DYSLEXIA : A Review of the Literature Pertaining to the Neurophysiology of Developmental Dyslexia.

Stephen Sexton


Dyslexia effects between 5-17 % of the population (Shaywitz,1998), and is a diagnosis often given to children or adults at the lower spectrum of reading ability in both speed and comprehension. Demb et al (1998) suggested in his article that “reading rate may be the most sensitive marker of dyslexia in adults with a childhood history of dyslexia and some level of compensation in adulthood”. While adults with a childhood history of dyslexia may have compensated for their learning disability by employing other cognitive skills to the task, the underlying abnormality in brain activity is still present, therefore maintaining their slow rate of reading (Demb et al, 1998).

Various theories have been presented regarding the underlying mechanism of dyslexia with the most popular theory being dysfunction of the M-cell transient visual pathway between M-type retinal ganglion cells and the posterior parietal cortex (Demb (98), Shaywitz (95), Stein (97), Beauchamp (97), Demb (94), Horwitz (98)). It has also been pointed out that deficits in the transient visual pathway may only be one component of a more generalized disorder of information processing (Farmer & Klein, 95). Demb (94) and Stein (97) hypothesized from their own and other studies that dyslexics may have a deficit in fast temporal processing of any stimulus, and further, that phonological, visual and motor deficits may all be affected by this fundamental deficit (Stein, 97). This could explain the difficulties experienced in reading and listening comprehension and visuo-spatial skills including general coordination and motor planning.

In addition to this, a number of authors have made reference to destabilized binocular fixation as being a possible explanation for the blurring and moving around of words or letters on the page (Demb (98), Stein (87), Stein (97), Carrick Institute (01)). Stein (97) reported that 67% of dyslexic children have poor vergence control “which leads to unstable sense of visual direction”, and that monocular occlusion for reading over a 6 month period resulted in an improvement in 51% of dyslexics with unstable vergence control. While there was no specific analysis regarding the cause of this deficit, the side of vergence weakness could be predicted in accordance to the theory of hemispheristic deficit where a decreased level of neuronal integration into oculomotor pools from the cortex, cerebellum or brainstem centres could be the underlying cause of destabilized binocular fixation. It is possible also that a dyslexic child or adult has deficits in cycloversional movements of the eye due to faulty ocular reflexes under cerebellar control, thus providing the perception of letters and words swirling about the page.

Fast temporal processing of auditory stimuli was also shown to be affected in dyslexics. Temple et al (2000) stated that dyslexics are particularly impaired in “phonemic awareness” – the ability to decompose words into their constituent speech sounds which affects their ability to relate visual input to phonological representations (ie reading comprehension). “The rapid processing hypothesis” (Wagner (87), Tallal (80), Merzenich (96)& Tallal (96)) of dyslexia therefore explains the impaired discrimination of acoustic cues “that are necessary to distinguish phonemes”. Nagarajan’s (99) research supported this hypothesis showing that an initial auditory stimulus produces excessive post-stimulus inhibition and therefore smaller neural activation following any new stimulus within a 200ms time window after the first stimulus – this can equate to deficits in comprehension or neural registering of the “intrasyllabic sound parts of words” (Nagarajan (99)). Therefore, dyslexics can have difficulties in both reading and listening comprehension.

Recent research in brain activity using brain imaging of dyslexic and control subjects has shown consistent changes in specific regions of the brain and subcortical circuits. Demb (98) compared results from tests that detect reading ability (including rate and comprehension) to motion perception tests (speed discrimination thresholds) and brain activity finding a strong three-way correlation, indicating that reading rate and speed discrimination thresholds could be an effective prediction of brain activity in dyslexics. Areas of brain receiving a predominance of M-pathway input such as the Middle Temporal area (V5) and surrounding regions (MT+) were found to have significant decreases in activity compared to controls (Demb, 98). These areas of brain are believed to be mainly involved in pursuit mechanisms and motion sensitive visual activity which may affect the smooth flow of successive saccades across the page when reading, and possibly reduce inhibition of the P-cell sustained visual pathway.

Shaywitz (95) discovered underactivity in the posterior regions of brain coinciding with Wernicke ’s area, the angular gyrus and striated cortex – areas involved in language comprehension and vision. They also found a reversal of brain activity associated with reading, such that non-impaired readers showed greater activity in the left hemisphere while dyslexics showed greater activity in the right hemisphere. Language abilities normally begin to develop in both hemispheres but will shift to the left hemisphere in 95% of individuals by the age of 5 (Carter,1998). Abnormal development at this stage in a child’s life may predispose them to difficulty in phonological awareness later in life when reading and writing become more important. Failure of activation of the left hemisphere could be the underlying cause of this developmental problem, and low frequencies of firing in the brain may prevent the expression of genes that are necessary for full development of canalised neural pathways.

The importance of intact fast temporal auditory processing abilities was also stressed by some authors (Nagarajan (99), Temple (00), Galaburda (94)). Galaburda (94) further identified changes to auditory anatomy in developmental dyslexia. Dyslexics had significantly smaller left sided Medial Geniculate Nuclear (MGN) cells compared to the right and a higher proportion of small neurons to larger neurons in this nucleus. The smaller diameter of the neurons could correlate with a slower speed of transduction and therefore a confusion or overlapping of consecutive auditory cues and less specification for transient auditory stimuli. Similarly, Livingstone et al (1991) found in a post-mortem study on dyslexic subjects that cells in the magnocellular layers of the Lateral Geniculate Nucleus (LGN) were on average 27% smaller than those of matched controls. Galaburda’s work supports a left hemisphere based phonological defect in dyslexic individuals. The increased proportion of smaller diameter neurons could also be related to a lesser frequency of firing of the presynaptic pools. Presynaptic pools to the medial geniculate nucleus include somatosensory, auditory and visual sensory areas (Kandel & Schwartz, p607-8). A similar relationship is noted in the anatomical connections of the Superior Colliculus and Lateral Geniculate Nucleus (LGN) of the visual system. The LGN receives 90% of axons from the retina and serves as the first major area of integration of visual input. The 90% of retinal ganglion cell axons that project to the LGN make up only 10 – 20% of the presynaptic pool of the nucleus. The majority of integration comes from the cerebral cortex and the reticular formation of the brainstem as sensory feedback (Kandel & Schwartz, p531-32). This could explain a large number of claims by patients that their hearing or vision improved following spinal manipulation or other modalities that would increase this type of integration into the thalamus and cortex. Measures of thalamocortical and cortical activity other than neuroimaging and electrical conduction have been proposed in the literature. A study by Carrick found a strong positive correlation between the side of decreased cortical hemispericity and non-spastic pyramidal paresis as determined by blind spot cortical mapping (by manual perimetry testing) and manual muscle testing (Carrick, 2001). The use of blind spot cortical mapping in determining the side of decreased hemisphericity (cortical activity) was outlined in an earlier study designed to determine the effect of cervical joint manipulation on brain activity (Carrick, 97). The results of this study showed that cortical activity could be increased by manipulation on the same side as the enlarged cortical blind spot which was contralateral to the side of decreased hemisphericity. The reverse was found to be true if the subject was manipulated on the other side.

Temple et al (97) showed that subjects with dyslexia could improve their sensitivity to rapidly changing auditory stimuli over a specific 33 day training program. Changes were noted in the response of the left frontal cortex to rapidly changing auditory stimuli on fMRI scanning. This shows that the pathways affected in dyslexia demonstrate plasticity. The follow up MRI did not demonstrate changes however in the abnormal response of the right cerebellum to this type of stimulus. Subjects showed a reversal of the normal response in this region to rapidly changing stimuli in that they responded much greater to a slow changing stimulus. Another study quoted by Temple (2000) on motor sequence learning showed decreased right cerebellar activity on PET (Positron Emission Tomography) in dyslexics compared to controls for prelearned and new motor sequences. These findings further support the model of global hemispheristic deficit in dyslexic subjects due to the direct relationships between right cerebellar and left cortical function.

Treatment aimed at improving cortical activity such as spinal manipulation, hemi-visual field stimulation (specific for the left sided M-cell pathway in most cases), eye, spinal or other motor and cognitive activities could be used specifically to improve the capacity of dyslexic subjects to learn. Chiropractic neurology is a specialty in chiropractic that utilizes these techniques to improve brain hemispheric function in patients demonstrating abnormal neurological control. Appropriate treatment and exercises should only be given following a full and comprehensive neurological assessment.



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