THE SPECTRA OF LEARNING DISORDERS:
AN INTEGRATIVE APPROACH

Presented to the Faculty of Saybrook Graduate School and Research Center
in Partial Fulfillment of the Requirements of the Degree of
Master of Arts of Psychology
by
Floyd S. Merchant

June 2002
San Francisco, California

Stanley Krippner, Ph.D., Chair

Ruth Richards, MD, Ph.D.
 

This masters thesis sought through a balanced and comprehensive review of contemporary and historically significant literature to evaluate the various types of learning disorders, especially the most familiar subset--termed learning disabilities (LD).

It is shown that the general accuracy of LD classification processes and efficacy of subsequent treatments in the public schools have repeatedly been called into question by numerous creditable authorities in the field. This thesis delved into the evolutionary/historical background of the subject as a method of understanding what might have contributed to present day dilemmas.

Informational patterns emerged within the clinical perspectives that resulted in the partitioning of the disabilities portion of learning disorders into three unambiguous, conceptual models: the educational, the neuroanatomical, and the biochemical. The remaining, non-clinical portion of this learning disorders picture was addressed by including two additional models: the developmental difference and the psychological.

Historically, a number of authoritative commissions met in order to formulate a definition of LD that could clarify clinical perspectives and classification methodologies. Trends in conceptualization and terminology emerged that, by the end of the 1980s, had brought about the general agreement that LD was intrinsic to the individual, presumed to stem from central nervous system dysfunction with the possibility of lifetime duration.

Coupled with incomplete nomenclature that makes it difficult for LD practitioners to look beyond neurological explanations, the presumption of central nervous system dysfunction builds on unproven assumptions and appears to circumvent scientific method.

Findings also revealed that little effort, if any--especially in the form of impact studies--has, to date, been expended to determine whether or not notification to guardians and children of disabilities involving central nervous system dysfunction is traumatic to, or has insidious effects upon, LD classified children.

Because LD nomenclature was found not to include mention of personhood and agency, there may be little incentive for LD practitioners to see beyond mechanistic-deterministic limitations. Among the array of shortcomings found to be implicit in the LD paradigm, practitioners may be led to overlook young learners’ capacities to contribute to their own successes. Consequently, the thesis recommends reinstituting, wherever possible and relevant, the underutilized, non-clinical developmental difference and psychological models as described therein.

CHAPTER 1: INTRODUCTION

This thesis examines learning disorders from a variety of standpoints. Within the entire array of learning disorders, I will present evidence suggesting that a pathological subset--termed learning disabilities (LDs)—has achieved much institutional recognition, especially in the United States. Therefore, the bulk of this exposition disproportionately concentrates on the clinically oriented, learning disabilities subset of learning disorders within the jurisdiction of the United States.

An illustrative scenario occurs in grade school and involves a student attaining unsatisfactory grades whose struggle has been brought to the attention of a learning disability specialist. The pupil is then evaluated via the application of a standardized test battery that will usually compare performance with a standard measure of aptitude. As a consequence, the student may be classified learning disabled and may become subject to whatever institutional adjustments are available.

Although I seek to delay, rather than intersperse, my opinions amongst the descriptions and findings, I do, however, offer brief evaluations at certain advantageous stages as they unfold throughout the thesis.

Evolution of Definitions

I examine the various implied and applied interpretations of LDs from the perspective of tracing historical development and evaluating the literal meaning of the current definitions. I present and explore the hypothesis that present day practices in the LD field have evolved from a reciprocity between theory, as expressed in the definitions of LD; and practice, as driven by human incentives as evidenced by advocacies, the tools at hand, and the states of the art.

Five Categories of Learning Disorder Perspective

After examining the literal aspects of LD theory, I partition learning disorders into five categories of perspective that either relate to diagnostic criteria or correlate with other practical concepts.

Three of the five learning disorder models introduced herein are deficit-based and potentially problematic. The reader should also keep in mind that a heterogeneity of conditions and/or causes may be subsumed in/by the LD categories. Two other constructs, by contrast, offer broader and more positive perspectives based on the function of the whole person and environment.

The Educational model

Students experiencing academic difficulties are LD classified according to how satisfactorily their academic performances (often measured through standardized testing) compare to expectations of their aptitudes as gauged by norm referenced intelligence measurements (Campbell, 2000). I alternately term this approach the psychometric model in educational settings where standardized testing drives LD classification processes. I predicate the educational model largely on the 1988, National Joint Committee on Learning Disabilities' position that children's central nervous systems are flawed and thus the cause of whatever form their heterogeneous learning difficulties happen to take (National Adult Literacy and Learning Disabilities Center, 2002).

The Neuroanatomical/Functional Model

The neuroanatomical (structural/functional) model also attributes learning disabilities to a malfunctioning central nervous system (CNS). As I will show, the educational model assumes rather than substantiates CNS causality. The neuroanatomical/functional model employs direct neuroimaging techniques in order to seek out and identify physical abnormalities and/or apply indirect neurological tests, such as, the Halstead-Reitan Battery (Lezak, 1983). It will be argued that definitions of LD that support intrinsic, CNS explanations, by virtue of their clinicopathologic basis, predispose investigative activities towards today's neuroimaging approaches (Gaddes and Edgell, 1994, p. 52).

The Biochemical Model: Coalescing around Attention-Deficit
and Disruptive Behavior Disorders

Pharmaceuticals are often administered to distractible and/or fidgety children who have either been diagnosed as having attention-deficit disorder (ADD) or attention-deficit-hyperactivity disorder(ADHD) (Diagnostic and Statistical Manual of Mental Disorders (DSM-IV, 1994). Children who report or display depression or anxiety may also be medicated (Kurtis, 2002). This approach is premised on the theory that a CNS chemical imbalance is responsible for these conditions. Again, one need not go beyond the premise that LD resides within the student in order to apply treatment, in this case, medicinal. Whereas the first three models concentrate on deficits within the child, the final two models offer an expansion in understanding and treating learning disorders.

The Developmental Difference Model

The developmental difference approach parallels the educational/psychometric approach in that each uses comparison techniques. Whereas the psychometric approach compares aptitude and normalized performance, the developmental difference approach compares age and performance. However, the emphasis is not on diagnosis, but rather on individuation and amelioration. At this stage, I delve beyond LD definitions that restrict discussions to a singularly intrinsic focus. One of the reasons I find it necessary to expand the scope of this analysis, as will be discussed, has to do with a developmental lag debate, that is, intervene early or await possible maturation.

Examining the pros and cons of intervention then introduces the question of where and how to intervene: in a clinical setting, in the classroom, or at the familial/custodial level? Because the classroom is where difficulties usually emerge, I focus on that setting for ongoing assessment, developmental adjustment, and possible intervention.

The Psychological Model

I compare theories of learning from behavioral, cognitive, psychodynamic, and humanistic perspectives and suggest that the benefits of philosophic orientations and techniques may vary amongst them. Believing that psychological perspectives are best chosen according to circumstances and settings, I examine combinations of approaches and conditions, finding strengths in some and weaknesses in others.

From a therapeutic standpoint, cases arise where the simple administration of psychiatric medication is either augmented by, or eschewed in favor of, what are sometimes termed "talking out" therapies (Reber, 1985). As in the developmental difference model, the emphasis stays with individual assessment and enrichment. The psychological approach centers on establishing helping relationships amongst school-based participants to investigate and offer supportive, rational discourse geared to each disordered student's emotional and intellectual level. Again as will be shown, an LD definition circumscribing therapies to neurobiological, intrinsic considerations disregards the fuller and therapeutic potential of psychology. Not only do background conditions emerge in this discussion, they may predominate over assumptions of CNS organicity.

The Author's View of Some Collateral Issues

I also attempt to assess the degrees to which various diagnostic and therapeutic approaches tend to recognize learners' autonomies with the question in mind as to whether or not researchers and practitioners exhibit stances one might consider to be overly deterministic and/or mechanistic.

I use this term to symbolize relevant types of learning difficulties accompanied by attributions as to cause--the entire range of potential contributing factors, both intrinsic and extrinsic; and whether, in addition, children’s ranges of intrinsic talents and motivations are also seen as part of their individual spectra.

In questioning what might be a preponderance of fractionated approaches, I suggest that researchers, practitioners, and educators consider incorporating all these standpoints and their contributing as well as detracting factors into the mix of assessments and treatments so as to better view each student as a unique person.

Conclusions and Recommendations

Having examined through the lenses of human incentives and advocacies, the tools at hand, the states of the art, and strengths and weaknesses in how our society addresses learning disorders, I summarize the situation and look to counteract weaknesses by offering alternative strategies that challenge the current practices that I have called into question. The antitheses, although not difficult to formulate, might gain momentum should new voices enter emerging arenas of public discourse.

CHAPTER 2: EVOLUTION AND APPLICATION OF LD DEFINITIONS

Background

The publications of James Hinshelwood, circa 1907, and Samuel T. Orton, two pioneer-investigators of reading disorders, contributed to a pathognomonic conceptualization of what was to be termed dyslexia (Coles, 1987). Hinshelwood, a Scottish schoolmaster, offered a telling case study about siblings who exhibited what was termed "word blindness." By focusing on his suspicions of congenital neurologic causation, Hinshelwood advanced the theory that learning difficulties had intrinsic rather than external origins.

In 1928, with his publication of, An impediment to learning to read: A neurological explanation of the reading disability, Samuel Orton, a neuropathologist, revived and reformulated Hinshelwood's theory with descriptions of students suffering from strephosymbolia, that is, reversal of symbols (Carter & McGinnis, 1970, p. 197). Orton, thanks to his scientific credentials, not only seemed to validate Hinshelwood's organicity hypothesis, but hypothesized that mixed dominance of the two cerebral hemispheres was the cause of dyslexia (Carter & McGinnnis, 1970, pp. 55-56), the clinical equivalent of Hinshelwood's word blindness.

Chronological Developments

In 1968, a multidisciplinary group, the National Advisory Committee on Handicapped Children, met in order to establish and define LD. The following construction, incorporating Hinshelwood's and Orton's emphasis on intrinsic causality became the standard for a decade (Coles, 1987):

The second sentence, in setting out symptomatology, has a behavioral bent. Structurally, CNS architecture is vaguely alluded to by mentioning perceptual handicaps, brain injury, dyslexia, developmental aphasia, and minimal brain dysfunction (MBD). Because the MBD term consists of an imprecise adjective coupled with two global nouns, I find it difficult to imagine how it could focus investigative activities in the interests of clinical diagnosis or scientific research.

The definition of MBD that appears in Diagnosis and Management of Learning Disabilities (Brown, Aylward, & Keogh, 1992), characterizes MBD as a "Subtle brain dysfunction in which a child exhibits a mixture of some or all of the following: learning disabilities, language disabilities, other inconsistencies among various cognitive functions, attention deficit disorder, gross, fine, and oral motor dyscoordinations [sic]" (p. 218). MBD is not to be found in the American Psychiatric Association's DSM-IV (1994), but Taber's Cyclopedic Medical Dictionary defines it as, "A poorly defined concept rather than a specific diagnosis" (Thomas, 1989, p. 1135). But MBD, in particular, has intimidating overtones and provides little, if any, denotative meaning. Its inclusion may be an attempt to differentiate LD from retardation so that when the latter is excluded, what's left over is MBD. I gather from the definitional scatter that it acts as a wild card, a place holder, for anything that might have been missed.

The final exclusionary sentence of the National Advisory Committee on Handicapped Children's definition of LD delves further into CNS structure by distinguishing between perceptual and sensorimotor deficiencies, excluding the latter. The exclusion of "environmental disadvantage" suggests extrinsic factors such as the home atmosphere may not need to be considered in this view, and if so, the quality of instruction is evidently left in an ambiguous state.

The failure to mention students’ motivations might be taken to suggest that either children are not credited with having an independent mental life, or if they are, it is of little consequence in learning. These definitional oversights remained extant for approximately nine years.

National Advisory Committee on Handicapped Children

As reported in their publication, "Learning disabilities issues on definition," the National Joint committee on Learning Disabilities (1990) reports that in 1977, the National Advisory Committee on Handicapped Children defined LD in this way:

Most of this definition is handed down from the previous one. Slightly better economy of words ensues by the blending of the preceding definition's first two sentences.

Again, the inclusion of such an indefinite expression as MBD ill serves the act of framing definitions.

More Definitions

Starting in 1985 and ending in 1988 with the currently adopted National Joint Committee on Learning Disabilities (NJCLD) definition, four more definitions were set forth.

This definition's use of the word "deficit" appears to place the CNS in the forefront of causality and, most significantly, carries with it the implied exclusion of other internal factors and all external factors.

Neurological causality is presumed and conspicuous. Employing the term, "presumed," when attributing brain dysfunction to children makes a weak argument for a serious allegation, and as this paper will show, its use is fated to have considerable ramifications.

Another notable expression is: "Throughout life, the condition can effect self esteem." The child is granted self esteem whereas intentionality goes unmentioned. Having alleged to the effect that slow learners are brain damaged, the definition further diminishes hope by raising the possibility of permanence.

This definition addresses the overall condition rather than component disabilities. "Presumed" has survived another iteration. The presumption of CNS causality overrules all other factors and now sets the boundaries that distinguish LDs. Inappropriate instruction appears to be set aside as (inexplicably) a component of "socioenvironmental" factors. Attention deficit disorders are also recognized and excluded from the definition. Children's volitional factors, had they been eluded to, now seem even more out of place as the tone becomes more mechanistic.

The next year, 1988, the National Joint Committee on Learning Disabilities (NJCLD) evidently modified the Interagency Committee on Learning Disabilities' definition so as to reassert lifetime chronicity and seemingly dismiss the relevance of "self-regulatory behaviors." Other than reinforcing what now seems to have become a deterministic stance, the NJCLD has copied the Interagency Committee on Learning Disabilities' definition almost word for word:

Analysis of the NJCLD Definition

As these definitions have emerged to indicate, the generally adopted NJCLD definition is the result of a gradual evolution of conceptualization in the LD field rather than either an inspired vision, such as Newton's Laws, or a research-driven attainment. Nevertheless, I will briefly treat the NJCLD definition as an entirety in order to better evaluate its salient points. At the outset, "disabilities" is defined in the plural as an umbrella term, citing six components (listening, speaking, reading, writing, reasoning or mathematical abilities) and are called a "heterogeneous group of disorders." One can infer that each disorder may be termed a specific disability, such as dyslexia, a reading disability. Following that, (what have subsequently turned out to be) important guidelines are set forth pertaining to causality, duration and limitation.

The DSM-IV (1994, pp. 46-53), opting to use the term "disorders" rather than "disabilities," classifies subtypes into the following developmental disorders: reading, mathematics, written expression, and not otherwise specified (NOS). Learning disorders/disabilities tend not to rise to the level of severity as do developmental disorders. More analogous in terms of degree, however, are another set of disorders, termed communication disorders (DSM-IV, 1994), and they must be considered because they equate so well with localized brain functions as will be described in the neuropsychological model: expressive language, mixed receptive/expressive language, phonological, stuttering, and NOS.

The DSM-IV, under the topic of differential diagnosis for learning disorders, states: "Learning Disorders must be differentiated from normal variations in academic attainment and from scholastic difficulties due to lack of opportunity, poor teaching, or cultural factors" (p. 47) but doesn’t offer diagnostic terminology for poor teaching, etc.

Levine (1983), writing in the 12th edition of the Textbook of Pediatrics confined his discussion to what he called, developmental dysfunction, and stipulated five areas of performance: reading, spelling, writing, mathematics, and social interaction (pp. 105-115). Under the area of diagnosis, he maintained, "Children with developmental dysfunction present complex and sometimes baffling diagnostic challenges. Their problems are not easily classified, each discipline tending to perceive problems in the context of its own subject matter" (p. 115). The disciplines he went on to mention are: educational, psychological, other specialties and the art of medicine.

The portion of the NJCLD definition that states, "These disorders are intrinsic to the individual, presumed to be due to central nervous system dysfunction, and may occur across the life span," denotes, what I consider, the most consequential and debatable elements. It excludes non-CNS problems such as poor self control and social deficiency which "do not, by themselves, constitute learning disabilities." By virtue of emphasis, the definition seems to rule out other intrinsic, but non-CNS (such as psychogenic and volitional) factors, implying that they either don't exist to measurable degrees, or are better off being dealt with in a different context. The remainder emphasizes that LD may not be attributed to extrinsic factors such as, poor classroom instruction or defective nurturing.

Ruling out insufficient instruction and childhood nurturing remains consistent with the previous assertion that the umbrella term, LD, or its components are "intrinsic." Whether or not one agrees, one must acknowledge that appropriate agencies, other vested groups, or authentic individuals who frame definitions of afflictions have the right (and the obligation) to set forth such boundaries as they see fit so as to differentiate between analogous disorders.

The CNS and permanency stipulations erect a double barrier, excluding: (a) all other intrinsic factors, especially connected with the existence of the self, such as volitional and attitudinal factors; and (b) all extrinsic causes.

Application of LD According to the NJCLD Definition

Putting these burdens aside for the meantime, I envision that there are four sets of concerns in approaching learning difficulties from a remedial perspective: the educational, tailoring curricula; the clinical, concentrating on each afflicted child's CNS; the rehabilitative, seeking to surmount those student's learning difficulties; and interventional, working on behalf of shortchanged students to remedy deprivations in the classroom or home.

In and of itself, the LD definition does not rule out the existence of an appreciable percentage of students failing to learn satisfactorily because of other, non-LD factors: intrinsically, psychogenic and volitional causes; and extrinsically, inadequate or traumatic conditions in the home or school.

Broadening outward categorically from this definition--but bearing in mind that a child may fall in more than one category--I can construct an expansion, which I henceforth term a spectrum, of seven populations of children experiencing "learning difficulties." Accordingly, I list seven potentially classifiable populations in an order of what might be their relative numerical prevalences: (a) those who, regardless of other hardships and/or disorders, are capable of performing were they so motivated, (b) those whose learning opportunities have been thwarted by deficient parenting, (c) victims of deficient teaching, (d) those trapped in socioeconomic difficulties with or without faulty peer associations; (e) students with psychogenic impediments that might underlie or intensify any of the above; (f) students who are intellectually ill-suited to the subject matters in question or handicapped in some other uncorrectable fashion; and (g) those who fall within the LD sphere and could be competent to learn under current conditions were it not for a fixed neurological defect that does not take on the dimensions of the previously-mentioned category.

There is nothing in the NJCLD definition that suggests what proportion of substandard learners meets the criteria for LD classification. Therefore, is there not a possibility that those students whose performances are diminished by either motivational roots or, what the LD definition terms "extrinsic influences (such as factors exerted within the home, the classroom, and peer associations)" are in abundance or even predominate over those with true CNS defects? How does one decide between neurological and other causalities when the NJCLD's use of the term, "presume," thanks to its essential immunity to analysis, frustrates any such attempt?

In a utopian school setting, a child exhibiting learning difficulties undergoes diagnostic procedures that attempt to identify causes in a sequence ruling out the most likely and working towards diminishing probabilities. In adhering to exclusionary criteria, an aspect of diagnosis, a child's home life might first be evaluated, then the teaching approach within that child's classroom might also come under scrutiny. In this ideal setting, only after having ruled out these external circumstances, is CNS causality suspected.

The above procedure parallels the clinical exclusionary approach whereby current suspicions or previous diagnoses, termed criteria, must be ruled in or out before other diagnoses under consideration are allowed (DSM-IV, 1994, p. 5). Differential diagnosis is a clinical comparison process (Thomas, 1989) employing exclusionary criteria so that procedural priorities take both vital and practical issues into account.

For instance when carrying out differential diagnosis along the lines of exclusionary criteria, one shouldn't attempt to diagnose X without first ruling in favor or against Y and maybe Z, etc. The priorities and immediacies of diagnostic evaluations vary along the lines of vital concerns combined with practical considerations and limitations. When following exclusionary criteria, questions one might ask are: Which potential maladies' prognoses deteriorate rapidly without immediate attention? What examination procedures are the most easily, accurately, and quickly performed (try to get them out of the way so their issues don't clutter up the picture)? What examination procedures are risky, invasive or otherwise undesirable (try to save them for last)? Which suspected disorders are more correctable or amenable to immediate treatment, but, later, may become refractory?

The application of exclusionary criteria sets clinical priorities of evaluation so that less consequential indispositions that mimic grave illnesses are exposed, or conversely mild afflictions are not diagnosed in lieu of critical care for aggressive diseases. The DSM-IV (1994, pp. 47-48) does apply a differential diagnostic approach to the process, but I will show that, thanks, in large part, to the incentive to spare parents and teachers embarrassment (Alessi, 1988), nearly all diagnoses attribute causality to the child's neurology rather than the child's circumstances.

Could it be that applying exclusionary criteria to learning disorders trivializes the differential diagnosis process? Firstly, in lieu of grave symptomatology, learning disorder diagnoses (perhaps better expressed as learning disorder classifications) are often rendered by non-medical professionals (Good, 1998), and in the arena of learning difficulties, exclusionary criteria no longer deal with life threatening concerns. Secondly, when students are not medically examined for LD, they are usually evaluated according to psychometric criteria, and CNS dysfunction is assumed rather than ascertained. Superficially, this argument weighs against applying exclusionary criteria in assessing LD. So what if an LD specialist tends to bypass extrinsic considerations, psychogenic concerns, or volitional considerations and assumes CNS causality of learning difficulties? What harm is done?

Attaching the expression, learning disabled, to a young learner has drawn criticism from various sources, (e.g., Coles, 1987; Gelzheiser, 1987; McGuinness, 1985). Isn't it legitimate to question any term with negative, global connotations, and when applied to a student, ask if such labeling is stigmatizing; and might this labeling have self-fulfilling effects, or be injurious in other ways?

Are there benefits to presuming, without confirmation, intrinsic, CNS causality over other factors? I don't perceive any for children, but any such definitional construct that might partially relieve LD administrators and specialists of the obligation of taking children's "extrinsic" circumstances into account when addressing their learning difficulties simplifies said LD practitioners' responsibilities. An anti-child abuse organization based in Wisconsin places "poor grades" at the top of a list of 19 behavioral "signs of child abuse and neglect" (Prevent Child Abuse, para. 3). Because poor grades can be restated as "achievement discrepancies," they may then be attributed to "intrinsic causalities" rather than extrinsic abuse or neglect on the part of parents or caregivers. In sourcing the problem to the child under the aegis of presuming CNS causality rather than to custodians, as direct evidence might suggest, LD specialists may benefit by not exposing themselves to controversy or parental retaliation.

"Bruises, welts or broken bones" (Prevent Child Abuse, para. 3) tops the list of physical signs of child battering. The above mentioned indications suggest that, for the sake of the child, intervention needs be undertaken. How often might it happen in school systems that do not want to get involved in litigation, that abused children's custodians are given benefit of the doubt? Combined with CNS dysfunction to explain poor performance, alternate explanations such as, youthful roughhousing, might rationalize evidence of battering and relieve school system personnel of the peculiar risks of "getting involved" in something that could turn nasty.

Aside from hardships that children with learning difficulties might experience during the LD classification process, is there an additional price the children and parents alike may pay for the assumption of CNS causality when the situation may be more benign? Whether or not it is evident that the CNS assumption is not without an emotional toll to parents and children, shouldn't advocates of such terminology be charged with the burden of proof? In an age where pejorative terms are being expunged from general usage, shouldn't the LD research community be tasked with the defense of an expression that may label a child with a second class mentality?

One might expect that concerns about the effects on children and their parents of being notified of a disorder that is "intrinsic to the individual, presumed to be due to central nervous system dysfunction, and may occur across the life span (National Adult Literacy and Learning Disabilities Center, 2002)," should arise amongst LD researchers. Such notification is not good news, and with it, hopes for the future might be dashed, possibly leading to guilt and depression on the part of parents and children. Worse yet, abusive custodians might blame the child and react accordingly.

The opposite may also occur. Well-intentioned parents may not challenge the LD process, even in cases where they believe their child has been misclassified. According to Wright (para. 5), a clinical social worker who, along with her husband, Peter, an attorney, works on special education legal matters, "Parents of special ed [sic] kids often say that they are intimidated, patronized and made to feel guilty and inadequate by the staff at their children's school. These parents feel helpless, frustrated, and defensive" (para. 5).

Therefore, I expect that someone in the LD field must have launched an impact study that queried children and their parents about any distress accompanying the news of the LD finding. My computer searches and other research efforts to uncover studies seeking to determine to what degree guilt and depression follow LD notification have led to naught. I sent E-mail communications to a number of credentialed authorities in the LD and special education disciplines asking them to access "studies on how psychologically detrimental or debilitating are the LD terminology connotations (brain causality, permanence, generality, etc.) .... to determine whether or not guilt and depression follow notification."

I received the following E-mail from Prof. Roland H. Good of the College of Education, University of Oregon, "I think you are examining a very important area. I believe the learning disability label carries the connotations you describe, and is likely to have the effects you describe, but I do not know of any empirical research documenting these effects" (personal communication, April 11, 2001).

The hypothetical question persists: Is the LD notification process traumatic to parents and children, and if so, how traumatic? Shouldn't at least one educational researcher care to know this? The jury is still out on whether or not any research-oriented educator has ever been curious enough to conduct such a study.

This leads me to two conclusions: (a) Considering that there well may be a psychological price to be paid by the LD-labeled students and their loved ones, exclusionary criteria should come into play during the learning disorder classification process. (b) Overdue are heavily-funded studies seeking to discover, whether or not, and to what degree, guilt, depression, and feelings of helplessness follow LD notification.

Theoretically, doesn't a division of resources where, early or late, the child is finally classified and treated according to whether or not learning disorders arise from the home, classroom, economic plight, psychological impairment, motivation, and/or central nervous system, make sense? Maybe so, but in practical terms, the incentive as demonstrated by advocacy groups, the tools, and the art must operate forcefully and efficiently enough so that all academically troubled students, regardless of which of the aforementioned categories they happen to fall in, have a fair chance of being accurately assessed and appropriately treated.

Experts in the field do not believe that this is what's happening (Armstrong, 1988; Coles, 1987). The following quotations indicate that, of the various categories, LD designations and approaches are over-applied whereas extrinsic factors in cases of shortchanged children should systematically trigger intervention but do not.

Gelzheiser (1987) observed, "Of course, when information is gathered only about the child, the cause of school failure can only be ascribed to the child, and it will often seem logical to identify the student as disabled" (p. 146).

Coles (1987), an outspoken opponent of LD practices in the schools states:

This leads to a critical question: how is it possible to appropriately classify uninspired, poorly cared for, or comparatively untaught students who carry (what might be construed as) LD patterns should there be, hypothetically speaking, no clinically or educationally befitting terms relating to a student's specific situation or condition? Even though the LD designation carries with it the burden of assumed CNS damage, it, along with "psychogenic" and "attention deficit hyperactivity disorder" seem to be the most frequently encountered learning disorder categories available. Just as the phoneme and morpheme are the basic elements of speech communication, and similarly, written communication rests on sets of graphemes for each language, each applied discipline has its own lexicon of terminology made up of what are termed, "lexemes." Without diagnosticians having suitable lexemes for classification, children whose opportunities to learn have been disrupted at home or attenuated in the classroom are likely to be misclassified as LD.

Of the various roots of learning disorders, such as, familial, instructional, CNS, and perhaps associational; only the CNS type seems to have been awarded an official, learning related designator. Thus, the Statistical Abstract of the United States (U.S. Bureau of the Census, 1995, p. 171) shows that, of the four million children who qualified for federal and state disability programs in 1980, 31.9 percent (1.278 million) were classified as being learning disabled whereas 29.6 percent (1.185 million) were speech impaired, and 21.7 % (0.869 million) mentally retarded. By 1993, the overall disability figure rose by 581 thousand to 4.586 million of which 51.3 percent (2.353 million) were classified LD, compared with 21.7 percent (995 thousand) speech impaired, and 11.3 percent (518 thousand) mentally retarded (Statistical Abstract of the United States, 1995).

While the total student disability population rose 14.5 percent, and the speech impaired and mentally retarded populations declined (16 percent and 40 percent respectively), the learning disabled count rose 84 percent. It is difficult to account for the disproportionate increase in LD over the period without questioning the accuracy of the LD, classification process.

This questioning inevitably leads me to a closer examination of the categories of classification, or lexemes. The major lexeme is the idiom: learning disability. Here is a category that can grow 84 percent in thirteen years while surrounding categories diminish!

"With its well-known problem of definition resulting in vague and ill-defined boundaries, it is relatively easy for a student to qualify as LD. The LD category has thus become a catch-all classification with little substantive foundation" (Kavale & Forness, 1998, p. 6). According to an entry in the Dictionary of Psychology (Reber, 1985) termed: Junk box labels, "The implications of the label are that the diagnostic category does not really represent a well-defined syndrome (or disease or condition) but rather is a loosely constructed conceptual 'junk box' into which all manner of individual cases are thrown."

There we have a possible answer to an 84 percent increase: LD is a category that must stretch to cover at least three other causes of learning difficulties, such as, unsatisfactory classroom instruction, poor parenting, and poor health care arising in the home and school that appear to have no dispassionate titles.

So, it appears that it is impossible to classify types of learning difficulties in adherence to exclusionary criteria when the names for at least three of the other categories don't exist. This leads me back the question: how important is it to practice exclusionary criteria in this milieu? I'll offer a possible answer with another question based on the assumption that unfounded beliefs in mental limitations act as disincentives to academic success. How important is it that numerous students, possibly stretching into the millions as I have deduced from the Statistical Abstract of the United States (1995), who may have no brain damage are not spuriously led into believing they do have brain damage? Not only may it be impossible to classify types of learning difficulties in adherence to exclusionary criteria without the categories that are missing, but if so, it becomes impossible to classify them at all. This may leave untouched the true causes of many, or even most, learning disorders. So lest the foregoing be the case, it is important, at least, to propose names for the missing categories.

Whatever terms are posited to fill volitional, home, and school lexeme deficiencies, they must be non-prejudicial lest they offend implicated adults and be declared: nomen dubium. Pejorative, would-be terms, such as "dysparentia," or, as in Armstrong's (1988) In Their Own Way, "dysteachia," might well occasion a backlash from parents and teacher's groups. "Dysnurtiad" or "dysinstructed" are not likely to fare much better in the face of vested, adult interests. Fortunately for the framers of the original term, LD, there were and are no children's organizations to point out the damage being done by the evident toxicity of such a term as "disabled." I leave it to those with better lexicographic abilities to propose terms clearing whatever obstacles parents and educators might erect.

On the face of it, considering the absence of other classification alternatives, is it wrong to posit such a draconian definition of LD where children's self images and self confidences are at stake? In theory, couldn't the LD definition be revised so as to be termed "learning challenged," or "learning disordered" and thus concurrently deal with all other, non-intrinsic learning difficulties under different, and perhaps more appropriate criteria? In practice, I don't doubt that many federal and state laws, policies, and regulations act as barriers to a changes of this sort.

Subtyping research, a discipline in itself, has developed from the heterogeneity aspects of LD. The DSM-IV partitions learning disorders into reading, mathematics, written expression, and not otherwise specified (1994, p. 46). Rourke (1991), a respected authority in the field of such LD research, edited a book titled: Neuropsychological Validation of Learning Disability Subtypes.

Rourke, himself, prefers age, verbal, nonverbal, and IQ grouping (pp. 3-11). Other classifications randomly pop up in this neuropsychological-research-oriented book such as dyslexia: p-type for slow, fragmented reading and l-type, for inaccurate reading (Bakker, Licht, & van Strien, 1991, pp. 124-139). Spelling, drawing, arithmetic-disabled by age, are identified as subtypes (DeLuca, Rourke, & Del Dotto, 1991, pp. 180-219), but I could not find any attempt to outline an overall taxonomy. Contributors Lyon and Flynn (1991, pp. 223-241) attempt to bring order to the situation with what they term, "current definitions of disability ... identified on the basis of different handicapping conditions (e.g., oral language, basic reading and reading comprehension, arithmetic calculation and reasoning and written language disorders)." After that respite from the frequent usage of inferential statistics that seems to typify Neuropsychological Validation of Learning Disability Subtypes, he text returns to ANOVAS, Mann-Whitneys, and the like.

Contributors Fiedorowicz and Trites (1991, pp. 243-266) come up with subtypes of the reading disabilities subtype: type-O (for oral), type-A (for intermodal-associative), and type-S (for sequential). Other groupings can be found in the overall text based on the subtests of the various test batteries employed. Coles (1987) dismisses such endeavors with, "subtyping research continues to serve the same LD pie, while only trying to slice it differently" (p. 64).

Gaddes and Edgell (1994) group all their subtypes according to traumatic vs. developmental. Along with sensory, motor pathway, and perceptual, the subtypes they suggest by their chapter headings are: "Attention Deficit Disorder; Language Development, Aphasia and Dyslexia," and finally, "Writing, Spelling, and Dyslexia."

Would that instructional and parenting deficiencies had been so assiduously explored, detailed with classification subtyping, and implanted within our social and legal discourse as varieties of childhood learning difficulties have been, might not the home and the school now provide more benign learning atmospheres for today's children?
 

CHAPTER 3: THREE DISABILITY APPROACHES

Of the five aforementioned learning disability models, the first three will be considered first. They are: the educational, the neuro-anatomical, and the biochemical. They all appear to meet the inflexible defining criteria of the NJCLD: (a) intrinsic, (b) CNS dysfunctional, and (c) life span reach.

The life span parameter, when added to the classification criteria shown in Table 1, then becomes the forecast or prognosis in all three of the upcoming categories, and this casts a pessimistic shadow over treatment. With such an abject limitation, treatment may seek more to accommodate than eliminate learning disabilities.

The Educational Model

Performance assessment for purposes of determining LD is a comparison process. The results of achievement test batteries are measured against aptitude test battery outcomes, and if achievement scores are less than aptitude test scores suggest they should be, the performance shortfall is termed a discrepancy (Francis, Espy, Rourke, & Fletcher, 1991).

Amongst the tests that are most often used to determine LD are: the Weschler Intelligence Scale for Children (WISC-III), and the Wide Range

Achievement Test (WRAT3) for children (Campbell, 2000). The WISC subtests establish three quotients: a verbal, a performance, and a combined IQ. The combined IQ is called the WISC Full Scale IQ (FSIQ).

There are two major considerations in setting the criteria with the educational, LD assessment process: (a) formulating a mathematical discrepancy model and (b) delineating the cutoff scores. The WISC-III, designed for 6 to 17 year olds, has both a test set to measure aptitude, termed verbal, and another set to measure achievement, termed performance (Campbell, 2000).

The scores from the six verbal subtests, five mandatory, are: Information, Similarities, Arithmetic, Vocabulary, and Comprehension; along with which the Digit Span subtest (reverse sequence Digit Span is optional) combines to produce verbal IQ scores (Kaufman, 2000). The performance scores from the five required achievement subtests; Picture Completion, Picture Arrangement, Block Design, Object Assembly, and Coding, and they combine to bring about a performance IQ. Mazes and Symbol Search are two optional, performance subtests (Kaufman, 2000).

The IQ difference between performance and expectations is termed a "performance discrepancy." This expression is an early entry to lexicon of LD, and, as cited in "Gifted children with learning disabilities" (Brody & Mills, 1997), the discrepancy model has been attacked from the outset as being insufficient to be the final arbiter of LD. As early as 1968, Krippner (1968) posited other factors, included among which were: poor auditory and visual skills, unfavorable educational experiences, and cultural deprivation that could account for similar outcomes. Nevertheless, performance discrepancy became the common standard for LD classification (Lezak, 1983). According to a state by state summary of early childhood special education in an eligibility chart compiled by the National Early Childhood Technical Assistance System (2001), cutoff scores of either 2.0 or 1.5 standard deviations are typical. The DSM-IV (1994, p. 46) suggests that performance discrepancy cutoff scores range between one and two standard deviations.

Although the completeness of the WISC-III provides a convenience, comparing its two subtest sets to determine discrepancies is not mandatory (Wilkenson, 2000). The WISC-III’s verbal, aptitude portion may be paired with performance batteries from other tests for performance discrepancy calculations. For instance, the WRAT3 has three achievement subtests that focus on the coding skills of reading, spelling, and arithmetic (Wilkinson). The WRAT3, with its seemingly better alignment with the WISC-III's, verbal portion, may be preferred over the WISC-III, non-verbal, problem solving performance battery for assessment of achievement (Campbell, 2000)

A recent counterpart to the WRAT is the Wide Range Intelligence Test (WRIT) (Glutting, Adams, & Sheslow, 1999). Its expanded age range is now from 4 to 80 years old.

Although Brown, Aylward, and Keogh (1992) identify the WISC-III as being inappropriate, Lezak (1983) wasn't impressed with the Weschler Adult Intelligence Scale (WAIS). "In short, averaged scores on a WAIS battery provide just about as much information as do averaged scores on a report card" (Lezak, 1983, pp. 242-243).

Kavale and Forness (1998) attribute the explosion of LD classified students to the success of advocacy groups, "One of the consequences of advocacy has been the elimination of identification criteria to the point where LD has essentially a single criterion, discrepancy, the difference between expected and actual achievement" (p. 6).

For example, the Learning Disabilities Association of America (LDA) was the first learning disorder, advocacy organization, founded in 1963 under the name of Association for Children with Learning Disabilities (Kavale & Forness, 1998).

Psychometricians interested in advancing internal validity, might insist that aptitude can only be tested by instruments whose elements make few "assumptions about specific prior learning experiences" (University of Illinois, 2001, para. 2). By contrast, achievement tests are expected to reflect standardized educational experiences. "In the real world the distinctions among these . . . tests are quite fuzzy. . . . It has been known for some time that the correlation between achievement and ability tests may be nearly as high as that between any two ability tests" (University of Illinois, 2001, para. 2).

Assessment formulations typically stipulate what is to be compared and do so according to a given mathematical relationship. In order to compare reading aptitude with comprehension, the psychometrician can normalize both sets of subtest scores according a standard frequency distribution curve and then, assuming that intermediate scores are proportionate, subtract the aptitude score from the comprehension score to see if there is a shortfall. He or she can then apply the standard deviation overlay and identify those discrepancies that exceed the cutoff points, such as, 1.5 standard deviations, as being LD.

Lezak (1983), Gaddes and Edgell, (1994), Rourke (1991), and Kavale & Forness (1998)--recognized experts in the learning disorder field--insist that, by application, aptitude and achievement tests are both arbitrary and psychometrically flawed:

But according to Lezak and others (Coles, 1987; Kavale & Forness, 1998; Brown, Aylward, & Keogh, 1992), the reliance on a discrepancy between performance and IQ is seriously tainted as a classification tool. If the difference between any two measures signals the approach to a pathological shortfall as it rises, isn't this another way of saying "the less the positive correlation between these two measures (aptitude and achievement), the greater the discrepancy, and thus the greater the performance shortfall?" Now, suppose all standardized measures of aptitude and achievement are already slightly correlated to some extent. This has been termed, "regression to the mean" (Francis, Espy, Rourke, & Fletcher, 1991, p. 19). Correlation offsets can be applied to raw scores to counteract regression but not without controversy, "Even when IQ and achievement scores are corrected for regression [to the mean], it is not clear that children with discrepancies in IQ and achievement have more specific disabilities than do poor achievers whose IQ scores are not discrepant" (Francis, Espy, Rourke, & Fletcher, 1991, p. 21). For instance, should the above two children achieve the same score on a performance subtest, and that score is marginal for purposes of LD classification; how they might be "treated" is: the child with the aptitude characterized by the IQ score of 112 (because of exhibiting a larger discrepancy) might sooner be classified as learning disabled than the one with the lower IQ score of 108. Lezak (1983) continued to describe how consequential to the life of the child any of the above inaccuracies might be:

Kavale & Forness (1998) find the discrepancy model poorly conceived:

Classification criteria and applications aside, what fate awaits the child after he or she is "pipelined" into special education? Although there are many possibilities, here are some of the more worrisome patterns that one may find in New Jersey.

"In Newark's schools, untrained substitutes were found overseeing special education classes on a regular basis" (Mooney, 2001, para. 2).

"Yet in urban and suburban systems alike, the state found widespread holes in how New Jersey's 220,000 disabled students are identified, placed and served--from a scarcity of programs and training to inadequate reporting of children's needs" (Mooney, 2001, para. 3).

"The US Department of Education cited New Jersey for long-standing, serious noncompliance" (Mooney, 2001, para. 4).

Special education students were originally slated to stay with their normal classroom settings, and only those who could not benefit from inclusion in regular education classrooms should be segregated into slow learner classes (Mooney, 2001). This ideal seems to be eroding in practice:

"'It is clear that the proper referral procedures (for classifying students) were not followed, and we heard that from a number of people,' said Barbara Gantwerk, the state's director of special education" (Mooney, 2001, para. 20).

"The state has shown it can identify noncompliance, but the question has always been whether it can correct it," said Diana Autin, director of the Statewide Parent Advocacy Network" (Mooney, 2001, para. 22).

"In Newark, New Jersey's largest district, fewer than one in five special education children are taught in inclusion settings. Among those students, parents 'felt that teachers did not have the necessary supports or the necessary supplemental aids and services that the students required,' the state's monitoring report said" (para. 26).

The Neuroanatomical/Functional Model

From a learning perspective, the "brain," referred to as the CNS, designates the larger of two globe-like structures in the head and is termed the cerebrum (Coles, 1987). Technically, the CNS encompasses the brainstem and spinal cord (Thomas, 1989). The cerebrum is alternatively named the forebrain as opposed to a miniature facsimile of same, called the cerebellum that is tucked beneath the cerebrum and is posterior to a part of the brainstem called the pons (Lezak, 1983). The cerebellum, along with the pons, regulate physical posture and fine motor control while academic learning, per se, transpires inside the cerebrum (Lezak, 1983).

The human brain is, under normal circumstances, unavailable for direct inspection and functionally complex beyond confident estimation. So the brain might not be expected to give up all of its secrets relating to reading ability. And it has not. Nevertheless, thanks to a historical background of physical examinations, x-rays, pathological case histories (especially related to diseases, blunt force traumas, penetrating wounds, and strokes) coupled with surgical accounts and autopsies, and data from mammalian experimentation; a store of brain-related knowledge had been accumulated by 1928. That's when Orton proffered his mixed dominance theory (Coles, 1987), contending that dyslexia results when "one hemisphere does not consistently lead the other in control over particular behaviors" (Reber, 1985, p. 214).

Elsewhere in early neuroscientific experimentation on the exposed surface of the brain during surgery, bodily movement and sensation had been stimulated by probing along opposite sides of a groove (the central fissure or fissure of Rolando) in the middle of each hemisphere (Waxman & deGroot, 1995). The bodily sensations and responses had been correlated with progressive positions--both along the central fissure and corresponding portions of the body (Waxman & deGroot, 1995). This demonstrable and repeatable effect led to success in functional mapping of that area of brain surface. Still very little of the above could be applied to assessments regarding the causes of dyslexia or other learning problems. By the middle of the 1930s, the prevailing hypothesis was that the wrong imbalances between the cerebral hemispheres caused dyslexia (Coles, 1987). One could hope that in the intervening years since Samuel Orton hypothesized CNS causality of reading difficulties (Carter & McGinnnis, 1970), a thorough understanding might have come forth as to exactly what malfunctioning areas within the brain, if any, cause dyslexia.

Perhaps opinion-makers in the educational establishment, having become impatient as a result of waiting almost half a century for an answer to Orton's conjecture, simply went ahead and stipulated a CNS defect (Coles, 1987). Although recent neuroscientific investigation shows some progress in establishing correlates, no fully understood connection between dyslexia and a disrupted neurology seems yet to have coalesced (Shapiro, 2000). Whereas the educational model assumes that the cause, or causes, of reading and mathematical difficulties are (a) CNS related and are (b) somewhat common across the population of poor learners, it stands to reason that the primary question neuroscientists have attempted to establish is: where, within the brain do learning difficulties arise? This quest for sites of causality is termed localization and has two components: brain-mapping and structural/functional, correlative analysis. Once the "wheres" are discovered, one might think, the "whats" and the "whys" might then follow.

Two general approaches to neuroanatomical localization are: the structural approach, localization by observing neuroanatomical abnormalities termed lesions coupled with known behavioral deficits; and the functional approach--the observational, correlative method in real time--localization by observing specifically stimulated behaviors compared with the site and extent of simultaneous, brain activity (Coles, 1987).

There are also degrees of precision starting from hemispheric considerations--such as the Wada test (Springer & Deutsch, 1989) to test cerebral dominance theories.

Advances in neuroimaging bring about ever higher spatial resolution seeking to isolate individual nuclei, which means, small groups of neurons serving common functions. Theoretically, the brain must be mapped in three dimensions, but except in a highly clinical venue, it's more efficient to orient viewpoints within a region or on a surface and relate positions to discernible features therein or thereon.

The processes of learning require perception, which amounts to "the integration of sensory impressions into psychologically meaningful data" (Lezak, 1983, p. 24), and this must be stored in a meaningful, retrievable way. To say that learning is a process depending on (a) sensory input, (b) associative integration, (c) memorization, and (d) expression, may be an oversimplification, but nevertheless, these elements seem to reflect gross CNS organization. For example, the surfaces of the brain are for the most part comprised of: sensory cortices, associative cortices, memory cortices (shared with interior structures such as the hippocampus and thalamus), and motor cortices (Waxman & deGroot, 1995, p. 273).

So for reasons that relate to comparative accessibility, I suspect cortical examination comprises the bulk of efforts for the localization of learning functions. Just as the spherical surface of the earth is usually mapped in only two dimensions, the outer surface of the brain can similarly be represented to good effect. Cerebral cortical brain mapping involves identifying enough "landmark" features so as to permit reproducible site identification and description for locales of interest throughout.

Superficially, the human brain (cerebrum) looks like an exposed walnut. The similarities between a brain and a walnut begin and end with a pair of wrinkled, hemispheric halves connected by a stalk-like, bridging segment. This representation is similar to human, invaginated, cerebral hemispheres connected by a relatively large, but short, bridge of neural fibers coordinating both hemispheres and arching around a rounded inner diencephalon. Said bridge is termed the corpus callosum (Waxman & deGroot, 1995).

The "wrinkles" in each half of the brain essentially mirror one another and delineate four matching divisions within each hemisphere known as lobes. The brain is mapped at the outer surfaces (lateral views) of hemispheric cortices and less frequently, at medial surfaces. What portions of the cerebral cortices are seen, plus greater areas that are hidden from view by "wrinkles" (Waxman & deGroot, 1995), all connect, through (white matter) systems of fibers and bundles of fibers, along with the vast architecture of the brain's hidden, internal neurostructure to project to other portions of the cortices.

Whereas the protruding folds on each side of a given "wrinkle" are called gyri, the crevices, themselves, vary in depth from what are termed furrows (sulci) to deep fissures. These alternating folds and creases in grey matter aid in the mapping that can register or enumerate (depending on the type of mapping) the sites of functional activities or lesions.

As seen from a left, lateral view (the left hemisphere is most often pictured for general maps of lobe locations), the overall outline of the hemisphere would be nearly elliptical with the major axis oriented horizontally (as is the case when a person looks towards the horizon) were it not for a notch in the lower left portion and a bulge in the lower right. The notch is where the eyes, nose and sinuses require space from the curve while the comparatively smaller occipital lobe, made up largely of the visual cortices, takes the form of a bulge at the lowest portion at the back of the cranium, beneath which resides the cerebellum.

The anterior notch with its emerging fissure is the most prominent landmark on each cerebral cortex and partitions corresponding hemispheric cortices to delineate the temporal lobes. The aforementioned fissure begins deep at the vertex of each notch (which happens to be near its corresponding temple) and runs almost horizontally towards the rear of the head. As this cleavage traverses from just beneath the corresponding temple on each side, it angles upwards along the side of the hemisphere in question and slightly above and behind the corresponding ear before losing definitional depth two thirds of the way from the origin towards the back of the crown of the skull. When discussing both sides, these two, bilateral crevices are termed, among other things, lateral cerebral fissures, and they divide the uppermost frontal and parietal lobes from the lower, horizontally oriented temporal lobes (Waxman & deGroot, 1995, p. 140). Their posterior terminus is bracketed by a small arching fold. Attached to that is another, short sulcus that runs posterior and downwards to make, some might think, the second arch of a tilted, letter, "m" as depicted and labeled in figure 10-5 in Waxman and deGroot (1995, p. 140). The bottom gyrus of the pair, termed the angular gyrus, has been linked to reading difficulties (Society for Neuroscience, April, 1999).

The aforementioned fissures of Rolando arch anteriorly from immediately behind the crown of the head of each hemisphere and, bending downwards towards the vertical while losing depth and definition as they nearly intersect the lateral fissures slightly above each ear. These central fissures partition the posterior, parietal lobes from the frontal lobes.

Immediately anterior to the central fissure on each side lie the primary motor areas and just posterior to these are the sensory association areas, but it is where the two main fissures almost meet just above the ear (especially in the left hemisphere for right-handed persons) that language skills are found to predominate (Waxman & deGroot, 1995, pp. 267-269).

The listening function is enabled by the ability to interpret audible language in the linguistically dominant hemisphere which is associated with a region slightly above and posterior to the ear in the temporal lobe. Essential for language comprehension, it is named Wernicke's area. The ability to produce meaningful spoken language in that hemisphere is associated with an area in front of Wernicke's area in the frontal lobe between the temple and ear and it is termed, Broca's area. The two language areas must be interconnected for a person to fully communicate, and this is accomplished by a bundle of fibers termed, the arcuate fasciculus. In order to connect Wernicke's area and Broca's area these fibers must bridge beneath, or vertically bypass, the deepest portion of the lateral fissure which separates the temporal and frontal lobes.

Terming each hemisphere's fissure of Rolando, "the central fissure," does not exaggerate its importance. The gyri on each side have consequently been named the post-central and pre-central gyri, and their motor and sensory cortices are what make their corresponding locations so vital in mapping. The anterior wall of the central fissure and adjacent precentral gyrus is also termed the primary motor cortex where contralateral muscular responses to stimuli applied there (face, hands, trunk, feet etc.) have long been mapped in progressively corresponding positions.

Contralateral organization, basic to the architecture of mammalian neuromuscular and neurosensory development, means that, because of a cross-over of projection fibers at various levels between the anterior corpus callosum of the diencephalon--basically the thalamus and hypothalamus (the portion of the cerebrum which underlies the cerebral cortex)--and the medulla, individual hemispheres control the motion of opposite limbs and are receptive of sensation in like fashion (Waxman & deGroot, 1995). Whereas, whenever the right hand is more developed to exert physical strength and dexterity than the left, the person's dextral dominance is classified as "right-handed." The contralateral combination of the left hemisphere and right hand seems, in the scheme of things, to have been preferred over the contralateral combination of the right hemisphere and left hand (Lezak, 1983).

A distinction must be made here so as not to confuse cerebral dominance with contralateral organization of sensorimotor, cerebral organization and control.

Dominance assumes such contralateral cerebral functioning; and besides its general application to sensorimotor functions, dominance also pertains to learning related specializations which tend to favor one hemisphere over the other (Waxman & deGroot, 1995, p. 272).

Associated with the processing of speaking and listening, two developmental aspects of reading ability, are the above-mentioned Broca's and Wernicke's areas that, when, by the measurements of their contours, are (especially in the case of right-handers) observed to be physically different than their opposite, hemispheric counterparts (Springer & Deutsch, 1989).

Also, according to Waxman and deGroot (1995), differences in physical development of related cerebral cortical areas accompany associated dominances. "The slope of the left lateral fissure is less steep, and the upper aspect of the left superior temporal gyrus (the planum temporale) is broader in people with left-hemisphere dominance [verbal functioning]" (p. 272). This does not mean, in general, that anatomical differences between hemispheric counterparts are always due to an increase in size of a dominant zone, such as might be assumed regarding Wernicke's area of the left hemisphere. Springer and Deutsch (1989) take care to establish that for right-handers, rather than neuronal growth singularly occurring in the left hemisphere; the non-dominant, right hemisphere can concomitantly lose bulk to account for the difference.

Ninety-five percent of right-handed people without any history of brain damage are left-hemisphere dominant in speech and listening (Springer & Deutsch, 1989); "so are 70% of left-handed people, while the remaining 30% of left-handed people are right-hemisphere dominant" (Waxman & deGroot, 1995, p. 272). So, hemispheric sites between handedness and verbal dominance tend to correspond in right-handers and cross over in left-handers. Lezak (1983, p. 221) offered similar proportions, "Approximately two-thirds of them [non- right-handers] show the pattern of lateral asymmetry that is characteristic for right-handers."

Of the major mammalian senses, sight and sound are probably the most essential for the processes of learning. The relative locations of human beings' primary auditory and visual cortices, which are located on the posterior surfaces of each occipital lobe, and their areas of association are good starting points to guide investigative activities.

As language elaborates in the developing child, two particular areas, Broca's and Wernicke's, differentiate whereby these areas appear larger in the dominant hemisphere. So, if these (seemingly) "beefed up" regions are not advantageously located with respect to handedness, might not transmission delays, especially through the corpus callosum, slow integration of neurosensory and neuromuscular activities?

Besides the brain's advantages of spherical design, I wonder if there might not be a type of allocation economy on--and between--the cortices. When entertaining that possibility, it's not surprising to find the primary auditory cortex residing in each temporal lobe immediately beneath the lower terminus of the sensorimotor cortex near where the lips, tongue and larynx are mapped (Waxman & deGroot, 1995). The organization of the arcuate fasciculus, lips, tongue and larynx sensorimotor cortices, and Broca's area, that arch over the auditory cortex offers a possible example. When verbal communication ensues, it may be that these areas can conduct fairly rapidly because they are not scattered about the surface of the brain, and that may be important for speed and accuracy of serial processing. In the less, well-organized brain, such as with the individual with mixed dominance, might not there be more of a tendency for borderline aphasia due to transmission delays? Whether or not that is possible, considering that listening does not require motor primary sensorimotor function as does reading, mixed dominance may be less likely to apply to phonemic awareness. But I would think that reading, with its necessity of controlling eye motions, and hand writing add new levels of complexity to the acquisition of communication skills, giving mixed dominance more opportunity to interfere with transmission.

The overall organization of each hemisphere shows that primary sensorimotor cortices border the central fissure, and adjoining these, in turn, are the association areas (Waxman & deGroot, 1995). Considering how the cortical regions appear to become more sophisticated in their functioning the farther away they are from the sensorimotor gyri bordering the central fissure, might it be that the further the distance anteriorly or posteriorly from the central fissure of any particular region, the more refined are its associational operations?

Moreover, it stands to reason that neurological disruptions of complex learning tasks might be found in associative regions that are not directly adjacent to the primary sensorimotor areas. The prefrontal cortices (behind the forehead) are said to host the highest cognitive activities. "We know now that the ability to perform many cognitive functions may be disrupted by frontal lobe damage" (Lezak, 1983, p. 79).

Efforts to attribute learning difficulties to either brain architecture, functioning, or both (brain physiology) have evolved from early results, hard-won over the limitations of direct examination (at autopsy or during surgery), to the more convenient and rewarding, present day imaging techniques.

Aside from the frequent necessity of injecting either radioactive or florescent contrast (Waxman & deGroot, 1995), some of these techniques are benign enough to allow the accumulation of scientific data which is not only open to corroboration but also subject to experimental control. Computerized tomography (CT) and magnetic resonance imaging (MRI) are employed for purposes of searching for neuroanatomical/functional deficits specific to whatever learning disorder is under investigation.

In the early 1970s, Electroencephalography (EEG) research was conducted under the controlled conditions of observing waveforms while reading-disordered subjects carried out various cognitive tasks during which their EEGs were cataloged as data. These task-evoked EEG responses, later termed evoked response potentials, were originally performed to gage hemispheric imbalance (Coles, 1987). But now with dramatic improvements in detail, evoked response studies employing sophisticated, color coded displays of EEG activity (termed BEAM scans for "brain electrical activity mapping; in Coles, 1987, p. 81), have shown promise in localizing abnormalities, essentially, looking for lesions. Because only association (not causality) can be attributed from relationships, correlation is the only product from such investigations (Coles, 1987).

A subsection of The Diagnosis and Treatment of Learning Difficulties is titled, "One must not treat without a diagnosis" (Bruknew, & Bond, 1955, p. 77). It may be that a learning disordered child is turned away without a diagnosis, but I suspect that clinicians who feel it is incumbent upon them to arrive at a diagnosis will find one. Thus, even as early as 1955, slow learning was likely to have been considered a pathology requiring a full-fledged diagnosis.

If, for instance, electrical activity, as displayed on BEAM, or cerebral blood flow, as shown on functional magnetic resonance imaging displays are seen to be abnormally low compared with the same areas in the brains of better readers, some sort of defect at that location may be thought to cause the reading deficiency. It may be the other way around, for instance, like the proverbial ninety pound weakling at the beach. Muscular underdevelopment isn't the sole cause of feebleness. Both can be rightfully attributed to a third factor, lack of exercise. Just as muscles become weak with neglect, so, according to Pribram (1971), does the brain's architecture and blood flow. Auditory cerebral dominance will not occur if the stimuli of hearing and vocalization do not keep pace (Pribram). Whereas dendrites proliferate under the spur of accomplishment, it seems that they dwindle when unemployed (Springer & Deutsch, 1989). So, it's not surprising to find functional, or even anatomical, CNS deficits in whatever areas of the brain are underutilized.

Nevertheless, observation or functional presentations of above mentioned under-utilization effects are termed "lesions (Waxman & deGroot, 1995)." I should think that the average person is likely to believe that a lesion is an open sore, or if not a wound in a state of festering, at least some anatomically observable formation of scar tissue. That is not so; lesions can even be assigned to functional deficits.

Is it not likely that the sequelae of strokes and head traumas have, at least historically, provided LD researchers with the bulk of their correlation information about various primary cortical difficulties? If so, in assessing learning difficulties might not associations between adult degenerative chronicity predispose diagnosticians to assume adult-like pathologies in youngsters without accounting for learning disordered children's youth-related resiliences? I believe--and base this belief on the NJCLD's 1988 pessimistic stipulation of life-span, CNS "dysfunction"--that when children present with either problematic behaviors or slow learning rates, their neurologies are as likely to become suspect as if they were adults. Has a pathologically-oriented bias conditioned the thinking of LD theorists to project clinical thought patterns on formative, more resilient neurologies without first looking outside the child for the answer?

The Biochemical Model

I can recall having encountered very few suggestions of chemical imbalances or neurotransmitter inadequacies during my comprehensive research of the above neuroanatomical model of LD. The anatomical term, lesion, however, cropped up repeatedly (Gaddes & Edgell, 1994).

By contrast, when researching ADD or ADHD, I cannot recall having encountered terms relating to the structural integrity of the brain--little or no mention of lesions. What was more often suggested under ADD or especially ADHD, were chemically based deficits in neurotransmission (Coles, 1987), which were correctable by dopamine agonists, especially the amphetamine, Ritalin (Norden, 1996). So, due to this dearth of anatomical support for ADD/ADHD, I favor the biochemical-ADD/ADHD association terminology. Furthermore, I will show (Kurtis, 2002) that treatments for ADD/ADHD are heavily weighted in favor of the amphetamine, Ritalin. Therefore, I've chosen to view attention deficits and hyperactivity through the lens of the biochemical without having the discussion spill over into the previously explored, neuroanatomical model.

Explaining the biochemical model

Section 314.00,01 of the DSM-IV (1994) presents a list of criteria, termed symptoms, for assessing attention-deficit/hyperactivity disorder that stipulates two, nine part sets of observable behaviors: the first cluster exhibiting inattention, and the other batch demonstrating hyperactivity-impulsivity.

"Reports from multiple informants (e.g., baby-sitters, grandparents, or parents of playmates) are helpful in providing a confluence of observations concerning the child's inattention, hyperactivity, and capacity for developmentally appropriate self-regulation in various settings" (DSM-IV, 1994, p. 83).

It stands to reason that inattention, in and of itself, can be an impediment to learning, and the DSM-IV presents a list of nine behaviors, any six of which amount to a problematic degree of inattention. The first item states that the child in question, "often fails to give close attention to details or makes careless mistakes in schoolwork, work, or other activities" (p. 83). Subsequent items dwell on supplementary instances of inattention--either in not sustaining sufficiently competent performance, exhibiting distractibility, or in not seeming to comprehend.

Following the attention deficit list, six indicators of hyperactivity are combined with three other characteristic behaviors indicative of impulsivity; and should any six of that total of nine be gleaned from observing a child's pattern of behavior, the DSM-IV's criteria for the hyperactivity-impulsitivity diagnosis has been satisfied. The DSM-IV's hyperactivity subsection leads off with the question as to whether or not the student, "often fidgets with hands or feet or squirms in seat" (p. 84). The three listed characteristics that constitute impulsivity are: (a) blurting out answers part way through questions, (b) difficulty awaiting one's turn, and (c) interrupting conversations (p. 84).

There exists an ADHD category that bypasses the rigor of finding six out of nine items in either of the above-mentioned categories: "When an individual's symptoms do not meet the full criteria for the disorder, and it is unclear whether criteria for the disorder have previously been met, Attention-Deficit/Hyperactivity Disorder Not Otherwise Specified should be diagnosed" (p. 80).

As the terms, ADD and ADHD entered the lexicon of clinical thought and practice, they were accompanied by laboratory-based efforts to operationalize embedded research constructs so as to improve upon diagnostic procedures (Forbes, 1998).

With that in mind, I suspect that, in general, initial studies seeking to validate ADHD diagnostic criteria emerged, not from the laboratory where confounding variables could be controlled or accounted for, but from the field (the home or school) where inconsistencies and subjectivities might emerge. At the outset, there was only the above mentioned, laboratory test that had limited utility in identifying ADD (Forbes, 1998). Meanwhile, other parent and teacher rating scales had appeared that sought to improve diagnostic objectivity and repeatability (Forbes, 1998).

Teachers' behavioral rating formats were also crafted, among which are the Revised Conners Teacher Rating Scale (RCTRS) and ADD-H Comprehensive Teacher Rating Scale (ACTeRS) (Forbes, 1998). Forbes mentions their prior use in selecting a sample population of ADHD children for experimental comparison purposes with another, more automated (CPT) test termed, Test of Variables of Attention (TOVA) (The description of which is deferred for the meantime). "Whenever possible behavioral ratings were obtained from teachers. Ratings from the Revised Conners Teacher Rating Scale (Goyette, Conners, & Ulich, 1978) were available for 94 subjects. Ratings on the ADD-H Comprehensive Teacher Rating Scale (Ullman, Sleator, & Sprague, 1991) were available for 51 subjects" (Forbes, 1998, p. 464). Forbes goes on to state that: