Drug Abuse Dsm
Drug Abuse Dsm

Mental Health Disorders: Schizophrenia
Schizophrenia affects around 1% of the population of this planet. It is a chronic, severe, and disabling mental disorder. It has also been recognized for centuries, maybe not with the same nomenclature, but most likely with the same symptoms. However, the complex mechanisms which cause this condition remain a mystery of their own… but for how long?
History of Schizophrenia: from demons to genes
The symptoms commonly associated with schizophrenia are on the records of many ancient civilizations, such as the Greeks, Romans and Egyptians. The causes for this mental disorder have been associated with demons, gods, poisonous substances, dark creatures and more – but until today, there are still no definite answers. There is evidence, however, to the different treatments tested (and used) in several patients. Drilling holes in a patient’s skull and performing dance rituals were some of them.
The term ‘Schizophrenia’ (derived from the Greek words ‘schizo’=split and ‘phrene’=mind) was only created in 1911 by Eugene Bleuler, a Swiss physician. Bleuler changed the term ‘dementia praecox’ created by Emile Kraepelin – the German physician who first classified mental disorders in categories – because the disorder was not a dementia. Later on, both scientists sub-classified schizophrenia into categories based on specific symptoms, three of which were delineated in the DSM-III (Diagnostic and Statistical Manual of Mental Disorders): disorganized, catatonic, paranoid, residual, and undifferentiated. Kraepelin’s classification remains influential and it is the basis of the DSM-IV.
Nowadays, it is believed that schizophrenia is caused by a mixture of gene interaction and environmental influence. However, it is not clear how much influence each of these causes wields.
The Symptoms
The symptoms of schizophrenia are divided into three categories: positive, negative and cognitive.
Positive symptoms are volatile, easy to recognise and normally involve some loss of contact with reality. Hallucinations (distortions of the human senses), delusions (false personal beliefs) and movement disorders are examples of such symptoms.
Negative symptoms are harder to recognise as they relate to some loss in abilities such as planning, speaking, expressing emotions or being motivated. These symptoms can easily be misconnected to laziness, depression or other conditions which involve similar behaviour. The term is referred as ‘negative’ due to the reductions in ‘normality’ – both emotional and behavioural.
Cognitive symptoms relate to problems in normal cognitive functions. In many cases these cognitive impairments are only detected through neuropsychological tests. Such symptoms include problems with memory, attention, decision-making and more.
The Causes
As previously noted, schizophrenia is believed to be caused by a mixture of gene and environmental influence. Davies stated that “schizophrenia appears to be caused by abnormalities in the development of the brain that become manifest in late adolescence or the early twenties, a time when a differentiation and maturation of the central nervous system is at its most complex” (Davies 2005 p. 210*).
However, the disorder is not characterised by a single predominant gene – it relies on the combination of a group of genes, each exerting a small effect. These gene combinations, along with the presence non-genetic factors such as exposure to viruses or drug abuse, play a key role of increasing vulnerability.
Current research is attempting to identify the genes which could be directly involved with the incidence of schizophrenia and psychotic episodes. There are candidate genes – however there is not enough evidence to prove that these genes in fact increase risk. “Some genes that have recently been associated with schizophrenia code for enzymes and proteins that help brain cells communicate with each other.
Some of these enzymes and proteins are involved in neurotransmitter systems that have long been implicated in schizophrenia, such as dopamine, glutamate and GABA. Other genes code for proteins involved in the brain development, while others code for proteins of yet undetermined function”. (NIMH – National Institute of Mental Health**).
Facts and the treatments
Schizophrenia is a chronic and disabling disorder, but nevertheless misinterpreted by the general population. In fact, between 25 and 40% of people who experience a psychotic episode not only recover, but never experience a second episode. In many instances, patients enter hospital care voluntarily, and are able to function normally when not experiencing an episode. Although people with schizophrenia are more likely to attempt suicide, they are not particularly prone to violence or crimes.
Over the last few years, new anti-psychotic medications have been developed – such as clozapine, risperidone and olanzapine. These drugs do not cure schizophrenia, but they effectively alleviate its symptoms and extrapyramidal side effects (such as rigidity, muscle spasms and tremors) which used to appear in older drug treatments.
Psychosocial treatment is also important in the management of schizophrenia. Rehabilitation and substance abuse treatment are helpful in integrating the patient to the society, and improving the patient’s capability to counteract the degenerative effects of the disease. Cognitive Behaviour Therapy (CBT) can also help. This treatment seems to be effective in reducing the severity of symptoms and decreasing the risk of relapse in patients which symptoms persist even when they take medication.
Furthermore, the efficacy of treatment can be vastly improved with the participation of family and friends. Because the positive symptoms of this mental illness are easy to distinguish, both patient and relatives are able to act when noticing the prevalence of different behaviour.
Overcoming schizophrenia: too far or too close?
The future of schizophrenia runs parallel to most research in mental health. With the advent of new brain mapping and scanning technologies, such as PET, MRI, fMRI and the developments in genetic research – scientists are narrowing their focus to the interaction between neurons and how each of our cognitive functions affect neurotransmission at a molecular level. With this in hand, there are expectations that the approach to schizophrenia will be more specific and efficient – but to predict cure at this stage, is a long shot.
Nevertheless, there may be more excitement in the other side of the spectrum. Identifying the exact gene combination which increases the incidence of this condition, and the role of non-genetic factors, may still seem distant. However, another solution could effectively help the vast population suffering from the symptoms of schizophrenia.
The general thinking is that the best way to combat an illness is to develop a cure. What about instead of finding the cure, combating the symptoms? That is the approach used for most illnesses which cure is yet to be discovered, and it could be a temporary solution to improve the lives of millions. Cognitive enhancers, such as nootropics (cited in a previous edition of this ezine) and cognitive enhancing methods – such as the use of electric waves in specific brain regions – could counteract some of the debilitating symptoms of schizophrenia.
Most of these techniques are still being tested, but they are much closer to reality and have already predictions to reach the market within a few years. Although there have been some studies in cognitive enhancing drugs, new drug classes are on the scene – and brain science and pharmacology are allowing further discoveries in the field. What will be the next step? That might not be the one million dollar question, but perhaps it holds the answer which over 65 million people have been waiting for.
Sources *Davies, J. (November 2005) A Manual of Mental Health Care in General Practice, Commonwealth Department of Health and Ageing, Canberra.
** National Institute of Mental Health Website (www.nimh.nih.gov/publicat/schizresfact.cfm).
About the Author
Pedro Gondim is a writer and publisher for the Australian Institute of Professional Counsellors. The Institute is Australia’s largest counsellor training provider, offering the internationally renowned Diploma of Professional Counselling. For more information, visit www.aipc.net.au/lz.
How to use differential differences and DSM-IV-TR together to diagnosis mood disorder/ drug abuse?
I need to know how to diagnosis a client who shows the symptons of mood disorder and with possible history of drug abuse using the differential difference and DSM-IV-TR coding system together
Hmm. Well if you are looking for some drugs for the client I highly suggest these:
· Anafranil**
· Asendin
· Aventyl
· Desyrel
· Effexor
· Elavil
· Ludiomil
· Luvox (SSRI)
· Marplan (MAOI)
· Nardil (MAOI)
· Norpramin
· Pamelor
· Parnate (MAOI)
· Paxil (SSRI)
· Pertofrane
· Prozac (SSRI)
· Remeron
· Serzone
· Sinequan
· Surmontin
· Tofranil**
· Vivactil
· Wellbutrin
· Zoloft (SSRI)
If you are not looking for drugs put the client under psychotherapy.
Good Luck!
Sincerly,
Jordan
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