Jeff and Cathy Romanczuk,
lukate@charter.netChapter 1
This introductory chapter includes a rationale for pursuing a bibliometric study of autism causation literature, a statement of the problem being investigated, and objectives of the research described. The rationale includes background on both autism causes and bibliometric studies. The problem statement describes the specific focus of this research, narrowly defining the topic while filtering out closely related issues. The objectives section briefly and broadly lays out what is more fully explained in Chapter 3, “Methods.” The section on objectives also clarifies the hypothesis being tested by this bibliometric investigation of autism cause literature.
The Diagnostic and Statistical Manual of Mental Disorders, 4th edition (DSM-IV), lists “autistic disorder” among those conditions “Usually First Diagnosed in Infancy, Childhood, or Adolescence.” Autistic Disorder is the first of the “Pervasive Developmental Disorders” discussed. Although links between these disorders and other general medical conditions—chromosomal abnormalities, congenital infections, structural abnormalities of the central nervous system—are mentioned, no causes of autism are supplied. Of course, the DSM-IV is principally a diagnostic tool, so causation is not emphasized. However, even Advocate—the bimonthly newsletter of the Autism Society of America (ASA)—mentions causes of autism only broadly in its “Definition of Autism” statement that appears in every issue: “The result of a neurological disorder that affects functioning of the brain, autism and its behavioral symptoms. . ..” Like the DSM-IV, Advocate stresses the characteristic, treatable symptoms over causation. The definition of autism has been refined often since Kanner first labeled the condition in 1943, after the Greek root “autos,” meaning “self” (highlighting the characteristic self-absorption of autistic individuals.) Some put autism’s origin before Kanner’s work. Beauchesne, writing in 1985, claims an origin in psychology dating back to E. Bleuler in 1911 “to describe a secondary dynamic symptom of schizophrenia. . . .. Bleuler viewed autism as a normal phenomenon, that of imaginary life. Bleuler’s students further described autistic thinking from the phenomenological perspective. L. Kanner (1943) described infantile autism antinomically, which caused mistakes in the term’s usage.” “Antinomically” means that Kanner was not only the first to describe autism independently of schizophrenia, but also that he allowed for psychological, neurological, or even genetic causations. This opened the way for the biggest problem with autism: that its etiology remains unknown. Bauman and Kemper observe that there is no metabolic, radiographic, or genetic marker yet identified to aid in the diagnosis or prediction of autism.
Most of the causal theories center on some brain defect, either in the development of a specific region or by an abnormal neural cell networking. Although it is not usually diagnosed until early childhood, many sources agree that autism begins during fetal development. Whether this aberrant brain development has a genetic link or could be triggered by environmental factors remains undetermined. Adding to the mystery, in the absence of laboratory tests to diagnose autism, the affliction has always been behaviorally determined. These diagnostic methods have kept open the possibility that autism has a psychological nosology. (Nosology is the branch of medical science that covers the classification of diseases.)
With such a range of possible etiologies to investigate, a bibliometric study of the causes that have been researched bears utility for both the biological and information sciences. An overall characterization of literature on the causality of autism would be useful to biological scientists because it could present fresh insights. These scientists tend to specialize in narrowly defined areas. Therefore, a presentation that includes not only how the various characterizations map out—but also how they overlap and intersect—could spark untried methods of research. Those involved in information sciences may gain another method for mapping information growth that is based not on author, journal, or citation usage, but on a specific position held by an author (or characterization of the literature being investigated).
Wallace suggests that “bibliometrics is the application of quantitative methods to the study of information resources.” He adds that although bibliometric studies have been conducted since early in this century, the term was not proposed until Alan Pritchard coined it in 1969 as an alternative to the unsatisfactory “statistical bibliography.” Scientometrics (“quantitative analysis of scientific productivity”) and citation analysis (“the practices and patterns of scholarly reference”) are closely related areas of study. Pao indicates that bibliometrics “uses mathematical and statistical methods to investigate and to quantify the processes of written communication.” Observable parameters in literature studies include publications, authors, citations, and journals. She offers three reasons for using bibliometrics: to identify literary areas with limited information, to predict trends, and to advance the “knowledge of communication.” Nicholas and Ritchie echo these reasons in quoting from Pritchard that bibliometrics’ purpose is “to shed light on the process of written communications and of the nature and course of a discipline. . .by counting and analyzing various facets.” These facets are to be counted in this study: causes being investigated; authors involved; countries publishing this work; publication years, formats, and sources; and the databases indexing these sources. The rationale for this bibliometric count and its objectives are explained in the next two sections.
Autism is a life-long developmental disability for which there is no cure. In fact, research into this condition has not yet reached a primary precondition (if not prerequisite) for finding a cure: consensus among those researching the disability concerning what causes autism. There are various suggestions, but as yet, no clearly supported generalizations.
While much time and effort have been devoted to the treatment of autistic symptoms, or managing autistic behaviors, comparatively little has been written about its cause or causes. Even less bibliometric work has been compiled concerning autism’s etiology, and this research has tended toward a narrow focus and year span to highlight a specific autism cause. However, a broader view of autism etiology research reveals many causes under investigation . If autism is caused by genetic, environmental, and brain development malfunctions coming together at some unfortunate opportunity, the research should reflect this mix. On the other hand, if autism is caused by any one of the three (or some other single biological, psychological, or autoimmune cause), this distinction should be borne out in the literature. While clarifying the relationships among suggested causes of autism and tracking their origins and growth will not necessarily lead the way to a cure, it is a fundamental step which could at least ease the way by clarifying the range of what has been said and done. For these reasons, the focus of this research is on the changing nature of autism etiology literature as it has followed the varying research being done into the possible causes of autism.
The researcher intends a bibliometric study of the international research into autism causes over a more than fifty year span, from the condition first being named in 1943 through articles published by the end of 1996. This research will track the growth, migration, and intermixing of various causal theories and test the null hypothesis that no one cause owns a majority percentage (that is, more than half) of the causes given for autism in articles published around the world.
The evolution of causal research literature will be tracked, primarily through secondary biomedical publications and bibliographic sources such as Index Medicus, Biological Abstracts, Excerpta Medica, the National Library of Medicine’s Current Catalog, and Psychological Abstracts (for the abstracts these five sources provide covering the early years of autism etiology research). For post-1965 coverage, the research will emphasize the medical online databases—MEDLINE, BIOSIS, EMBASE, and PsychLIT/PsychINFO. The main intent of using both print and online databases is not so much to expose gaps and confirm duplication as to ensure complete coverage. However, any implications that such gaps and duplication highlight will certainly be incorporated into the overall discussion.
The purpose of this investigation is to map the research into autism causes. Finding a cure for autism has been elusive because there are many probable causes. The hypothesis to be tested is that no one cause will dominate the literature: that is, no single cause will be advanced in the scientific literature statistically more frequently than any other possible causes. There should be much evidence of the four most popular causal theories—neurobiological impairment, genetic influence, psychological causes, or environmentally induced autoimmune malfunctions—with some intermixing of several popular theories, but no clearly identifiable single cause. A bibliometric mapping of the autism cause research results published should demonstrate this multidirectional attack on autism, as well as this lack of causal consensus.
The research will also test the hypothesis that specific causal research categories tend to group together for a certain time span, or by a certain country or journal, before giving way to autism etiology research in a different vein. Goffman’s “epidemic theory of communication” is basically that ideas spread like diseases; they are transmitted mainly by direct communication and spread among a susceptible population. He adds that the journal population is the controlling factor; that is, the number of authors is directly related to the number of journals that publish on a subject. Also, the number of “quality” authors is proportional to the total number of authors in the field. However, the importance of Goffman’s work lies in its “predictive power.” Just as statistics are predicted for epidemics, as a research topic emerges Goffman’s mathematical analysis may be applied to predict controlling conditions, dimensions of growth, and the rate of slow down. Another value of Goffman’s work is that it points out the “infectious nature of ideas.”
Goffman believed, too, that the information retrieval process is more than “strictly a matching procedure” and makes the point that what is learned along the way affects subsequent documents. For him, then, information retrieval becomes a dynamic process of intercommunication and interrelationships. Once all of the data are collected for the fifty plus years of autism cause research, application of Goffman’s epidemic theory will provide what should be an interesting framework for some exciting discussion about the direction of autism causation research.
This introductory chapter laid out a rationale justifying the necessity for pursuing a bibliometric study of autism cause literature. The statement of the problem being investigated gave background on both autism causes and bibliometric studies. It also delineated what the issues are and what they are not. The objectives section broadly described the research plan. However, this early indication of how and where the data are to be collected is worthwhile since it is the heart of the research at hand. The section on objectives also clarified the hypothesis being tested by this bibliometric accounting of autism causation literature.
The literature review to be described in the next chapter distinguishes among the three groups of sources necessary for review: secondary biomedical publication’s abstracts, bibliometric background literature, and material explaining the various theories about autism’s etiology. The latter is the primary focus of Chapter 2, while the former two will be expanded on as needed to clarify points made in Chapter 3, “Methods” and Chapter 4, “Results.”
lukate@charter.net