Evidence-Based Practice of the Correlation between Schizophrenia and Cannabis Addiction - Essay Example

? Evidence-based analysis of the correlation between Schizophrenia and Cannabis addiction PART INTRODUCTION During the practice of scientific medicine the established rules of evidentiary analysis must be applied with even more rigor, in the interest of preserving human life. In the 1980’s the term ‘evidence-based practice’ was used to describe the application of scientific evidence to determine the best practice. (Bayea & Slattery, 2006) In addition, it can be stated that it “Aims to apply best available evidence to clinical decision making.” (Holland, 2010) Also vital is the need to ‘match the expertise and level of provision with the severity of the case.’ (Royal College of Psychiatrists, 2005) This can include what is known as Research Utilization, in which an analysis of research findings is used to inform clinical practices. DEFINITIONS AND BRIEF IMPORTANCE OF CLINICAL PRACTICE The term evidence-based practice (EBP) or empirically-supported treatment (EST) refers to preferential use of mental and behavioral health interventions for which systematic empirical research has provided evidence of statistically significant effectiveness as treatments for specific problems. (Thomas & Pring, 2005) A way in which this benefits medicine would be in studying the effects of cannabis. This drug has been found to share commonality with schizophrenia. Immunology research has found common receptors located in in immune cells, spleen macrophages, to be specific. These have the ability to alter immune cell migration and cytokine-release within body tissues and in the brain, these receptors tend to be abnormal in schizophrenia patients. More findings that hint at a larger relationship between, not cannabis itself – but receptors it depends on, and a biological predisposition towards schizophrenia. Research such as this can bring nurses and medical technologists more fully into the treatment of psychiatric care. (Cabral & Staab, 2005) (Gong et al, 2006) An additional definition would be: "Evidence based medicine is the conscientious, explicit, and judicious use of current best evidence in making decisions about the care of individual patients. “Sackett et al's (1996, 71-72) And in this clinicians must integrate personal clinical expertise with the most cutting-edge external clinical evidence from systematic research. Another vital factor in Evidence-based practice is quality or performance improvement; how to streamline services in order to maximize the most efficient use of resources? (Bayea & Slattery, 2006) By definition: Performance Improvement (PI) is a method for analyzing performance problems and setting up systems to ensure good performance. PI is applied most effectively to groups of workers within the same organization or performing similar jobs. (Intrahealth.org 2011) A possible example would be to make systematized evaluations of patient needs based on probabilities. For instance, schizophrenics have a 25% higher proclivity towards illicit drug abuse than the general population. (Jablensky, 2000) Also, in studies of the neuropathology of the psychiatric disorder schizophrenia, findings have emerged which link the condition to brain receptors that are actually susceptible to molecules of cannabis. Schizophrenia is a challenging psychiatric disorder with a lifetime prevalence of 0.4% amongst the general population. (Desfosses et al. 2010) This can inform clinical choices, and influence the circumstances under which certain batteries of tests are ordered, and for whom, saving time and money. PART 2 ASPECT OF PROFESSIONAL PRACTICE AND RATIONALE I have chosen for the exploration of Evidence-based Practice a linkage between susceptibility to cannabis, and the neurological disorder, schizophrenia. Clinical research has established a connection, and where such associations occur, it behooves clinicians to explore the phenomenon to aid diagnostic tools. Among the atypical antipsychotics used to treat schizophrenia, there are risks factors. Among these medications is clozapine (Clozaril). It is a very effective medication that treats psychotic symptoms, hallucinations, and breaks with reality, such as delusions of grandeur. Clinical observations of a particular patient, designated ‘Patient X’ included agranulocytosis, a loss of pathogen-fighting leukocytes (white blood cells). For the clinicians involved, regular cell-count checks are prescribed in order to monitor his condition, and avert potential complications. Generally, clozapine is a good, 'last-resort' strategy for those that do not respond to conventional antipsychotic medications. For the reasons mentioned above, it is necessary to monitor/screen such patients for illicit drug abuse, as well. Despite the white blood cell risks, Clozapine has been found effective for the treatment of substance abuse, in particular cannabis smoking, in schizophrenia patients (Drake et al. 2000). In tests with rats, clozapine influenced the binding activity of a selective CB1 agonist (CP,55940) in the nucleus accumbens. The nucleus accumbens serves as a 'pleasure center' of the brain, and is believed vital to addiction-maintenance. This binding activity was not observed with other antipsychotics (Sundram et al. 2005) PART 3 To identify the most current clinical evidence of the linkage between these two phenomenon, an online search was conducted of Pub Med.gov, and the Cochrane schizophrenia group trials. The term ‘Cannabis & Schizophrenia’ were searched for. Articles found concerning endocannabinoid receptors are primary research. Presently, etiological models attempting to explain the biological bases of these two disorders are numerous, including models of neurodevelopmental, neurodegenerative or cortical-subcortical disconnection. There is wide agreement that schizophrenia is associated with many comorbidities spanning disciplines, from the study of addiction, towards immunology, endocrinology, and neurology. There is considerable motivation to deliver a cogent explanation for this aggregation of symptomology from a neurobiological perspective. A menagerie of medications have been developed over time to manage the symptoms. EXTENT OF THE DIFFERENT TYPES OF EVIDENCE In qualitative terms, there are real differences in the brains of schizophrenics that must inform medical decisions. It has been found that the chemical family of what can be termed, endocannabinoids, including anandamide and 2-arachydonoylglycerol (2-AG) react differently in schizophrenic brains. Endocannabinoids are lipids that derive naturally from membrane precursors with binding affinity to cannabinoid receptors (CB1, CB2). The disruption of this endocannabinoid system is part of the pathophysiology of schizophrenia. It is fair to say that there is a connection between schizophrenia and polymorphisms of the CB1 receptor gene. In addition, the density of CB1 receptors is greater in the prefrontal cortex, basal ganglia, and hippocampus of patients with schizophrenia. Quantitatively, levels of anandamide are higher in the cerebrospinal fluid (CSF) and serum of schizophrenia patients. This is also true during the prodromal state, which suggests that anandamides may function to maintain psychosis homeostasis. Schizophrenics are more prone to substance abuse in general, as reported above, when compared to the population at large. (Regier et al. 1990) Arguably, this proclivity is due to an interrelationship on a neurochemical level. The study of illicit substances, specifically cannabis abuse is important here for highlighting that interrelationship. A randomized, controlled study by van Nimwegen, investigated subjective 'well-being' and cannabis addiction symptoms, in terms of craving over a 6-week period. The study was double-blind, and randomized. The purpose was a statistical analysis of neural receptor sites normally targeted by cannabis; the occupancy of these sites would then have the effect of blocking the cannabis molecule with two antipsychotics drugs. Olanzapine and Risperidone; in the double-blind study, both had indistinguishable benefits towards reduction of cravings. Based on observations, and a drug-desire questionnaire, either treatment was equally effective at altering cannabis dependency. (van Nimwegen, et al. 2008) As noted above, Risperidone and Olanzapine have been previously known for years. These atypical antipsychotics have been used in the treatment of schizophrenia. Binding, or affecting these sites, as well as moderating symptoms of the psychosis, also has an effect on cannabis abuse/addiction. The pattern is clear for a neurophysiological interrelationship. Additional pre-clinical studies with atypical antipsychotics found that Risperidone increases the binding of the CB1 receptor in the rat amygdala, caudate nucleus, and hippocampus. Olanzapine, as well significantly diminished CB1 binding in the dorsal vagal complex of the medulla (brainstem) in ex vivo tests in rats. (Secher et al. 2010) In another randomized, double-blind, placebo-controlled study, intra-venously administered tetrahydrocannabinol, abbreviated as ?9-THC administered to healthy human participants controls produced both positive (hallucinatory delusions) and negative symptoms (blunted affect and social withdrawal). Cognitive effects are apparent as well; suggesting its effectiveness as a valid model for the understanding of psychosis. Related evidence indicates that inhaled ?9-THC has been shown to impede verbal memory, as well as selective attention and sustained focus in both healthy subjects and schizophrenia patients. (D’Souza et al, 2004) (Henquet et al, 2006) Systemic review shows that cannabis-triggered delusions and schizophrenia both show promising responses to antipsychotic treatment. Considering the cannabinoid hypothesis of psychosis, we can suppose that the Cannabinoid receptor system is not only connected with psychosis but also in the effects of antipsychotics. In human studies, clinical remission of symptoms is followed by a sharp decrease of anandamide levels following olanzapine (atypical antipsychotic) treatment and in addition by reductions of messenger RNA for two types of cannabis-susceptible receptors. (De Marchi et al. 2003) Other studies have tried to piece together the role the aforementioned endocannabinoids, which are natural. Studies show indicate that schizophrenia patients treated with typical antipsychotics exhibited similar CSF (cerebrospinal fluid) and anandamide levels, compared with healthy controls (Giuffrida et al. 2004). It is presumed from this result that antagonism of the receptor labeled D2 decreases excess cannabinoids, with is consistent with other, preclinical data, while agonism of the D2 receptor induces synthesis of anandamide in limbic and motor regions. By contrast, schizophrenia patients treated with atypical antipsychotics experienced higher anandamide levels, which is the same as drug-free schizophrenia patients. Thus, the disturbance of the anandamide-cannabinoid receptor system is only affected by the 'typical' antipsychotics. This effect was specific to the nucleus accumbens, which in addition to the addiction-activity, is also thought to have involvement in psychosis. But no effect was observed in the hippocampus, the frontal cortex, or the striatum. This result seemed limited to rats, but supports the idea that clozapine may be beneficial in dual-diagnosis patients. There is uncertainty concerning the underlying mechanisms of clozapine's activity on CB1 receptors. (Fukudome et al. 2004) For humans, there is growing attraction to the perceived potential applications of the Endocannabinoid (ECB) system for the development of a new generation of antipsychotic drugs. For that purpose, a functional magnetic resonance imaging study showed that 7-day administration of rimonabant (CB1 antagonist) to healthy participants lowered their subjective experience of reward (anhedonia) and their neural responses in another brain reward region, namely the ventral striatum. (Horder et al. 2010) But in a randomized, placebo-controlled study involving adults with schizophrenic disorders, rimonabant did not improve psychotic symptoms in a statistically significant way. (Meltzer et al. 2004) But the connection between the psychotic disorder, and the neuro-physiological system affecting it does give considerable ammunition for future modification of the condition. PART 4 FACTORS THAT COULD FACILITATE AND HINDER THE IMPLEMENTATION OF EVIDENCE-BASED PRACTICE 1.) Practical limitations on the clinician/practitioners’ ability to utilize research products. 2.) Lack of research on the process itself and the outcome of empirically tested treatment modalities and existing facilities used for different purposes. 3.) Lack of research on available products for end-users. 4.) Lack of research concerning the integration of science and practical applications throughout higher education. 5.) Economic, cost-based realities that impede evidence-based decision-making. 6.) Inability to translate theories derived from research into actionable clinical practice. (Addis, 2002) Many of these issues could be addressed by increased education by both administrators and staff, and to steep clinicians in a culture of research. Forming contacts with researchers and manufacturers can ease the transitions between theory and practical application. Larger hospitals may look into the feasibility of dedicated personnel to comb recent medical research to proactively hunt down and adapt the latest knowledge for medical benefit. CONCLUSION In real life as well as clinical practice, ignorance and prejudice are also impediments to the evidence-based practice of scientific medicine, and pharmacology. The medical facts underlying, and connecting these two conditions must inform policy-makers as well as the public, to avoid ignorant misclassification of this (and other) disorders. Lay-persons should not be mis-educated to the point that they will simply lump in a serious, neurophysiological condition such as this with environmentally encouraged, ‘therapist-couch’ issues that can be talked through. One cannot psychoanalyze a schizophrenic, and for decades it has been known that drugs were the only option. Cost is another factor; smaller institutions may be limited in the quality and education of the personnel they can attract, and the batteries of tests they can run in a limited time. Here, education is important, both in terms of universally more capable persons at a variety of medical institutions, but also of the public as well, to prevent misunderstandings that will delay the proper care, and waste resources. Patients too, must be informed of the nature of long-term conditions requiring considerable care, that they can play a role in their own healing. References Addis, Michael E. 2002. 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