Prevalence Rates of Schizophrenia from Available Research
Question:
Discuss about the Pharmacokinetics and Treatment of Schizophrenia.
The purpose of this paper is to describe the neurochemical theories that are associated with schizophrenia and the accompanying treatment modalities of schizophrenia. This paper will also describe the prevalence rates of Schizophrenia from available research. The history of theories of that describe and explain Schizophrenia will be properly described within the paper. Schizophrenia in itself is a complex and chronic mental disorder that is accompanied by a myriad of symptoms which include hallucinations, disordered or disorganized thoughts and a decrease in cognitive ability (Patel et al, 2014). Schizophrenia is a syndrome –meaning it is a collection of symptoms.
The condition (schizophrenia) has an early onset and progression within the families of individuals. In this regard, schizophrenia creates a very high proportion of disability within the population. The types of schizophrenia within the general population include: catatonic schizophrenia; disorganized hebephrenic schizophrenia; paranoid schizophrenia; simple schizophrenia; residual schizophrenia and undifferentiated schizophrenia (Townsend et al, 2017).
According to McGrath (2008) the prevalence of Schizophrenia has been identified to be fifteen point two percent for every one hundred thousand people. Schizophrenia has a devastating national and global consequence. Schizophrenia not only disables the individual from progressing with activities of daily living appropriately but also decreases the quality of life for the individual in question. Studies have not conclusively defined the spread of schizophrenia within population and the information obtained from such studies varies from one study to another (Simeone et al, 2015).
According to Simeone (2015) the significant disparity in terms of proportion of people affected by schizophrenia from study to study is due to: the study method used during the study; the geographical location of the study in question; the time when the assessment was done and the quality score of the study in question. Muggah (2013) also supports this assertion, of disparity in the studies previously conducted, to ascertain prevalence of schizophrenia within populations. The study method such as cohort or cross-sectional studies played a key role in the results obtained during estimation calculation of the prevalence of schizophrenia from location to location (Muggah, 2013).
The wide variability in the spread and distribution of schizophrenia within populations may be attributed partly to the inherent complexity that is associated with schizophrenia. The diagnosis of schizophrenia has also changed significantly- the current version of DSM-V (Diagnostic and Statistical Manual of Mental Disorders) advices physicians who diagnose schizophrenia to grade it along the range of severity from the less severe delusional disorder all the way to the more severe, schizoaffective disorder (Bhati et al 2013). The progression of a patient with schizophrenia is promising if early diagnosis and treatment is performed.
The etiology of Schizophrenia is not known. Many studies have tried to identify the cause but have not been able to identify its cause conclusively. In the early 20th century, most studies that were performed tried to identify the pathologic basis of Schizophrenia –mainly through autopsy. During the period of the 1950s to 1960s studies were focused more on the psychological and psychosocial aspects that were related to the origin of Schizophrenia (Coyle et al, 2016). Interpersonal theorists suggested that Schizophrenia originated from the effects of dysfunctional and disordered relationships during the early period of life and adolescents. However, none of the interpersonal theories already developed has been proven. In contrast, most of the current studies that have been performed have come to support the neurologic or neurochemical theories (Coyle et al, 2016).
History of Theories of Schizophrenia
The current scientific studies demonstrate that schizophrenia resulted from a type of brain dysfunction. The neurologic or neurochemical theories are backed up by the cumulative effects of antipsychotic medications to control the associated effects of psychotic symptoms. In addition, it has been seen that the brain of individuals suffering from schizophrenia is different from those without schizophrenia (control subjects) through the use of neuroimaging tools (Coyle et al, 2016).
With the use of non-invasive techniques in the last 25 years such as magnetic resonance imaging, scientists have been able to view the normal brain function. From the investigations performed it has become clear that individuals with Schizophrenia poses lower levels of cerebrospinal fluid than the control groups (Olabi et al, 2012). The study of the brain structure (neuroanatomy) has provided substantial information about individuals suffering from schizophrenia. In addition to lower levels of cerebral spinal fluid within these individuals, it was also identified that individuals with schizophrenia presented with relatively less brain tissue (Olabi et al, 2012). These aspect significantly represents an occurrence of failure during development or an associated pathology that could have initiated the loss of tissue.
Computed tomography scans have elaborated the syndrome further. Scans have displayed enlarged ventricles in this individuals and signs of cortical atrophy. Glucose and oxygen are diminished when a positron emission tomography is performed in these individuals. Oxygen levels are within lower levels within the cortical structures of the brain. Research that has been performed in the subject matter, continuously conclude that a decrease in brain volume with abnormal brain operation within the frontal and temporal areas is evident in individuals with schizophrenia. This development is associated with the positive signs of schizophrenia within individuals from different studies. The positive signs of schizophrenia such as psychosis (which affects the temporal lobe) and negative signs (which affect the frontal lobe) such as lack of volition or lack of motivation support this assertion (Patel et al, 2014)
However, it is not clear whether failure in the functioning of the frontal and temporal areas of the brain is due to a failure in the areas to develop or if there is a correlation between its function and infection by a virus or trauma, or if an immune response can lead to such damage (Patel et al, 2014). The effect of intrauterine influences and effects are being studied as one of the causative effects. Such intrauterine influences include poor nutrition during pregnancy, the use of tobacco and high stress levels which could bear a significant effect on neuronal development and thus lead to a the pathological findings in the brain of people who have schizophrenia.
Neurochemical theories have continuously shown that the alterations within the neurotransmitter systems of the brain in individuals affected by schizophrenia. The neuron networks are responsible for the transmission of information or electrical signal from a nerve cell through the entirety of the axon, Golgi apparatus and the pre and post synaptic receptors along the nerve cells show signs of malfunction. A complex of biochemical reaction occurs during the transmission of a nervous signal within the synapse. The studies have shown that the cumulative activities of serotonin, norepinephrine, dopamine, acetylcholine, and several neuromodulator peptides play a critical function in the activities that occur along the synapse (Maletic et al, 2016).
Complex and Chronic Symptoms of Schizophrenia
The most significant theories that have been developed to explain this hypothesis of the development of schizophrenia deal with and involved the actions of dopamine and serotonin. One of this essential theories denotes that dopamine excesses are the cause of the abnormal behavior evident in schizophrenia patients. The theory came into actualization as a result of the association of two observations. The observations that the theory was based on are: firstly, the medications and drugs which increase the activity within the dopaminergic area or system, which include: levodopa and amphetamines are sometimes found to elicit a paranoid or psychotic reaction that is similar to that found in schizophrenia. Secondly, the drugs that are responsible for blocking the postsynaptic dopamine receptor have the ability to reduce the psychotic symptoms and reactions, the more the ability of the drug to lead to a substantial decrease in the activity of the dopamine receptors, the greater its effectiveness in decreasing the symptoms that are associated with schizophrenia (Patel et al, 2016).
The existence of abnormal activity within the sites found along dopamine receptors, mainly D2, has been postulated to be one of the key reasons why schizophrenia occurs. There are four dopaminergic receptors that have been identified to play a key role in the actualization of schizophrenia in patients and this are the nigrostriatal pathway (motor symptoms are elicited in this pathway when dopamine levels are decreased), the mesolimbic pathway (positive symptoms of schizophrenia are elicited in this pathway when dopamine levels are in excess), the mesocortical pathway (cognitive deficits are found to be elicited when the dopamine is in low levels within this pathway) and the tuberoinfundibular (amenorrhea, galactorrhea and reduced levels of libido are evident when this pathway is blocked) (Patel et al, 2016).
Another theory that has been recently postulated in regard to the neurochemical theories that come hand in hand with schizophrenia is that associated with serotonin. The serotonin theory came into being as a result of the identification of the lysergic acid diethylamide enhanced effects of serotonin in the brain. In regard to this theory serotonin is effective in controlling the excesses in amounts of dopamine. Other researches tend to presume that serotonin in itself leads to the development of schizophrenia and its associated symptoms (Patel et al, 2016). Drug formulations with the ability to control the resultant effects of positive and negative effects of schizophrenia and operate on both serotonin and dopamine have been developed in recent years.
In addition to the theories developed dealing with the activities of serotonin and dopamine, yet another theory that describes the effects of glutamate within the system has been postulated. Glutamate is the major excitatory neurotransmitter within the brain and plays a key function in the transmission of electrical impulses within the brain. The theory came into being when it was recently identified that phenylciclidine and ketamine, which are two of the glutamate antagonist played a key role in the development of schizophrenia within patient bodies. The theory tried to explain why the schizophrenic patients experience negative symptoms and the associated cognitive symptoms, based on the fact that the glutamate antagonist receptors/NMDA are inactive in the normal state of functioning and modulation of the mesocortical dopamine neurons (Patel et al, 2016).
Types of Schizophrenia within the General Population
Antipsychotics such as clozapine and chlorpromazine are the drugs used to treat schizophrenia. Clozapine is an atypical neuroleptic. Clozapine is highly recommended as the drug of choice for schizophrenia. However, clozapine is not recommended as the first-line treatment because of the cumulative extrapyramidal side effects that accompany it (Takekita et al, 2016; Kar et al, 2016). Clozapine is advantageous in that it improves psychopathology, the affect of the patient among many advantages. Clozapine has a high affinity for serotonin and alpha 1-adrenargic receptors but has a cumulative weak affinity for the D2 receptors (Maletic et al, 2016).
Few studies have been done to examine the pharmacokinetics and the cumulative pharmacodynamics of clozapine in patients with schizophrenia. The parameters in pharmacokinetics and pharmacodynamics of clozapine have been variable within the studies performed. time to reach peak plasma concentrations 1.1 to 3.6h|The time to reach peak levels within the blood plasma have been found to be between one point one and three point six hours, the elimination and half life are nine and seventeen hours respectively, the clearance is eight to fifty three hours, the volume of distribution is one point six to seven point three liters per kilogramme.
Clozapine is metabolised through the hepatic microsomal enzyme system into two main metabolites: clozapine N-oxide and demethyl-clozapine. Clozapine, according to recent studies has binding to D4 receptor subtype. Patients should however, be continuously monitored for extrapyramidal effects.
On the other hand Chlorpromazine is a low potency typical neuroleptic. Chlorpromazine has a high affinity for dopamine D2 antagonism and low serotonin antagonism (Li et al, 2016). The basis of operation of the actions of clozapine and chlorpromazine is the ability or affinity to block the dopamine and serotonin receptors in the brain. However, research is not conclusive in determining the mechanism of actions of the antipsychotics (Maletic et al, 2016).
Food does not interfere with the absorption of Chlorpromazine. It easily passes into the brain and has a large volume of distribution. These agents readily pass into the brain, have a laIt binds well to plasma proteins and is metabolized at different areas especially by the cytochrome P450 within the liver. It produces some amounts of tolerance. However, chlorpromazine has little physical dependence attached to it.
Conclusion
It can be seen from the above paper that there is clearly a generalized need for more and more research on schizophrenia. This is owing to the fact that the research that has been performed is not yet conclusive to support proper management for schizophrenia as a disease. The gaps in research into schizophrenia have promoted the fact that schizophrenia currently does not have a cure. The myriad of symptoms that accompany schizophrenia need to be studied further and a method and means to eliminate the symptoms identified.
A disparity also exists between different research articles and among different researchers about the prevalence and spread of schizophrenia within populations from research to research. A conclusive research should also be performed to deal with and describe the actual distribution schizophrenia within population. The identification of the actual spread of schizophrenia will enable health care providers and researchers manage and understand any causative causes of schizophrenia within populations.
In addition the cumulative theories that have been formulated have led to a great disparity in the management processes. The effect of serotonin and its association with dopamine should be assessed further. The studies performed on serotonin assume that it could be a causative factors to schizophrenia. However, these studies fail to give conclusive evidence to the association between serotonin and dopamine in the formation and development of schizophrenia. The availability of treatment modalities have also failed to yield complete eradication of schizophrenia and relapse has been noted to occur- this aspect shows that more and more research is needed. There is a lot of disparity and gaps in the data researches performed. More needs to be done in researching schizophrenia as a disease.
References
Bhati, M. T. (2013). Defining psychosis: the evolution of DSM-5 schizophrenia spectrum disorders. Current psychiatry reports, 15(11), 409.
Coyle, J. T., Balu, D., Puhl, M., & Konopaske, G. (2016). A Perspective on the history of the concept of “disconnectivity” in schizophrenia. Harvard review of psychiatry, 24(2), 80.
Kar, N., Barreto, S., & Chandavarkar, R. (2016). Clozapine monitoring in clinical practice: beyond the mandatory requirement. Clinical Psychopharmacology and Neuroscience, 14(4), 323.
Li, P., L Snyder, G., & E Vanover, K. (2016). Dopamine targeting drugs for the treatment of schizophrenia: Past, present and future. Current topics in medicinal chemistry, 16(29), 3385-3403.
Maletic, V., Eramo, A., Gwin, K., Offord, S. J., & Duffy, R. A. (2017). The Role of Norepinephrine and Its α-Adrenergic Receptors in the Pathophysiology and Treatment of Major Depressive Disorder and Schizophrenia: A Systematic Review. Frontiers in psychiatry, 8, 42.
McGrath, J., Saha, S., Chant, D., & Welham, J. (2008). Schizophrenia: a concise overview of incidence, prevalence, and mortality. Epidemiologic reviews, 30(1), 67-76.
Muggah, E., Graves, E., Bennett, C., & Manuel, D. G. (2013). Ascertainment of chronic diseases using population health data: a comparison of health administrative data and patient self-report. BMC public health, 13(1), 16.
Olabi, B., Ellison-Wright, I., Bullmore, E., & Lawrie, S. M. (2012). Structural brain changes in first episode Schizophrenia compared with Fronto-Temporal Lobar Degeneration: a meta-analysis. BMC psychiatry, 12(1), 104.
Patel, K. R., Cherian, J., Gohil, K., & Atkinson, D. (2014). Schizophrenia: overview and treatment options. Pharmacy and Therapeutics, 39(9), 638.
Simeone, J. C., Ward, A. J., Rotella, P., Collins, J., & Windisch, R. (2015). An evaluation of variation in published estimates of schizophrenia prevalence from 1990? 2013: a systematic literature review. BMC psychiatry, 15(1), 193.
Takekita, Y., Fabbri, C., Kato, M., Koshikawa, Y., Tajika, A., Kinoshita, T., & Serretti, A. (2016). HTR1A polymorphisms and clinical efficacy of antipsychotic drug treatment in schizophrenia: a meta-analysis. International Journal of Neuropsychopharmacology, 19(5).
Townsend, M. C., & Morgan, K. I. (2017). Psychiatric mental health nursing: Concepts of care in evidence-based practice. FA Davis.
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