Is there a way to think about the etiology, the de-coding/unwrapping and possible treatment options of schizophrenia which avoids the single model approach? Considering the multiple memoirs from insiders (patients and therapists) and theoretical and medical approaches I have already reported, and considering the fact that we have not yet “solved” the schizophrenia “dilemma”, how might we pull together bits and pieces of data into some understandable systemic whole? In my previous post I referred to Harrington’s statement that a group of researchers in 2008, who identified and critically assessed all known facts about schizophrenia concluded that the facts did not, as a group, lead logically to any coherent explanation of schizophrenia. She also said that these same researchers in 2011 claimed that the field seemed to be operating like the fabled six blind Indian men groping different parts of an elephant and coming up with different conclusions. “In fact they admitted, in the current state of knowledge, one could not rule out the possibility: ‘that there may be no elephant, more than one elephant, or many different animals in the room'” (p.182). I will propose a possible way through this dilemma.
Why am I interested in schizophrenia? While studying psychology in undergraduate school , I worked as a counselor at The Lawrence School for emotionally disturbed children in VanNuys, California (1959-1961), and as a volunteer on the children’s ward at the Camarillo State Hospital in Camarillo, California. The Lawrence School was one of the first of its kind in the U.S. Our objective was to take children in early elementary school grades and prepare them to be mainstreamed after the sixth grade. If they were too disturbed and /or organically impaired, so that the prognosis was not positive, we could not take them and the only option for them usually was a state hospital. We did not typically place diagnostic labels of these children, but many were likely on the autism spectrum, with several other disturbances, some with possible symptoms of schizophrenia. While it is not thought that schizophrenia shows up before adolescence, there may have been pre-psychotic symptoms with some of our children. While working in the children’s ward at the Camarillo State hospital, I had access to the records of the children I worked with. Most were given a diagnostic label of “Schizophrenia Reaction, Childhood Type”. I believe that this was because psychiatrists at that time knew almost nothing about how schizophrenia might affect children. Since most children had obvious psychotic symptoms or were extremely autistic, the label was used as a “holding place” until more was known. Meanwhile, these children were essentially being “housed” in an institution because their families could not manage them. Treatment options were minimal. I don’t remember if the children were medicated as were the adults at the hospital. I do remember that I was fascinated with trying to communicate with the most disturbed children. One boy had become a Bumble Bee and would buzz the ward non-stop. The staff ignored him. I decided to buzz alongside him to see if he would notice and perhaps talk to me. He definitely noticed, but he never talked. This at least hinted to me that he was aware of what was happening around him, while he was living as a bee.
Many years later, while I was in graduate school, I was studying with Gregory Bateson and using some his ideas for my dissertation. I became intrigued with his development of the “double bind theory”, which came out of the research with families with schizophrenia that he, Don Jackson, Jay Haley, and John Weakland, had done from 1952-1954 through Stanford University. I have posted earlier on the double bind theory. Bateson’s idea about this actually goes well beyond the research with families, but it was the family dynamics around mental illness which provided observable material for this theory. While this research was very influential for the family therapy and family systems movement, the emphasis on the etiology of schizophrenia resting with family dynamics and particularly on the influence of the mother, caused ongoing backlash from families with schizophrenia in their midst. It is true that the interpersonal psychotherapy psychiatrists also identified the mother as a primary agent within a family unit, but their interpretation was based more on developmental psychology and the early mother-child relationship. The Bateson group noticed the roles played by each member of a family grouping, and in families where a father was mostly absent and ineffective, the burden for raising children fell mostly on the mother. This was certainly true of the Galvin family in Colorado Springs. What I learned from revisiting the papers that Bateson published about schizophrenia in “Steps to an Ecology of Mind”(1972) is that he considered the possibility of genetics influencing the occurrence of schizophrenia within families, though this genetic influence will still need environmental or interpersonal influence as well. In posing the dilemma between genetics and environment, Bateson asks if simply noting which family member becomes hospitalized with schizophrenia will tell us that they have a particular gene for schizophrenia:
“We cannot simply assume that the hospitalized members carry a gene for schizophrenia and that others do not. Rather, we have to expect that several genes or constellations of genes will alter patterns and potentialities in the learning process, and that certain of the resultant patterns, when confronted by appropriate forms of environmental stress, will lead to overt schizophrenia” (p.259). This statement and Bateson’s next one ( part of his 1959 lecture delivered at the Institute for Psychosomatic and Psychiatric Research and Training in Chicago), presages current thinking about the relationship between genetics and environment in the etiology of schizophrenia: “In the most general terms, any learning, be it the absorption of one bit of information or a basic change in the character structure of the whole organisms, from the point of view of genetics, the acquisition of an ‘acquired characteristic.’ It is a change in the phenotype, of which that phenotype was capable thanks to a whole chain of physiologic and embryologic processes which lead back to the genotype”(p.259).
My interest in schizophrenia comes from my work with emotionally disturbed children and from the family systems research and from the mystery of the etiology and treatment approaches.
I propose a systems approach to understanding schizophrenia, which includes genetics and biochemistry, vulnerability markers or endophenotypes, impairments in sensory gating, early parental-child relationships, family dynamics, and communication theory. I will explain the connections among these variables in my next post…