Paranoid schizophrenia is an acute disease and the most prevalent form of schizophrenia. Since paranoid schizophrenia has no cure, the treatment plan should focus on lifelong strategies aimed at addressing psychosis features such as post-traumatic stress disorder, substance abuse, aggression, depression, and suicide. The reason psychosis treatment is the primary target in paranoid schizophrenia symptoms is that, notwithstanding the type, psychosis has a close relationship with suicide considering that 50% of paranoid schizophrenia patients commit suicide and 45% obtain depressive symptoms during the first five years of living with the disease (American Psychiatric Association, 2006). According to Bartlett (2014), treatment for paranoid schizophrenia should be comprehensive, abide by best practices and individually tailored to meet specific patients' needs. The treatment goals for paranoid schizophrenia goals include, and not limited to:
- psychotic symptoms amelioration
- preventing secondary morbidity
- reducing the risks of relapse
- self-efficacy and positive self-concept retention
- maximizing the quality of patient's lives
- promoting and maintaining recovery from incapacitating impact from the disease to the optimum level possible
Medication
Since paranoid schizophrenia treatment is lifelong, pharmacotherapy forms the building block of the intervention strategies which include specialty care coordination and psychotherapy. The pharmacological therapy for neurotic schizophrenia patients is available in two forms; use of typical or atypical antipsychotics. The criteria for choosing the medication has the basis of efficacy, cost, availability, and side-effects of the drugs (Viron, Baggett, Hill, & Freudenreich, 2012). Furthermore, the choice of medication depends on age, stage of the disease, symptom severity, and intensity, previous medical history of the patient. Viron, Baggett, Hill, and Freudenreich (2012) add that the choice of medical practice must be stage and age-appropriate, a principle which affects both psychosocial and pharmacological interventions.
Typical Antipsychotics
Typical, standard, traditional or conventional antipsychotics are the most common form of tranquilizers thus earning the attribute as conventional antipsychotics considering that they have been in use in addressing psychosis since the 1950s. The working principle of the typical psychosis is that it blocks the brain's chemical receptors namely serotonin and dopamine. Since the first antipsychotic used in treating schizophrenia was chlorpromazine (Thorazine), it serves as the basis of categorizing other drugs through potency measurements. Potency, by definition, is the indication of the amount of medication necessary for achieving desired outcomes to those that 100 mg of chlorpromazine (Thorazine) would produce (Lehman, 2010). Therefore, typical antipsychotics can fall into law, medium and high potency categories. Low potency antipsychotics include Thioridazine (Mellaril) and Chlorpromazine (Thorazine) while Trifluoperazine (Stelazine), Thiothixene (Navane), Perphenazine (Trilafon), Molindone (Moban) and Loxapine (Loxitane) represent medium potency antipsychotics (American Psychiatric Association, 2006). On the other hand, Zuclopenthixol (Clopixol), Fluphenazine (Prolixin) and Haloperidol (Haldol) are examples of high potency typical antipsychotics.
Atypical Antipsychotics
Atypical antipsychotics came in as an attempt to reduce the potential side effects of conventional antipsychotics such as nasal congestion, hypotension, sedation, constipation, cognitive impairment, urinary hesitation, dry mouth and blurred vision. Examples of atypical antipsychotics include ziprasidone, olanzapine, clozapine, quetiapine, and risperidone. The preference of atypical antipsychotics medication follows their ability to reduce negative and positive psychotic symptoms (Meltzer & Basu, 2009). The capacity of a drug to antagonize H1 receptors predict its sedating potential. In that criteria, the ranking of the atypical antipsychotics in order their increasing their ability to block H1 is haloperidol, risperidone, fluphenazine, quetiapine, chlorpromazine, olanzapine, and clozapine.
Both medications are currently in use in managing paranoid schizophrenia in its initial phases. Analysis of both medication forms shows that atypical antipsychotics achieve the criteria of minimum or mild side-effects, unlike typical antipsychotics. However, atypical antipsychotics are the most preferred choice because of their lower side-effects profile and costs. Despite the lack of proof that typical antipsychotics are superior, Divac, Prostran, Jakovcevski and Cerovac (2014) say that preference may be due to attribute that any typical antipsychotic has the potential of antagonizing dopamine subtype 2 receptor (D2). In many cases, quetiapine and risperidone are atypical medications used as first-line drugs in addressing paranoid schizophrenia. Different research studies have reasons for the preference of atypical drugs. For instance, Wright and O'Flaherty (2014) rationale for choosing atypical medication over typical intervention is to reduce the chances of the patient's extrapyramidal system disruption, a characteristic linked with the use of conventional drugs. Extrapyramidal system's function as the primary controller of the motor function thus its disruption through the use of standard medication may trigger akathisia defines an inner restlessness, parkinsonism which causes unsteadiness, rigidity, and tremor. Other negative attributes of standard drugs include repetitive postures and tardive dyskinesia whose prevalence upon the use of conventional medications is approximately 30% (Meltzer & Basu, 2009). Not all atypical antipsychotic drugs reduce extrapyramidal effects as amisulpride, olanzapine and risperidone increase the chances of impaired motor functioning. However, using typical antipsychotics in low doses may not produce serious side-effects thus making them suitable choice in small quantities.
Expected Outcomes
Despite both typical and atypical medications present in the patient's treatment plan, the choice of the category to utilize is dependent on their possible outcomes. According to Wright and O'Flaherty (2014), atypical antipsychotics drugs as the most recently developed medications have little risks of causing tardive dyskinesia (TD), one of the most severe side-effects of antipsychotics. Typical medicine predisposes individuals with TD. Although the choice of atypical antipsychotics is most appropriate drugs, they have side-effects such as possible weight gain. Furthermore, in the case where administration of the drug is not age-appropriate or where there is high dosage, it can cause issues such as withdrawal and movement disorder resembling Parkinson's disease. Meltzer and Basu (2009) suggest that despite the attributes of atypical antipsychotics as advanced solutions in treating paranoid schizophrenia, their consideration as optimal intervention is subject to ongoing research studies.
There is a persuasive demonstration that antipsychotics are the primary treatment intervention for paranoid schizophrenia because of positive symptoms as demonstrated in Whitaker (2010) and Leucht et al. (2012) studies. When illness proceeds, there is little knowledge regarding the outcomes and effectiveness of antipsychotic medication especially three years after the onset of illness as their efficacy deteriorate with time, a characteristic which Leucht et al. (2012) consider to be a prevalent phenomenon while treating any schizophrenia, asthma, cancer and other somatic disorders. On the other hand, Whitaker (2010) provide a suggestion that because there is no cure for paranoid schizophrenia, the use of antipsychotics in long-term serves as an iatrogenic trigger of schizophrenia chronicity leading to patients' well-being and health deterioration. Systematic reviews in Sohler et al. (2015) study confirms Whitaker's (2010) findings. Despite the rarity of studies investigating the outcomes of antipsychotics medication, available evidence suggests that drugs have more good than harm considering that paranoid schizophrenia has no optimal medical solution at present. Criticisms only arise from the contention regarding antipsychotics efficacy.
References
American Psychiatric Association. (2006). On an engaging patient with paranoid schizophrenia. American Journal of Psychiatry, 154(8), pp. 1178a-1178.
Bartlett, J. (2014). Childhood-onset schizophrenia: what do we really know? Health Psychology and Behavioral Medicine, 2(1): 735-747. DOI: 10.1080/21642850.2014.927738.
Divac, N., Prostran, M., Jakovcevski, I., & Cerovac, N. (2014). Second-Generation Antipsychotics and Extrapyramidal Adverse Effects. BioMed Research International, 1(2): 1-19. http://dx.doi.org/10.1155/2014/656370.
Lehman, A. F. (2010). Practice Guide: Treatment of Patients With Schizophrenia. Washington DC: American Psychiatric Association.
Leucht, S., Tardy, M., Komossa, K., Heres, S., Kissling, W., Salanti, G., & Davis, J. (2012). Antipsychotic drugs versus placebo for relapse prevention in schizophrenia: a systematic review and meta-analysis. Lancet, 379(9813): 2063-2071.
Meltzer, D. O., Basu, A., & Herbert Y. Meltzer. (2009). Comparative Effectiveness Research For Antipsychotic Medications: How Much Is Enough? Health Aff (Millwood), 28(5): w794-w808. DOI: 10.1377/hlthaff.28.5.w794.
Sohler, N., Adams, B., Barnes, D., Cohen, G., Prins, S., & Schwartz, S. (2015). Weighing the evidence for harm from long-term treatment with antipsychotic medications: a systematic review. American Journal of Orthopsychiatry, http://dx.doi.org/10.1037/ort0000106.
Viron, M., Baggett, T., Hill, M., & Freudenreich, O. (2012). Schizophrenia for Primary Care Providers: How to Contribute to the Care of a Vulnerable Patient Population. The American Journal of Medicine, 125(3): 223-230. https://doi.org/10.1016/j.amjmed.2011.05.002.
Whitaker, R. (2014). The case against antipsychotic drugs: a 50-year record doing more harm than good. Medical Hypotheses, 62(1): 5-13.
Wright, P., & O'Flaherty, L. (2014). Antipsychotic drugs: atypical advantages and typical disadvantages. Journal of Psychological Medicine, 22(2): 20-29. https://doi.org/10.1017/S0790966700007497.
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