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Thomas A. Ban: Recent Advances in the Biology of Schizophrenia

Thomas A. Ban: Recent Advances in the Biology of Schizophrenia
Charles C. Thomas, Springfield, 1973. (119 pages)

Presented by Thomas A. Ban

INFORMATION ON CONTENTS: This monograph is divided into two parts (Part One: Etiology and Part Two: Treatment) and eleven chapters: 1. Descriptive Classifications (chapter 1), Conditional Reflex Correlates (chapter 2), Neurophysiological Findings (chapter 3), Biochemical Hypotheses (chapter 4), Genetic Factors (chapter 5), Present Status (chapter 6), Pharmacotherapy with Neuroleptics  (chapter 7), Prediction of Neuroleptic Effects (chapter 8), Neuroleptics Versus Other Treatments (chapter 9), Other Pharmacological Treatments (chapter 10) and Present Status (chapter 11).  Chapter 1 is preceded by a Preface and Acknowledgements, and chapter 11 is followed by Concluding Remarks, Bibliography and two Indexes (Authors and Subjects).

                      In Chapter 1 (Descriptive Classifications), the controversy of the 1950s is addressed, namely whether the different forms of schizophrenia are progressive stages of one generalized disorder of the brain, as perceived by Klaus Conrad, or distinct, localized disorders of the brain, affecting one or more neurological system simultaneously, as perceived by Karl Kleist and Karl Leonhard.

In Chapter 2 (Conditional Reflex Correlates) findings with conditioning test batteries, in the 1960s, are presented. It was noted that in 1962 Christian Astrup described the differential conditional reflex profiles of Carl Schneider’s three different forms of “acute schizophrenia” and Karl Leonhard’s eighteen different forms/sub-forms of “chronic schizophrenia”.

In Chapter 3 (Neurophysiological Findings), findings with surface electroencephalography (EEG) and averaged evoked potentials (AEP) are discussed. It was noted that no “exclusive EEG signs” of schizophrenia could be identified, but there was a relative excess of fast activity (EEG) and a greater variability in auditory evoked potentials (AEP) in schizophrenic patients than in normal subjects.   

In Chapter 4 (Biochemical Hypotheses), numerous biochemical theories and speculations about the “cause” of schizophrenia are reviewed. They include: (1) normal products of phenylalanine metabolism, such as norepinephrine (NE) and dopamine (DA); (2) abnormal  products of phenylalanine metabolism, such as 3, 4-dimethoyphenylethylamine (DMPEA), adrenochrome and adrenolutin; (3)  psychotoxic dimethylated products of tryptophan metabolism, such as bufotenin and dimethyltryptamine; (4) transmethylation, i.e., the metabolic process itself; (5) nicotinamide adenine dinucleotide deficiency; and (6)  a plasma protein factor that interferes with the conversion of glucose into pyruvic acid (in vitro).  While none of these hypotheses were borne out by evidence, supportive of the role of dopamine in the pathogenesis of schizophrenia or at in the pathogenesis of some of the symptoms or syndromes of schizophrenia, are findings which indicate that all neuroleptics with demonstrated therapeutic efficacy in the treatment of schizophrenia antagonize some of the central effects of dopamine.

In Chapter 5 (Genetic Factors), the role of heredity in schizophrenia is examined. Findings in traditional twin studies, in studies in adopted away children of schizophrenic parents, and in biochemical genetic investigations are reviewed. It was noted that in Pollin’s biochemical genetic investigation, urinary excretion levels of catecholamines were higher in both members of monozygotic twins discordant for schizophrenia than in normal subjects, whereas 17-OH steroid levels were higher only in the schizophrenic members of the pairs.

In Chapter 6 (Present Status), Part One concludes as follows:”There is sufficient evidence to believe that schizophrenia is a genetic disease, although neither the nature of the genetic disturbance, nor the mode of transmission has been demonstrated to date. Similarly, there is sufficient evidence to believe that there are biochemical disturbances in schizophrenia, but whether they are the causes or the effects of the psychopathological manifestations is not known”.    

In the remaining five chapters the focus in the monograph shifts from “etiology” to “treatment”.

In Chapter 7 (Pharmacotherapy with Neuroleptics), the status of pharmacotherapy in schizophrenia with neuroleptics in the early 1970s is reviewed; findings related to neuroleptic dose requirements in the treatment of schizophrenia are presented; and information on neuroleptic dependence, toxicity and teratogenicity is discussed.  

In Chapter 8 (Predictors of Neuroleptic Effects), possible predictors of treatment outcome with neuroleptics are examined, without success of identifying any. It was noted that early relapse after neuroleptic withdrawal might be predicted by the absence of a startle response.

In Chapter 9 (Neuroleptics Versus Other Treatments), findings in efficacy studies in the treatment of schizophrenia in which neuroleptics are compared with other non-pharmacological treatments are reviewed. It is shown that neuroleptics compare favorably in the treatment of schizophrenia to milieu therapy, psychotherapy, insulin coma and electroshock.

In Chapter 10 (Other Pharmacological Treatments), findings in the Canadian Mental Health Association Collaborative Studies on nicotinic acid in the treatment of schizophrenia are reviewed. It is shown that treatment with nicotinic acid in megadoses has no therapeutic effect in schizophrenia.  

In Chapter 11 (Present Status), Part Two (Treatment) concludes as follows:” In the foregoing modern biological treatments of schizophrenia were reviewed. It was noted that since the introduction of chlorpromazine at least 50 neuroleptics had been clinically investigated. While most of these new drugs ………………are successful pharmacological agents in the control of psychopathological manifestations of schizophrenia, the fact remains that neuroleptics may alter the course but cannot cure the disease”.

AUTHOR’S COMMENTS: This monograph is an expansion of my presentation at a Symposium on Schizophrenia, organized and chaired by Nathan S. Kline that was held at the Arizona State Hospital  in Phoenix, on November 12, 1971. The material was also presented in my lectures on the Biology of Schizophrenia to postgraduate students in psychiatry, McGill University, at the Douglas Hospital in Verdun, Quebec, during the month of January, 1972.

Thomas A.Ban

June  5, 2014