Aim of the Study
Review of the Literature
Conclusion & Recommendations.
First and foremost, thanks to ALLAH, whose magnificent help is the first factor in every thing we can do in our life.
I wish to express my indebtedness and my gratitude to the faculty of nursing Menoufyia University, for giving me the opportunity to pursues my post graduate studies.
I would like to express my deepest gratitude and sincere thanks to my Prof. Dr. Dalal Khalil Eshera Prof. of Nursing Education, Faculty of Nursing, Menoufyia University, for her sincere advices and remarkable comments made the accomplishment of this work possible. I am greatly appreciating her valuable suggestion and supervision.
I am especially grateful and specially indebted to Prof. Dr. Nefissa Mohamed Abd El-Kader Prof. of Mental Health Nursing and Director of Nursing Research and Development Center Faculty of Nursing, Cairo University, for her constructive keen supervision, fruitful criticism, continuous support and encouragement to complete this work. she sacrificed a good deal of his time for accomplishment of this work. I express my heartful thanks for submitting his effort and help to me, and for the time spent on overcoming any obstacle.
I am particularly Indebted to my Prof. Dr. El-Sayed Abd El Hamid Gad, Prof. & Chairman of Neuropsychiatric Department Faculty of Medicine, Tanta University, for his close observation, generous guidance, valuable supervision, and great support.
I am particularly Indebted to Dr Ahmed Gamal Abo El Azayem, consultant of Neuropsychiatry and Prof. Dr Samir Abo El Magid Professer of Neuropsychiatry, faculty of medicine, Cairo University, for their effort to offer their help and skills that made the completion of this work possible
My great thanks and gratitude to all members of nursing staff and patients at Tanta mental hospital for their cooperation and I would like to thank them for all what they have done to make the accomplishment of this work possible
I would like to express my sincerest gratitude to my family for their love, understanding and caring and to my Husband, my daughters for their encouragement love, support and sacrifices.
LIST OF FIGURES
Figure (1) : Range , mean and +SD of total improvement regarding dependent variables improvement in experimental group
Figure (2) : Range , mean and +SD of total improvement regarding dependent variables improvement in control group
Figure (3) : Differences between total mean and + SD of experimental and control groups regarding their improvement in study variables
Schizophrenia has significant impact on patient’s lifestyle due to its effect on patients’ cognition, perception, attention, physical function and their psychosocial skills. Cognitive behavioral therapy is a part of treatment modalities developed recently for treating schizophrenic patients. The cognitive behavioral therapy and psychosocial intervention in many studies proved its effectiveness in preventing relapse, improving coping skills, developing better social & vocational functioning and abilities to function more independently.
The aim of the present study was constructing a technique of cognitive behavioral therapy related to schizophrenic patients, implementing this program & finally evaluating its impact on patients’ developing more adaptive ways of thinking & behavior and ability to acquire social skills essential for social interactions & functioning.
The sample consisted of 40 schizophrenic patients from inpatient department of Tanta Mental Health Hospital, Ministry of Health. Five instruments were used to collect the data for the current study. Sociodemographic & personal characteristics sheet, Breif Psychiatry Rating Scale (Overall,& Gorham, 1962), Taylor Anxiety Manifest Scale (arabic copy translated by Ghaly & reviewed by Swiff 1962) ,the arabic version of Wechsler Adult Intelligence Scale (WAIS) developed by Mellika, (1990) and Observational Behavioral Assessment Sheet developed by (Omar, 1993)
After assessment the sample was classified into two group (experimental group) & (control group). A constructed cognitive behavioral intervention was developed by the researcher &implemented with experimental group on 24 sessions, twice weekly, 45-60 minutes for each.
Data were statistically analyzed &results revealed that there was a significant difference between experimental & control group regarding their reduction of psychotic symptoms, Anxiety level & information processing. In addition to increased abilities of experimental group in social skills acquisition. So, the study concludes the effectiveness of cognitive behavioral therapy in patients’ developing adaptive ways of thinking and the effectiveness of psychosocial skills training in developing abilities of schizophrenic patients to acquire skills & function independently. The study recommended that conducting in service training and educational programs for nurses on C.B.T. and developing centers for rehabilitation to meet the need of schizophrenic patients.
Key words: Schizophrenia, Patients, cognitive behavioral therapy, disorders, symptoms management.
Schizophrenia is a devastating illness marked by hallucinations, delusion, emotional withdrawal, and poor social functioning. Also, it comprises a group of behaviors whose prominent common features include retreat from reality, emotional blunting and disturbances in thinking these features vary in severity from patient to another. (Kane & Mc.Gllshan. 1995).
Schizophrenia originally meant “split diaphragm” because classical photospheres thought that mind was in the mid riff. A popular misconception is that schizophrenia is a split personality (Phrenos” means mind and Schiziph. Means split mind). Actually, split or multiple personality is a form of dissociation found among certain types of neurotics.
The mean age illness onset is in the mid-20s and fewer than 60% of patients achieve full symptoms remission (Shepherd, Watt, Falloon and Smeeton, 1989). Many patients with schizophrenia have residual psychotic symptoms and social disability that persist through their adult lives (Bustillo, Lauriello and Keith, 1999).
Schizophrenia treatment has been focused on anti-psychotic medications, which have been available since the mid-1950s. Psychotherapy continues to be practices that it is perceived to be of value to patients with schizophrenia (Coursey, Keller and Farrell, 1995). Research into the use of cognitive behavioral therapy (CBT) in schizophrenia have been increased significantly over the past 5 years. It suggested that cognitive behavioral therapy is an effective treatment using supportive techniques which concentrate on patients’ signs and symptoms and described as an essential component in the management of schizophrenic patients (Janes & Kane, 1996).
Over the last two decades, effective cognitive behavioral therapies (CBT) have been developed for depression and anxiety disorders (Beck, Rush, Shawand Emery, 1979; & Barlow, 1988). Recently there has been renewed interest in cognitive B.T, for more serious psychiatric disorders including severe depression (Scott, 1996; Scott and Wright, 1997), bipolar disorders (Basco and Rush, 1995; PerryTarrier, Morriss, McCarthy and Limb, 1999), and personality disorder (Beck & Freeman, 1990; Linehan., Armstrong, Suarez, Allmon and Heard, 1991). Building on earlier case reports, cognitive behavior therapies have also been developed for schizophrenia (Perris, 1989; Alford and Correia, 1994; Fowler, Garety and Kuipers 1995; Chadwick , Birchwood, and Townsend, 1996; Beck and Rector, 1998).
A major impetus for the CBT for schizophrenia includes the facts that ant psychotic medications lead to incomplete clinical improvement for many patients. When CBT applied to schizophrenia. It targets to replace psychotic symptoms (especially delusion and Hallucination) with more adaptive thoughts. The proponents of C.B.T. report significant success using this therapy because the basic premise of C.B.T is that perception, personal meaning and cognitive appraisal drive emotions (Wako field and Pallister, 1997, Townsend, 2000).
Besides theoretical strengths and positive outcome study data, proponents of C.B.T also under score cost effectiveness, shorten duration and packageability as advantages to its use with schizophrenic patients (Janson and Kane 1996 & Dickerson, 2000).
Abdel Kader, (1986), Said that nurses can help schizophrenic patients to develop independent living skills, adequacy in interpersonal relationship, and coping resources and thus help meet their needs. Furthermore, Boston & Farrell 1998 commented that nurses have become involved in psychological treatment approaches including psychotherapies and cognitive behavioral therapy. Nurses are among several disciplines increasingly trained in cognitive behavioral techniques in such cases, they act as primary therapist for patients with schizophrenia in both inpatient and outpatients. Settings. Also, the cost benefit of employing nurses as a behavioral therapist was calculated and it was found that people treated by nurses used fewer health care resources (Ginsberg and Manks, 1977).
Nurses faced with schizophrenic patients may have great difficulties in dealing with them that is because they exhibit marked disturbance in their cognition, perception, affect , behavior and socialization , therefore nurses can focus on close observation of patient’s behavior regularly monitor patients, perceived responses and feelings and adopt an accepting attitude toward the patients in order to allow them the security and freedom to examine all aspects concerning them as a total human being.
Furthermore, nurses can offer reassurance, maintain patients contact with reality and administer prescribed ant psychotic medications (Stuart & Sundeen, 1995; Gold, Teicher and Spelic 1998) fortunately over the past decade a number of effective treatment has been developed as well as various form of counseling approaches target schizophrenia including C.B.T. which become an increasingly important components of the nurses’ role and need to be more aggressively integrated into the role of psychiatric nurses that because they are the frontline provider of care, the group most often called to carry out selective reinforcement, modeling extinction skill training , shaping and role playing. Also, because they are indirect and consistent contact with patients, they are the best able to observe patients, assess problems area and recommend targets for cognitive behavioral interventions (Sturat,& Sundeen, 1995; Townsend, 2000).
Significance of the study:
Considering the importance of cognitive behavioral therapy as a cost-effective treatment with various forms of psychiatric illness, the devastating consequences precipitated by schizophrenia on individual, family and society added to the emphasis on psychiatric nurses’ role as a behavioral therapist and lack of local research about this therapy, are the main causes for conducting this study.
The conduct of this study will have a paramount effect on increasing nurses’ awareness, knowledge, and skills regarding this cost-effective treatment modality (cognitive behavioral therapy).
Therefore, it is important to study the impact of structural intervention of cognitive behavioral therapy on schizophrenic patients and evaluate its effectiveness as a treatment modality in changing the maladaptive thoughts and behaviors into adaptive ones.
AIM OF THE STUDY
The aims of the study are:
1- To construct a technique of cognitive behavioral therapy related to schizophrenic patients.
2- To implement the treatment intervention of cognitive behavioral therapy.
3- To evaluate the effectiveness of treatment intervention on changing the maladaptive thoughts and behaviors of schizophrenic patients into adaptive ones.
§ Assessing that patient are otherwise receiving adequate clinical care including antipsychotic mediations, the following research hypotheses were formulated to answer the research questions.
§ H1 Schizophrenic patients who will be subjected to the cognitive behavioral therapy intervention will develop adaptive ways of thinking more than the control group.
§ H2 Schizophrenic patients who will be subjected to the cognitive behavioral therapy intervention will develop adaptive ways of behaviors more than that of those who don’t participate (Control group)
§ H3 Schizophrenic patients who will subjected to psychosocial skill training can acquire the targeted social skills than other subjects (Control group).
REVIEW OF LITERATURE
The Historical view and Concept of Schizophrenia
An illness like schizophrenia has been variously described over the years. Falvet in 1851 called it Folie circulaire, Hecker in 1871 called it Hebephrenia, Kahlbaum in 1874 described Catatonia (a movement disorder) and Paranoia. Kraepelin in 1878 pulled the various concepts together into one disease entity which he termed Dementia praecox and said there were four types: simple, paranoid, hebephrenic and catatonic, depending on the clinical presentation. Simple dementia praecox involved a slow social decline, with apathy and withdrawal rather than florid psychotic symptoms - such people became drifters or tramps. Paranoid dementia praecox involved fear and systematized persecutory delusions. The Hebephrenic type was silly and facetious.
Catatonic patients were those with predominant motor symptoms - increased muscle tone, preservation of posture (patients could be manipulated like passive mannequins into unusual postures which they would maintain for hours), waxy flexibility, and fear. Despite their persistent immobility such catatonic patients were acutely aware of their surroundings. Before suitable pharmacological treatments arrived, unless the catatonic episode aborted spontaneously the patient would die through starvation, or thirst unless carefully nursed.
Bleuler, in 1908, criticized the use of the term dementia praecox, because he said that there was no global dementing process. He first used the term schizophrenia and said that there were four characteristics: blunted affect, loosening of associations , ambivalence and autism
These characteristics were called the 'fours A's'. blunted affect referred to a restricted range of affect, loosening of associations referred to the thought disorder present in schizophrenia, ambivalence, or an inability to make decisions was often seen in untreated cases while patients might hover for hours on the threshold of a doorway, uncertain whether to come in or go out (sometimes called impendence).
The four characteristics symptoms called autism referred, not to the childhood condition, but to a retreat into an inner world, incomprehensible to the outsider.
The four diagnostic criteria of Bleuler have been revised over the years. Kurt Schneider listed the so-called 'first rank features' of schizophrenia in 1959. One of these, in the absence of organic disease, persistent affective disorder, or drug intoxication, was sufficient for a diagnosis of schizophrenia. third person auditory hallucinations (running commentaries on the patient's actions or thoughts, or arguments about the patient) , thought echo [echo de la pensée], thoughts spoken out loud [gedankenlautwerden] , passivity phenomena (made actions, made emotions, made impulses) , thought insertion, withdrawal, broadcasting and delusional perception .
However, the criteria were criticized for being too narrow and only looking at a 'snapshot' of a patient at one point in time.
The current guidelines used are those of ICD-10 from 1992:
"A minimum requirement is one of the following symptoms: thought echo, insertion, withdrawal, broadcasting, passivity phenomena, delusional perception, third person hallucinations, and persistent delusions - all in clear consciousness.
Other symptoms used to make the diagnosis (2 must be present) include persistent hallucinations in any modality, thought blocking, thought disorder, catatonic behavior, negative symptoms and loss of social function."
Symptoms should have been present for at least one month. This emphasis on the form of the illness helps exclude patients with transient psychotic symptoms or signs. Affective disorder should have been excluded. Symptoms should be present in the absence of overt brain disease, drug use, or epilepsy (which can all mimic schizophrenia). ICD-10 lists the following types of paranoid, hebephrenic, catatonic, residual (a chronic state) and simple.
Disease definition, Natural History, and epidemiology:
A. Clinical features:
Schizophrenia is a major psychotic disorder. Its essential features consist of a mixture of characteristic signs and symptoms that have been present for a significant length of time during a 1-month period (or for a shorter time if successfully treated), with some signs of the disorder persisting for at least 6 months (A.P.A, 1994&2003). The symptoms involve multiple psychological processes, such as perception (hallucinations), ideation, reality testing (delusions), thought processes (loose associations), feeling (flatness, inappropriate affect), behavior (catatonia, disorganization), attention, concentration, motivation (a volition, impaired intention, and planning), and judgment. no single symptom is pathogenic of schizophrenia. These psychological and behavioral characteristics are associated with a variety of impairments in occupational or social functioning. Although there can be marked deterioration with impairments in multiple domains of functioning (e.g., learning, self-care working, interpersonal relationship, and living skills), the disorder is noted for great heterogeneity across individuals and variability within individuals over time. It is also associated with an increased incidence of general medical illness (Karasu, Waltzman, Lindenmayer, & Buckley,1980) & (A.P.A.2003) and mortality, especially from suicide, which occurs in up to 10% of patients (Dingman & McGlashan, 1986) (McGlashan ,1988). (Kaplan & Sadok, 1998; Carson, 2000)
The characteristic symptoms of schizophrenia have often been conceptualized as falling into two broad categories. Positive and negative (or deficit) symptoms? with a third category, disorganized, recently added because statistical analyses have revealed that it is a dimension independent of the positive symptom category, where it was previously included. The positive symptoms include delusions and hallucinations. Disorganized symptoms include disorganized speech (Docherty, DeRose,& Andreasen, 1996) (Townserd 2000; Carson 2000) thought disorder and disorganized behavior and poor attention. Negative symptoms include restricted range and intensity of emotional expression (affective flattening), reduced thought and speech productivity (a logia), anhedonia, and decreased initiation of goal directed behavior (a volition) (McGlashan,& Fenton ,1992) . (Kaplan &Sadok 1998 , AP.A, 2003)
According to DSM-IV, subtypes of schizophrenia are defined by the predominant symptoms at the time of the most recent evaluation and therefore may change over time. These subtypes include paranoid type, in which preoccupation with delusions or auditory hallucinations is prominent; disorganized type, in which disorganized speech and behavior and flat or inappropriate affect are prominent; catatonic type, in which characteristic motor symptoms are prominent; undifferentiated type, which is a nonspecific category used when none of the other subtype features are predominant; and residual type, where there is an absence of prominent positive symptoms by continuing evidence of disturbance (e.g., negative symptoms or positive symptoms in an attenuated form) (McGlashan, &Fenton, 1991) Although the prognostic and treatment implications of these subtype are variable. The disorganized type tends to be the most severe and the paranoid type to be the least severe ( Fenton,& McGlashan, 1991).
Other mental disorders and general medical conditions may be comobrid with schizophrenia. Along with general medical conditions, the most comorbid disorder appears to be substance use disorder, especially abuse of alcohol (Drake, Osher,& Wallach, 1989) and stimulants, such as cocaine and amphetamines (Brady, et.al 1990). Other commonly abused substances are nicotine, cannabis, and phencyclidine (PCP) ( Dixon, Haas, Wediden, Sweeney,& Frances, 1990) & (McGlashan, & krystal, 1995) . Such comorbidites can worsen the course and complicate treatment.(Test, Wallisch, Allness, & Ripp ,1989) & (Zisook, et.al ,1992). Symptoms of other mental disorders. Especially depression but also obsessive and compulsive symptoms, somatic concerns, dissociative symptoms, other mood or anxiety symptoms, may also be seen with schizophrenia. Whether they represent symptom or disorder levels of comorbidity, these features can significantly worsen prognosis (Fenton, & McGlashan, 1986) and often require specific attention and treatment planning. General medical conditions are often present, and individuals may be at special risk for those associated with poor self-care or institutionalization (e.g. tuberculosis), substance use (e.g., emphysema and other cigarette-related pathology, HIV- related disease), and antipsychotic-induced movement disorders. Some individuals with schizophrenia develop psychosis-induced polydipsia, which can lead to water intoxication and hyponatremia.
Furthermore, social dysfunction is a hall mark of schizophrenia. Indeed, impairment in social functioning is included as one of the defining diagnostic criteria for schizophrenia. In the DSM-IV (APA, 1994). So considerable attention is now being given to enhancement of social skills in their patients. (Towersend, 2000)
Maller, 1989 stated that behavioral disorders of schizophrenic are directly contributing to social changes include the inability to communicate coherently, loss of drive and interest, deterioration of social skills, personal hygiene and mistrust. In addition, direct social changes may be influenced by the patients poorly formed ego and body boundaries, and an inability to filter stimuli.
Chronic low self-esteem is a persistent problem for persons with chronic mental illness, they see themselves as ineffective and helpless; many are very much aware of their own deviance. Persons with chronic mental illness who experience small successes resist making further attempts for fear of failure (Lefley, 1987;Drew, 1991; Rawnsley, 1991 and Townsend , 2000)
Aksu, and Myers, (1994) found that when brain changes (possibly in the frontal area) occur so that the patient exhibits a lack of drive and motivation, this can also have social consequences. If a person is experiencing a preponderance of negative symptoms, he or she may lack the energy to nurture relationships. It takes a certain amount of energy to initiate activities with others and follow through with social or vocational commitments.
Shaheen, and El-Rakhawy, (1971) view that the basic manifestation in schizophrenia is the failure of communication which if established through defective use of a socially functioning language. This is a mechanism to avoid any relation with a threatening external reality. The patient starts to acquire a special code which is not understandable to others. A word may have a meaning to the patient different from its common meaning. A wall of seclusiveness is built gradually between the patient and reality.
As stated by El-Rakhawy, (1992); Kaplan and Sadock, (1994 and 1998) the patient may begin to feel perplexed at the onset of the disease.
The family and friends may eventually notice that the person has changed and is no longer functioning well in occupational, social, and personal activities.
B. Natural History and Course:
The onset of schizophrenia typically occurs during adolescence or early adulthood. It affects men and women with equal frequency. The peak age at onset for males, however, is the early 20s, and for women it is the late 20s and early 30s (McGlashan, 1988). The majority of patients alternate between acute psychotic episodes and stable phases with full or partial remission.
Inter-episode residual symptoms are common. This often-chronic illness can be characterized by three phases that merge into one another without absolute, clear boundaries between them. These phases form the structure for integrating treatment approaches.
- Acute phase. During this florid psychotic phase, patients exhibit severe psychotic symptoms, such as delusions and / or hallucinations and severely disorganized thinking and are usually unable to care for themselves appropriately. Negative symptoms often become more severe as well. (A.P.A.,2003)
- Stabilization phase. During this phase, acute psychotic symptoms decrease in severity. This phase may last for 6 or more months after the onset of an acute episode.
- Stable phase. Symptoms are relatively stable and, if present at all, are almost always less severe than in the acute phase, patients can be asymptomatic; others may manifest nonpsychotic symptoms, such as tension, anxiety, depression, or insomnia. When negative (deficit) symptoms and / or positive symptoms, such as delusions, hallucinations, or thought disorders, persist, they are often present in attenuated, nonpsychotic forms (e.g., circumstantiality rather than looseness, illusions rather than hallucinations, overvalued ideas rather than delusions). (A.P.A.,2003)
The onset of the first psychotic episode may be abrupt or insidious, but many individuals display some type of prodromal phase manifested by the slow and gradual development of a variety of signs and symptoms (e.g., social withdrawal, loss of interest in school or work, deterioration of hygiene and grooming, unusual behavior, outbursts of anger).
Eventually a symptoms characteristic of the active phase appears, marking the disturbance as schizophrenia. Before a patient in the stable phase replaces there is usually a prodromal period in which there may be nonpsychotic dysphoric symptoms, attenuated forms of positive symptoms or idiosyncratic behaviors. This prodromal period usually lasts for several days to a few weeks but may last for several months. (A.P.A, 2003)
Most longitudinal studies of schizophrenia suggest that its course is variable, with some individuals free of further episodes, the majority displaying exacerbation and remissions, and a small proportion remaining chronically severely psychotic (Bleuler ,(1978); (Huber, Gross, Schuttler,& Linz ,(1980); (Ciompi 1980) ( Tsuang, Woolson, Winokur, & Growe, (1981); (Harding, Brooks, Ashikaga, Strauss,& Breier (1987). Because of the differences in diagnostic criteria used in studies, an accurate and comprehensive summary of the long-term outcome of schizophrenia is not possible. Complete remission (i.e. a return to full premorbid functioning) is not common in the disorder. Of the patients who remain ill, some appear to have a relatively stable course, whereas others show a progressive worsening associated with severe disability. Early in the illness, negative symptoms may be prominent and apparent primarily as prodromal features. Subsequently, positive symptoms appear.
Because these positive symptoms are particularly responsive to treatment, they typically diminish, but in many individuals’ negative symptoms persist between episodes of positive symptoms. There is some suggestion that negative symptoms may become steadily more prominent in some individuals during the course of the illness (McGlashan,& Fenton, (1993) . There are some prognostic variables that are of value in predicting long term outcome. and example , better outcomes are associated, on average , with female gender, family history of affective disorders, absent family history of schizophrenia, good premorbid functioning , higher IQ, married marital status, acute onset with precipitating stress, fewer prior episodes (both number and length), a phasic pattern of episodes and remissions, advancing age, minimal comorbidity, paranoid subtype, and symptoms that are predominantly positive (delusions, hallucinations)( and not disorganized (thought disorders, disorganized behavior) or negative (flat affect, alogia, avolition) (Tsuang, Woolsaon, Winokuwer & Crowe (1981) ; (McGlashan, & Fenton (1991); Fenton & McGlashan (1991); & (McGlashan & Fenton(1993). It appears that the course is influenced by culture and societal complexity, with better outcomes in developing countries.
In summary, a minority of a fifth of patients with a first episode of schizophrenia have a good prognosis. The majority have multiple episodes, and about half have chronic impairment of function affecting their ability to form relationships and work. Schizophrenia can therefore be seen as an chronically disabling disorder with important family and social consequences. (A.P.A, 2003)
Schizophrenia is a term used to describe a group of mental illnesses which are diverse in nature and cover a broad range of cognitive, emotional and behavioral disturbances. It is a common disorder with up to 600,000 sufferers in the UK. The incidence and prevalence rates are consistent Worldwide at 0.15-0.20 per 1000 per year and 2-4 per 1000 per year, respectively. The lifetime risk of schizophrenia in the general population is about 1% but for first-degree relatives of sufferers this is increased to 10%. ( APA ,1994) & (McGuffin P., et al., 1995)
Okasha, ( 1985) Stated that schizophrenia is believed to affect 0.85% of 3% of the population and represents the major social problem of our time accounting for approximately 50-60% of our admission to mental hospital a 50-70% of long stay patients. By predominantly affecting young adults, there are often disastrous sequelae. Loss of working ability, breaking up family life & sometimes leading to antisocial and Frankly criminal behavior.
Lifetime prevalence of schizophrenia varies, but the results of most studies collectively average out to a rate of slightly less than one case per 100 persons in the population (Huper, Gross, Schuttner & linz, 1980); (Eaton, Day & Kramer 1988); (Wyatt, Alexander, Egan, Kirch (1988).
The disorder appears to be uniformly distributed worldwide, although pockets of high or low prevalence may exist (Wyatt, Alexander, Egan, Kirch (1988) The risk of developing schizophrenia is enhanced if one’s relatives have the disorder, especially if they are first-degree relatives or if more than one of affected; Dohernwend,& Egri (1981) .(Waton, Day, Kramer (1988). Wyatt, Alexander, Egan, Kirch (1988); (McNeil (1988) Because schizophrenia usually appears early in life and can often be chronic, the costs of the disorder are substantial. Schizophrenia accounted for 2.5% of total direct health care expenditures, or about $ 16-$19 billion, in 1990 (Rupp & Keith (1993). Indirect costs from such factors as loss of productivity and family burden are estimated at $64 billion (Rupp, Keith (1993); (Wyatt, Henter, Leary& Taylor (1995). Unemployment rates can reach 70%-80% in severe cases Attkisson,et.al (1992) and it is estimated that schizophrenic patients constitute 10% of the totally and permanently disabled (Rupp & Keith, (1993). Homelessness and schizophrenia have been linked, it has been estimated that about one-third of homeless single adults suffer from severe mental illnesses largely schizophrenia (Attkisson,et.al (1992).
The A etiology of Schizophrenia
The cause of schizophrenia is unknown. During this century various theories have been proposed to range from social and psychological ideas to biological, genetic and environmental hypotheses. A brief overview some of these theories is presented below.
In 1948 Fromm-Reichmann suggested a 'schizophrenogenic' mother, one who is both overprotective and hostile to her children, caused schizophrenia. Lidz proposed the disorder was the consequence of 'marital skew 'and' marital schism. (Lidz , 1949;Lidz, 1968) Marital skew describes the situation where one parent dominates the other. Marital schism is when parents have contrary views which are thought to cause a child to have divided loyalties. However, subsequent studies failed to confirm such ideas (Ferreria & Winter 1965; Sharan , 1965). and it is suggested the findings were the result, as opposed to the cause of schizophrenia. Disorders of communication within families have also been suggested to be of a etiological significance. (Bateson ,1956; Wynne &Singer. 1963)
Life events have been proposed to be a cause of schizophrenia. This suggestion is based on the finding that schizophrenics experience significantly more life events in the three weeks prior to the onset of the illness and that life events appear to precipitate relapses . ( Norman & Malla. 1993); (Kaplen &Sadok, 1994 & 1998); (Towersend, & Carson, 2000).
Biochemical theories of schizophrenia include the dopamine and glutamate hypotheses. (Carlsson, 1999). The dopamine hypothesis was based on the pharmacological findings that the drugs stimulating central dopamine receptors, can produce a disorder indistinguishable from schizophrenia, and that anti-psychotic drugs block dopamine receptors. All the new information produced by studies into schizophrenia, however, cannot be accounted for simply by abnormalities with dopamine.
Family, twin, adoption, and epidemiological studies provide considerable evidence for the genetic contribution to the aetiology of schizophrenia. Washington, APA (1994) (McGuffin P., et al., 1995) However, despite numerous linkage and association studies with candidate genes for schizophrenia no one gene for schizophrenia has been found and results have largely been negative or inconsistent. (Portin et al., 1997) The possibility that schizophrenia is a single gene disorder has been excluded (O’Donovan , 1999) and transmission is now thought to involve multiple susceptible loci. (McGuffin P., et al., 1995) Although twin studies provide compelling evidence for genetics in the causation of schizophrenia they also establish the importance of environmental influences. The findings that both affected and unaffected monozygotic twins pass the same increased risk of development of schizophrenia to their children; (Gottesman, 1989 );(Dixon, Haas, Weidwn, Sweeney,& Frances (1990).( Kendler K.S. Diehl 1993) (McGlashan, & Krystal, (1995).;; Kaplan & Sadok, 1994 & Carson 2000 & Townserd, 2000) and in monozygotic twins discordant for schizophrenia the affected twin has larger ventricles and less temporal lobe grey matter than the unaffected twin (Test, Wallisch, Allness, & Ripp, (1989). (Suddath , 1990; Reveley et al., 1990) (Zisook, Heaton, Moranville, Kuck &, Jernigan (1992) & suggests the involvement of more than just genetics in the aetiology of the disorder.
Also, the environmental factors implicated in the aetiology of schizophrenia.
The neurodevelopmental hypothesis of schizophrenia proposes that a proportion of schizophrenia is the result of an early brain insult, either pre or perinatal, which affects brain development leading to abnormalities which are expressed in the mature brain. (Weinburger , 1987; Bloom , 1993) This idea is not new, Kraeplin and others throughout the 20th century argued that some cases of schizophrenia probably resulted from insults that cause cerebral maldevelopment. (Southard, 1915; Kraeplin, 1919) (Ciompi (1980). The cause of the brain lesion is postulated to be either from the inheritance of abnormal genes, which impair brain development, or from some fetal or neonatal adversity.
Neuropathological, Clinical and Epidemiological Findings
Firstly, reports of neuropathology will be evaluated followed by data from studies of premorbid children with abnormalities which are interpreted to represent cerebral maldevelopment. The third section reviews studies that have attributed the cerebral abnormalities to specific etiological factors. Finally, there will be a discussion of the mechanisms proposed to explain how and why the onset of the illness is delayed until 20-30 years after the initial insult.
Post-mortem and brain imaging studies into schizophrenia have shown the disorder to be associated with disturbances in cerebral structure. However, researchers have reported different brain regions to be affected to varying extents. A meta-analysis of 40 MRI studies (Lawrie, 1998) described the following abnormalities in the brains of schizophrenics: Volume reductions, Whole Brain (3%), Temporal lobe (left 6% right 9.5%) and Amygdala/hippocampal complex (left 6.5%, right 5.5%). In the other hand, volume is increased in the lateral ventricles (left 44%, right 36%) , grey matter is reduced but white matter volumes may be increased
These brain abnormalities are thought to be neurodevelopmental in origin, as opposed to neurodegenerative, because of reports they are found in newly diagnosed patients as well as chronic schizophrenics, (Bogerts, 1990, Tuner, 1986, DeLisi, 1991, Degreef, 1992, Lieberman, 1993, Noupoulos, 1995,). and as they appear to be non-progressive. (Nasrallah, 1986, Vita, 1988, Illowsky, 1988 (Abi-Dargham, 1991). (Jaskiw, 1994, Marsh, 1994,, Also, it is argued that if the disease process of schizophrenia were progressive then so would be the neuropsychological profile; but the cognitive deficits found in schizophrenia show no deterioration over the course of the illness. Stephens (1978 )& (Hyde , 1994). However, reports of changing brain volumes in schizophrenia are inconsistent (Chua, 1995)., and since 1989 there have been both positive ( Kemali , 1989, Woods, 1990, Davis, 1998) and negative (Hoffman, 1991, Sponheim, 1991) longitudinal computed tomography findings of progressive volume loss in schizophrenia; and both positive (DeLisi, 1995, DeLisi, 1997, GurReet, 1998,) and negative (McGlashan,& Bardenstein (1990);( Bromet, ; (Jaskiw, 1994, Vita, 1994) longitudinal magnetic resonance imaging results in follow-up investigations of first episode schizophrenia.
In addition, there is evidence for progressive ventricular enlargement in childhood-onset schizophrenia. (Rapoport, 1997). Moreover, the failure to find conclusive evidence of brain volume loss over time is not proof that neuronal degeneration does not occur in schizophrenia unless it is assumed that there is a temporal relationship between degeneration and symptomatic illness.
Many imaging studies also report the presence of excessive extracerebral CSF in schizophrenia. (Wyatt, Alexander, Egan & Kirch,1988); (Woods, 1991, Gur, 1991) This is difficult to explain using a model of an early static defect in brain development as brain volume triples between birth and the age of five years and any increase in extracerebral volume would tend to be filled up by the outward growth of the brain. (A.P.A, 2003) ( see figure)
Nevertheless, compelling evidence in support of the neurodevelopmental hypothesis comes from studies of cortical cytoarchitecture which discovered neurons in schizophrenic brains to be misplaced, mis-sized and disorganised. (Jakob, 1986, Arnold, 1991, Benes, 1991, Abkarian , 1993) Such findings are difficult to explain in any other than neurodevelopmental terms as they are suggestive of impaired neuronal migration which takes place during the second trimester of pregnancy. However, the findings remain controversial. (Zaide, 1997).
Gliosis is the neural scarring which accompanies brain lesions other than those which occur during early development and is regarded as a characteristic feature of neuronal degeneration. In schizophrenic brains the balance of neuropathological evidence is strongly against excessive gliosis being characteristic of schizophrenia. Bogerts, 1983; Roberts, 1987 and Stevens, 1988); (Roberts, 1986; Benes, 1986; Falkai, 1988; Bruton, 1990; ( Frank, & Gunderson (1990); (Attkisson, et.al (1992); (Rupp, & Keith (1993); (Amador, et.al(1994); ( Wyatt, Henter, Leary, & Taylor, (1995) .
Also, there is no evidence of increased glial membrane turnover signals in magnetic resonance spectroscopy in either chronic schizophrenia or at the time of
disease onset. (Herz, et.al (1996) (Bertolino , 1996) This is supportive of the idea that the damage to the brain in schizophrenia occurs early in life and is not due to a neurodegenerative process.
However, earlier studies of schizophrenic brains did report gliosis, (Stevens, 1982);( Marder, et.al (1994) although this could be explained by technical issues; with results being dependent on specific staining procedures (Marder,& Meibach (1994) (Arnold, 1996) or vulnerability to long fixation times . Herz (1985) (Selemon , 1995).
In addition, some researchers report that the brain can respond to injury with gliosis as early as the 20th week of gestation (Roessmann, 1986) ; (Weiden, et.al (1994) and certainly throughout the third trimester (Robert, 1991) suggesting that any perinatal brain injury should result in gliosis.
Human Brain Asymmetries
In schizophrenia there is a failure to develop normal cerebral asymmetries. (Petty, 1995; Crow, 1989; Bilder, 1994; Falkai, 1995; Falikai, 1992 and Rossi, 1992) Since normal human brain asymmetries are formed early in development, during the second trimester of gestation, these findings suggest the occurrence a pathological event interfering with this stage of development. However, such findings remain controversial and are only suggestive, not conclusive, of deviant neurodevelopment. (Kullynych, 1991; and Bartley, 1993; Flaum, 1995).
In some studies, pathological changes appear to affect the left side of the brain more severely than the right. (Crow, 1989; Kendler , 1993; Waddington 1993 and Shenton, 1995; Aidel, 1997, ,) This is potentially explicable in neurodevelopmental terms as the left hemisphere of the brain is thought to develop more slowly than the right hemisphere during early to mid-gestation and so could be more vulnerable to injury or vulnerable for a longer period of time.
Further evidence in support of the neurodevelopmental hypothesis is the aberrant expression of developmental and plasticity associated markers such as the embryonic isoform of the neural adhesion molecule (NCAM) (Barbeau, 1995) and the growth-associated protein 43 (GAP-43) (Perrone-Bizzozero, 1996) in the brains of schizophrenics.
Finally, sulcal-gyral abnormalities have been reported in some post-mortem studies of schizophrenic brains . (Jakob, 1986; Jakob, 1989) Since gyrification in the human brain is largely intrauterine between weeks 16 and 29 (Armstrong, 1995) such abnormalities are highly suggestive of a process affecting the fetal brain at this stage of development. However, these studies were not conducted blind and may not have accounted sufficiently for the sex differences in the sulcal-gyral pattern. (Gentleman, 1991) Nevertheless, the findings have since been confirmed in a later study (Kikinis, 1994).
The Premorbid Child
If schizophrenia is caused by an aberration in the developing brain, then it is reasonable to expect some subtle abnormalities of neural function and developmental anomalies to be present in early life.
Several lines of circumstantial data support this possibility. Pre schizophrenic children have a higher incidence of: neuromotor abnormalities; delayed attainment of developmental milestones; and behavioral and intellectual abnormalities. (Walker, 1994; Jones, 1994; Foerster, 1991 and Eoerster, 1991).
They are also often described as having 'schizoid' personality traits such as being socially withdrawn, aloof and preferring to play alone. (Jones, 1994 Done, 1994) One study, using old home movie tapes, revealed that in the first two years of life children who were to become schizophrenic had reduced responsiveness, less positive affect, and less eye contact. (Walker, 1990) Another study reported that children who go on to develop schizophrenia perform less well than their contemporizes in tests of neuropsychological and academic performance. (Aylward, 1984) 75% of people who go on to develop schizophrenia have 'soft' neurological signs as children. These include slightly abnormal gaits in children; dysgraphaesthesia; proprioceptive errors; tics; twitches and epileptic attacks. (Walker, 1994; Jones, 1994) The results of these studies are consistent with the possibility of brain maldevelopment.
Nevertheless, despite all these reports, many children who go on to develop schizophrenia have shown high levels of social, academic, and occupational functioning. So, it appears there is a subgroup of schizophrenics who have been subtly impaired for years before the onset of overt positive schizophrenic symptoms, implying a proportion of schizophrenia is attributable to a neurodevelopmental defect.
Schizophrenic patients are also reported to have a higher prevalence of minor physical anomalies than the general population. (Green, 1994) Dermatoglyphic asymmetry, (Bracha, 1992 and Mellor, 1992 Fananas, 1996) and cerebral anomalies, such as agenesis of the corpus callosum and cavum septum pellucidum, and developmental cysts, (Lweis, 1996) are both found more commonly in schizophrenics and are both indicative of disturbed intrauterine development. Additionally, minor physical abnormalities including low set ears; furrowed tongue; high arched palate; curved fingers; greater distance between the eyes and a single palmer crease are also found more frequently in schizophrenics, particularly in males and in those with a positive family history. (Green , 1989 ;Green, 1994, &2002) Both the skin and the central nervous system are derived from the ectodermal tissue in utero, so such visible anomalies can be considered as external markers of damage to ectodermal structures of the fetus and as such can be interpreted as indirect support for the occurrence of aberrant neurodevelopment. Such anomalies are also found in other disorders of neurodevelopment such as Down's syndrome and intrauterine viral encephalopathies. However, this theory remains controversial (Murphy, 1996) with the true frequency of these abnormalities in schizophrenia unknown and uncertainty as to whether all the morphological characteristics reported are actually pathological.
If schizophrenia is a neurodevelopmental disorder the causes must act early in development. It is feasible that genes may be involved in the genesis of the brain abnormalities and the finding that environmental risk factors associated with schizophrenia act pre- or perinatally offers further support for the neurodevelopmental hypothesis. However, the presence of risk factors early in life does not necessarily mean that schizophrenia must be developmental in an overall sense, for example, there are early risk factors for stroke. (Green, 2002)
People who develop schizophrenia are born in winter and spring slightly more frequently than the general population. (Hare, 1988; Kaplan & Sadk 1994 &1998) and several studies indicate that the increased risk for winter births is enhanced among those born in large cities and is greater the colder the winter. (Lewis, 1992, Takei, 1995) The possibility that this observed seasonality could be a statistical artifact or merely an accentuation of the seasonality seen in general births has generally been refuted. (Sham, 1992) The findings suggest the influence of some intrauterine factor that varies seasonally.
Environmental factors proposed include infectious agents, nutritional factors, and the temperature variations at the time of conception. Maternal infection could affect fetal brain development through in utero infection; maternal fever; maternal antibodies crossing the placenta and acting as fetal anti-brain antibodies; or maternal use of analgesics. Support of infection as the cause of this phenomenon are the reports that viral entry into the CNS is promoted by exposure to cold (Benn-Nathan, 1991) and the demonstration by rubella that viral infection in a pregnant women can cause permanent damage to the fetal nervous system.
Maternal infection with the influenzas is also claimed to be associated with the later development of schizophrenia in the unborn child, particularly in females. (Mednick, 1988; Barr, 1990 O’Callaghan, 1991; Cooper, 1992; Sham, 1992; Kinugi, 1992; and Adams, 1993) However, the existence and importance of this effect remains controversial, (Crow, 1991; Kendell, 1991) as although ecological studies show an association between schizophrenia and the timing of the great influenzae epidemics there is yet to be a convincing demonstration of this effect in individuals known to both have been exposed to influenzae in utero and to have developed schizophrenia. The mechanism by which maternal influenza increases the risk of schizophrenia in the unborn baby is not established. It is possible it is mediated through maternal antibodies to influenzae cross-reacting with neuronal proteins, a mechanism that has been observed in rabbits (Knight, 1991) or that certain mothers are genetically predisposed to produce a harmful immune response (Wright, 1993) Any theory attempting to explain this association must also account for why only a minority of mothers infected with influenzae during pregnancy have a child who becomes schizophrenic.
Several studies have found that obstetric complications during antenatal life or delivery are more frequent in patients with schizophrenia, especially in male, early onset schizophrenics. (Lewis, 1987; Owen, 1988; Eagles, 1990; O’Callaghan, 1992; Gunther-Genta, 1994; Guregje , 1994; Cantor-Graae, 1994 and McNeil, 1994; Kungi, 1996). However, a meta-analysis of such studies suggests that there may be considerable publication bias in the literature and that prospective, population-based studies tended to be largely negative. (Geddes, 1995) Acute late onset and female schizophrenic subjects do not seem to share the excess of obstetric complications which may be one reason why not all studies show such an association. (Done, 1991; McCreadie, 1992 and Buka, 1993) Ischemia is the mechanism by which obstetric complications have been proposed to increase the risk of the later development of schizophrenia.
Obstetric complications causing hypoxic ischemia in the pre- or perinatal period can lead to intraventricular or periventricular bleeds, resulting in ventricular enlargement. (Murray, 1985) Furthermore, the pyramidal cells in the CA1 region of the hippocampus are among the most vulnerable in the human brain to mild ischemia.
Excitotoxic damage associated with perinatal hypoxia could also account for some of the neurochemical abnormalities that are found in schizophrenia. (Jerwin, 1992) However, pre-existing brain dysfunction may predispose to obstetrical complications and some investigators have interpreted the association between obstetric complications and schizophrenia as being an indication of fetal abnormality. (Goodman, 1988)
Maternal malnutrition in early gestation (Susser, 1992; Susser, 1996;) is another intrauterine environmental event which appears to increase the risk of developing schizophrenia in a dose dependent way.
However, this study (Susser, 1992) did not control for the implication of social class both in access to food and on risk for schizophrenia.
Nevertheless, four lines of evidence support prenatal nutritional deficiencies as a plausible set of risk factors for schizophrenia: (Brown, 1996). Their effects are not incompatible with the epidemiology of schizophrenia, they have adverse effects on brain development, general malnutrition results in neuropathological anomalies of brain regions, implicated in schizophrenia, prenatal malnutrition affects maternal systems critical to the developing fetal and nervous system.
In the light of the widely accepted data that genetic factors convey susceptibility to schizophrenia, it is not surprising that there has been speculation about genetic factors that may affect brain development in schizophrenia. Since approximately 30% of the genome is expressed in the brain (Sutcliffe, 1984) and many genes are turned on and off during discrete phases of brain development, there are many potential candidate genes for aberrant neurodevelopment. It is suggested a mutation in a gene relating to brain development could result in the neuropathological deviations found in the developing brain. (Murray, 1992) Alternatively, it is hypothesized a genetic defect could predispose the schizophrenic brain to be adversely affected by intrauterine or perinatal environmental events. Another possibility is that the genetic control of brain development may be disrupted by adverse environmental events which results in the cerebral pathologies found in the brains of schizophrenics. (Bloom, 1993).
Mechanisms of delayed onset
It is easy to see how the neuronal abnormalities in the frontal and temporal lobes could result in an abnormal pattern of cortical connections and cause the premorbid abnormalities in children and the social and cognitive defects shown by schizophrenic adults. However, the neurodevelopmental hypothesis proposes that such pre or prenatal lesions can produce the positive symptoms of schizophrenia 2-3 decades later.
Animal studies have demonstrated that a brain lesion sustained in early life can remain quiescent until early adulthood after which time in influences behavioral and neuropharmacological phenomena that mimic schizophrenia. For example, neonatal damage in the temporal lobe has little effect in juvenile monkeys but leads to behavioral and pharmacological abnormalities in adulthood. (Beauregard, 1995; Green, 2002) Also, prenatal lesions in the hippocampi of rats remain apparently silent until adult life. (Lipska, 1993; Lipska 1993; Flores, 1996; Lipska, 1995; Lipska, 1995 and Sams-Dood, 1997).
Nevertheless, although these studies do show that a defect in development can result in a latency before the onset of symptoms, they do not demonstrate spontaneous late deterioration of function after an early lesion which is what occurs in schizophrenia.
A study in monkeys have been interpreted as showing that prenatal lesions of the dorsolateral prefrontal cortex can remain undetected until sexual maturity when deficits in neuropsychological tests arise. (Goldman, 1971) However, careful examination of the study does not support this interpretation; the performance of the 'lesioned' monkeys in the tests did not become poorer as they progressed from infancy into adulthood, the 'non-lesioned' monkeys just performed better. It should also be noted that the performance of monkeys who sustained lesions in infancy was always superior to those who sustained lesions in the juvenile period which is implies some degree of compensatory organization. Therefore, this study, although frequently cited as supporting the neurobiological plausibility of the neurodevelopmental hypothesis, in fact it does not.
It is possible that a similar process as is occurring in these animals with early brain lesions explains why pre schizophrenic children do not show the positive symptoms of schizophrenia until early adult life. (Pulowsky, 1991).
A large proportion of all the cells generated in the developing nervous system die by the time it is mature. After peaking during childhood, synaptic density in the human frontal cortex declines by 30-40% by adulthood. A process of selective neuronal death and progressive synaptic elimination appears to operate throughout adolescence to eliminate early errors of connection and it is suggested that this sculpting of this nervous system might be abnormal in schizophrenia. (Feinburg, 1983; Hoffman, 1997; Hoffman, 1989 and Keshaven, 1994) .
Integrating this idea with the neurodevelopmental hypothesis results in the suggestion that the maldevelopment in utero sets the stage for secondary synaptic disorganization in adolescence. This hypothesis has been supported by: phosphorus-31 magnetic resonance spectroscopy studies of neural membrane phospholipid turnover. (Pettegrew, 1991; Stanley, 1995)
Alternatively, it is possible that lesion remains dormant until the normal processes of brain maturation in adolescence lead to the use of neuronal circuits that are not greatly developed in children. In support of this idea, it has been found that in humans the development (myelination) of circuitry to and from the hippocampus is only complete in adolescence, providing a mechanism whereby a lesion affecting this area may not be apparent until these pathways are mature. (Green, 2000) Also, proposed have been the possibilities of abnormalities of neuronal sprouting or adverse effects of stress related neural transmission. (Bogerts, 1989) Finally, support for the neurobiological plausibility of the latency period in schizophrenia comes from studying human developmental disorders which also exhibit this phenomenon. Both temporal lobe epilepsy and metachromatic leukodystrophy provide a 'mock-up' of schizophrenia. (Roberts, Done, Buton & Crow, 1990, Hxde, Ziegler & Wein Burger 1992).
Treatment Modalities in schizophrenia:
People with schizophrenia can benefit from a variety of psychological interventions, including individual and group psychotherapies, behavior therapy, social skills training, family intervention, vocational rehabilitation, psychopharmacology, adjunctive treatments, assertive community treatment, and case management.
Antipsychotic drugs have effectively treated the symptoms of schizophrenia for over 40 years, and they are still the first choice for most patients with schizophrenia.9 (Johns,& Thompson, 1995) Psychosocial therapy enhances the efficacy of antipsychotic medications, and patients cooperate better with psychosocial therapy when psychotic symptoms are under control.
Antipsychotic drugs, also called neuroleptics or major tranquilizers, treat both acute and chronic symptoms and prevent exacerbation of positive symptoms of schizophrenia. Conventional antipsychotics include chlorpromazine (Thorazine) and haloperidol (Haldol).5 (Dixon, & Lehman,& Levine, 1995) Common side effects include the anticholinergic manifestations of dry mouth, blurred vision, constipation, and urinary retention, as well as those listed in "Medication Side Effects." The unpleasant side effects often cause noncompliance.
Antiparkinsonian agents, such as trihexyphenidyl (Artane) and benztropine mesylate (Cogentin), are generally prescribed with neuroleptics to counteract extrapyramidal symptoms. These drugs are cholinergic blockers, producing the same anticholinergic side effects as neuroleptics.3 (Townsend, 1996).
Newer antipsychotic agents such as clozapine (Clozaril), risperidone (Risperdal), and olanzapine (Zyprexa) have much lower risk of the side-effects of tardive dyskinesia and neuroleptic malignant syndrome. (Buchanan, 1995; Umbricht, & Kane, 1995 and Littrell,& Peadbody & Littrell. 1996) Like traditional antipsychotics, these drugs control the positive symptoms of schizophrenia; they apparently also alleviate the negative symptoms. (Buchanan, 1995; Umbricht, & Kane, 1995 and Lehman, 1995) But clozapine causes a risk of agranulocytosis; patients taking this drug must have their white blood cells and differential count monitored.10 (Buchanan, 1995).
Various other medications serve as adjunctive treatments for schizophrenia, as does electroconvulsive therapy (ECT). Medication alternatives include benzodiazepines such as diazepam (Valium), carbamazepine (Tegretol), lithium carbonate (Eskalith), and various antidepressants.3,9 (Townsend, 1996 and Johns & Thompson, 1995) ECT may be helpful for chronic, neuroleptic-resistant patients.9 (Johns & Thompson, 1995)
2- Individual psychotherapy:
In which a patient has one-to-one contact with a therapist, may be either dynamically oriented psychotherapy, which typically seeks to increase insight, or supportive psychotherapy, which typically seeks to build self-esteem.7 (Scott, & Dixon, 1995) The primary focus in all cases must be to decrease anxiety and increase trust.3 (Townsend, 1996)
Once a therapeutic interpersonal relationship has been established, the therapist emphasizes reality orientation by looking at the patient’s interactions and relationships. Education helps the patient identify sources of stress and ways of reacting appropriately. Such therapy also emphasizes methods for improving interpersonal communication, emotional _expression, and frustration tolerance.3 (Townsend, 1996)
Individual psychotherapy requires a long-term commitment from a therapist who is extremely patient and has no need to prove himself or herself by changing the patient. Generally, treatment lasts for many years before patients can function independently. (Townsend, 1996). Group therapy has been most helpful over the long-term course of the illness, particularly during residual phases. When leading groups in rehabilitation programs, nurses can remember that therapeutic effects because of the social interaction, sense of cohesiveness, identification, and reality testing achieved in the group setting. (Townsend, 1996)
Behavior modification can help reduce the frequency of bizarre, disturbing, and deviant behaviors and increase appropriate behaviors. Techniques include Clearly defining measurable goals, consistently applying clear positive and negative consequences to adaptive and maladaptive behavior, reinforcing even incremental success, and using instructions to elicit the desired behavior.
Social skills training increases motor and interpersonal skills, using methods and principles derived from social learning theories. (Scott, & Dixon, 1995) Nurses can focus on the social skills like eye contact, interpersonal distance, voice intonation, and posture, helping patients adapt interactions to the situation. (Townsend, 1996)
Social skills training involves analyzing complex behaviors and separating them into discrete behavioral elements, then using behavioral techniques such as role playing to train patients in those behaviors. (Scott, & Dixon, 1995) For example, a typical scenario may find a nurse educating the patient by saying "See how I nod my head up and down and look at your face while you talk," then giving the patient a chance to role play. Emphasize functional skills that are relevant to daily living and are likely to draw positive response. (Townsend, 1996) and (Scott, & Dixon, 1995)
Evidence suggests that family interventions can delay if not prevent relapse for people with schizophrenia who have significant family contact. (Dixon& Lehman,1995)
3- Family therapy:
Aims to help family members understand the illness, reduce stress, develop social networks for family interactions, and begin to solve long-term problems. (Dixon& Lehman,1995 and (Townsend, 1996) Nurses should identify the level of family function and assess the family’s communication patterns, relationships between members, role expectations, and problem-solving skills, and should find out what outside support systems are available.
This program can enhance a schizophrenic person’s vocational activities, but they do not significantly improve a person’s ability to hold a job after leaving the programs.8 But improvements in vocational functioning are correlated with a reduction in symptoms and relapse. (Lehman, 1995).
5- Case management and Assertive community treatment (ACT)
To function in their communities, many schizophrenic patients need a variety of treatment, rehabilitation, and support services. Assertive community treatment (ACT) draws on a multidisciplinary, community-based team to provide a comprehensive range of treatment, rehabilitation, and support services. (Scott, & Dixon 1995) The staff of ACT programs meet patients and start their support systems. The approach relies heavily on home care, high staff-to-patient ratios, staff continuity, and brief but frequent contacts. (Scott, & Dixon 1995)
Case management, which is generally more narrowly focused, uses a relationship between a patient and a case manager to enhance continuity and coordination of care. Through this relationship, the patient receives expanded access to services, whether these are provided directly or contracted through outside agencies. (Scott, & Dixon 1995)
Case managers traditionally have five core functions: assessment, planning, advocacy, linkage, and monitoring. Different models emphasize certain functions. Some models work with large caseloads, contracting services from other providers and agencies. In other models some services are provided while others are contracted out, and the caseloads may be smaller. (Scott, & Dixon 1995)
Both ACT and case management programs reduce hospitalization and increase use of community mental health services that usually cost less than hospitalization . (Scott, & Dixon 1995) ACT and case management approaches can be seen as being at opposite ends of a spectrum, though some programs may overlap. ACT directly and intensively provides nearly all treatment, rehabilitation, and support services, while case management offers a limited array of direct services delivered with less intensity than ACT programs. (Scott, & Dixon 1995)
Psychosocial rehabilitation models with the core values of self-help and empowerment aim to help patients function in the community as well as possible. (Thompson, & Strand, 1994) Nurses working in such programs are typically responsible for some specific nursing functions; they also help patients with goals such as finding an apartment, learning to care for an infant, and making friends.
For many clients, the most effective treatment appears to be a combination of psychotropic medication and psychosocial therapy . Towensend, 2000; A.P.A., (2003)
This review Considers evidence for the efficacy of psychological interventions of persons with schizophrenia including cognitive behavioral and psychosocial skill training.
Cognitive Behavioral Therapy
What is Cognitive Behavioral Therapy?
Cognitive Behavioral Therapy is a psychotherapeutic approach which is used by psychologists and therapists to help promote positive change in individuals, to help alleviate emotional distress, and to address a myriad of psycho/social/behavioral issues.
Basic concepts & its definitions:
Wright and Beck (1994) state, the general thrust of cognitive therapy is that emotional response is largely dependent on cognitive appraisals of the significance of environmental cues. Basic concepts include automatic thoughts and schemas or core beliefs.
1- Automatic thoughts. Automatic thoughts are those that occur rapidly in response to a situation and without rational analysis. These thoughts are often negative and based on erroneous logic. Beck, Rush, and Shaw (1979) call these thoughts cognitive errors. Following are some examples of common cognitive errors.
1. Arbitrary inference. In a type of thinking error known as arbitrary inference, the individual automatically concludes about an incident without the facts to support it, even sometimes despite contradictory evidence to support it. Example: Two months ago, Mrs. B. sent a wedding gift to the daughter of an old friend. She has not yet received acknowledgement of the gift. Mrs. B. thinks, they obviously think I have poor taste. (Townsend, 2000)
2. Overgeneralization (Absolutistic Thinking). Sweeping conclusions are overgeneralizations made based on one incident-a type of “all –or-nothing” kind of thinking. Example: Frank submitted an article to a nursing journal, and it was rejected. Frank thinks,” nor journal will ever be interested in anything I Write” (Townsend, 2000).
3.Dichotomous Thinking. An individual who is using dichotomous thinking views situations in all or nothing, black –or-white good, or bad terms. Example: Frank submits an article to a nursing journal and the editor returns it and asks Frank to requite parts of it. Frank thinks, “I’m a bad writer,” instead of recognizing that revision is a common part of the publications process. (Townsend, 2000)
4.Selective Abstraction. A selective abstraction (sometimes referred to as mental filter) is a conclusion that is based on only a selected portion is usually the negatives evidence or what the individual views as a failure, rather than any successes that have occurred. Example: Jackie just graduated from high school with a 3.98/4.00 grade point average. She won a scholarship to the large state university near her home. She was active in sports and activities in high school and well-liked by all her peers. However, she is very depressed and dwells on the fact that she did not earn a scholarship to a prestigious Ivy league college to which she had applied.
5.Magnification. Exaggerating the negative significance of an event is known as magnifications. Example : Nancy hears that her colleague at work is having a cocktail party over the weekend, and she is not invited. Nancy thinks, she doesn’t’ like me. (Townsend, 2000)
6.Minimization. Undervaluing the positive significance of an event is called minimization. Example: Mrs. M is feeling lonely. She calls her granddaughter Amy, who lives in a nearby town, and invites her to visit. Amy apologizes that she must go out of town on business and would not be able to visit at that time. While Amy is out of town, she calls, Mrs., M twice, but Mrs. M still feels unloved by her granddaughter. (Townsend, 2000)
7.Catastrophic Thinking : always thinking that the worst will occur without considering the possibility of more likely, positive outcomes is considered catastrophic thinking. Example: On Janet’s first day in her secretarial job, her boss asked her to write a letter to another firm and put it on his desk for his signature. She did so and left for lunch. When she returned, the letter was on her desk with a typographical error circled in red and a note from her boss to redo the letter. Janet thinks, this is it I will surely be fired now. (Townsend, 2000)
8. Personalization. In personalization, the person takes complete responsibility for situations without considering that other circumstances may have contributed to the outcome. Example: Jack, who sells vacuum cleaners’ door to door has just given a two-hour demonstration to Mrs. W. At the end of the demonstration, Mrs. W tells Jack that she appreciates his demonstration, but she won’t be purchasing a vacuum (when in fact, Mrs. W’s husband lost his job last week and they have no extra money to buy anew vacuum cleaner at this time). (Townsend, 2000)
Schemas (Core Beliefs):
Beck and Weishaar (1995 ) define schemas as: Cognitive structures that consist of the individual’s fundamental beliefs and assumptions, which develop early in life from personal experiences and identification with significant others. These concepts are reinforced by further learning experiences and in turn influence the formation of other beliefs, values, and attitudes.
These schemas, or core beliefs, may be adaptive or maladaptive. They may be general or specific and they may be latent, becoming evident only when triggered by a specific stressful stimulus. Schemas differ from automatic thoughts in that they are deeper cognitive structures that serve to screen information from the environment. For this reason, they are often more difficult to modify than automatic thoughts. However, the same techniques are employed at the schema level as at the level of automatic thoughts. Schemas can be positive or negative, and they generally fall into two broad categories. Those associated with helplessness and those associated with immovability (Beck, 1995).
Cognitive therapy has its roots in the early 1960s research on depression conducted by Aaron Beck (1963,1946). Beck had been trained in the Freudian psychoanalytic view of depression as “anger turned inward.” In his clinical research, he began to observe a common theme of negative cognitive processing in the thoughts and dreams of his depressed clients (Beck & Weishaar, 1995).
Several theorists have both taken from and expanded upon Beck’s original concept. The common theme is the rejection of the passive listening of the psychoanalytic method in favor of active, direct dialogues with clients (Beck &Weishaar, 1995). The work of contemporary behaviorists (Bandura, 1977; Meichenbaum, 1977) has also influenced the evolution of cognitive therapy, Behavioral techniques such as expectancy of reinforcement and modeling are used within the cognitive domain.
Richard Lazarus (1966), upon whose premise of personal appraisal and coping the conceptual format of this book is founded, has also contributed a great deal to the cognitive approach to therapy. The model for cognitive therapy is based on cognition, and more specifically, the personal cognitive appraisal by an individual of an event, and the emotions or behaviors that result from that appraisal. Personality which undoubtedly influences our cognitive appraisal of an event is viewed as having been shaped by the interaction between innate predisposition and environment (Beck & Freeman, 1990). Whereas some therapies may be directed toward improvement in coping strategies or the adaptiveness of behavioral response, cognitive therapy is aimed at modifying distorted cognitions about a situation.
What are the goals of Cognitive Behavioral Therapy?
The goals are to restructure one's thoughts, perceptions, and beliefs. Such restructuring facilitates behavioral and emotional change. During therapy, coping skills and abilities are assessed and further developed.
What kinds of techniques are used in Cognitive Behavioral Therapy?
Some specific techniques that the therapist may use include, but are not limited to: Challenging irrational beliefs, Relaxation education and training, Self-monitoring, cognitive rehearsal, thought stopping, communication skills training, assertiveness skills training, social skills training, bibliotherapy and homework assignments
The phases of therapy:
To understand how this has become possible, we need to look at how therapy typically proceeds. Several researchers have tried to clarify this issue. Among the most widely accepted findings have been those of Prof. Kenneth I. Howard and his associates at Northwestern University 2003.
Howard, 2003 has collected data over several decades of psychotherapy research that suggest the following three phases, which I will use his own words to describe: Remoralization. Some patients are so beset by problems that they become demoralized and feel that they are at their "wits' end." This type of experience is pervasive and severely disrupts a person's ability to mobilize his or her coping resources. The person begins to feel frantic, hopeless, and desperate. Demoralization tends to respond quickly to psychotherapy; remoralization is usually accomplished in a few sessions.
Remediation : A second phase of therapy is focused on remediation of the patient's symptoms, the symptoms that led the person to feel so upset and demoralized that he or she had to seek treatment. During this second phase, treatment is concerned with refocusing the patient's coping skills in a way that brings symptomatic relief. The attainment of symptomatic relief is more gradual and typically requires about 16 sessions (depending on the type and severity of these symptoms).
Rehabilitation.: The third phase of treatment is probably what has traditionally been thought of as "psychotherapy" in that it is focused on unlearning troublesome, maladaptive, habitual behaviors and establishing new ways of dealing with various aspects of life (e.g., problematic relationship patterns, faulty work habits, and trouble-causing personal attitudes). During psychotherapy, the rehabilitation of life functioning is quite gradual, and the number of sessions required is dependent on the severity of the disability and the area of problematic functioning (e.g., work, family, or self-management).
How is the therapy conducted?
Clients are first evaluated to obtain a thorough history and background information to better understand the nature of the difficulties for which treatment is being sought. Clients may also be asked to complete assessment tools or questionnaires. Treatment usually takes place on a weekly basis, focusing on current issues. A Treatment Plan is completed to set goals and to monitor progress. The number of sessions varies with the type of difficulties being treated. Clients are expected to be active participants in their own therapy.
1-Cognitive modification (automatic thoughts)
“Automatic thoughts” are thoughts that come to mind involuntarily and effortlessly. You may not even notice them unless you make a point of looking for them. They may or may not have an appreciable effect on your feelings, moods or behavior. When they do, their effects may be beneficial, harmful or neutral.
Most of our thoughts are automatic they just happen, without being planned or intended. Nearly all the time, this is an advantage. However, some automatic thoughts can cause serious mischief. CBT helps you learn to recognize and deal with them, so they stop causing trouble. Sometimes automatic thoughts turn out to have a shared theme (called a “schema”) that you may or may not have ever put into words or even be aware of.
- Quote paper
- Amal Khalil (Author), 2004, Impact of Cognitive Behavioral Therapy on Thought and Behavioral Disorders of Schizophrenic Disorders, Munich, GRIN Verlag, https://www.grin.com/document/1150965