The, Back From Madness : A Struggle For Sanity Essay

Former U.S president Ronald Reagan was shot by a man named John Hinckley in the year 1981. The president along with many of his entourage survived the shooting despite the heavy infliction of internal and external injuries. The Hinckley case is a classic example of the 'not guilty by reason of insanity' case (NGRI). The criminal justice system under which all men and women are tried holds a concept called mens rea, a Latin phrase that means "state of mind". According to this concept, Hinckley committed his crime oblivious of the wrongfulness of his action. A mentally challenged person, including one with mental retardation, who cannot distinguish between right and wrong is protected and exempted by the court

Schizophrenia is a complex and highly debilitating mental illness that we are currently unable to treat in any way that guarantees success or return to previous function. It affects around 1% of the population and is associated with a thirteen-fold increase in the likelihood of suicide, so its effective control is paramount (Gogos et al., 2015). There have been several hypotheses as to the cause of schizophrenia. Many link genetic and environmental factors, and dysregulations of neurotransmitters dopamine, glutamate, and serotonin (Egbujo, Sinclair, & Hahn, 2016). The dopamine hypothesis currently suggests that hyperactive dopamine transmission in the basal ganglia leads to psychosis and underactive dopamine transmission in the prefrontal

The major support and refutation of the dopamine hypothesis has come from the examination of dopamine receptors in these regions of the brain. There are two main types of dopamine receptors, D1 and D2. However, within the category of D2 receptors, there are three subtypes, D2, D3, and D4. (5) Through PET scan analysis of dopamine usage in the brain and post-mordum molecular analysis of brain tissue, researcher were able to determine relative levels of dopamine receptors in patients with schizophrenia compared to non-schizophrenics. Overall analysis of dopamine

The introduction of Clozapine, marked a turning point in the treatment of schizophrenia, as the first "atypical" antipsychotic drug lacking the propensity to produce ‘extra-pyramidal symptoms’ (associated with the older antipsychotic agents) (Kane et al. 1988). Even though, Clozapine has not conclusively demonstrated its significantly superior record or efficacy for psychosis (Gardner et al. 2005), it has proven exceptional effectiveness, compared to other more traditional antipsychotics (Claghorn et al. 1987). However, Kane et al. (1988) and others have concluded, 30–60% of all schizophrenic patients who fail to respond to typical antipsychotics may respond therapeutically/effectively to Clozapine (Breier et al. (1994) & Iqbal et al. (2003)). This is especially apparent for refractory schizophrenia (Kane et al. 1988), treatment-resistant schizoaffective disorders (Zarate et al. 1995) and aggression (Cohen & Underwood, 1994).

The vast majority of medications currently in the marketplace or under development to treat schizophrenia/psychosis focus on dopamine in one way or another. Most of the medications that are currently used to treat this condition affect dopamine in a direct way. These drugs specifically target this substance because historically, psychosis has been linked to unusually high levels of dopamine in the part of the brain that is known as the stratum (Nauert, 2010). Moreover, there is a fair amount of research that indicates there is a direct correlation between levels of glutamate, which is another substance the brain produces and is found in the hippocampus, and dopamine in individuals who eventually develop schizophrenia.

Kaboom! In the matter of seconds a fun time can turn into a panic of terror. Looking around, seeing the sheer excitement on everyone's face. Not one of us had second guessed this idea. It was completely silent, not one cricket chirped, in the dried out grass clearing. Although it is a peaceful little place, it's not going to be so soothing and tranquil any longer. Now came the roar of the explosion, echoing through the wood. A violent blast of burning hot air hit my face. Shrapnel of glass bottle pierces my skin. Gunpowder and debris from the oak wood tree dusted my lips, having a bitter disgusting flavor. A blinding flash of light dazed me, white spots began to spread around my line of sight. The sounds of laughter at the campfire, cars passing by, and the wind whistling through the trees suddenly all went quiet, but a rising tone of a broken amplifier replaced all the other noises, causing us to become disorientated. Not even being able to hear the crackling of leaves beneath our feet, over the insane ringing.

There are primary neurological brain abnormalities in individuals with schizophrenia. According to Fusar-Poli (2009), schizophrenia is delineated by prefrontal activity and elevated striatal dopaminergic functions. These elevations in striatal dopamine activity and prefrontal cortical dysfunctions (Fusar-Poli, 2009). Along with other abnormalities in white matter as well as, having been observed in the right superior frontal gyrus, left middle frontal gyrus, bilateral parahippocampal gyrus, adjacent to the right caudate head, right thalamus, left insula, left lentiform nucleus, left fusiform gyrus, and bilateral claustrum (Antonius, 2011). The study of these findings may assist us to understand their role in the severity of the schizophrenia disorder symptoms (Antonius, 2011).

Schizophrenia is a life-long disorder that affects about one percent of the population (Mueser & McGurk, 2004). The cause of this mental illness is still unclear. Studies have suggested that Schizophrenia does not arise from one factor but from a combination of genetic, environmental, and social factors (Liddle, 1987). People diagnosed with Schizophrenia struggle to deal with a multitude of symptoms that make it difficult to function (Mueser & McGurk, 2004). Antipsychotic medications are a popular treatment of the symptoms of Schizophrenia (Mueser & McGurk, 2004). Research is constantly being done to develop these medications to enhance the quality of life of those diagnosed with Schizophrenia.

Schizophrenia research has examined many glutamatergic components, which has altered the Glutamate Hypothesis many times; nonetheless, the updated hypothesis explains Schizophrenic symptoms as the result of the malfunctioning of NMDA (n-methyl-d-aspartate) receptors, which are ionotropic glutamate receptors (Howes et al., 2015). For instance, a psychopharmacological study by Krystal et al. (1994) examined the effects of Ketamine, an NMDA non-competitive antagonist, on behavior. They observed the behavior of three groups of healthy adults that were administered a placebo or a high or low dose of Ketamine via an I.V. injection. Subsequently, those injected with Ketamine presented dose-dependent schizophrenia-like behaviors that were similar to positive and negative symptoms (Krystal et al., 1994). Similar studies have replicated these findings; however, to ensure that these behaviors are not only related to acute treatment, other studies have looked at prolonged use. Stone et al. (2014) compared the mental states of a group of chronic Ketamine users with a group of poly-drug users, and found that six of the fifteen chronic Ketamine users were formally at-risk for a psychotic episode, while none of the poly-drug users fit such criteria. Secondly, they used proton magnetic resonance spectroscopy (H-MRS) to measure the activity of glutamatergic system proteins, such as glutamine, creatine, and N-acetyl aspartate (NAA), in

One major hypothesis, the dopamine hypothesis, postulates that dopaminergic overexpression in the brain is associated with schizophrenia onset. This explanation was originally based on studies that observed the significant interaction between psychostimulants and increased dopamine transmission (Abi-Dargham, 2012). An alternative hypothesis is the glutamate hypothesis, which attributes schizophrenia development to hypoactivity of glutamate receptors. This hypothesis was based on psychostimulants’ antagonism to glutaminergic N-methyl-D-aspartate (NMDA) receptors. And, specific genes that act as modulatory sites for NMDA receptors are believed to increase risk for schizophrenia (Moghaddam, 2005). Likewise, the overexpression of other receptors, such as serotonergic receptor 5-HT2A, has been implicated in the etiology of schizophrenia. More likely, however, the dynamic imbalance between dopaminergic and serotonergic transmission contributes to the pathogenesis of this disease. This two-pronged explanation is the foundation for theories regarding the mechanism of action of second-generation antipsychotics (Roth & Meltzer,

The Dopamine Hypothesis theorizes that the symptoms portrayed in Schizophrenia is can be explained by abnormal function of dopamine in the brain. There have been three versions of the Dopamine Hypothesis. The first version of the hypothesis focuses on the dopamine receptors. Antipsychotic drugs that impact the metabolization and reabsorption of dopamine where found to be effective in treating the symptoms. It was theorized that if the symptoms of a Schizophrenic episode can be treated by the use of dopamine

The Dopamine Model (DM) has been around since the twentieth century (Preston, O’Neal and Talaga, 2017). The model believes that the cause of schizophrenia symptoms is from abnormal dopamine in the brain (Preston, et al., 2017). The premise is based off two observations. The first one is that antipsychotic drugs are able to bind and block the dopamine receptors (Preston, O’Neal, et al., 2017). The second observation is that the antipsychotic drugs increases dopamine which create paranoid schizophrenia symptoms (Preston, et al., 2017).

The period of time a patient experiences any issues before receiving any form of drug treatment has found to be a significant predictor of any long term effects. Lieberman et al. (1990) reported this as an indicator that neuron degeneration is progressive, resulting in a diminished response to the antipsychotic medication. Provide treatment too late, and it can result in amount of neuronal damage being too severe to allow for a full recovery. Biological theorists have over time proposed a variety of possible causes for any neural damage, as next for discussion. This is useful as it provides an indicator as to the possible development of schizophrenia as it is significant, empirical

In regard to proposals put forth to explain what dysfunctional mechanisms are causing schizophrenia, the dopamine hypothesis has been one of the most prevailing. The earliest versions of this hypothesis proposed that dopamine producing neurons in the brain were hyperactive (Haracz, 1982). An updated hypothesis, version II, described which specific areas were producing too much dopamine (Davis, 1991). Since that publication, thousands of other ideas have been put forth to test the dopamine hypothesis. Advancements in neuroimaging techniques have created a pool of information ripe for another iteration of the hypothesis.

Lu Xun’s story “Diary of a Madman” serves to demonstrate his discontent with traditional Chinese cultural, not only by the fact that it clearly addresses the incidence of cannibalism that is believed to have occurred but also symbolizes the oppressive nature of Confucian principles.Lu Xun’s madman has the ability to recognize the oppressive elements of Chinese Confucian culture serves to mock established but out-dated traditional scholarship and symbolizes the greater wisdom of cultural reform, especially as it is advanced by modern intellectuals of the period.