|Year : 2008 | Volume
| Issue : 1 | Page : 11-13
Early psychosis in Indian context
Prof. Emiritus, Deccan College of Medical Sciences, Hyderabad, India
Prof. Emiritus, Deccan College of Medical Sciences, Hyderabad
Source of Support: None, Conflict of Interest: None
|How to cite this article:|
Khan M. Early psychosis in Indian context. Indian J Psychol Med 2008;30:11-3
Understanding of Psychosis went through many developmental phases. Take for instance Schizophrenia. A breakaway came from the conventional thinking on Kraepilian after 100 years. Dementia Precox became to be known as schizophrenia and with further observations, four sub- types, Paranoid, Simple, Catatonic and Hebephrenia were described.
Another promising land-mark study was known as Camberwel family study where three types of expressed emotions- Hostility, Critical and overinvolvement were supposed to cause relapses in all psychiatric disorders. There was a study described in The Singapore Medical Journal way back in 1996 /37, 82-85 by Azhar M & Verma S.L entitled Relationship of Expressed Emotion with relapse of schizophrenia patients in Kelantan. In our culture , we know that in a joint family setting negative emotions can be very damaging. It seems to have lost its relevance in western culture. Now Expressed emotions do not find a place even in modern psychiatry text books.
Through the study of expressed emotions, domain of negative symptoms emerged in full bloom. Initially it was thought that negative symptoms could be due to the use of antipsychotics. Later came the development of good phenomenology by the revised versions of DSM. The use of measuring scales like PANSS and others, improved the understanding of the symptom domains. Negative state got further clarified into emotions and intellect. Finally Cognition has emerged as a fundamental process, heralding early psychosis.
To-day, dysfunction of cognition is understood as a part of the disease process itself and forms a major component of Schizophrenic illness. This has now become a hall mark of Schizophrenia and many other symptoms are being understood in the context of cognitive impairment like disordered types of thinking, perception and insight. I feel that in Indian context , decline in cognitive faculties can be noticed in very early stages like complaints from the teachers.
As diseases in general are getting recognized and clinically staged in early stages, there is a tendency in psychiatry too to stage them in terms of their progression. This has certainly been happening in the field of Schizophrenia. The pioneers in the field have been Australian Psychiatrists, who were advocating early treatment of Schizophrenia.. Tuck Schulz from Minnesota presented large data of teenager schizophrenics below the age of 18 who were put on anti-psychotics. He presented these findings in the American Psychiatric Association meeting in Washington in 2008. Such a study has been last done in 70s. There is convincing evidence that early intervention does halt the disease progression.
From then on tremendous advancements have been taking place in the recognition of Early Psychosis particularly in Schizophrenia. More recently for the first time, early stages of Bi-polar disorder is also described.. Refer to RAP study by Barbara Cornblat in Long Island, New York (Paper presented in APA 2008). RAP stands for Recognition and Prevention.
Against this background of massive Western experience and literature, I wish to understand it in the Indian context. Do our patients too behave in the same way and exhibit the same symptom profile? Patho-Physiology is universal but symptom profile do differ because of our culture.
In this connection the seminal work of Patrick McGorry of University of Melbourne, cannot be underestimated and his work has certainly inspired me to take interest in this new area of development, which I feel is neglected in India.
I must mention Hafner of Germany who in 2005 showed that the prodrome of Schizophrenia was indistinguishable from that of major depression in its early stages. Negative and "basic Symptoms" have also been described in prodromes.
Way back in 1997, Kloster Kokker had mentioned that basic symptoms in early psychosis, refer to subjectively experienced abnormalities in the realms of cognition, attention, perception and movement and are thought by many to be important precursors of schizophrenia.
As we were still grappling with the phenomenon of early psychosis, many more advancements in understanding of early psychosis have taken place. Earlier to early psychosis and prodrome, high risk cases and UHR - Ultra High Risk category is getting recognized by virtue of latest imaging techniques. Changes in the grey matter of high risk children have been described long before the development of frank psychosis.
Tuck Shulz in his study showed teenagers diagnosed as schizophrenics had enlarged ventricles. (APA 2008)
What Krapelin described was the phenomenology of established cases of Schizophrenia and Manic Depressive Psychosis. No body had thought of early psychosis and it was not possible to support the observation with any hard investigative evidence, which is now available.
Mc Gorry and Yung in 2006 talked about staging and said that at the heart of the concept is the differentiation of initial and mild clinical phenomenon from those that accompany illness extension, progression and chronicity.
He goes on to explain the prodrome concept and its implications for early diagnosis. Treatment runs into problems due to the wide variability between individuals and the lack of specificity of many of its features.
Many prodromal symptoms and signs are non specific and could be the result of a number of conditions, such as major depression, substance abuse and even physical illness.
On the other hand, Titel in 1991 and Van O set al in 2001 had noted that isolated and attenuated psychotic symptoms do not necessarily develop into frank schizophrenic phenomenon due to false positives.
This is also true that many patients who do develop frank psychosis do have sub-threshold psychotic features over a long period of time. In our Indian context this is very true. Neglect of personal hygiene is a pointer.
Against this background, Indian psychiatrists have an unenviable task of defining prodromes.
How do I maneuver the various care pathways laid down so admirably, in my clinical practice.. First, I must try and understand what the Neuro Scientists have been doing in the realm of psychosis in general and Schizophrenia in particular. There are innumerable number of excellent research works done but how do I gather all this in my mind to guide me through. This has been my constant dilemma.
In my own reckoning, the most impressive break through has been the capacity to visualize various changes in a living person through the agency of more and more sophisticated imaging techniques ranging from Magnetic Resonance imaging and functional MRI to proton Magnetic Resonance Spectroscopy and more and more powerful image intensifiers.
The first wonder came not when the human genome was successfully cracked but when scientists were able to actually see what happens in a living cell. Relate the changes in a cell to the environment and you will understand a lot from the missing links.
The structural abnormalities in the shape of grey matter deficits and enlargement of ventricles came through morphological photometry but did not connect it to the actual process of psychosis.
While beautiful multi-coloured live images were flashed on suspected areas and culprit Neurocircuits were getting identified, work was going on in the growing field of molecular biology and scientists were zeroing in on various neuro receptors, but the connection between these observations and clinical symptoms are still missing. D2 has been the most favourite destination for everyone from Neuro Scientists to Clinicians . Block D2 receptors became the main slogan in treating Schizophrenia.
In my mind I was not able to relate abnormal chemical changes and structural changes and the emergence of Psychotic symptoms, until now.
John Tebage from Canada, has been working for the past 10 years on glutaminergic Neurotransmission. I got more confused but Tebage was able to show a connection between the presence of abnormal chemicals and their role in causing Neuro toxicity.
I had difficulty in understanding the role of glutamine and glutamate in Neuro transmission.
Glulamine seems to be more important than glutamate. He was able to estimate the level of glutamine in various suspect areas like Cingulate gyrus and Thalamus. He says that glutamate - glutamine circuit is a specific circuit in the brain, whereas glutamte is found in many areas of the brain.
The specific cycle gets activated in early psychosis and level of glutamine goes up. But the disease progresses with or without the use of antipsychotics, the level after doing a certain amount of damage comes down and hence the damage is not progressive but static.
This has to a large extent clarified my doubt.
In early psychosis it is the neuro chemical change which is important and the cognitive deterioration starts to manifest. In our Indian population, youngsters developing early cognitive decline first show as failing academic performance and drop outs. After this they begin to withdraw socially. Social withdrawal has to attend to promptly through enhancement of social skills, to prevent fast deterioration. For this initial psycho social education is crucial.
We must begin to spot early psychosis through the schools and close relatives and launch extensive psycho-education progammes to check deteriorating sociability.
I feel decline in sociability is the hall mark of early psychosis in Indian Population.