Introduction The History Of Schizophrenia Psychology Essay

Introduction The History Of Schizophrenia Psychology EssaySchizophrenia from the classical word (schizo) means split and (phrenia) means mind is a psychiatric disease characterised by despotic, negative and cognitive dysfunctions (Andreasen, 1997 Meltzer, 1999a, b Meltzer et al., 1999 Weinberger and G onlyhofer, 1997). These symptoms argon characterized by delusions, h on the wholeucinations, loss of abstract thinking and difficulty to differentiate between ingenuousness and fantasy. In general, symptoms differ from one person to another.Schizophrenia has been known to homo since the ancient Egyptians. The ancient Egyptians described disturbances in thought and behaviour which is seen in dementia praecox. Many of the dementia praecox symptoms have been described in ancient Greek, Romans and Chinese scripts. During that sequence, these societies had an awareness of psychotic disorders and believed they were caused by demons and evil spirits. Treatment of psychotic disorders w as exorcising of the demons which varied enormously from mild and safe treatment much(prenominal) as exposing the enduring to certain music to more invasive and fatal treatment such as drilling into the tolerants skull (Schizophrenia.com, (nd). The History of Schizophrenia.online Available http//www.schizophrenia.com/history.htm. Last accessed 13 declination 2009).Our belowstanding and differentiation of schizophrenia from other mental disorders alterd and influenced by Huglings-Jacksons postulations in 1984. His possibleness influences most of schizophrenia researchers until now such as (Andreasen et al., 1995 Meares, 1999a, b). He classified psychosis as a neurological disorder and categorize excessive behaviour as positive symptoms and absence in emotions, obstetrical delivery and social withdrawal as negative symptoms. The most chief(prenominal) of his hypothesis is that he proposed that negative symptoms are caused as a result of abnormalities in the brain and positi ve symptoms result from cognitive deficits (as cited in Beck, 2009)Another important scientist is Emil Kraepelin, a German psychiatrist, who introduced the term dementia praecox in 1896. He observe a number of young patients and came to a conclusion from his extensive clinical observation with three symptoms hebephrenia (purposeless, disorganised) catatonia (immobility and anxiety) and paranoia (delusions and h every last(predicate)ucinations). He grouped them under dementia praecox (early dementia) as he observed these symptoms in young bighearted patients. He also identified works store deficits, attentional deficits and lack of organisation (Kraepelin et al., 1919)The instituteing father of schizophrenia is Eugen Bleuler, a Swedish psychiatrist, who introduced the schizophrenia term and classified schizophrenia as a mental disorder (Bleuler and Zinkin, 1950) and went beyond Kraepelins observations. He characterised schizophrenia symptoms into primary symptoms and secondary s ymptoms. Primary symptoms involve social withdrawal and attentional deficit and were benefaction in all schizophrenia patients and had brain abnormalities causes. Secondary symptoms which include delusions, hallucination, catatonia and these symptoms were not natural for diagnosis and they had no pathological brain abnormalities. He proposed that there is a link between underlying neurological pathology that results in the manifestation of the symptoms (as cited in Beck, 2009)Besides the positive and negative symptoms experienced by schizophrenia patient cognitive deficits are also one of the core symptoms experienced by schizophrenia patients. Cornblatt and his colleagues (1997) pointed out(p) that attentional deficits and other cognitive deficits observed in patients are part of the disorder symptoms but they are independent of the positive and the negative symptoms and do not respond to treatment (Cornblatt et al., 1997). cognitive deficits frequently lead to the expression of psychosis (Erlenmeyer-Kimling et al., 2000) and tend to be no deterioration of the symptoms all over time (Albus et al., 2002). Cognitive deficits present even after subsidence of psychosis and unaffected(p) by antipsychotic treatment (Harvey and Keefe, 2001 Keefe et al., 2007).Measurement and Treatment Research to alter Cognition in Schizophrenia (MATRICS)As a result of the devastated logical implication of this disorder, research has now started to focus on developing drugs to meliorate erudition in schizophrenia patients and also to improve social and employment. This led the case Institute of Mental Health (NIH) to the initiation of the MATRICS (Marder and Fenton, 2004). The MATRICS initiative aim is to improve current treatment and also to develop new drugs that help improve science in patients. (Green et al., 2004) MATRIC Program (nd) MATRICS.ucla.edu. online Available http//www.matrics.ucla.edu/.htm. Last accessed 13 December 2009).MATRICS create a consensus that concluded the of import common features of cognitive deficits found in schizophrenia patients. These seven cognitive deficits are oral learning and shop, visual learning and depot, reasoning and problem solving, speed of processing, works memory and social cognition. These seven domains should be represented in a cognitive battery to evaluate the effects of new drugs on cognition in schizophrenia (Nuechterlein et al., 2004).In order to develop new drugs to deepen cognition in schizophrenia, preclinical test batteries are required to imitate schizophrenia cognitive domains in vivo. Floresco and his colleagues (2005) considered two methods for developing cognitive range and animal models to mimic schizophrenia symptoms by (i) using lesions or drugs intercession to alter systems which fetchs to schizophrenia disorder and (ii) to develop animal models that characterise schizophrenia symptomatology (Floresco et al., 2005)Animal models to mimic schizophrenia in Laboratoryphencycl idine hydrochloride was first of all used as a surgical anaesthetic but it was found to cause schizophrenia-like symptoms in patients after surgery (Morris et al., 2005). PCP antagonises non-competitively N-methyl-D-Aspartate (NMDA) receptor (Anis et al., 1983). It binds to post within channel pore which is accessible when the pore is open and antagonism is use use-dependent (Morris et al., 2005). PCP also antagonises other ion channels such as voltage-dependent sodium and potassium channels and nicotinic acetylcholine receptor in the same stylus as the NMDA receptor but not use-dependent(Oswald et al., 1984). It also antagonises membrane proteins of sigma receptors and all dopamine and noradrenaline transporters (Garey and Heath, 1976 Pubill et al., 1998). These actions of PCP are less potent than its actions on the NMDA receptor. Yet, schizophrenia patients show reduced CNS nicotinic receptors activity and elevated limbic dopamine level and compromised sodium and potassium cha nnel function (Morris et al., 2005). Thus, these actions contribute partially to the schizophrenia symptoms and action at NMDA receptor remains the main site of action (Morris et al., 2005)Showing PCP and ketamine to cause schizophrenia-like symptoms in healthy patients ((Adler et al., 1999 Allen and Young, 1978 Krystal et al., 1994 Luby et al., 1959) led to hypothesis that schizophrenia is related to NMDA hypofunction in the limbic system (Olney and Farber, 1995) which is supported by post-mortem examination studies in schizophrenia patients screening evidence of decreased expression of NMDA receptor subunits and associated proteins in the brain of schizophrenia patient compared to control (Noga et al., 1997 Sokolov, 1998)Thus, PCP has been used to model cognitive deficits in animal models (Jentsch and Roth, 1999 Mandillo et al., 2003 Sams-Dodd, 1998). Sub-chronic administration of PCP has been found to produce schizophrenia-like symptoms in rodents (Jentsch and Roth, 1999). Cogni tive dysfunction induced by sub-chronic injection of PCP results in deficits in works memory and inhibtitory in control in rodents and monkeys (Jentsch and Roth, 1999).In the present champaign, we are only concerned with works memory. The term working memory was first introduced by David Olton and Werner Honig in the 1970s (as cited in Dudchenko, 2004).Working memory is defined the retrieval of information learnt over a delay of time within sessions but not necessarily between sessions (Dudchenko, 2004).The holeboard task was developed by Oades in1978 and this behavioral test is useful as it allows each in the test to develop its own method of finding food injection (Oades and Isaacson, 1978) making this behavioural test a good experimental initiation to assess spatial working memory in rodents. This test curse on intact hippocampus and performance was impaired following lesions in the ventral tegmentum (Oades, 1982)The test can only be carried out in rats. The test apparatus consisted of an arena 70-70-50cm with 16 holes 3.5cm wide and 2cm deep (Oades and Isaacson, 1978). The animals are left to explore the arena to adapt to the apparatus with food beingness placed in all of the holes, the animals deprived from food before the number one of the test and this time food is only allocated at 4 holes out of the 16 holes (Oades and Isaacson, 1978)The test which have been developed to mimic deficits in working memory seen in schizophrenia patients are useful to assess working memory in rodents but with difficulties and confliction in defining working memory between rodents and humans make it hard to model this cognition in animal models and to assess the effect of antipsychotic drugs.The core aim of this study was to assess the effects of sub-chronic PCP treatment on the spatial working memory using the 16-hole. It is expected that sub-chronic treated rats will perform indisposed in this task as sub-chronic PCP induce deficits in working memory in animal models (Jentsch and Roth, 1999).Objectives of this experiment is firstly is the habituation of 16 female rats to the 16-hole-board for 3 days and the food is available in all of the 16 holes, then the food will be placed in only 4 holes and the animals will be trained to eat and call down these holes only for 7 days and is then followed by the administration of sub-chronic PCP (2mg/kg, n=8) or vehicle (0.9% saline, n=8) intraperitoneally for 7 days followed by washout of the drug for 7 days and then carrying out the behavioural test.