Biological theories of dyslexia

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Main articles: Dyslexia and Dyslexia research

The primary symptoms of dyslexia were first identified by Oswald Berkhan in 1881.[1] The term 'dyslexia' was coined in 1887 by Rudolf Berlin,[2] an ophthalmologist practicing in Stuttgart, Germany.[3] Since then generations of researchers have been investigating what dyslexia is and trying to identify the biological causes. (See History section of the Dyslexia article.) The theories of the etiology of dyslexia have and are evolving with each new generation of dyslexia researchers, and the more recent theories of dyslexia tend to enhance one or more of the older theories as understanding of the nature of dyslexia evolves.

Theories should not be viewed as competing, but as attempting to explain the underlying causes of a similar set of symptoms from a variety of research perspectives and background.[4][5]

Cerebellar theory[edit]

The cerebellar theory asserts that a mildly dysfunctional cerebellum can cause dyslexia. The initial cerebellar hypothesis suggested that a signal scrambling impairment of cerebellar origin secondarily impaired brain processors.[6] In attempting to explain all the many known reading and non-reading dyslexic symptoms, therapies and theories as well as the presence of only cerebellar and related vestibular neurophysiological signs in dyslexics, the cerebellum was postulated to fine-tune in time and space all signals (visual, auditory, tactile, proprioceptive, motion) entering and leaving the brain as well as signal interconnections. The quality and severity of the many symptoms characterizing each dyslexic was reasoned to depend on the diverse cerebral cortical and other brain processors receiving scrambled signals due to a cerebellar dysfunction, the degree of signal- scrambling as well as the compensatory descrambling capability of specific brain processors. Helpful therapies were reasoned to enhance cerebellar fine tuning (e.g.,the use of cerebellar-vestibular stabilizing antimotion sickness medications) and/or improve descrambling and other compensatory cognitive capabilities (e.g.,tutoring, biofeedback). Most other theories equate the dyslexia disorder with impaired reading comprehension and so attempt to only explain the latter. Another cerebellar proposal indicated that articulation problems can contribute to the phonological deficits that can cause dyslexia. The cerebellum also contributes to the automitisation of learned behaviors, which can include learning the grapheme-phoneme relationships when reading texts.[4][7] However, some have suggested that cerebellar dysfunction alone may not be a primary cause of dyslexia and that dysarticulation and phonological deficits appear unrelated.[8][9][10]

Evolutionary hypothesis[edit]

This theory considers that reading is an unnatural act carried out for a very brief period in human evolutionary history. It has only been in the last hundred years that reading a visual form of speech has been promoted as a major form of communication, and subsequently a lack of time for reading behaviors to evolve. In many societies around the world the majority of the population do not use the visual notation of speech as a form of communication, and do not use reading skills, and therefore have no dyslexia.[11]

Many developmental dyslexics significantly compensate for their cerebellar-vestibular determined symptoms and signs over time and most normal young children evidence age-appropriate "dyslexic-like" symptoms and cerebellar-vestibular(CV) "immaturities." It was thus hypothesized that genetic dyslexia may represent an ontogenetic recapitulation of a pre-reading state in phylogeny and that ontogeny extended beyond the embryo into childhood and occasionally beyond, thus perhaps explaining late and even late-late blooming.[12] The development of reading and related writing and spelling functioning, as well as the corresponding ontogenetic CV-cerebral developmental lag hypothesis of dyslexia, is indirectly supported by studies suggesting that "the cerebellum has enlarged between three and fourfold in [only] the past million years of evolution [together with a corresponding spurt of the cerebrum]."[13][14]

Magnocellular theory[edit]

The Magnocellular theory attempts to unify the Cerebellar Theory, the Phonological Theory, the Rapid Auditory Processing Theory, and the Visual Theory. The Magnocellular theory proposes that the magnocellular dysfunction is not only restricted to the visual pathways but also includes auditory and tactile modalities.[4][15] Support for the magnocellular deficit theory of dyslexia is mixed. While studies of contrast sensitivity are highly conflicting with this theory,[16] studies of visual evoked potentials are mixed. Subjects' age (10-46), differences in experimental design, small sample sizes (<10 dyslexic subjects in prominent studies), and the presence, absence, or failure to assess for comorbid ADHD might explain these contradictory findings.[17] There is neither widespread support nor opposition for this theory and further investigation is needed.

Naming speed deficit and double deficit theories[edit]

The speed with which an individual can engage in the rapid automatized naming of familiar objects or letters is a strong predictor of dyslexia.[18] Slow naming speed can be identified as early as kindergarten and persists in adults with dyslexia.

A deficit in naming speed is hypothesized to represent a deficit that is separate from phonological processing deficit. Wolf identified four types of readers: readers with no deficits, readers with phonological processing deficit, readers with naming speed deficit, and readers with double deficit (that is, problems both with phonological processing and naming speed). Students with double deficits are most likely to have some sort of severe reading impairment.

Distinguishing among these deficits has important implications for instructional intervention. If students with double deficits receive instruction only in phonological processing, they are only receiving part of what they need.[19]

Perceptual visual-noise exclusion hypothesis[edit]

The concept of a perceptual noise exclusion deficit (impaired filtering of behaviorally irrelevant visual information in dyslexia or visual-noise) is an emerging hypothesis, supported by research showing that subjects with dyslexia experience difficulty in performing visual tasks (such as motion detection in the presence of perceptual distractions) but do not show the same impairment when the distracting factors are removed in an experimental setting.[20][21] The researchers have analogized their findings concerning visual discrimination tasks to findings in other research related to auditory discrimination tasks. They assert that dyslexic symptoms arise because of an impaired ability to filter out both visual and auditory distractions, and to categorize information so as to distinguish the important sensory data from the irrelevant.[22]

Phonological deficit theory[edit]

The phonological deficit theory proposes that people with dyslexia have a specific sound manipulation impairment, which affects their auditory memory, word recall, and sound association skills when processing speech. The phonological theory explains a reading impairment when using an alphabetic writing system which requires learning the grapheme/phoneme correspondence, the relationship between the graphic letter symbols and speech sounds which they represent.[4]

Rapid auditory processing theory[edit]

The rapid auditory processing theory is an alternative to the phonological deficit theory, which specifies that the primary deficit lies in the perception of short or rapidly varying sounds. Support for this theory arises from evidence that people with dyslexia show poor performance on a number of auditory tasks, including frequency discrimination and temporal order judgment.[4]

Visual theory[edit]

The visual theory represents a traditional perspective of dyslexia, as being the result of a visual impairment creating problems when processing information from letters and words from a written text. This includes visual processing problems such as binocular, poor vergence, and visual crowding. The Visual Theory does not deny the possibility of alternative causes of dyslexia[4]

Benign paroxysmal positional vertigo[edit]

Physician Tapani Rahko has tested some 10 000 patients aged 3,5 years to 94 during over 10 years with his positional vertigo tests. The reading speed of patients was measured before and after positional treatments in some 3500 cases to obtain information on the effect. The reading speed of dyslexic patients was increased by an average of 40% after the treatment. The research identified benign paroxysmal positional vertigo causing dyslexia through increasing the amount of involuntary rapid eye movement, making it difficult for patients to focus on a word prior to treatment. Treating the vertigo reduced the involuntary eye movement, easing reading. Multiple Finnish schools are in process of testing vertigo treatment in helping dyslexic children to great effect.[23][24][25]

An independently validated study by Frank and Levinson in 1973 indicated that 97% of 115 dyslexics evidenced neurological and electronystagmographic signs of a dysfunction within the inner-ear and its supercomputer—the cerebellum.[26] Dyslexia was postulated to occur when impaired ocular-motor fixation and sequential tracking due to a subclinical nystagmus of inner-ear and cerebellar origin scrambled the letter and word signals during reading and thus secondarily interfered with their cerebral cortical and related brain processing. A follow-up study of 4,000 learning disabled and dyslexics in 1988 further validated the hypotheses.[27] Utilizing an optokinetic instrument, dyslexics were shown to have significantly reduced ocular-motor fixation, sequential tracking and visual span capacities as well as abnormal signal scrambling vs controls.[28][29] Inner-ear-enhancing anti-motion sickness medications were clinically recognized to improve most all reading and non-reading dyslexic symptoms and mechanisms.[30][31][32][33] Later research suggested that a majority of those with fears, phobias and related anxiety disorders have cerebellar-vestibular determinants and deficits as well as related abnormal optokinetic tracking, visual span and signal capacities vs controls.[29][34][35]

References[edit]

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