Essay On Phencyclidine

For the past fifty years treatment of schizophrenia has been marked by its basis on the dopamine hypothesis for schizophrenia. However, this model for the disease and its subsequent treatment have left many patients without relief or help in dealing with this disease which has lead to a search for a better model. The dopamine model lacks the recognition of a whole range of symptoms associated with the disease and therefore can not be an accurate basis for treatment. More recently, there has been a shift to the glutamate hypothesis which has been shown to more accurately characterize the wide range of symptoms experienced by patients living with this disorder as well as the possibility in improvements for drug treatments.

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

Over the last few decades Schizophrenia has become embedded in mainstream vernacular as any behavior or emotional response that is out of touch with reality. However even with its popularity heightened through movies and headline news stories, schizophrenia is still one of the most enigmatic and least understood disorders of the brain. With current research focused on the role of neurobiology and functioning on a cellular level, investigative analysis has merited new innovations towards its source, however a single organic cause for the disorder still eludes scientists. Although the foundation of the affliction is still unknown, its effects are well documented and over the next few pages will show the changes in the brain as the disease

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.

This paper defines schizophrenia from a biological and psychological perspective and also provides treatment to help combat symptoms of schizophrenia. This paper has three important contributions. First, by defining and expanding on schizophrenia from a biological perspective, I can identify the nature related predispositions. After expanding from a biological approach, secondly, I will analyze schizophrenia from a psychological aspect by determining if there is any environment or nurturing externals that can result to schizophrenia. Lastly, I will provide treatment details and also reveal early signs to schizophrenia. This paper is important because schizophrenia is an epic mental disease and it is crucially important to bring awareness to the public of how we can limit the illness. It is unclear whether schizophrenia have only a biological background or psychological background, but what was discovered is that both contribute to schizophrenia. Positive and negative treatment can be combatted undergoing pharmaceutical and psychotherapy,

A Review of " Intrinsic Hippocampal Activity as a Biomarker for Cognition and Symptoms in Schizophrenia"

An excess in dopaminergic, and a deficit in glutaminergic (specifically NMDA) signalling correspond to positive and negative symptoms respectively. The NMDA antagonist MK-801 is used in animal models of schizophrenia, while paranoid and persecutory delusions are typical of methamphetamine users. In those with an

From the biological perspective, there is a new suggestion that autoimmune diseases and schizophrenia are related. In fact, in one report individuals that had an autoimmune disease paired with hospital contact for an infection were at increased incidence rate than those without an autoimmune disorder treated for infection (Benros, Nielson, Eaton, Dalton, & Mortensen, 2012). This perspective is possibly the oldest in regards to the investigation of schizophrenia, beginning

Over the years, experiments have produced evidence to suggest that dopamine plays a role in the development of Schizophrenia (Howes, McCutcheon, & Stone, 2015). Dopamine is a neurotransmitter that is produced in the substantia nigra and ventral tegmental regions of the brain. The belief that dopamine was involved in Schizophrenia arose after multiple studies performed with compounds produced an increase in extracellular concentrations of dopamine (Lieberman, Kane, & Alvir, 1987). The patients that were administered these compounds had similar symptoms to those observed from patients who were diagnosed with Schizophrenia (Lieberman et al., 1987).

Schizophrenia is a chronic and severe neurological brain disorder characterized by disruptions in perception and reality and disturbances in emotions and language. This disorder is extensively studied by researchers, however the specific mechanisms and factors behind its development are still not completely understood. Most cases of schizophrenia arise in men between the ages 16-30, though the disorder is not confined to this group. Additionally, studies have identified over 100 genes associated with schizophrenia, making the causes of the disorder difficult to elucidate.What is better understood about the disorder is that there are changes in brain structure and communication.

Schizophrenia is a severe mental disorder that “disrupts the function of multiple brain systems, resulting in impaired social and occupational functioning” (Lewis & Sweet, 2009, pg. 706). Lewis (2009) suggests these functions usually consist of the confluence of disturbance in perception, attention, volition, fluency and production of language, recognition and expression of emotion, and capacity for pleasure. Schizophrenia has calamitous effects on people, and such devastating illness afflicts “0.5%-1% of the world’s population” (Lewis & Sweet, 2009, pg. 706). Lewis (2009) states that people with schizophrenia are at high risk of cardiovascular disease as well as excessive nicotine, alcohol, and

Prepulse inhibition is a measure of sensorimotor gating. Impairment of prepulse inhibition is frequently found in patients with schizophrenia and other neuropsychiatric disorders. A number of rat models have been developed using this known dysfunction to study the neurological pathophysiology that underlie these disorders. Two models that are known to be highly valid models in the study of schizophrenia are maternal immune activation and adolescent stress. Maternal immune activation is an environmental risk factor in the development of schizophrenia. In rat and mice models, it has been successful in producing deficits in sensorimotor gating. A number of cytokines have been identified as having a role in the neurological changes that result in behavioural and cognitive abnormalities in offspring. Adolescent stress is also considered an environmental risk factor in the development of schizophrenia. The adolescent brain is considered to be more vulnerable to stress than other stages of life. It is believed that a combination of maternal immune activation and adolescent stress is responsible for a larger effect size in humans. This is known as a two-hit model. To our knowledge, a two-hit model has not been applied to Long Evan Rats. It is our belief that using this combination will result in a stronger and more

A growing body of literature has shown that a deficit in the GABAergic system is involved in a variety of psychological disorders, including schizophrenia, anxiety, and depression (Lydiard 2003; Costa et al. 2004). The decrease of GABAergic signaling was considered to be one of the most robust pathologies observed in schizophrenia (Lodge et al. 2009). In addition, glutamic acid decarboxylase (GAD), which is an enzyme that catalyzes the decarboxylation of glutamate to GABA in interneurons, was markedly reduced in schizophrenia patients (Hashimoto et al. 2003). Dysfunction of GABAergic neurons has

Schizophrenia is a psychiatric disorder that affects about 1% of the adult population and carries a high disease burden involving a number of health comorbidities and an average decrease in life expectancy by 12-15 years. Current drug treatments for schizophrenia primarily target the positive symptoms such as hallucinations and delusions, but usually fail to treat negative symptoms such as social withdrawal, difficulty focusing, and lack of motivation. A major research challenge is to better understand the causes of schizophrenia so that more effective prevention and treatment plans can be developed.

Schizophrenia is a severe brain disorder that involves seeing objects that are not there, disordered or disrupt thinking and deficiencies in cognition. People affected by it may experience agitation as well as hours without talking. Doctors have studied for years in order to determine the actions that lead to this neural illness so far it is known to start in early adulthood. There is still not one specific cause of it. In this review, I will interpret the areas of the brain affected by this illness, its implications, psychological effects, its physical effect on individuals, and treatments that have been proposed. Human brain scans have provided facts representing the prefrontal cortex, limbic system, and the basal ganglia are affected.