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From the 1 October 1993 issue of Smart Drug News [v2n5]. Copyright (c) 1993, 2009. All rights reserved.
by Steven Wm. Fowkes
What do allergies, hyperactivity, phobias and dyslexia have in common? On first appraisal, we might be tempted to think that such varied and disparate conditions are completely unrelated. But they arent. They may all be related to disturbances of the inner ear that adversely influence brain function.
Many pediatricians now believe that inner ear infections play a significant role in learning disabilities. They theorize that infection-related fluid (effusion) in the middle ear interferes with hearing, which in turn interferes with auditory perception and processing.
In 1987, Randi Hagerman and Alice Falkenstein reported a connection between hyperactivity (attention deficit disorder) and inner ear infections (otitis media). Among the children referred to a child development group for failure in school, hyperactive children had a significantly increased history of ear infections.
Among children evaluated as hyperactive by two or more raters, 89% had three or more ear infections and 74% had eleven or more infections. Among non-hyperactive children, the incidence of ear infections was 50% for three or more and 20% for eleven or more. When Hagerman and Falkenstein examined the hyperactive children requiring medication, they found the same strong association: 94% with three or more ear infections and 69% with eleven or more infections. This data shows a highly significant association between early ear infections and the subsequent development of hyperactivity. Seventy-nine percent of the eleven-or-more group experienced recurrent otitis before age 1.
Other researchers have found associations between recurrent otitis and impaired speech [Silva 1986, Hubbard 1985, Teele 1984] and language development [Roberts 1988, Teele 1984].
The otitis media connection is still controversial. Many of the studies, including the one cited above, were done with highly selected groups. Many studies have contained methodological flaws, and methods for assessing hyperactivity and the past incidence of otitis media have not been precise. Other studies have found no association [Lous 1988, Fischler 1985].
The inner ear is much more than the site of hearing. It is also one of our most primitive methods of orientation. The main vestibule (chamber) in the ear contains beds of sensory hair cells which support calcium carbonate crystals. The pull of gravity on the crystals is felt by the hairs, allowing the brain to determine our vertical orientation.
Also attached to the inner ear vestibule are three semicircular canals (a, b, c) which are oriented at right angles to each other (see illustration). In other words, each canal lies in a different plane (also a, b, c) of three-dimensional space (see following illustration). As the head moves in different directions, the movement of the fluid in each canal is sensed by a tuft of hairs. Actually, it is the semicircular canals which are moving; the fluid tends to remain stationary. Either way you look at it, the brain can determine an acceleration frame of reference by comparing fluid movements in all three planes.
Also attached to the main vestibule is the cochlea, a long, gradually tapering tube which is spiraled into a snail-like coil. The cochlea contains tiny hairs which gradually diminish in size down the length of the tube, and which vibrate in response to different frequencies of sound that resonate down the tube. The cochlea is responsible for our sense of hearing.
The nerve connections from the inner ear to the brain attach to the cerebellum, a primitive part of the brain that sits right on top of the spinal cord and which deals with balance, equilibrium and muscular coordination. The cerebellum pays close attention to the signals coming from the inner ear so that imbalance can be detected and quickly corrected through movements.
Imbalance is fundamentally unsafe. When climbing a tree or rock, a fall can be deadly. To prevent this, the brain responds to imbalance by releasing adrenalin and norepinephrine (NE) two neurotransmitters which focus attention and speed up reaction time. Ideally, the quicker the response, the more likely a fall can be prevented. NE also stimulates the learning process. This means that a successful correction to the state of imbalance will be remembered for future reference.
When the inner ear malfunctions by sending out spurious signals, the cerebellum reacts as if there were a real state of imbalance. This is exactly what happens in vertigo (pathological dizziness). Vertigo sufferers experience movement (vestibular stimulation) without any corresponding physical movement. The resulting dizziness and disorientation are extremely distressing.
Many people experience a milder form of the same type of disorientation in motion sickness. When the vestibular frame of reference from the inner ear does not match the visual frame of reference provided by the eyes, car sickness and sea sickness can result. Motion sickness distress can often be diminished by looking at the passing scenery (instead of reading in the car) or standing on the open deck of a ship and gazing at the horizon (instead of staying in cabin below decks). This strategy tends to match the visual and inertial frames of reference and serves to restore orientation and equilibrium.
How does the cerebellum know the difference between signals from the inner ear which mean balance and ones that mean imbalance? The answer is: by trial and error. When were born, we dont know how to move our heads, sit up, crawl, stand, walk or run. We have to learn each in turn by trying, and noticing the difference between what works and what doesnt.
Through each of these stages, the cerebellum learns to recognize patterns of inner ear sensation which accompany falling down (imbalance) and not falling down (balance) and match them with patterns of movement. This leads to coordination. Practice makes perfect.
Chronic inflammation from food allergies, and repeated or unresolved middle-ear infections, can interfere with the proper functioning of the inner ear. When this interference happens in early life, while the brain (cerebellum) is supposed to be patterning vestibular signals, incomplete, inhibited and erroneous patterns can be formed.
The resulting cerebellar dysfunction (otherwise known as dyslexia) can interfere with sensory information processing and the ability to read, write, speak, or follow spatial or sequential directions. The disorientation, dizziness, and stress of trying to reconcile conflicting frames of reference can lead to motion-related phobiasfear of heights, open or confining spaces, the dark, driving vehicles, or riding elevators or planes.
Because of the similarities between dyslexia and other diseases known to be due to disruptions of high-level (cerebral cortex) brain functions, many researchers argued that dyslexia also resulted from cortical dysfunction. After all, both conditions impair the ability to recognize without impairment of seeing. But the absence of identifiable cortical abnormalities prompted a few researchers to look elsewhere. Given the numerous cerebellar dysfunctions that were observed in dyslexics and learning disadvantaged children, Dr. Harold Levinson set up blind neurological examinations of normal and dyslexic children. These research programs found a 96-97% incidence of cerebellar-vestibular dysfunction in dyslexics. The incidence of cortical dysfunction was only 6%.
Even with the cerebellar-vestibular understanding of the roots of dyslexia, the diagnosis of dyslexia remains problematic. Traditional use of reading deficiencies as an indicator of dyslexia miss those dyslexics with enough native intelligence to adequately compensate for their handicap. Such reading-score-compensated dyslexics have been identified by Dr. Levinson to exhibit such related symptoms as headaches, temper tantrums, enuresis (bed wetting), abdominal pain, obsessive and compulsive neuroses, phobias (those related to school, heights and motion), and various misbehaviors (acting-out and delinquency). They all experienced assorted difficulties with writing, spelling, mathematics, memory, directions, balance and coordination. Dr. Levinson estimates that 15-20% of the middle-class population suffers from cerebellar-vestibular-based dyslexia.
The role of cerebellar-vestibular disturbances on the development of dyslexia is further supported by Dr. Levinsons successful use of anti-motion-sickness drugs to treat the disabilities associated with dyslexia.
Dyslexia is also being successfully treated with repatterning exercises at the Stillman Dyslexia Institute. These exercises involve repetitive head movements in particular directions that are designed to reinforce patterning that should have taken place in early childhood.
We have received numerous reports from Smart Drug News subscribers who have used nutrients and smart drugs to alleviate the disabilities of dyslexia and overcome learning disabilities. In addition to personal accounts of adults self-treating themselves, we have also received reports of parents treating their children. Most of these people have expressed frustration at not being able to find open-minded professionals to supervise their treatments.
The involvement of food allergies in hyperactivity has been obvious to many parents and therapists for years. It is now becoming established in the literature [Crook, 1980]. The link between food allergies in early infancy and later dyslexia is just now being explored in a rigorous manner. For parents dealing with the trauma of dyslexic children, it provides an avenue for discovering and eliminating potential causes of the condition. Food allergies (sometimes called food insensitivities) may be quite common in infants, children and adults. The inflammatory cascade which results from exposure to problem foods may be every bit as much a disruptive influence on cerebellar patterning of vestibular signals as overt inner-ear infections. Many parents are ill-prepared to recognize such problems in their children. And many professionals still deny that foods may pose such risks.
With the recognition of cerebellar dysfunction as the primary source of dyslexia and other dyslexia-related learning difficulties, dyslexia can now be diagnosed in non-reading-impaired children that have figured out an adaptive strategy for compensating for their conditions. In addition, milder forms of dyslexia can be identified and treated, with significant enhancement of learning, academic achievement, and overall success in life.
Crook WG. Can what a child eats make him dull, stupid, or hyperactive? Journal of Learning Disabilities 13(5): 53-8, May 1980.
Fischler RS, Wendell T and Feldman CM. Otitis media and language performance in a cohort of Apache Indian children. Am J Dis Child 139: 355-60, 1985.
Hagerman R and Falkenstein AR. An association between recurrent otitis media in infancy and later hyperactivity. Clinical Pediatrics 26: 253-57, May 1987.
Hubbard TW, Paradise JL, McWilliams BJ, Elster BA, and Taylor FH. Consequences of unremitting middle-ear disease in early life: Otologic, audiologic and developmental findings in children with cleft palate. The New England Journal of Medicine 312(24): 1529-34, 13 June 1985.
Levinson HN. A Solution to the Riddle Dyslexia, Springer-Verlag, New York, 1980, 1981 (ISBN: 3-540-90515-4).
Lous J, Fiellau-Nikolajsen M and Jepesen AL. Secretory otitis media and language development: A six-year follow-up study with case-control. International Journal of Pediatric Otorhinolaryngology 15: 185-203, 1988.
Silva PA, Chalmers D and Stewart I. Some audiological, psychological, educational and behavioral characteristics of children with bilateral otitis media with effusion: A longitudinal study. Journal of Learning Disabilities 19: 165-69, 1986.
Stillman Dyslexia Institute, 16133 Ventura Blvd., Suite 905, Encino, CA 91416. Phone: 818-789-1111.
Teele DW, Klein JO, Rosner BA, and The Greater Boston Otitis Media Study Group. Otitis media with effusion during the first three years of life and development of speech and language. Pediatrics 74: 282-87, 1984.