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Post by alison on Mar 3, 2016 10:01:37 GMT
I found it disturbing to read the chapter on deactivation syndrome (Breggin). I confess I wasn’t aware that the current use of the term ‘anti-psychotic medication’ isn’t strictly accurate – nor that the lobotomy-like effects of neuroleptic drugs were widely written about when these drugs first came into use. I recognize there are individual and public safety issues for consideration, but it seems the words ‘control’ and ‘management’ are more appropriate than ‘treatment’ in relation to the use of neuroleptic drugs. As per this paragraph: “…these patients and inmates sometimes seem less obviously in emotional pain, and they are almost always more manageable. But the effect has nothing to do with treating a psychiatric disorder. Instead the patients have been rendered emotionally and neurologically disabled by the drugs” Breggin, p41 My view is that certain circumstances will require medication as a necessary component in the treatment of schizophrenia – but this should always be within a broader context of psychosocial treatment. I found this to be an interesting summary of psychosocial interventions: www.ncbi.nlm.nih.gov/pmc/articles/PMC3181651/Research suggests the exact causes of schizophrenia are unknown, but that a combination of physical, genetic, psychological and environmental factors can make people more likely to develop the condition. And that people fare better in the long-term if medication is avoided (in favor of psychosocial interventions) at the first episode. My heart sinks when I think about the implications of budgetary cuts, not just in acute mental health services, but broader social support and 'prevention' services, day centres, children's centres..... etc etc etc. I think Chris's earlier post (Cartesian... leadership... boarding/public school.....) was an insightful post in relation to this topic |
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tutor
New Member
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Post by tutor on Mar 6, 2016 6:47:55 GMT
Hi Alison
I agree this is a very worrying situation. We seemed to be moving in the right direction with early intervention approaches to psychosis. However some of these teams have been disbanded because of budget cuts.
There is a saying - "The way to judge a civilisation is how it treats its weakest members."
Tutor
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Clare
New Member
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Post by Clare on Mar 8, 2016 14:21:52 GMT
The prevalence of schizophrenia is approximately 1%. Research has recognised that the aetiology is a complex puzzle with the consensus concluding that
• Aetiology involves environmental and genetic factors
• Multiple developmental pathways lead to the onset
• Maturational process play a role in the aeitiological process
(Maddux J. 2016)
There are many theories for the onset of schizophrenia, Maddux 2016 Chapter 17 has a very in depth and up to date collection of research which I will attempt to summarise into a bite size view:
There have been countless adoption studies to provide enough evidence for a genetic component and found that psychosis was significantly higher in adoptees that had biological mothers with schizophrenia. This genetic vulnerability was mainly expressed in a disruptive adoptive environment compared to the adoptees grown up in a stable environment. These findings support genetic vulnerability interacting with environment.
There is also the effect of the neurotransmitter’s dopamine and glutamate (mainly the N-methyl-D-aspartic NMDA receptor). The enhancement of this receptor can reduce negative symptoms in schizophrenia but why and how is unknown.
However, further research into gene expression and understanding of neurotransmitter abnormalities is needed.
Treatment:
According to Maddux (2016), the treatment of schizophrenia can be divided into 3 phases:
• The acute (4-8 weeks duration)
• Stabilisation (6 months)
• Maintenance
Pharmacological interventions are with a group of second generation antipsychotics, blocking the dopamine nueurotransmitter, and vary in the way that they affect serotonin, glutamate and other neurotransmitters. There is an elevated risk of weight gain, new onset or worsening diabetes mellitus and lipid abnormalities. (Newcomer, 2005).
Psychosocial interventions including family therapy has substantial benefits, particularly for the prevention of a relapse it is about working with the individual and their family to create a support network.
A very interesting topic, and a specialised area of expertise. Optimal treatment would be a combination of pharmacological and psychosocial approaches tailored to the individual needs. Schizophrenia itself a complex and differs in its complexity in every individual. The individual may lead a “normal” life if this right balance is achieved.
Maddux. James et al (2016). Psychopathology. Foundations for a Contemporary Understanding. 4th ED. Routledge London & New York
Paris. J (2015). The Intelligent Clinician’s Guide to the DSM-5. 2nd Ed. Oxford University Press
Newcomer J (2005). Second Generation antipsychotics and metabolic effects: A comprehensive literature review. CNS Drugs, 19, 1-93
Bach D et al. (2012). Long term effects of brief acceptance commitment therapy for psychosis. Behavioural Modification, 36(2), 165-81
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Post by liliana on Mar 9, 2016 17:58:44 GMT
Both, Alison and Clare, mentioned a number of factors that, together, in various combinations, could cause schizophrenia. But, as Cornblatt et al. observe in the Oxford Textbook of Psychopathology (2009), after nearly 100 years of study, the cause of what is largely accepted as a disease of the brain, namely schizophrenia, remains a mystery. What is widely observed and accepted is that schizophrenia runs in families. It is still not clear, though, whether shared genes or shared environments are to blame. The tendency was first to search, in the psychoanalytic tradition, for the environmental factors, parenting and other family interactions being seen as source of schizophrenia. In the last four decades, though, the focus has fallen on the genetic component of schizophrenia and the other environmental factors impacting genes, mainly family environment and early development in individuals with genetic predisposition to develop the illness.
I would add that, in terms of the aetiology of schizophrenia, apparently the strongest known risk factor is genetic, Gottesman and Shields (1982), and then Gottesman (1991) explain the existence of a so called ‘gradient of genetic risk’ for schizophrenia, according to the proximity of the genetic relationship to the schizophrenic proband, the closest genetic relationship being to a monozygotic twin. Indeed, the gradient of risk for schizophrenia in the general population is just 1%, but it increases gradually the closer one gets on the scale of genetic relationship to the proband. So, for example there is a 4% risk of a nephew developping the illness if a grandfather was affected, 10% when brother or sister suffer from schizophrenia, 13% when one parent has schizophrenia, and 46% when both parents have it.
There is 50% risk of a monozygotic twin developing schizophrenia, but the 50% discordance in these genetically identical individuals is usually used as evidence in favour of environmental factors. This is supported by the neuroimaging studies of monozygotic twins who are discordant for schizophrenia and who show some brain abnormalities (in general, the temporal lobe volume is smaller, and the fluid-filled parts of the brain, or ventricles, are larger) in the affected compared to the non-affected of each of the twins (Gregory, 2004). The idea is that the non-affected twin still carries a great risk of schizophrenia, that he or she possess a genetic vulnerability, and could later show features of schizophrenia without meeting diagnostic criteria for the illness itself.
In term of non-genetic factors that actually may contribute to increase the risk of schizophrenia, I would mention the seasonality of birth, so called ‘season of birth effect’ for schizophrenia (in the Northern hemisphere only), though I am not very convinced of that. Other causal factors could be related to advancing paternal age, maternal stress during pregnancy, pregnancy and birth complications, exposure to influenza type A2 during the second trimester of pregnancy, etc.
There is also some research that focuses on the use of cannabis as a possible cause of schizophrenia in genetically vulnerable individuals. It is a well-known fact that cannabis can cause psychosis-like symptoms, but more research needs to prove that there is a direct link between the exposure to cannabis and schizophrenia.
Meanwhile, I have also read some passages from Breggin (2007) about the use of neuroleptics in the treatment of schizophrenia and the terrible effects in some patients. This is shocking indeed. I share Alison’s view that medication must be paired with psychosocial interventions.
There is also the idea that there are a number of advantages in treating pre-psychotic cases psychotherapeutically in the prodromal phase of schizophrenia by only addressing the patient’s current problems. Such early interventions can make, in some cases, a difference but not always and great caution is necessary (Sharma and Harvey, 2006).
I assume that a multidisciplinary team is always required from the very moment that someone is diagnosed with schizophrenia. The approach of treating schizophrenia should be consistent over time, with relapse-preventing strategies, and family and patient psychoeducation is vital. Psychological therapies, including specific treatments targeting medication adherence, social anxiety, depression, social skills, may also help, and should be available and included in the treatment plan. The most researched seems to be the use of CBT framework in helping people with schizophrenia to deal with ‘medication-resistant’ delusions and hallucinations. It has proved successful especially for delusions.
This is uncharted territory but I am sure psychotherapy can offer more than that and help to improve the quality of life of these people, and their families. I would really like to be able to look more closely into this.
References:
Cornblatt, B. A. et al. (2009) Schizophrenia: Etiology and Neurocognition. In Blaney, P.H. and Millon, T. (Eds.) Oxford Textbook of Psychopathology (pp. 298-333). New York: Oxford University Press.
Gregory, R. L. (Ed). (2004). The Oxford Companion to the Mind. New York: New York University Press.
Gottesman, I. I. (1991) Schizophrenia genesis: The origins of madness. New York: Freeman.
Gottesman, I. I. and Shields, J. (1982). Schizophrenia: the epigenetic puzzle. Cambridge: Cambridge University Press.
Sharma, T. and Harvey, P. D. (Eds.) (2006).The Early Course of Schizophrenia. New York: Oxford University Press.
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Post by alison on Mar 10, 2016 10:20:30 GMT
Thank you liliana, an interesting read. I think your comments on causal factors related to paternal age, maternal stress during pregnancy, pregnancy and birth complications are a very useful inclusion. Reminded me of the presentation by Prof Ray Iles at the NCHP conference 2014 (on impact of maternal stress in pregnancy). I think this is a very interesting area of research.
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Post by Chris on Mar 11, 2016 0:36:41 GMT
"I think Chris's earlier post (Cartesian... leadership... boarding/public school.....) was an insightful post in relation to this topic" Thank-you, Alison. My instinct and observation regarding this subject is that in the main, schizophrenia is caused by childhood misery - probably working in conjunction with a slight genetic predisposition to the condition. Recent research at the universities of Liverpool and Utrecht seemed to show that children exposed to severe trauma were three times more likely to develop schizophrenia than children with an uneventful upbringing: www.sciencedaily.com/releases/2012/04/120419102440.htm |
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