Anatomical Regions of Dyslexia

by Kristen Matthews

     Dyslexia is a behaviorlly diagnosed syndrome,
presumed to manifest from a central nervous system
disfunction(Hynd and Semrud-Clikeman, 1989).
     The specific anatomical sources of dyslexia remain
unclear, though many regions participate, and are
affected by reading behavior. Although there are cases in
which visual problems are the source of impaired reading,
most have concluded the underlying problem of dyslexia to
be a phonological deficit(Paulesu et al, 1996). There is
an inability to relate the sequences of sounds of letters
seen, of word sounds, and the spelling of words.  The
anatomy of this system includes Broca’s area, Wernicke’s
area, the insula, the supramarginal gyrus, and the
arcuate fasciculus(Paulesu et al, 1996).
     These ideas were tested when adult dyslexics were
asked to perform rhyming and short term memory tasks
using letters of the English alphabet. Positron Emission
Tomography (PET) revealed only a subset of brain regions
that are nornally active during phonological processing
to be involved in these same processes in dyslexics.
Broca’s area was stimulateed during rhyming tasks, and
the tempo-parietal during the short term memory tasks.
These areas were not activated in sync, as they were in
the controls. When one area was active, the other region
was only weakly activated. This provides evidence of a
weak connection between anterior and posterior language
areas as the source of dyslexia. The left insula was
never activated during these tasks, which may be the
anatomical connection between these areas, as well as the
source of disfunction.
     Neuropsychological and pathological investigations
have found a deficit of the left tempo-parietal region in
dyslexic subjects(Rumsey et al, 1992). PET scans were
measured in men with severe dyslexia during phonological
and auditory attention tasks. Non-dyslexics stimulated
the left tempo-parietal lobe during rhyme detection
tasks, but not during attention tasks. No activation
occured in the left tempo-parietal regions in dyslexic
subjects for rhyming tasks, however both groups showed
similar activity in this area during rest and attention
tasks(Rumsey et al, 1992).
     Cerebral blood flow was later measured in the right
frontotemporal regions during rest and a tonal memory
task also in dyslexic men(Rumsey et al, 1994).The control
group showed significant stimulation in the right
frontotemporal and left temporal areas. Opposingly,
dyslexic men made more errors, and showed less activity
in the right frontotemporal regions. Mid and anterior
temporal cortex activity remained the same for both
groups. It may be concluded that the right, as well as
the left temporal corticies are involved with
dyslexia(Rumsey et al, 1994).
     The size and symmerty of hemspherse has been
recorded to detect any differences between dyslexics and
control subjects(Duara et al, 1991). Magnetic resonance
imaging (MRI) was used to measure segments of left and
right hemispheres, a horizontal brain section, and
divisions of the corpus callosum. Dyslexics had a greater
asymmetry, with the right side being larger than the left
in the midposterior segment of the angular gyrus. The
opposite was true of the non-dyslexic subjects. Dyslexic
subjects also had a larger splenium in the corpus
callosum, and derceptual processes(Vallar et al, 1996).
     This distinction of processes is significant in
determining at what stage in processing do certain
deficits occur. Two patients were cited as having left
hemisphere lesions which which precursed visual
extinction on the right, but difficulty reading the left
side of words. One patient also had difficulty naming the
letters in the words. Results indicate an alternative
source to general deficits in visual perception and
attention(Katz, 1989). This type of reading difficulty
may manifest after general perceptual processes have
taken place, but before phonological and semantic access.
It is proposed the deficit takes place in one of the
three levels of letter perception(Katz, 1989). These
three processing levels consists of the feature level,    
            the letter level, and the word level.
Detection of individual letter features occurs at the
feature level.The letter level identifies each letters
position within a string of letters. Finally, the word
level identifies the string of letters as words(Katz,
1989). Each level stimulates the next, beginning with the
feature level and ending with the word.  It is unclear
where these patients deficits lye within this processing
system. Generally, the problem seems to affect the
ability to recognize the initial letterd in words.
     In summary, the biological basis of dyslexia is
incomplete, though growing. A deactivation of the left
hemisphere seems to occur in people with this syndrome,
though cases have seen the right side effected as well.
Parts of the corpus callosum are larger, which may
account for a deficit in the lateralization of function.
Finally, specific stages of processing may be the key to
understanding the origins of this syndrome.



WORKS CITED

Duara, R., Kushch, A., Gross-Glenn, K., Barker, W.,
Jallad, B., Pascal, S., Loewenstein, D., Sheldon, J.,
Rabin, M., Levin, B., Lubs, H.  Neuroanatomic Differences
Between Dyslexic and Normal Readers on Magnetic Resonance
Imaging Scans.  ARCHIVES OF NEUROLOGY, 1991, 48 (4),
410-416.

Ellis, A., Young, A. HUMAN COGNITIVE NEUROSCIENCE. 
Lawrence Erlbaum Associates: Hove (UK) 1994.

Flynn, J., Deering, W., Goldstein, M., Rahbar, M.H.
Electrophysiological Correlates of Dyslexic Subtypes. 
JOURNAL OF LEARNING DISABILITIES, 1992, 48 (4), 410-416.

Hynd, G., Semrud-Clikeman, M.  Dyslexia and Brain
Morphology.  PSYCHOLOGICAL BULLETIN, 1989, 106 (3),
447-482.

Katz, R.  Positional Dyslexia.  BRAIN AND LANGUAGE, 1989,
37 (2), 266-289.

Paulesu, E., Frith, U., Snowling, M., Gallagher, A.
Morton, J., Frackowaik, R.S.J., Frith, C.  Is
developmental dyslexia a disconnection syndrome? Evidence
from PET scanning.  BRAIN, 1996, 119 (pt. 1), 143-157.

Rumsey, J., Andreason, P., Zametkin, A., Aquino, T.,
King, C., Hamburger, S., Pikus, A., Rapoport, J., Cohen,
R.  Failure to Activate the Left Temporoparietal Cortex
in Dyslexia. An Oxygen 15 Positron Emission Tomography
Study.  ARCHIVES OF NEUROLOGY, 1992, 49 (5), 527-534.

Rumsey, J., Andreason, P., Zametkin, A., King, A.,
Hamburger, S., Aquino, T., Hanahan, A., Pikus, A., Cohen,
R.  Right Frontotemporal activation by tonal memory in
dyslexia. An O15 PET Study.  BIOLOGICAL PSYCHIATRY, 1994,
36 (3), 171-180.

Rumsey, J., Casanova, M., Mannheim, G., Patronas, N.,
DeVaughn, N., Hamburger, S., Aquino, T.  Corpus Callosum
Morphology, as Measured With MRI, in Dyslexic Men. 
BIOLOGICAL PSYCHIATRY, 1996, 39 (9), 769-775.

Vallar,  G., Guariglia, C., Nico, D., Tabossi, P.  Left
Neglect Dyslexia and the Processing of Neglected
Information.  JOURNAL OF CLINICAL AND EXPERIMENTAL
NEUROPSYCHOLOGY, 1996, 18 (5), 733-746.  

Copyright © 1997, Dr. John M. Morgan, All rights reserved - This page last edited March 17, 1997
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