demonstrated decreased volume of specific brain areas, neuronal loss, and other changes in the limbic system, basal ganglia, and frontal cortex. Dopamine (DA) remains the neurotransmitter most likely to be involved in schizophrenia, although t here is also evidence for disturbances of serotonin and norepinephrine. Post-mortem and positron emission tomographic studies suggest an increased number of D2 DA receptors in some schizophrenics. Neuroendocrine studies reinforce the role of DA in schizophrenics. Viral infections and autoimmune disturbances may be responsible for some types of schizophrenia, but there is no firm experimental evidence to support either hypothesis. The possibility that mixtures of structural abnormalities and functional changes involving DA occur in the same patients rather than independently as part of two syndromes (Type I, II) seems attractive. The symptoms of schizophrenia patients appear to be diverse, with different elements of the disease having different impacts on different individuals. Since Bleulers (1950) conception of the schizophrenias as a heterogenous disease composed of symptomaticlly different subgroups, attempts have been made to identify biological correlates of specific behavioral dysfunction. Diagnosis of the illness could be seen to have been fraught with difficulties. The initial lack of differentiation between the manic episodes of bipolar affective disorder and schizophrenia still presents as being greatly problematic within studies published within the literature, and subsequent attempts to differentiate between subgroups of schizophrenics have yielded no discrete classification system. The search for an etiology has also been bedeviled by this lack of distinct classification. Nevertheless, the publication of and the conduction of a number of biological theories have contributed to an understanding o f schizophrenia by identifying specific dysfunctional neural areas in determining biochemical changes associated with symptomatology and in formulating new etiological hypotheses. Neurological correlation between neurological studies and the effects of schizophrenia have been examined by research conducted through the use of magnetic resonance imaging, computed and positron emission tomography, and, also postmortem morphological changes (Koning et al, 2010). Studies of cognitive function in association with metabolic and cerebrovascular activity have contributed to the identification of discrete neural dysfunction. In addition, development of the dopamine theory and its relationship to positive symptoms has assisted in diagnostic differentiation, while recent studies on the modulatory role of neuropeptides on neurotransmitters have expanded the scope of the dopamine theory. Several biological theories have been proposed for an etiology of schizophrenia. (Krabbendam et al, 2004) Perinatal complications and viral infection have been suggested either in isolation or in conjunction with genetic factors. Low birth weight has also been proposed as a predisposing or associated factor in the subsequent development of schizophrenia. The viral hypothesis has received impetus from recent research into retroviruses capable of genetic transmission and causing latent disease onset. It is also recognized that factors other than biological, in particular, Psychosocial influences may play an etiological role in schizophrenia. Discussion of these factors, however, will not be discussed in great detail in this paper due to time restrictions. The difficulty of diagnosis As etiological studies rely to a large extent on accurate diagnosis, it is important initially to identify diagnostic problems because this aids an understanding between the interplay between biological and psychological effects, which can be noted in schizophrenics. It has long been recognized that the term schizophrenia incorporates a heterogeneous collection of subgroups, possibly with different etiologies, disease processes, and outcomes. The subsequent categorization of such patients into meaningful groups therefore relies upon differences in symptomatology and long term outcome, and fall broadly into three categories- paranoid versus nonparanoid, negative versus positive, and chronic versus acute (Goldstein Tsuang, 1988) The literature proposes that paranoid groups show a better premorbid adjustment, cognitive performance, and prognosis than the nonparanoid group (Kumra and Schulz, 2008), it has been suggested that this represents a measurement artifact and depends on whether absolute or relative measures of paranoia are used. Studies using absolute predominance measures to the exclusion of other symptoms reject many subjects displaying both sets of symptoms. Many nonpredominance studies show no differences between the groups of an increase in negative outcome as paranoid symptoms increase. Other researchers have proposed that schizophrenics could be categorized into two types placed into their category upon the basis of positive or negative symptom preponderence. Type I, or the positive symptom group, display some of the Schneiderian first rank symptoms of hallucinations and delusions, while Type 2, or the negative symptom group, show affective loss or extinction, speech content poverty, psychomotor deficits, and a general loss of drive or will. One of the problems with this categorization is that many schizophrenics display both sets of symptoms and that schizophrenics with primary positive symptoms often develop negative symptoms over time (Phillips and Silverstein, 2003). This would mean that studies using young subjects showing predominantly Positive symptoms may not be adequately differentiating between groups. Recent refinements of the positive/negative dichotomy have led to a redefinition of negative symptoms congruent with familial genetic factors, developmental dys- function, and the development of psychometric scales to measure relative symptomatology (Pickett-Schnenk et al, 2006). However, the influence of neuroleptic drugs on attentional and extrapyramidal functioning could also contribute to the development of differential symptoms. Furthermore, the effects of early environmental factors, such as perinatal trauma and familial environment, and of concurrent disorders, such as depression, are not adequately taken into account in such studies. Thus, this highlights the difficulties, which can be seen when trying to relate the biological and psychological effects of schizophrenia to a certain pathological aspect of brain development. Within the Diagnostic and Statistical Manual of Mental Disorders (DSM-III-R; APA, 1987) chronicity is defined as persistence of disturbance for more than two years with further residual diagnosis if subsequent symptoms are primarily negative. It is assumed to be associated with negative symptoms within Crows typography (Crow, 1980). This classification is the most common in the literature because of its basis in psychiatric diagnosis and its relationship to poor prognosis and to biological and cognitive deficits. For the purpose of biological research, the argument appears to be somewhat circular however because, for example, research attempts to find biological correlates of subgroups that are often operationally defined by their biological correlates. Moreover, there is significant overlap between the two groups in that many initially acute schizophrenics subsequently become chronic (by definition). While researchers across the literature publications acknowledge the heterogeneity of the disease, they continue to rely operationally on a dichotomous diagnosis. Multiple research strategies on the same subgroup would assist in isolating behavioural and biological attributions and in refining diagnostic criteria. Biochemical research and the impact on our understanding of the effects of schizophrenia Disruptions of neural biochemical processes have been extrapolated both from the effects of psychomimetic drugs and from the actions of symptom-reducing neuroleptic drugs. Drugs such as amphetamine and L-dopa, which cause psychotic conditions (e.g., hallucinations and paranoia), are known to involve excesses of dopamine release (Goodwin, 1972). Although different classes of neuroleptics are known to block acetylcholine, noradrenaline, or serotinin transmission, all of them block dopamine, and symptom reduction is thought to emanate from the latter (Millar et al, 2001). Within the dopamine theory two models of dysfunction have been proposed: autoreceptor excess, and postsynaptic receptor mechanism deficit. Different classes of neuroleptics vary in whether action is pre- or postsynaptic, but an inhibition of dopamine transmission is effected by all classes. Two classes of dopamine receptors have been identified-D1 and DP as previously mentioned, and it is believed that they are related to schizophrenia and neuroleptic effects. Distinctions between the two are based upon their actions on adenylate cyclase: stimulatory for Dl and distinct or inhibitory for D2 (Murray et al, 2008). Dl neurons, which project from the substantia nigra to the corpus striatum, are implicated in Parkinsons disease. Inhibition of Dl receptors is believed to be the origin of neuroleptic side effects, such as tardive dyskinesia and parkinsonianism. D2 receptors are associated with the antipsychotic effects of neuroleptic drugs and form the mesolimbic dopamine system which projects to the frontal cortex and some limbic forebrain structures (Tseng et al, 2008). The proposition that schizophrenic symptoms are caused by an excess of D2 receptors was initially difficult to substantiate due to drug effects and disease process. In most postmortem studies showing higher densities of dopamine receptors, previous antipsychotic drug use is also implicated (Seeman, 1986). However, in several studies subjects had never been treated with neuroleptics and still evinced increased dopamine receptor density (Trower et al, 2004). The role of dopamine receptor anomalies has also been studied using differential effects of classes of neuroleptics on dopamine receptors. In vivo Positron Emission Tomography (PET) research using the ligand [Cl raclopride has indicated that diverse classes of neuroleptic drugs administered in clinically effective doses block D2 dopamine receptors in the putamen. suggesting increased D2 dopamine density in schizophrenic subjects (Thompson et al, 2001). Research on the role of the atypical neuroleptic, clozapine, on dopamine receptors has however yielded inconsistent results. It is thought that the relative absence of extrapyramidal side effects with clozapine administration is due to a selective effect on D2 dopamine activity in the ventral tegmental area and nucleus accumbens but not in the substantia nigra or striatum. Haloperidol, on the other hand, reduces dopamine activity in both areas. The effects of both drug classes have been observed in rats using in vivo extracellular sing le-unit recordings (Tseng et al, 2009). However, clozapine also acts antagonistically on cholinergic, a-adrenergic, his- tamine, and serotonin receptors and, in addition, the combination of haloperidol with the a-noradrenergic antagonist, prazosin, produces similar effects to clozapine administration, namely, reduced basal dopamine release in the striatum but not in the nucleus accumbens (Thimm et al, 2010). Studies on cerebrospinal fluid (CSF) levels of prolactin following clozapine administration have also yielded inconsistent reslults. Prolactin release is inhibited by dopamine and increased by conventional neuroleptics. However, in at least one study it has been found that administration of clozapine to human schizophrenic subjects produced no significant increase in prolactin levels 11 hours after administration, despite moderate to marked therapeutic effects (Meltzer, Goode, Schyve, Young, Fang, 1979). Several recent studies have also implicated Dl receptor blocks in the therapeutic effects of clozapine. A further obstacle to the initial acceptance of the dopamine theory has been the time discrepancy between drug administration and antipsychotic symptomatic effects. PET studies have shown immediate binding to dopamine receptor sites, yet their clinical effect is often delayed for several weeks (Tarrier et al, 1999). There have been suggestions that receptors blocks produce an initial overactivity of dopamine release to compensate for inhibition. Further evidence for the dopamine theory has come from measurements of CSF, and plasma levels of the dopamine metabolite, homovanillic acid (HVA). Although findings in unmedicated patients have not yielded consistent differences in HVA levels between schizophrenics and controls, neuroleptic treatment increases HVA levels (Abubaker et al, 2008). In unmedicated patients, a correlation between low HVA levels and cortical atrophy and ventricular enlargement has been found in at least one study. This has led to the suggestion that dopamine excess is related to Type 1 schizophrenia, an interpretation which is supported by a good response to neuroleptic drugs in this group (Crow, 1985). In addition, Allen et al (2008) has suggested a possible deficiency of dopamine in Type 2 schizophrenics. However, the Type l-Type 2 typography has not been fully supported, and there is evidence that neuroleptic drugs elicit response in negative symptom sufferers (Allen et al, 2008). From the evidence there is little doubt of the biological role of dopamine within some forms of schizophrenia. The influence of serotonin in schizophrenia was suggested by the antagonistic activity of the psychomimetic drug, D-lysergic acid diethylamide (LSD), on serotonin transmission (Addinton and Addington, 1993). This has been studied in CSF by measuring levels of the serotonin precuresor, tryptophan, and the metabolite 5- hydroxyindole acetic acid (5-HIAA). At least one study has found reduced levels of 5-HIAA in schizophrenics and no difference between those on and off neuroleptics, but the latter group had only been drug free for a short time (three weeks). Therefore residual effects cannot be discounted. It was not stated whether subjects were also suffering from depression, which is known to decrease serotonin levels (Akbarian and Huang, 2009). Neither increasing nor decreasing serotonin levels have had a beneficial effect on schizophrenic symptoms (Akbarian and Huang, 2009). Monoamine oxidase (MAO) metabolizes dopamine, serotonin, and noradrenaline, as well as endogenous stimulants or hallucinogens such as phenylethylamine and diethltryptamine. It has therefore been hypothesized that decreased MAO activity could be contributory to schizophrenia. Studies have been conducted into platelet MAO activity in schizophrenics with varying results. Meltzer and Arora (1980) found that decreased MAO platelet activity was positively correlated with paraniod and positive symptoms. Other studies have found no un- usual MAO platelet activity in paranoid or hallucinating schizophrenics (Arts et al, 2008) Recent research has also considered the role of neuro-peptides in modulating CNS functions and the possible implications for schizophrenic symptomatology. Endorphins have been the subject of the most intensive study because of their association to proposed neural deficit areas both in biochemical and neuropathlogical research. The B, y, and (Y endorphins originate in the basal hypothalamus and modulate neurotransmitter activity in several structures of the limbic system and brain stem. Of all the biochemical theories of schizophrenia, the dopamine hypothesis has been the most consistently substantiated in research. The implication of other neurotransmitters, however, suggests a possible diffuse dysfunction with dopamine eliciting the most severe disruption. Efforts have been made to control for medication, but residual drug effects cannot be discounted. Many studies now use chlorpromazine equivalents to control for the effects of varying medication levels. The problem with this method is that, although different classes of neuroleptics all reduce dopamine levels either pre- or postsynaptically, they do not have equivalent effects on serotonin, MAO, or noradrenalin. Further problems are encountered when attempts are made to ascribe an etiological function to neurotransmitter activity. It is equally probable that any such changes are caused by the disease process rather than their being causal. Structual brain abnormalities The neuropathology of schizophrenia has received considerable recent interest in the light of positron emmission tomography (PET), postmortem, cognitive function and cerebral blood flow (CBF) research. While PET scans and postmortem investigation have concentrated on structural measurements, cognitive studies have provided tacit support for such structural changes. It has been hypothosized that neuropathological abnormalities identified in subgroups of schizophrenics could be in vitro developmental disorders either genetically transmitted or resulting from prenatal trauma (Ashburner et al, 2008). The most consistent findings across the publications within the literature have been differences in ventricular size, in some sections of the temporal limbic and nigrostriatal systems and basal ganglia, and in the prefrontal cortex. Measurements of ventricular size have however, shown considerable inconsistency, with some studies finding no significant difference between subjects and non-schizophrenic controls (Bles et al, 2010), and some reporting significant differences between chronic paranoid and hebephrenic subjects and normal controls (Bales et al, 2010). Evidence to date suggests that ventricular enlargement is only salient for a small subgroup of schizophrenics subject to chronicity or other, as yet unidentified, factors. Inconsistency in the results could be due to deviations in subject samples. It has been proposed that atrophy of specific neural areas could account for some schizophrenic symptoms. While some evidence has come directly from postmortem studies. Abnormalities have also been inferred from the results of PET and CAT scans and CBF measurements performed in conjunction with cognitive tasks designed to activate specific neural areas. Postmortem studies have identified significant cortical atrophy in the lateral nigro-striatal area (Birchwood et al, 2004) and in the limbic portions of the temporal lobe, specifically the amygdala, hippocampus, and parahippocampal gyrus (Birchwood et al, 2004). Psychotherapies and social treatments The psychological effects and impacts of schizophrenia must be emphasized. Due to the impact of the different, aforementioned parts of the brain and the CNS in schizophrenia, the psychological impact of the disease is obviously one, which takes great effect as previously mentioned. Psychotherapies are thought to be important within the current treatment lines in schizophrenia and although antipsychotic medications are the mainstay of treatment for schizophrenia, pharmacotherapy alone produces only limited improvement in negative symptoms, cognitive function, social functioning and quality of life. Additionally, it has been found that a great number of patients continue to suffer from persistent positive symptoms and relapses particularly when they fail to adhere to prescribed medications. This underlines the need for multi-modal care including psychosocial therapies as adjuncts to antipsychotic medications to help alleviate symptoms and to improve adherence, social functioning and qu ality of life (Patterson and Leeuwenkamp, 20008). A short review of the evidence that has accumulated on the efficacy of the major modalities of psychosocial treatment highlights that treatments involving social skills training, psychoeducation and cognitive behavioural therapies (CBTs) can all have a role in the treatment of individuals with schizophrenia. The reasoning behind the success of each treatment can give guidance into the psychological effects of the disease. For example, Psychoeducational interventions provide information about the disorder and its treatment to patients and their family members, and additionally inform the patients and family members about strategies to cope with schizophrenic illness. From the literature findings, it is evident that an extensive body of literature has accumulated regarding the efficacy of these interventions. Meta-analyses suggest that these interventions reduce high expressed emotion among relatives, and decrease relapse and rehospita lization rates (Pitschel et al, 2002; Giron et al, 2010). In general, interventions that include family members are found to have a much greater level of success (Pharaoh et al, 2006). Multi-family psychoeducation group approaches, which provide family psychoeducation and additionally offer an expanded social network, are found to reduce rates of relapse as are peer-to-peer education programs for families and patients (Chien et al, 2006). Cognitive Behavior Therapy (CBT) About a third of patients with schizophrenia continue to suffer from persistent psychotic symptoms despite adequate pharmacotherapy. Cognitive Behavior Therapy (CBT) has therefore been presented as a system of treatment which has emerged to address this need, and is based on the hypothesis that psychotic symptoms such as delusions and hallucinations stem from misinterpretations and irrational attributions caused by self-monitoring deficits. CBT seeks to help patients rationally appraise their experience of disease symptoms and how they respond to them, thereby reducing symptoms and preventing relapse (Turkington et al, 2008). Meta-analytic evaluations of this data have found CBT to be effective in ameliorating positive symptoms (Rector and Beck, 2001) although effect sizes of CBT have been noted to be inconsistent across studies and a recent meta-analysis of six blinded studies (Lynch et al, 2010) found CBT to be ineffective in reducing any symptoms of schizophrenia or in preventing relapse; the fairness of this analysis has been questioned (Kingdon et al, 2010). CBT is reported to be ineffective in targeting negative symptoms and its effects on other treatment domains are not well studied. Although CBT is recommended as a standard of care for persons with schizophrenia (NICE, 2009) the results are thought to give the best outcomes in patients who are willing to comply with treatment. Cognitive remediation A substantive proportion of schizophrenia patients have impaired cognition, particularly in the domains of psychomotor speed, attention, working memory and executive function, verbal learning and social cognition. These deficits are robust and persist during the illness, and serve as rate limiting factors for functional recovery (Tandon et al, 2009). Several cognitive remediation approaches have been developed over the past two decades which involve compensation strategies to organize information, use of environmental aids such as reminders and prompts, and a range of techniques designed to enhance executive function and social cognition (Eack et al, 2010). Earlier reviews and meta-analyses which have been presented and published within the literature findings have suggested that cognitive remediation leads to modest improvements in performance on neuropsychological tests but has limited generalization to functional outcomes (Pilling et al, 2002) One large meta-analysis published by McGurk et al, (2007), however, found that cognitive remediation was associated with significant improvements in cognitive performance and symptoms, as well as psychosocial functioning in schizophrenia. Cognitive remediation has been found to be more effective in studies that provided adjunctive psychiatric rehabilitation in addition to cognitive remediation. Thus, it appears to be the case that the durability of benefits of cognitive remediation are not yet set in stone. Social skills training (SST) Schizophrenia patients manifest deficits in social competence and these contribute to poor outcome. The goal of SST is to improve day-to-day living skills by focusing on components of social competence such as self-care, basic conversation, vocational skills, and recreation. These skills are practiced mostly in group settings using techniques based on operant and social learning theory. Historically, token economy was the first such intervention that sought to improve the social behavior of patients with psychiatric illness. While effective, the results did not generalize beyond the therapeutic setting. A recent meta-analysis of randomized controlled trials of social skills training in schizophrenia showed a large effect size for improvement in skills, a moderate effect size for performance-based social and community skills and for community functioning, and a small effect size for symptoms and relapse (Kurts and Mueser, 2008) Conclusions Thus, in conclusion, and in review of the findings published within the literature, it si clear that the impact of both biological aspects of the disease and psychological impacts are prevalent within the schizophrenic population. In summary, research on psychosocial approaches to treatment of schizophrenia has yielded incremental evidence of efficacy of CBT, SST, family psychoeducation, ACT and supported employment. Relatively few rigorously conducted trials of psychosocial interventions have been reported in the early course of schizophrenia, a phase of the illness when effective interventions may yield long-term outcome benefits . More hypothesis-driven research is needed to examine active ingredients of the therapeutic modalities that work, to identify the synergistic effects of combinations of interventions, and to use the knowledge which we have gained from the biological impact of the disease and the understandings of the neurological circuitry and its implications in schizoph renia to aid the development of new methods of reducing the effects of schizophrenia on the patient population.