SCHIZOPHRENIA

0 Comments

Schizophrenia is a very rare and dreaded mental illness that has plagued mankind for countless years. Researchers have explained that of all psychiatric conditions, schizophrenia, with a lifespan pervasiveness of 1% globally, is the most complicated to understand and treat. It is associated with constant hallucinations, delusions, thought disorders, apathy and self-withdrawal. People suffering from schizophrenia are unable to differentiate between real and unreal experiences, think logically, have normal emotional reactions and even behave in a normal manner in social situations. Most people with schizophrenia live with the condition for the rest of their lives, requiring frequent and long periods of hospitalization.

In the early years, schizophrenia was looked down upon. People didn’t know it was a disease and as such was associated with demon possession. Most cases were overlooked, terming them as nervous breakdowns or split personalities. Robert Louis Stevenson in his fictional novel, “The Strange Case of Dr. Jekyll and Mr. Hyde” popularizes the concept of multiple personality, a factor that is totally unrelated to the schizophrenia. This can be backed up by evidence that clearly explains development of multiple personality being witnessed early in life and often as a result of child hood trauma whereas schizophrenia develops in early adulthood or late adolescence.

Over the years countless studies have been carried out by scientists worldwide to investigate the cause of the illness and establish a cure. In fact, schizophrenia has been the most investigated psychiatric disorder, with scientists spending the most time, money, energy on research towards this illness than on all other psychiatric disorders combined. The unfortunate truth is that despite all the countless studies, our ignorance concerning its causes and treatment is still abysmal. The onset of the illness is usually in the early 20’s and even with medication and therapy; it usually persists throughout the entire adult life. The best we can ascertain is that several theories have been developed over the years each one seeking to resolve the issues underlying schizophrenia. Little satisfaction can be achieved in the fact that psychiatry, in its bid to understand schizophrenia, is still more backward than oncology is on its vigorous research in cancer. Evidence suggests that the main obstacle in understanding schizophrenia is the fact that most researchers have failed to know the significant questions to ask and how to achieve the correct answers to these questions.

In the U.S for example, approximately 2.2 million of its citizens suffer from schizophrenia. In terms of ratio, this means that 8 out of every 1000 people suffer from the illness, with almost 900,000 people having schizophrenia ending up not being treated. This staggering large number of untreated people suffering from schizophrenia is not a new thing to our ears.

History of Schizophrenia

In the olden ages, Greek mythology associated schizophrenia as madness and even went on to the extent of associating it to a punishment from God. Greek physician Hippocrates (460-377 BC) decided to put schizophrenia into scientific speculation. He argued that this ‘madness’ may be as a result of an imbalance in bodily humors which through consuming the right diet and blood lettings, could be reversed. Greek philosopher Aristotle (384-322BC) and physician Galen (129-216 BC) went further to expound on Hippocrates humeral theory, both playing an important role in establishing schizophrenia as Europe’s dominant medical role.

“Only from the brain springs our pleasures, our feelings, our happiness, laughter and jokes, our pain, our sorrows and tears. This same organ makes us mad and confused, inspires us with fear and anxiety” – Hippocrates, The Holy Disease.

It is until the late 18th century that beliefs in modern psychiatry started to surface, resulting to people viewing schizophrenia as a disease. In 1887, Dr. Emile Krapelin, a German physician, became the first person to identify the disease as a discrete mental illness, terming it as “dementia paradox” to explain the symptoms in patients that we now term as schizophrenia.

Schizophrenia not only affects the people suffering from it but also their close relatives and friends. A person having schizophrenia will always have mixed reactions to everyday normal situations. This unfortunately takes a toll on the people who are closest to him as they have to continuously deal with a wide range of difficult emotions, including fear, guilt, anger, hopelessness and frustration. Many of them, worried about the stigma that is related o mental illness, are confused and embarrassed by the strange behaviors that they cannot understand. They opt to try and hide their loved ones illness from others. This supports the evidenced large number of untreated individuals suffering from schizophrenia. Unfortunately, this isolation and denial only compounds the problem.

It is argued from a highly biological basis of studies that schizophrenia is inherited. These studies have therefore revealed the existence of a gene that plays a major role in its onset. Hereditability however only applies to a very small percentage of those suffering from schizophrenia, as a majority of those suffering from it do not possess any family history to the disease. We cannot however condemn the studies undertaken in relation to schizophrenia. Positive steps have been achieved over a number of years including the development of newer antipsychotics. These antipsychotic drugs have been able to provide the people suffering from schizophrenia with at least some measure of relief and ability to live their lives. However, most of these medications come with a wide range of side effects which may disable the individual.

 

Publication about Schizophrenia

Of all the factors associated with development of schizophrenia in patients, imperative evidence suggests that genetics play a major role. According to Annabel Bligh (2014) in her publication, “The genetics behind schizophrenia are more complex than we thought”, a recent study to understand the genetics of schizophrenia was carried out with scientists sampling blood from almost 7000 Swedes and Bulgarians. The blood samples were obtained from patients diagnosed with schizophrenia and their parents. The samples were thoroughly examined and compared on the basis of those who had a history of the disease. Findings from this study were very fruitful as they not only isolated patterns relevant to the biology that underlies the disease but they were also able to locate genetic mutation sites primarily responsible for its advent. However, as Bligh further expounds, the conclusion from the study stated that the disease possessed a very complex genetic basis. This invalidated the assumption that specific genes are responsible for the disease, and posed a major drawback in discovery of the schizophrenia gene despite the concerted efforts. On the contrary, the research established that a number of genetic mutations are implicated in the development of schizophrenia.

In developing a treatment and prevention strategy for schizophrenia, it is important to identify the cause(s) of the disorder. As research in understanding the disease is progressing over the years, improved understanding of the disease has been evidenced. For example, scientists have been able to identify possible genetic and environmental causes that they believe result to development of schizophrenia in patients.

 

 

 

Models explaining the causes of schizophrenia

Scientists have developed various models suggesting biological and environmental causal factors of schizophrenia. These models however vary in range, a factor attributed to the variety of ways in which schizophrenia manifests itself (Peralta & Cuesta, 2000). Onley and Faber (1995) suggested that NDMA receptor hypo function could provide reliable insight, both physiological and biological; to the symptoms of schizophrenia (cited in Keshavan et al., 2008). Their theory had a good number of similarities to the genetic causes of schizophrenia scientists had previously documented. However, compelling evidence to support the validity of their model lacked (ibid.)

Crow (1995) came up with another model in which he suggested “a desynchrony of hemispheric development due to genes involved in evolution of language”. His model played an important role in explaining a number of aspects related to schizophrenia. Another model was yet suggested, claiming that stress may be the trigger to schizophrenia (Concoran et al., 2003). This model however failed to answer the question of why a number of people are prone to the disease whereas others are not. As a result of these models, along with many others, it was suggested that a clear model to explain schizophrenia would remain being an overwhelming drawback, reason being; the assumption that schizophrenia is a single disease may be false (Keshavan et al., 2008). This proposal maintains its validation from the fact that a wide range of manifestations can be witnessed in persons diagnosed with schizophrenia.

Another proposal put on the table was that “as long as the question of heterogeneity fails to be understood and answered at clinical levels, heterogeneity would be difficult to resolve at further pathological and etiological levels (Peralta & Causeta, 2000, p.253). In a nutshell, it suggested that until we are able to see the symptoms of schizophrenia earlier enough and more clearly, it will be much harder to ascertain the proper cause model explaining the cause of schizophrenia.

In the recent years, newer and more informed models have been created, with the examples off the stress-diathesis model and bio-psychosocial model. The bio-psychosocial model aims at unifying both the biological, physiological and social caused that may bring about schizophrenia (Harris, 2010). The model also tries to categorize the causes of schizophrenia by whether they are triggered, predisposed or keep the disorder continuing (ibid.) hence allowing for the creation of a table that can assist in organizing the broad causes of schizophrenia. The stress-diathesis model on the other hand relates stress factors in the environment to the onset or trigger of the disease to individuals suffering from it (Jones & Ferynhough, 2007). In as much as these two models seem to differ, they both agree to the fact that schizophrenia is a very complex disease, having a broad list of causal factors that can expose individuals to it or trigger it on them.

 

Genetic Causes of Schizophrenia

Research has shown that both environmental and genetic vulnerability when combined can lead to schizophrenia, and that genetic problems resulting to this disease are caused by different genes and other factors (Harrison & Owen, 2003). It has however been hard to estimate hereditability of schizophrenia due to the complexity of separating the environmental and genetic problems (O’Donovan et al., 2003). A recent research that was done on twins revealed a high level of heritability in both of them and suggested that gene factors may be the main cause of the disease (ibid). This theory of genetics suggests that schizophrenia possesses complex heritability and subsequently, research has primarily focused in establishing these particular genes that are assumed to be responsible for this mental illness (Owen et al., 2005). Other studies have revealed that some patients suffering from schizophrenia have deletions or duplications of their DNA sequences. These duplications affect genes that are responsible for neuronal signalization of the brain development (Walsh et al., 2005) and this result to psychotic disorders such as schizophrenia. Whenever the structural sequence of the brain is not normal or becomes unchanged, e.g. a difference in volume of the grey matter in some of the sections of the brain, reduction in the number of neurons occurs, causing psychotic syndromes (Hoffman & McGlashan, 2001).

With advancement in technology, high resolution brain imaging processes have been made possible. Scientists have been able to observe that there exists a common abnormal connection of different gene networks in schizophrenic patients (Broyd et al., 2009). These observations have revealed a rivalry between neural networks leading to deactivation of one of them, hence disrupting functions in some parts of the brain. These results have been pivotal in explaining most symptoms related to schizophrenia such as loss of memory, attention disorders and social cognition (ibid.) Research on the cause(s) of schizophrenia has stressed particular attention to the function of dopamine in the mesocortical and mesolimbic pathway of the brain. Seeman et al. (2005) explains that based on drug experiments, the “dopamine hypothesis of schizophrenia” show that a malfunction in this area results to the disorder symptoms. Evidence is derived from findings which show that genes coding for mechanisms involved in dopamine function are usually more prevalent in individuals diagnosed with schizophrenia (Arguello & Gogos, 2008).Later research however revealed that dopamine function may not be the cause of schizophrenic symptoms, and in contrast, low levels of glutamate, another neurotransmitter, has been the one found to produce the similar effects.

Drug Use

Compelling evidence has suggested that use of certain drugs, can trigger the onset or relapse of schizophrenia in individuals, with cannabis being the main drug of focus, with amphetamines and hallucinogens also being included. Despite this, a comparative relationship between drug use and schizophrenia is yet to be established. Studies carried out on cannabis suggest that the drug increases the risk of developing schizophrenia, but these findings have not been sufficient in establishing it as a contributing factor in the development of the disorder (Arsenault et al., 2004). From a review of studies conducted by Arsenault et al., it can be casually assumed that 8% of cases in the overall population of schizophrenic patients result from use of cannabis, which is believed to double the risk of developing the disease. Amphetamines on the other hand tend to worsen symptoms of schizophrenia since the drugs triggers the release of dopamine (Laurelle et al., 1996). Excessive use of hallucinogens has also been found to trigger the onset and relapse of schizophrenia, explains Meuser et al. (1990). Unfortunately, all these drugs have failed to produce significant factors in explaining their relationship with schizophrenia but nevertheless have been stated to trigger schizophrenia (Laurelle et al., 1996).

 

 

 

 

 

Conclusion

The unfortunate truth that dawn on us is that schizophrenia has no cure. Despite having medication for the illness, the medication only serves to reduce the symptoms related to schizophrenia and not to treat the illness itself, and once individuals suffering from schizophrenia stop taking them, all the symptoms return. Also, it’s quite disturbing that despite the countless efforts and hours scientists all over the world have put in trying to understand the disease; it still remains a complex disorder. The complexity in interrelated factors causing schizophrenia, genetics being at the peak of it among other environmental factors and drugs use have been sufficiently examined, with no major breakthrough yet. Seaman (2010) argued that all roads to schizophrenia lead to dopamine sensitivity”. All responsible research bodies worldwide should aim at unification of the numerous research findings, if a similar diagnosis for schizophrenia is to be achieved. At the moment, no known cure exists, but there is only hope that constant in-depth research will provide a lasting solution to those suffering from schizophrenia, enabling them to live normal and healthy lives.

 

 

References

Arguello, P. A., Gogos, J. A. (2008). A signaling pathway AKTing up in schizophrenia. J Clin Invest,118, 2018–2021.

 

Arsenault, L., Cannon, M., Witton, J., Murray, R. M. (2004). Causal association between cannabis and psychosis: examination of the evidence. Br J Psychiatry, 184, 7-110.

 

Broyd, S. J., Demanuele, C., Debener, S., Helps, S. K., James, C. J., Barke, E .J. S. (2009). Default-mode brain dysfunction in mental schizophrenia disorders: a systematic review. Neurosci Biobehav Rev, 33, 96-279.

 

Corcoran, C., Walker, E., Huot, R., Mittal, V., Tessner, K., Kestler, L., Malaspina, D. (2003). The stress cascade and schizophrenia: etiology and onset. Schizophrenia Bull, 29, 92-671.

 

Harris A. (2010). Pharmacological treatment of schizophrenia [Lecture on the Internet]. (2010). Sydney: University of Sydney [cited 2010 Nov 8]. Available from: http://sydney.edu.au/medicine/psychiatry/workshops/presentations/pharmacological_treatment_schiz.pdf

 

Harrison, P. J., Owen, M. J. (2003). Genes for schizophrenia? Recent findings and their pathophysiological implications. Lancet, 361, 9-417.

 

Hoffman, R. E., McGlashan, T. H. (2001). Neural network models of schizophrenia. Neuroscientist, 7, 54- 441.

 

Janssen, I., Krabbendam, L., Bak, M. et al. (2004). Childhood abuse as a risk factor for psychotic experiences. Acta Psychiatr Scand, 109, 38-45.

 

Jones, S. R., Fernyhough, C. (2007). A New Look at the Neural Diathesis Stress Model of Schizophrenia: The Primacy of Social-Evaluative Schizophrenia and Uncontrollable Situations. Schizophrenia Bull, 35, 177-1171.

 

Keshavan, M. S., Tandon, R., Boutros, N. N., Nasrallah, H. H. (2008). Schizophrenia, “just the facts”: what we know in 2008 part 3: Neurobiology. Schizophrenia Res, 106, 89-107.

 

Laruelle, M., Abi-Dargham, A., Van Dyck, C. H., Gil R., D’Souza, C. D., Erdos, J., McCance, E., Rosenblatt, W., Fingado, C., Zoghbi, S. S. et al. (1996). Single photon emission computerized tomography imaging of amphetamine-induced dopamine release in drug-free schizophrenic subjects. Proc Nat Acad Sci USA, 93, 40-9235.

 

O’Donovan, M. C., Williams N. M., Owen, M. J. (2003). Recent advances in the genetics of schizophrenia. Hum Mol Genet, 12, 33-125.

 

Owen, M. J., Craddock, N., O’Donovan, M. C. (2005). Schizophrenia: genes at last. Trends Genet, 21, 25-518.

 

Peralta, V., Cuesta, M. J. (2000). Clinical Models of Schizophrenia: A Critical Approach to Competing Conceptions. Psychopathology, 33, 28-252.

 

Seeman, P., Weinshenker, D., Quirion, R., Srivastava, L. K., Bhardwaj, S. K., Grandy, D.K., Premont, R.T., Sotnikova, T. D., Boksa, P., El-Ghundi, M., et al. (2005). Dopamine super sensitivity correlates with D2High states, implying many paths to psychosis. Proc Nat Acad Sci USA, 18-3513.

 

Walsh, T., McClellan, J. M., McCarthy, S. E., Addington, A. M., Pierce, S.B., Cooper, G. M., Nord, A.S., Kusenda, M., Malhotra, D., Bhandari, A., Stray, S. M., Rippey, C. F., Roccanova, P., et al. (2008). Rare structural variants disrupt multiple genes in neurodevelopment pathways in schizophrenia. Science, 320, 43-539.

"Are you looking for this answer? We can Help click Order Now"

UK BEST WRITING