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DYSLEXIA-- A CEREBELLAR-VESTIBULAR HYPOTHESIS AND SOLUTION

BACKGROUND -THE CEREBRAL CORTICAL THEORY Ever since bright children failing to acquire normal reading & related writing & math skills were first recognized in the late 1800's, there developed the natural assumption & conviction that these reversal-prone dyslexics suffered from the very same dominant cerebral cortical defect proven responsible for acquired alexia in adults. In other words, it was believed that deficient cerebral processors could neither recognize nor comprehend the normal reading-related signals received in both developmental dyslexics & acquired alexics. However, there remained a major scientific dilemma. The expected presence of similar localizing & diagnostic neurological signs reflecting cerebral cortical impairment found in alexics defied detection in dyslexics, despite intensive & extensive century-old studies by gifted clinicians & researchers to find them.

A SURPRISING CEREBELLAR-VESTIBULAR (CV) DISCOVERY In a determined clinical effort to detect the elusive "hard & fast" cerebral cortical deficit signs in dyslexia evading all others, two neuropsychiatric and psychoanalytic clinicians were led to neurologically examine & reexamine 1,000 dyslexic children during 1966-1970. Upon a retrospective analysis of the resulting data, the expected "hard-&-fast" evidence of a primary cerebral deficit was nowhere to be found. Instead, 75% of the sample unexpectedly demonstrated the so-called "soft" signs indicative of delayed or impaired balance, coordination, rhythm, equilibrium...Although also reported by most other neurological investigators, these signs were invariably dismissed as diagnostically unimportant. By contrast, the CNS dysfunctioning signs were suddenly recognized by Frank & Levinson to be hard & fast evidence of a cerebellar-vestibular(CV)dysfunction. Significantly, all future clinical studies demonstrated only CV impairments in over 96% of thousands of neurophysiologically examined dyslexics--further supporting a primary CV role in determining this disorder. Thus the evolving clinically-derived evidence clearly suggested that dyslexia & alexia have different neurological origins & are thus different disorders.

CIRCULAR LOGIC & REASONING. Circular reasoning in dyslexia research appeared motivated by the unshakable conviction, really assumption, that dyslexia = alexia & so is of cerebral origin. Thus the presence of soft signs in an individual is solid evidence that the CNS is impaired or developmentally delayed. And the mere co-existence of a reported reading disorder is considered proof that the impairment resulting in dyslexia is due to an underlying alexic-like cerebral deficit or dysfunction, even in the complete absence of any hard & fast diagnostic cerebral signs. In other words, an assumption --belief--is unwittingly used to prove the very same assumption.

A CONCEPTUAL REVERSAL-- THE CV HYPOTHESIS OF DYSLEXIA How can one possibly explain the apparent paradox whereby a cerebral-like reading disorder might result without an alexic-like cerebral impairment in the presence of only a CV dysfunction? To do so another conceptual reversal of previously accepted convictions was crucially needed. And the hypothetical solution offered was elegantly simple: As opposed to alexia, dyslexia was postulated to result when normal cerebral structures & functions secondarily failed to process the CV-determined scrambled reading & related sensory signals received.

CONFIRMING THE CV FINDINGS A follow-up prospective research study published by Levinson & his mentor Jan Frank in 1973 found 97% of 115 dyslexic children to exhibit only CV dysfunction. Importantly, pediatric neurologists reported an even greater incidence of only "cerebellar deficits" in the subsample of 17(~98%) referred dyslexics they "blindly" examined. (Paradoxically, they often diagnosed these dyslexics with reported "cerebellar deficits" as having cerebral dysfunction despite the complete absence of any validating cerebral signs.) Vestibular or inner-ear- determined ocular-motor & related abnormalities were independently noted by neurotologists in 87%(26/30) of referred dyslexics in "blinded" studies utilizing electronystagmography or ENG testing.

VALIDATING THE CV HYPOTHESIS The initially proposed CV determined signal-scrambling concept of dyslexia was shown valid by utilizing a newly designed 3-D Optical Scanner. This latter instrument demonstrated that previously recognized word & sentence signals, when accelerated, blurred-out or scrambled significantly more rapidly in dyslexics relative to normal reading controls when compensatory mechanisms were minimized.

NEW SCREENING/DIAGNOSTC TOOLS In addition to the 3-D Optical Scanner, 3-D Auditory & Tactile Scanners were designed to measure the rapid signal-scrambling of auditory & tactile sequences reported in dyslexics & others with CV dysfunctioning. Levinson also developed a highly reliable diagnostic/screening questionnaire that was fully capable of encompassing all the proven CV- determined symptoms found characterizing dyslexia.

A NEW MEDICAL TREATMENT Most important, Frank and Levinson demonstrated in clinically-based pharmacological studies that varied side-effect- free combinations of CV-enhancing medications and nutrients were able to rapidly, significantly and often dramatically improve the symptoms found characterizing dyslexia in 75 to 85% of treated cases. Moreover, there resulted a wide range of improved reading & non-reading CV-determined symptoms and mechanisms suggesting that the pre-treated dyslexic disorder was far greater in scope and depth than anyone had previously recognized & defined. MEDICAL PREVENTION By successfully treating the CV-determined balance, coordination, speech...impairments in young children with CV enhancing medications, it became possible to medically prevent the typical dyslexic reading, writing...symptoms from later appearing once school & academics began. A UNIQUE RESEARCH TOOL--FAVORABLE MEDICAL RESPONSES By highlighting changes in dyslexics via their reported and observed favorable responses, the CV-enhancing anti-motion sickness & related medications served as an invaluable and highly unique research tool with which to dissect and analyze  the previously hidden CV dysfunction & the many diverse symptoms & compensatory mechanisms resulting from this impairment. AN EXPANDED CV PERSPECTIVE---HIGHER CEREBELLAR FUNCTIONS Based on the cerebellar concepts derived from animal studies & especially the favorable response patterns of dyslexics to the CV-enhancers: The cerebellum was reasoned to play a vital role in modulating all sensory, motor and primitive thinking, feeling and communication capabilities  as well as related signal transmissions via its discovered mechanisms of selective facilitation and inhibition (i.e., speeding up or slowing down signal and transmission speeds). THE DYSLEXIA SYNDROME. Contrary to initially expecting only reading and motor improvements in medically treated samples of dyslexics, there occurred a completely unanticipated consistent and reproducible favorable response pattern involving hundreds of improved CV-determined symptoms in varying intensities. These diverse symptoms were grouped within 15 major areas of dysfunctioning that involved: reading, writing spelling, math, memory, direction& space, time, speech, grammar, concentration/distractibility and activity (ADD/ADHD), phobias and related panic/mood, behavior, balance/coordination and rhythm, psychosomatics, self-esteem and body image. As a result of these insights, dyslexia was recognized to be a complex syndrome encompassing all the above mentioned symptoms rather than just an alexic-like reading comprehension disorder. COMPENSATION Because a normal cerebral cortex was found highly capable of compensating for the CV- determined signal-scrambling in dyslexia, there resulted a favorable prognosis for both it's reading & non-reading symptoms. By contrast, the cerebral reading processor is structurally defective in alexia & so cannot compensate for its own impairment, thus leading to a poor prognosis. THE READING DISORDER IN DYSLEXIA The favorable responses of dyslexics to the CV-enhancers unexpectedly highlighted a wide range of previously unrecognized CV-determined reading symptoms and mechanisms which frequently overlapped with one another. These included: memory instability, ocular fixation and sequential scanning difficulties, ocular perseveration, tunnel vision,  orientation & spatial instability, delayed/scrambled visual & auditory processing,  gyroscopic slanting, light sensitivity and overloading, a wide range of corresponding impairments in auditory perception, phonetic memory & sequencing as well as deficient integration and coordination with corresponding visual reading symbols, primary and/or secondary impairments of concentration and distractibility, & secondarily Impaired comprehension. By contrast, a primary alexic-like reading comprehension impairment is seldom if ever present A NEW DEFINITION  & ENHANCED CONCEPT Because dyslexia was recognized to be a dynamically changing complex syndrome of many and diverse primary CV-determined symptoms in equilibrium with compensatory mechanisms, Levinson proposed the following fully encompassing clinically-based definition: As opposed to alexia: Dyslexia is a CV-determined syndrome of many and diverse reading and non-reading symptoms co-existing in varying degrees of intensity. This syndrome may include difficulties with reading as well as impairments with writing, spelling, math, memory, speech, sense of direction and time, concentration/distractibility and activity, balance/coordination and rhythm, psychosomatics, mood/anxiety, self-esteem, etc. The presence and even degree of each and every symptom is a resultant of primary CV dysfunctioning vs. secondary and perhaps even primary cerebral & related CNS compensatory forces within the context of  total brain functioning. Accordingly, symptoms may change and vary from one extreme to another over time. And reading may even normalize or become superior. EXPLAINING ALL THE DYSLEXIA SYMPTOMS & THERAPIES According to the expanded CV hypothesis of dyslexia, one CV-determined fine-tuning impairment may result in hundreds of qualitatively diverse symptoms in varying intensities depending upon: 1) the type of CV dysfunction and impaired mechanisms, 2) the pattern and degree of signal scrambling, 3) the specific CNS processors receiving scrambled signals, and 4) the ability (and/or inability) of the brain’s cerebral cortical and related CNS processors for descrambling and/or compensatory reprogramming. Thus any & all therapies which decrease CV-determined signal scrambling &/or enhance cerebral & related CNS compensation will result in improvements. THE FALLACIOUS READING-DEPENDENT DEFINITION

With increased clinical experience, it became readily apparent that the disorder called dyslexia cannot be logically defined in terms of only severe degrees of only one of its many & diverse symptoms as is currently mandated. Nor is it reasonable to call both the disorder of many & varied symptoms & only its severe reading impairment by the very same name -- dyslexia. FEARS/PHOBIAS/ANXIETY/PANIC Unexpectedly, CV dysfunctioning dyslexics who responded favorably to CV-enhancing medications often spontaneously reported improvements in their fears/phobias, anxiety & panic. Follow-up studies showed that 90% of fears/phobias were of a primary CV origin. And for the first time, the specific shape, form, combination, onset & intensification of these symptoms could be reliably explained by CV -dysfunctioning mechanisms & triggers. As noted, these anxiety symptoms respond favorably to CV-enhancers. DEVELOPMENTAL DYSLEXIA VS ACQUIRED/OR INTENSIFIERS OF DYSLEXIA Although the vast majority of dyslexics appear to be of genetic and/or developmental origin, the dyslexia syndrome was recognized to be newly acquired and/or intensified at any age following a dysfunction within the CV (or inner-ear) fine tuners. These impairments may be due to infections (i.e., ear/sinus infections, mononucleosis, Lyme’s disease, etc.), injuries (whiplash, concussions, etc.) as well as allergic, toxic degenerative, metabolic and other disorders. In fact, transient fatigue and stress and even spinning or rotation and zero gravity may physiologically trigger temporary dyslexic states, including “space dyslexia” as termed by Levinson and reported in astronauts, thus further validating clinically the CV hypothesis. MANY DISORDERS--ONE CV CAUSATION A wide range of differently named signal-scrambling impairments were all proven to be part and parcel of the CV-determined (dyslexia) syndrome and so could also be effectively treated and compensated for. These include: LD (poor learning), ADHD (poor concentration and activity), dysgraphia (poor writing), dyscalculia (poor math), dysphasia and dysnomia (poor/impaired speech and word recall), dyspraxia (poor balance/coordination), pervasive developmental delay (severe dyslexia and dyspraxia), Asperger syndrome (social dyslexia), psychosomatic disturbances  (i.e.,headaches, dizziness, motion sickness, stomachaches, etc.), phobias (motion, sensory-motor  and related CV triggers), and many other previously misunderstood disorders discussed and clarified within Levinson’s works. MIXED DYSLEXIA A CV signal-scrambling dysfunction was found to often play a hidden co-existing minor role in a series of major primary processing disorders such as mental retardation, Down’s syndrome, whiplash, concussion and brain injury, cerebral palsy, autism, schizophrenia, etc. And by decreasing the signal-scrambling in these major processing disorders utilizing CV-enhancing medications and related non-medical treatment modalities, it is possible to obtain overall functional benefits, especially when combined with therapies specifically designed for improving the major processing impairment. ENCOMPASSING/CRITIQUING DYSLEXIA THEORIES The value of any dyslexia theory rests entirely on its ability to encompass and explain all known related data while leading to new and unique insights and discoveries never before anticipated. As noted, the CV hypothesis of dyslexia was formulated and expanded so as to include and explain all the typical and atypical as well as the expected and unexpected signs, symptoms, mechanisms and insights obtained by Levinson’s first-hand clinically-based neurophysiological examinations, follow-up & medical treatment of more than 35,000 dyslexic or LD children and adults, a majority responding favorably to CV-enhancing medications. Even all the fMRI findings, especially those reported within the cerebral cortex highlighting both dysfunction &/or compensatory reorganization, can now be dynamically and more objectively examined and analyzed as to their primary and/or secondary( CV) causes. INDEPENDENT CEREBELLAR VALIDATION Although Levinson's cerebellar/dyslexia research was long supported by many distinguished clinicians & researchers, including cerebellar Nobel laureate Sir John Eccles, independently initiated cerebellar validation did not seriously occur & escalate until1999 & the new millennium---three decades later than anticipated. And the new fMRI cerebellar findings remained isolated from the pre-millennium insights. RESISTANCE TO A SOLUTIONCEREBELLAR DENIAL To explain a wide range of puzzling psychologically-determined phenomena both creating the dyslexia riddles & then hampering their solution, Levinson wondered: Was and is a subconsciously motivated defense mechanism called cerebellar denial in active play? Are there others?