A Critical investigation of the etiology of Developmental Dyslexia:
A Critical investigation of the etiology of Developmental Dyslexia:
The long disputed debate about the primary cause of dyslexia is still very much alive in the field of psychology. Dyslexia is commonly characterized as a reading and writing impairment that affects around 5% of the global population. The disorder has frequently been hypothesized to be the result of various sensory malfunctions. For over a decade, studies have made major contributions to the disorder's etiology; however, scientists are still unclear of its specific causal. Initially, dyslexia was thought to be a reading disorder in children and adults (1). Later it was suggested to consist of both a visual and writing component, therefore characterizing it as more of a learning disability which affected people of normal intelligence's ability to perform to their fullest potential (5). In the current research, cognitive and biological perspectives have often been developed independently of one another failing to recognize their respective positions within the disorder's etiology.
The Phonological Deficit and Magnocellular theory are two of the most dominant theories in dyslexic research. Various theories have been suggested to explain the nature and origin of dyslexia, however, they often served as additional support for either the phonological or magnocellular theories. The Double Deficit theory suggested that dyslexic symptoms were the result of speed-processing (7). The Genomic theory posed that dyslexia was a highly heritable disorder that can be localized to a specific genetic component, Finally, the Cerebellar Deficit theory suggested that dyslexia was the result of an abnormal cerebellum exist (2). With the constant debate of the biological nature versus the cognitive nature of the disorder's causal, scientists have had major problems explaining the disorders' etiology based on one individual theory. While it was important to locate the specific cause of the disorders' manifestations, it seemed that the most effective results would be achieved by a collective approach. This kind of approach would encompass ideas placed forth by both the cognitive and neurological theoretical ideas which currently existed in the current research of the etiology of dyslexia.
The phonological deficit hypothesis of dyslexia is one of the most long standing explanations existing in psychological research. The theory was coined by a man known as the father of dyslexia, Pringle-Morgan in 1896. Morgan viewed reading as a process that critically involved the segmentation of text into graphemes (1). These graphemes served as the earliest precursors to phonemes (the small unit of language), such that grapheme to phoneme conversion is equivalent to the whole sound of a word (1), (5). The process is said to both require that a reader assemble and address a word's phonology. Dyslexics are said to have phonological deficits which caused phonemic representation difficulties; they would often fare worse than others when it came to mapping sounds into letters in the brain, and with phonemic recall (1,5). Deficits in dyslexics' ability to retain short-term word memory and problems with segmentation of words into phonemes (e.g., auditory discrimination), lent support to these ideas (5).
A study by Petra Georgiewa and colleagues investigated the phonological
theory using advance scientific techniques. In the study, 17 adolescent
children were subjects; 9 dyslexics & 8 controls. Dyslexic subjects
were diagnosed based on the discrepancy between non-verbal IQ and
read/spelling performance (1).
All subjects were matched for age and intelligence level (IQ > 85)
and the mean age was 13 years old. During the study each child was
given a series of word and non-word displays on a computer screen to
read silently. The experimental condition contained words and non-words
and the control condition contained words and non-words with an
asterisks. All words were either 1 or 3 syllable nouns accumulated from
a basic 10 year old vocabulary. Each word and non-word was presented
one per 2000 milliseconds and remained on the screen for 1800
milliseconds for the completion of the task. A blocked fMRI design was
used so that the tasks consisted of 8 blocked segments with a total of
four blocks of experimental reading and four blocks of control
condition reading which were alternated over the 20 minute duration of
the experiment. The usage of fMRI (functional Magnetic Resonance
Imaging) and ERP (Event Related Potentials) were used to compare
differences across the dyslexic and control groups' performance.
Additionally, observations of a behavioral task was collected with a
similar word blocking before the experiment allowing subjects to read
aloud allowing both groups to form familiarity with the task a provide
Subjects silently read similar linguistic stimuli for both the fMRI and the ERP data collection. The ERP's however, were measured in a separate session where the stimuli and control words were displayed in a pseudorandomized order that was all presented in one session (1). Five images were taken from every 2.5 minute session totaling 40 total images for fMRI analysis. These data were collected by simultaneous electrodes at critical time periods for linguistic processing (100- 180ms, 180-250ms, 250-350ms, 350-500ms, and 500-600ms after word presentation). All ERP data were analyzed over a 2000ms timeframe.
Results from the fMRI data revealed significant activation in the left inferior frontal gyrus (IFG) for control subjects during the task (1). However, the dyslexic subjects display three areas of activation of dyslexic readers (1). Dyslexic readers' had activation in the left IFG, the posterior left thalamus, and in a part of the left caudatus nucleus (1). In addition, dyslexics displayed a significant hyperactivaion in the Broca's area (found in the anteriror insula and in the lingual gyrus [right tempro-occipital region]) in comparison to control subjects (1).
The data collected in Georgiewa's study provided significant support for the phonological hypothesis. Data from the behavioral study worked to demonstrate that dyslexics had increased problems with phonological decoding (most decoded at a slower rat which required a greater amount of effort) which was seen even during out loud reading tasks. Group differences in the activation of the Brocaas area are said to be reflective of increased effort concerning phonological coding, due to the Brocaas area's involvement in phonological decoding and lexical identification; piecemeal/ assembled phonology (1). And lastly, the activation of three separate areas of the brain during phonological decoding is suggestive of insufficient sensory function and of possible compensatory efforts to more efficiently do a task that is generally localized to one area of the brain.
While the phonological theory of dyslexia provided a sufficient explanation of the etiology of dyslexia through the usage of a cognitive framework, the magnocellular theory provided the field of dyslexia with a grounded biological origin for the cognitive manifestations that were observed in dyslexia. This theory did not refute the findings of the phonological deficit theory, rather, it tried to validate it by providing neurological evidence linking cognitive symptomologies to brain abnormalities. Moreover, this theory suggested that dyslexics suffer from an auditory deficit which also can be seen in the manifestations of the disorder. The magnocellular theory was coined by Stein in 1997 and was based on the idea that there exists a division of the visual system into two neural pathways: the magnocellular and the parvocellular pathways (6). It is suggested that dyslexics suffer from abnormalities in the magnocellular pathway that cause visual and binocular difficulties (6). The impairments of these neural pathways are believed to cause auditory and visual deficits. With both auditory and visual deficits, the magnocellular theory suggests that dyslexics suffer from difficulty in processing rapid temporal properties of sounds which leads to phonological deficits (5).
A 2002 study investigating temporal processing by Rey, De Martino, Espesser & Habib was done in light of both the phonological and magnocellular theories and lends support to a neurological temporal deficits in dyslexics described by the magnocellular theory. This study accessed 13 developmental dyslexic children ranging from 9.8- 13 years and 10 normal readers ranging from 11.5-13 years old. Dyslexic subjects attended a school specialized for dyslexic while controls attended regular junior high school. Subjects were match for age and IQ. During the experiment subjects were asked to complete a Temporal Order Judgement (TOJ) task which used the succession of two (p/s) within a cluster, these clusters, in addition there were two sections where either the stimuli was artificially shortened or lengthened during the TOJ task (4).
Results from the experiment supported a possible deficit in temporal
functioning as a component of dyslexia. Dyslexics did significantly
worse on the consonant brevity trails (shorting), preformed somewhat
better on the consonant lengthening, and displayed normal performance
(for their age and intelligence) when given 200% lengthening of
The absence of significant effects of consonant ordering, suggested
that temporal processing difficulty work to impair the dyslexic
student's ability to perform to the best of their ability. Similar
findings of Bradlow's 1999 study support these deficits. Bradlow's
electrophisological manipulations (slowing or lengthening) of the
presentations of each phoneme along the da-ga continuum revealed grave
differences among dyslexic and normal subjects. It was found that
common deficits of slowed temporal processing were minimized when there
was an increase in phonemic presentation (increases of 40 milliseconds
to 80 milliseconds) (4).
It may be inferred through both the Rev, atl and Bradlow findings that
there does exist clinical evidence for a magnocellular deficit in
dyslexics which is inclusive of the presence of a phonological
deficiencies, but also recognizes an additional temporal processing
Though both theories provide acceptable rationale for possible causal of dyslexia it is difficult to give preference to either theory. While the phonological deficits theory addresses important cognitive impairments that are detected in the majority of adults and children who suffer from dyslexia, it fails to account for the many other legitimate sympotomologies displayed in the greater population of dyslexia (7). To address this shortcoming, in 2002 Maryanne Wolf and Partrica Bowers proposed the idea of the double deficit theory. This theory proposed two subtypes of dyslexic readers; one with a single deficit (name-speed or phonological deficits) and others with a double deficit (both naming speed and phonological deficits (7). Through their research they discovered that phonological deficits were just one source of reading dysfunction and that naming speed deficits were also a major source of problems in dyslexic readers (7). Further, it was suggested that dyslexics with double deficits were among the worse reading due to their limited compensatory routes for reading efficiently. This research was the result of a growing number of dyslexic children who had not been diagnosed because their symptomologies were not "just" phonological in nature. Though the phonological deficit theory provides us with a firm idea of the core manifestations of dyslexia, it should be revisited to account for the various subtypes which occur throughout the spectrum of dyslexia. Accounting for these variations would allow clinical diagnoses to be a more flexible processes that acknowledges a wider variety of co-occurring symptomologies.
In accordance, the magnocellular theory, though useful in the localization of cognitive symptoms to core neurological abnormalities neglects to address common symptoms displayed in dyslexics which are not the directly the result of visual or auditory pathway abnormality. Difficulties in handwriting, clumsiness, automating skills are among a few commonly found symptoms which are present in over 90% of dyslexics (2). Many of these symptoms have been proposed to be the result of a ceberallar abnormality which effect dyslexics fine motor, balance and the ability to automate skills. From this idea, researcher Nicolson, Fawcett, and Dean proposed the cerbellar deficit theory as an additional cause of dyslexia and found promising results from a 2001 experiment which suggested that the core deficits; reading, writing and spelling, could be all be linked to abnormal functioning of the cerebellum (2). They further proposed that cerbellar deficits encompassed and addressed phonological deficits while paralleling magnocellular abnormalities; suggesting that some dyslexic children displayed either or both magnocellular and cerebellar abnormalities which served as a core source of the manifestations of their phonological deficits.
In light of the current research of the double deficit and cebellar deficit theories, it is necessary that the traditional theories of dyslexia be revisited. Though both the phonological and magnocellular deficit theories provide key components which are helpful in the long standing investigation of dyslexia, they both are lacking in major ways. Using the both the double deficit and cerbellar theories in conjunction with these dominant theoretical models, however, may be useful in obtaining a more holistic understanding of the true nature of the disorder. Accounting for the major phonological deficits with the phonological theory, the disorders neurological origin through the use of both the magnocellular and cerbellar theories, and assessing the various subtypes of dyslexia through the double deficit theory would be the ideal strategy for efficient investigation of the etiology of dyslexia. In conclusion, a model which works to incorporate these four facets of investigation could potential advance the research and treatment of dyslexia, by broadening the current diagnostic spectrum of dyslexics and evoking varying styles of intervention which work to target the multitude a dyslexic symptoms and subtypes.
1)Sciencedirect, Great article on brain imaging in subjects who suffer from dyslexia.
2)Sciencedirect, Great article which explains the cerebellar deficit hypothesis of dyslexia.
3)Infotrac, Article about cerebellar deficits in dyslexics which lends support to the hypothesis of cerebellar deficit in dyslexia.
4)Sciencedirect, Article which give an in-depth explanation of temporal processing and phonological deficit theory of dyslexia.
5)Nature.com, Article discussing the two most prevalent theories of dyslexia; the magnocellular and phonological theories.
7) Infotrac, Article describing the double deficit hypothesis of dyslexia.
NON-WEB REFERENCES6).To see but not read; the magnocellular theory of dyslexia. Stien, J. & Walsh, V. TINS v20 1997 pages 147-152.
Anyway, if anyone knows anything about it, or if it might be related to bipolar disorder, I would greatly appreciate any information you can give me ... Rhonda McBride, 27 March 2007