Abstract
Clearly, the value of any theory—dyslexia or otherwise—depends entirely on its encompassing and explanatory powers as well as its ability to lead to new insights and discoveries.
This is a preview of subscription content, log in via an institution to check access.
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Notes
- 1.
Although there have been some who recognized the limitations of the dyslexia = alexia brain damage theory of dyslexia, and a few have offered diverse versions—including Orton’s 1920 impaired dominance concept—no one else has proposed a concept that completely refutes all hypotheses that rely on the above dyslexia = alexia = “dyslexia”concept, even when partially modified. And for the sake of keeping a valid discussion simple, I have used my analysis of Critchley’s theory’s positives and negatives to highlight the dynamics applying to just about all other theorists and their resulting concepts.
- 2.
Quite recently, a neuroimaging study reported differing patterns of thinking brain functioning in dyslexics vs. normal individuals. Accordingly, the authors reasoned that the differences measured in the thinking brain support a cerebral cause. However, these theorists failed to take cognizance of a simple alternative explanation: If dyslexics’ inner-ear/cerebellar systems send scrambled signals to their thinking brains, isn’t it reasonable to consider that an initially normal thinking brain, via compensatory adaptations, will handle these abnormal signals differently from normal ones? Perhaps there may even be impaired cerebellar-cerebral circuits? So further testing is vital.
As will be discussed in Chap. 18, neuroscientist Paula Tallal and colleagues who developed Fast ForWord may have made a couple of unwitting assumptions—and errors: (1) believing this linguistic phonological defect was of a cerebral vs. CVS origin, and (2) possibly confusing the efficacy of their Fast ForWord reading method to remedy the one rapid word-processing defect they found in speech and reading disorders. Improving just one of many mechanisms may not significantly improve the total reading disorder as simply as Tallal assumed.
- 3.
The magnocellular theory of dyslexia, especially as eloquently explained by Professor John Stein, appears to be a modified, albeit significantly incomplete, replica of my CVS concept. Thus, Stein recognizes that the cerebellum is the head ganglion of the magnocellular systems. He cites the visual and auditory systems to be smaller in dyslexics and so likely assumes it contributes to timing difficulties with binocular fixation and to inner speech for sounding out words. Both these impairments decrease orthographic skills and so explain the reading impairment—mistakenly equated with the dyslexia syndrome. In other words, dyslexia = “dyslexia.” He also cites the language areas of the right and left dyslexic thinking brains to be abnormally symmetrical—suggesting a primary linguistic component to the dyslexic reading impairment. If proven valid, might this finding be secondary to the CVS impairment? The latter assumption of mine is supported by two considerations: (1) Were this abnormal symmetry primary to determining the dyslexic reading symptom, then CVS enhancers couldn’t be helpful since they can’t reverse this stated defect. (2) Nor would rotation, vertigo, and other CVS triggers be able to intensify dyslexic symptoms, reading included. And as you will read in the paragraph below, the abnormal embryonic cells found by Galaburda within this lower brain area were also found wherever the assumed cause of the alexia-like reading disorder was traditionally assumed to be.
Thus, for example, Galaburda and colleagues initially found atypical embryonic cells in the thinking brain’s reading processor of one dyslexic adult many years ago, mistakenly believing this proved the alexia theory of dyslexia, e.g., dyslexia= alexia. Then these large abnormal cells, referred to as brain “warts “ (ectopias) by Stein and others, were found in the brain’s language centers and then later on within the visual and auditory magnocellular systems (and elsewhere) in others. These cells, and the assumed impairment they represent, were then also mistakenly assumed—believed—to cause linguistic and later visual and auditory processing defects in dyslexia.
According to my critique within A Scientific Watergate—Dyslexia, Chapter 18, pages 341–355, I reasoned that these and all other neotraditionlist theories insufficiently and/or incorrectly explained only one or two of many reading mechanisms and absolutely none of the other non-reading symptoms characterizing dyslexics and their complex syndrome. So I initially reasoned that the brain “warts” may be secondary or even irrelevant phenomena since they do not correlate with, nor explain, the symptoms and mechanisms that dyslexics voice. Rather, they seemed erroneously used to support the mistaken traditionalist theory “du jour.”
Because of its importance, allow me to repeat what was just said above, but in a slightly different way: The CVS-enhancing meds can improve all known reading symptoms and mechanisms in dyslexia but can’t remove/dissolve Galaburda’s embryonic cells nor grow Stein’s missing magnocellular cells nor normalize the cerebral language asymmetry within the right and left brains. So clearly, the phonological and magnocellular theories are seriously deficient—especially since stopping the meds cannot restore these structural abnormalities once dyslexic symptoms return!
Unfortunately, these brilliant theorists and their fascinating experimental findings were never reconciled and so never integrated with my CVS theory of the dyslexia syndrome and clinical findings. Had these academic researchers used my clinical findings to devise objective experiments, their resulting concepts would have better explained the reading disorder as well as all other dyslexic symptoms in a valid, solidly grounded and holistic context. In other words, their research would have been far more productive had it been directed to further elaborate and/or modify my CVS theory, rather than mistakenly used to prove the mistaken neotraditionalist ones. And had these gifted researchers properly referenced my clinical research—as just explained—I believe follow-up investigators would have likely avoided needless similar dead ends and thus more significantly and rapidly advanced their altruistic aims.
On later thinking, perhaps Galaburda’s embryonic cells support one of my long-held concepts described at the end of Chapter 9: that dyslexia may result from delayed and/or abnormal embryonic development. Do not all very young children normally manifest all the symptoms characterizing the dyslexia or CVS syndromes? Thus these cells may likely be non-specific embryonic markers, explaining their appearance throughout the CNS. Accordingly, Galaburda was correct, albeit partially so. And I was wrong, although partially so. This is the zigzagging needed to advance. Hopefully, the above back-and-forth reasoning illustrates that discoveries do not often occur in straight lines and that mistakes are a dime-a-dozen. Yet their admission and correction—rather than denial—are vital.
- 4.
Developing a holistic theory of dyslexia dependent on expertise in multiple complex medical/scientific disciplines is infinitely more difficult than it might seem. Thus, for example, apparently considering dyslexia to be primarily a reading disorder—as most do—neurotologist Tapani Rahko independently validated the presence of benign paroxysmal positional vertigo (BPPV) in dyslexics. So he recognized that the resulting increase in involuntary rapid eye movements caused impaired focusing and thus “dyslexia.” And by treating the BPPV and by increasing the reading speed of dyslexics, he apparently also found improvements in visual (increased visual span during reading), auditory processing, “ADHD,” and “dyscalculia”—postulating that this vestibular mechanism interferes with other brain functions. So he apparently hadn’t read of all, or perhaps any, of the other reading and non-reading mechanisms I described resolving and defining the dyslexia syndrome. And I never previously read of his fascinating research—or I would have added it to mine, albeit in modified form.
Although Rahko did propose an important inner-ear theory and treatment for dyslexics, he apparently failed to comprehensively explain and encompass most of Kathy’s symptoms and mechanisms, albeit he appeared far better in doing so than all the non-CVS theorists.
Accordingly, Rahko’s important research also highlights the difficulties gifted clinicians and investigators have in properly integrating their findings with those of others. And the reason is simple. As a neurotologist, Rahko does not really understand dyslexia as I do. And as a psychiatrist, I do not really understand neurotology, especially as he does. And no doubt, this same difficulty holds for all attempting to solve the dyslexia riddle. In retrospect, I was forced to become a jack of all trades, sacrificing true expertise in most. But it took me 50 years to do it imperfectly, but sufficiently. Thus, I’m a slow learner! But there was lots to learn about dyslexia—including neurotology—and even more mistaken assumptions and convictions to unlearn. And nature holds onto her secret insights, using kryptonite to help out.
Because I could not obtain an English translation of Rahko’s research, only a summary, it was difficult to be sure of his concepts or what exactly he knew of my prior research, albeit I was referenced. And he failed to respond to my communications. Thus I footnoted his theory and therapy here until I understood them more accurately, rather than discussing this content within the main text.
(Tapani Rahko (2003). “Alleviating dyslexia by treating benign positional vertigo and eye movement disturbances, saccades.” Finnish Medical Journal. 39: 3883–3886.)
- 5.
Because the reading scores in dyslexics may vary from one extreme to another, two brilliant and productive dyslexia researchers at Yale (Sally E. Shaywitz, M.D., and Bennett A. Shaywitz, M.D.) questioned dyslexia’s existence. Similarly, this observation led many laymen to believe that dyslexia is a fiction—representing just the severe end of a normal bell curve distribution of reading capabilities in otherwise normal individuals. However, both groups failed to recognize that dyslexia is a CVS syndrome of many reading and non-reading symptoms. And both failed to fully realize that the quality vs. severity of the reading impairment in dyslexia is diagnostically significant. Yet this concept may have merit, since it is explained by my embryonic CVS dyslexia theory.
Author information
Authors and Affiliations
Rights and permissions
Copyright information
© 2019 Springer Nature Switzerland AG
About this chapter
Cite this chapter
Levinson, H.N. (2019). Kathy and the Mistaken Theories of Dyslexia. In: Feeling Smarter and Smarter. Copernicus, Cham. https://doi.org/10.1007/978-3-030-16208-5_8
Download citation
DOI: https://doi.org/10.1007/978-3-030-16208-5_8
Published:
Publisher Name: Copernicus, Cham
Print ISBN: 978-3-030-16207-8
Online ISBN: 978-3-030-16208-5
eBook Packages: MedicineMedicine (R0)