The term schizophrenia was coined in 1908 by the Swiss psychiatrist Eugene Bleuler. The word was derived from the Greek ‘skhizo’ (split) and ‘phren’ (mind). Schizophrenia results from a variable combination of genetic predisposition, biochemical dysfunction, physiological factors, and psychosocial stress. (Sadock & Sadock, 2003). The DSM V (APA, 2013) identified the Schizophrenia spectrum as a psychotic disorder and is defined by idiosyncrasies that are seen individually or multiply. The idiosyncrasies seen are delusions, hallucinations, disorganized thinking (speech), grossly disorganized and catatonia, and negative symptoms. Therefore, in the DSM-V, two criterion (A) symptoms are required for any diagnosis in schizophrenia and there is a precondition for a person to now have at least one of three positive symptoms of schizophrenia (APA, 2013). Schizophrenia is categorized by the interference visibly seen in cognition and emotion, which affects language, thought, perception and the individual’s affect. The assortment of symptoms exhibit psychotic expressions, such as hearing internal voices or undergoing other sensations such as distorted beliefs (APA, 2013).
The symptoms seen in Schizophrenia are divided into two systems positive and negative. Positive symptoms appear to reflect an excess or distortion of normal functions which contribute to the presence of hallucinations. Hallucinations are exaggerations of perception in all senses (APA, 2013). This can contribute to abnormal behavior and disorganized thinking. Disorganized speech/thinking, (thought disorder) is usually assessed primarily based on the person’s speech and thus, the behavior of the Schizophrenics is catatonic. This behavior shows a decline in reaction to one’s environment (Sadock & Sadock, 2003). The decline in behavior demonstrates negative symptoms which reflect a loss of normal functioning. Negative symptoms display a lack in abilities such as lack of emotion to appreciate activities as one did before, low energy and interest and social isolation , flat affect and alogia (not verbally responsive) (APA,2013).
The DSM-1V-TR (APA, 2000) identifies various types of schizophrenia which are disorganized, catatonic and paranoid schizophrenia. In disorganized schizophrenia, onset of symptoms is usually before age 25 years, and the course is commonly chronic. Behavior is markedly regressive and primitive. Contact with reality is extremely poor. Catatonic schizophrenia is characterized by marked abnormalities in motor behavior and may be manifested in the form of stupor or excitement (Sadock & Sadock, 2003). Paranoid schizophrenia is characterized mainly by the presence of delusions of persecution or grandeur and auditory hallucinations related to a single theme. The individual is often tense, suspicious, and guarded, and may be argumentative, hostile, and aggressive. Onset of symptoms is usually later (perhaps in the late 20s or 30s) (APA, 2000).
Residual schizophrenia is when the individual has a history of at least one previous episode of schizophrenia with prominent psychotic symptoms which demonstrate symptoms like social isolation, eccentric behavior, impairment in personal hygiene and illogical thinking (Townsend, 2005 &; Sadock & Sadock, 2003). Schizoaffective Disorder is manifested by schizophrenic behaviors, with strong element of symptomatology associated with the mood disorders (mania or depression). The prognosis for schizoaffective disorder is generally better than that for other schizophrenic disorders but worse than that for mood disorders alone (Sadock & Sadock, 2003).
The cause of schizophrenia is still uncertain (Townsend, 2005). Most likely no single factor can be implicated in the etiology rather the disease probably results from a combination of influences including biological, psychological, and environmental factors. .
Environmental influences and socio-cultural factors play a role indeed. Epidemiological statistics have shown that more individuals from the lower socioeconomic classes experience symptoms associated with schizophrenia than do those from the higher socioeconomic groups (Ho, Black & Andreasen, 2003). Explanations for this occurrence include the conditions associated with living in poverty, such as congested housing accommodations, inadequate nutrition, absence of prenatal care, few resources for dealing with stressful situations, and feeling of hopelessness for changing one’s lifestyle of poverty. Also, it is know that extreme stress can precipitate psychotic episodes (Sackeim &Mukherjee, 1992).
Physiological influences viral infection; the epidemiological data indicates a high incidence of schizophrenia after prenatal exposure to influenza. Other studies suggested that the exposure is most significant if it occurs during the second trimester of pregnancy. Further research is required into this hypothesis of psych immunology as an etiological implication for schizophrenia. (Townsend, 2005). Also, anatomical abnormalities and structural brain abnormalities have been observed in individuals with schizophrenia. Ventricular enlargement is the most consistent finding however; sulci enlargement and cerebellar atrophy are also reported. Studies have also revealed a decrease in frontal lobe size, in studying brains of clients with schizophrenia they found a disordering or disarray of the pyramidal cells in the area of the hippocampus.
A look further into the physiological and biological approach to schizophrenia can reveal a lot about its etiology. For one, we know that multiple neurotransmitters have been implicated in schizophrenia. Dopamine and Glutamate have been hypothesized to be associated with the pathophysiology of schizophrenia.
Dopamine is a hormone and a neurotransmitter. In the brain, it functions as a neurotransmitter that plays a major role in rewards, motivational behavior, motor control and controlling the release of several other important hormones. The Dopamine hypothesis of schizophrenia is a model, which attributes symptoms of schizophrenia (i.e psychosis) to excessive activities at dopamine synapses in specific areas of the brain. There is strong evidence that support this theory. Firstly, drugs that block dopamine reduce schizophrenic symptoms. During the 1950s, psychiatrists discovered that chlorpromazine (Thorazine) reduces the positive symptoms of schizophrenia in most patients. Researchers, later uncovered that antipsychotic drugs related to the phenothiazines and the butyrophenones families blocks dopamine synapses (Kalat, 2008).
Secondly, high and repetitive doses of methamphetamine, cocaine and amphetamine induce substance- induced psychotic disorder, which mimics the positive symptoms (hallucinations and delusions) of schizophrenia (Connell, 1958; Kalant, 1966; Tatetsu, 1964). These substances increase the activity at the dopamine synapses. Substance-induced psychotic disorder is a model for schizophrenia, in the same way that antipsychotic drugs blocks substance-induced psychosis it also reduces schizophrenic symptoms. Although the evidence supporting ‘The Dopamine hypothesis of Schizophrenia’ is strong there are still limitations to this theory. Drugs that block dopamine receptors act quickly. However, patients with schizophrenia begin to experience relief after 2 or 3 weeks on the drug. Also, the effects of antipsychotic drugs may be indirect; these drugs may influence other neurotransmitters that may have a greater impact on schizophrenic symptoms other than dopamine. For example, clozapine, blocks receptors for dopamine and serotonin. Lastly, methamphetamine, cocaine and amphetamine do not only increase dopamine levels but they also alter other neurotransmitter levels.
Glutamate, an amino acid precursor, is the most common excitatory neurotransmitter in the brain and spinal cord. There are two general ways that glutamate can be damaging to neurons and the brain. First, abnormally high concentrations of glutamate can lead to overexcitation of the receiving nerve cell. Second, the receptors for glutamate on the receiving nerve cell can be oversensitive, such that less glutamate molecules are necessary to excite that cell (S. Lou, 2011). Recently, researchers have discovered that deficient activity at glutamate synapses also results to neurodegeneration and has been implicated in the causes of schizophrenia. According to the glutamate hypothesis of schizophrenia, schizophrenia is linked glutamatergic dysfunction. Several pieces of evidence have supported this hypothesis. Persons with schizophrenia have lower than normal release of glutamate and fewer than normal receptors in the prefrontal cortex and hippocampus (Akbarian et al., 1995; Ibrahim et al., 2000; Tsai et al., 1995). Further support for this hypothesis comes from the effects of dissociative drugs, such as, phencyclidine (PCP or angel dust) and ketamine (Special K). Both substances can cause psychotic symptoms in individuals without schizophrenia and can worsen symptoms in persons with schizophrenia.
PCP, a drug that inhibits the NMDA receptors (N-methyl-D-aspartate, a glutamate receptor) can produce both the positive and negative symptoms associated with this illness. NMDA-receptor abnormalities have been hypothesized in schizophrenia. Schizophrenia is believed to have a Neurodevelopmental component, and the NMDA receptor is critical in guiding axons to their targets in development. NMDA receptors may be important in processes that lead to synaptic pruning seen in adolescence, which has been hypothesized to be abnormal in schizophrenia. Cognitive functioning depends on the plasticity mediated in part by NMDA receptors, and schizophrenics often have cognitive deficits. Finally, the reduction of gray matter in several brain regions seen in schizophrenia has been suggested to be the result of neurotoxicity mediated by NMDA receptors (Meador-Woodruff & Kleinman). Schizophrenia is a complex disorder. Probably both dopamine and glutamate play important roles in this illness, but to different degrees varying by individuals.
Are there regions of the brain that are especially implicated in schizophrenia? While much about schizophrenia is still unknown, there is evidence that show that certain brain regions are affected more than others. Research has revealed that the prefrontal cortex, basal ganglia, auditory system, occipital lobe, hippocampus, and the amygdala, all are affected by this illness (Keshavan et al., 2008; Shenton et al., 2001; Tamminga et al., 2002; Weinberger, 1997).
Individuals with schizophrenia have a reduced volume of gray matter in the brain, mostly in the temporal and frontal lobes (Lawrie &Abukmeil, 1998). Recently neuroscientists have detected gray matter loss of up to 25% (in some areas). The damage starts in the parietal, or outer, regions of the brain but spreads to the rest of the brain over a period of time. Patients with the worst brain tissue loss also have the worst symptoms, which includes hallucinations, delusions, and bizarre and psychotic thoughts.
Although the biology of an individual is significantly impacted in Schizophrenia, other factors still play a role in the disorder. How cognition is implicated in schizophrenia and the psychosocial and environmental aspects that factors into the etiology of schizophrenia will be addressed.
Schizophrenia is a mental disorder that affects the brain, which indicates that cognitive impairment is seen in the brain. Cognitive impairment affects the brain in two parts: psychotic cluster and disorganization (Kalat, 2008). Delusions affect cognitive impairment which specifically heightens a false perception of a schizophrenic patient. Hallucinations are sensations or sounds that only exist in the person’s mind but, it also affects the senses of the individual (Kalat, 2008). The senses in hallucinations that are impaired in schizophrenia patients are auditory hallucinations (hearing), olfactory hallucinations (tasting), tactile hallucinations (feeling) and visual hallucinations (seeing). Another perspective to consider is disorganized cluster which are thought disorders, speech impediments and/or abnormal behaviors that contribute to a decline in attention and working memory (Kalat, 2008). Schizophrenia affects disorganized behavior when there is a daily decline in routines thus, indicating an unpredictable emotional response and impulsive behavior which shows a lack of self-consciousness.
According to Psychiatric disorders in America: the epidemiologic catchment area study (1991) stated that schizophrenia patients exhibit cognitive impairment through the increased activity in the thalamus, hippocampus and a part of the cortex. Schizophrenics display impaired cognition in confined thoughts. The neurological development of schizophrenic patients is not only seen in the hippocampus or thalamus but, it is demonstrated in deficits in the left temporal and frontal lobe of the cortex which confirms abnormalities in the prefrontal cortex (Brisch et al, 2014). Thus, the effect of cognitive impairment provides evidence to indicate a decrease in brain activity in schizophrenics. The decrease in brain activity demonstrates the incapability to mask the comprehension of information or make rational decisions (Robins, & Regier, 1991).
Lederbogen et al., (2013) stated that stress demonstrates abnormality in the Hypothalamus ‘Pituitary Adrenal cause sets of dysfunction in the neurotransmission of dopamine and neural circuits. This is due to high levels of stress. Schizophrenia is affected by many factors, which plays on the onset of the mental disorder is various environmental stressors. The massive array of environmental factors has been found to be allied with schizophrenia and the particular effects of the disorder.
Environmental factors, such as the influenza, malnutrition before birth and socioeconomic status all interact with development of Schizophrenia. Schizophrenia is affected before birth when the fetal hypoxia which is linked with the reduction of grey matter and it increases the cerebrospinal fluid in schizophrenics (Leask, 2004). However, a response to malnutrition is improper infrastructure emplaced and poor socioeconomic status to sustain oneself. Persons suffering from schizophrenia have difficulty finding revenue and maintaining their health. Socioeconomic status is predicament in treatment because it decreases the patient’s mental state (Versola-Russo, 2006). A schizophrenic patient condition diminishes after one is unable to afford proper treatment. The worst possibility to consider is the patient’s health when one is non-complaint with taking prescribed medication. A long term prognosis is that not only the symptoms become more sever but they can risk becoming harmful to themselves or another person (Versola-Russo, 2006).
The causes of mental disorder are diverse and not fully understood. The majority of psychological disorders are believed to be caused by a combination of biological and/or psychosocial influences. However, this role can be characterized differently from person to person. Persons who suffer from schizophrenia display a large level of psychosocial stressors which indicate a low level of competency. The inability to function in a normal social environment can be an indicator of the lack of maintenance in interpersonal skills and relationships. Persons who are suffering from schizophrenia are incapable of adapting. Schizophrenia patients are unlikely to focus and maintain function on a job, which can contribute to isolation. Isolation leads schizophrenic patients to be less active in the community or in social programs and this exhibits a decline in their social skills. Lederbogen et al., (2013) provided evidence that rapid growth in stress can affect the pathology of this mental disorder. Lederbogen et al., (2013) further states that stress is a high level of emotional disturbance and lack of comfort in the home along with relatively low family support (Lederbogen et al., 2013). High levels of stress can be attributed to the lack of family involvement and interaction in psychoeducational settings. There is a need to incorporate family structure in the process for those coping with long prognosis of schizophrenia. This can be prevented with proper treatment and interventions.
Schizophrenia is a complex disorder that has a variety of treatment options which mental health professionals can prescribe. The treatment for this disorder is a reflection of the symptoms that arise which disrupt the everyday life of the patient. The symptoms which are typical of schizophrenia include hallucinations and delusions. As stated earlier, Brisch et al., (2014) discussed the original dopamine hypothesis which provides an explanation for why these hallucinations and delusions occur.
The main support for the dopamine hypothesis is the fact that antipsychotic drugs which block dopamine receptors are the most effective against schizophrenia (Kalat, 2013). This shows that this neurotransmitter is associated with schizophrenia. According to Kalat (2013) pharmacologic treatment for schizophrenia which includes antipsychotic drugs is what is typically used to relieve both positive and negative symptoms of schizophrenia. However, there are different antipsychotic drugs which have been effective for the positive symptoms of schizophrenia and the negative symptoms of schizophrenia.
Miyake, Miyamoto and Jarskog (2012) described two different types of antipsychotic drugs: first-generation antipsychotics (FGAs) and second-generation antipsychotics (SGAs). FGAs was developed based on the dopamine hypothesis of schizophrenia, thus we know these drugs blocked dopamine receptors. In 1952 Chlorpromazine, a popular FGA was introduced for the treatment of schizophrenia. The authors noted that this drug along with other FGAs was shown to be effective for treating the positive symptoms of schizophrenia, but are limited in that it does not benefit the negative symptoms or the cognitive impairments of schizophrenia. Also, FGAs produce a number of side effects including acute extrapyramidal side effects (EPS), hyperprolectinemia and tardive dyskinesia (Miyake, Miyamoto and Jarskog, 2012).
As one could imagine, along with having schizophrenia, the severe side effects produced by FGAs can make the recovery process much more challenging. Also, there are still the untreated negative symptoms that the patient has to deal with. Researchers noted the limitations of the FGAs and in 1990 Miyake, Miyamoto and Jarskog (2012) stated that Clozapine was introduced as the first set of SGAs. These drugs were found to be more effective than FGAs in the treatment of schizophrenia and had the benefit of not causing EPS (Miyake, Miyamoto and Jarskog, 2012). SGAs do have some side effects which the authors explained are metabolic side effects such as weight gain, dyslipidemia and glucose dysregulation. However, SGAs produce fewer neurological side effects and could be beneficial in cognition, relapse prevention and quality of life for schizophrenic patients.
As stated earlier the common symptoms that schizophrenics experience can disrupt everyday life. There symptoms can make it difficult to differentiate between what is real and what is imagined. While on antipsychotic medication, the mere fact of having to take this day to day drug can put a damper on one’s mood which can affect daily functioning. There needs to be more than just pharmacological treatment to help these people live a fulfilling life. Psychosocial interventions should be included as a complimentary treatment to pharmacotherapy. According to a bulletin on effective health care by the University of York, there are several forms of psychosocial interventions for schizophrenia. In particular, to help patients adjust to everyday life, skills training should be implemented as a part of the treatment program along with pharmacotherapy.
Skills training can include many different levels to help one cope. Life skills training teach you how to function independently in everyday life. Life skills such as managing money, running a home and personal self-care are taught. Social skills training aim is to help schizophrenic patients reduce distress and difficultly which will allow them to enhance their social performance. Components of this training include behaviorally-based assessments of social and interpersonal skills, verbal and non-verbal communication and learning how to respond to social cues. Vocational skills training consist of two programs: pre-vocational training and supported employment. Pre-vocational training allows the person to be supported in a type of sheltered work before getting a job in the real world. Supported employment assists people who have real-world jobs.
In the treatment of a schizophrenic person, there should be a combination of pharmacological treatment with a psychosocial intervention, particularly SGA drugs (as they are more efficient) and skills training. Also, there needs to be some form of family therapy for this person to have support from their loved ones and others in the community. A combination of treatments in schizophrenia will not only allow one to be able to cope with their illness but, also give them the necessary skills and support needed to function normally and have a fulfilling life.
As if battling schizophrenia for even the toughest patients isn’t rough enough , it has been proven that having a schizophrenic disorder places an individual at much greater risk for developing a mood disorder. In fact, Judd et al., (2009) stated that mood disorders are so prevalent in persons affected by this disorder that they may be considered a fundamental characteristic of schizophrenic disorders. This strong relationship has been controversial, with some maintaining that mood disorder comorbidities in schizophrenia are actually a manifestation of schizophrenia and not a simple, by chance, co-occurrence with schizophrenia.
The most common comorbidity would be that of substance abuse. Mood disorders including anxiety and depression follow next in line for its commonality.
The abuse of alcohol and/or illicit drugs by patients with schizophrenia is a remarkably common phenomenon (Bull, 2009). According to Kalat (2013) many of the positive symptoms of schizophrenia can develop from prolonged use of amphetamine, methamphetamine, cocaine and more. Someone who may stop using these drugs is likely although not completely certain to recover from these symptoms. Simply, substance abuse comorbidity is common and is deleterious to the course and outcome of schizophrenia. Substance abuse is associated with relapse of psychosis, multiple hospitalization, violence, social isolation and mainly non compliance with medication. Caton et al., (2005) stated that cannabis abuse worsens positive symptoms, sometimes making their hallucinations more intense and can increase disorganization within our patient.
Next, we look at depression and how it can add to the already detrimental nature. Schizophrenia Bulletin (2009) stated that depression can cause secondary negative symptoms, panic attacks and drive paranoia. Patients with schizophrenia are at increased risk of developing depression relative to the already high lifetime prevalence of depression in the general population (Bartels and Drake, 2012). In addition to depression, anxiety symptoms may sometimes occur spontaneously or intermittently or even as a side effect or response to antipsychotic medication which would only be prescribed by the psychiatrist.
Implacably, because schizophrenia is a chronic illness that influences virtually all aspects of life of the affected person, one recommendation would be that the treatment planning be made out with 3 specific goals in mind. Those would be to reduce or eliminate symptoms, maximize the quality of life and adaptive functioning and promote and maintain recovery from the debilitating effects of the illness to the maximum extent possible. Recommendations for this would be a pharmacological treatment and a psychosocial intervention in the form of skills training. Both pharmacological treatment and psychosocial intervention can significantly decrease relapse rates for a schizophrenic patient. Adequate assessment and treatment is important to improve the prognosis of the schizophrenic patient. Systematic assessment and efficient medication is essential for management of the comorbidities of schizophrenia. Significantly, psychosocial treatment has been proven to be effective on several comorbid conditions (Lehman, Lieberman & Dixon, 2010).
Another recommendation would be that engagement of the family and other significant persons with the patients permission is recommended to further strengthen therapeutic effects. Family therapy can significantly decrease relapse rates for the schizophrenic family member.
Concluding, cultural recommendations would include, further developing research around schizophrenia in the Bahamas. We believe that we lack this initiative and we can’t safely say that there is no one among us suffering from this psychological disorder. We must develop centres apart from The Sandilands Rehabilitation Centre to simply cater to those Bahamians among us that may be suffering and try our endeavour best to develop treatment plans that will appeal to them. As a culture we must develop a mindset and mandate to not stigmatize those that may suffer from this condition among us. Besides the effect of a supportive family, studies show that a supportive community and social atmosphere can reduce the relapse rate in patients suffering from schizophrenia. Therefore we think it is vital to our countries development in psychology that we take a look at those around us and to list and consider alternative solutions. Also, to select and implement the consensual best solution for those in our culture that may be suffering.
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