Dear Canice McGivern
we have been looking ar saccadic intrusions and binocular stability in normla
control subjects aged 7 to 28y and in dyslexics age 7 to 15y. I am currently
working at the MS, but part of the data have been published
Strabismus 8, 119-122 (2000). I am sending the published text below.
We found that fixation stability improves over age until adult age and that
about 50% of the dyslexics suffer from fixation instability by intrusions
and 25 % by binocular drifts. We are currently trying to give the children a
daily practice to stabilize their fixation control system
Best regards
Burkhart Fischer
Stability of Gaze Control in Dyslexia
Burkhart Fischer and Klaus Hartnegg
Brain Research Group, University of Freiburg
Key Words: Saccade - Antisaccade - Reaction Time - Fixation - Binocular
Control
Mailing address:
Prof. Dr. B. Fischer
Brain Research Group
Hansastr. 9
D - 79104 Freiburg
e-mail: [log in to unmask]
www.brain.uni-freiburg.de/fischer/
Abstract
The neurobiological basis of saccade control has at least 3 components:
fixation, reflexes, voluntary control. It was found in earlier studies that
the voluntary component of saccade is specifically impaired in dyslexics as
compared with controls of the same age. In this study we searched for evidence
of fixation instability by analyzing the eye movements of 99 control subjects
and 262 dyslexics (age 7-17y) performing an overlap prosaccade and a gap
antisaccade task. The percentage of intrusive saccades was counted for each
subject during a period of the trial where stationary fixation was required.
Both groups show improvements of fixation stability with age, but the dyslexic
group exhibits developmental deficits. It is discussed whether these deficits
could be interpreted as consequences of deficits in the magnocellular pathway.
Introduction The neurobiological basis of low level vision and saccade
control is well studied in primates and human subjects. It was found that the
visual pathway divides into two systems, the parvo- and the magnocellular
system. Fixation and saccade control require the cooperation of several
subcortical and cortical structures to provide stable vision. In large studies
it was further found that many of the visuomotor functions still develop with
age above 7 years. For example the generation of antisaccades may last until
the age of 18 years (4). Dyslexic subjects exhibit developmental deficits in
dynamic, transient vision (7); (8); (2); (3) and in voluntary saccade control
corresponding to a delay of 2 to 4 years on average (1). These deficits may be
compensated to a large extend and in most dyslexic children by daily practice
of perceptual tasks requiring fixation and/or saccadic eye movements (6).
Binocular coordination as tested by the dunlop test exhibits deficits in
dyslexia as well (11). These deficits as well as problems in the auditory
system of dyslexics have been interpreted as a consequence of a poorly
developed magnocelluar system as reviewed earlier (10).
In this study we searched for evidence for visual instability in dyslexia
eventually caused by deficits in eye movement control. We reanalyzed the data
of control and dyslexic subjects by counting the number of intrusive saccades
as an index of instability.
We used the data of children who were tested in our laboratory for deficits in
saccade control. The original data were reanalyzed for the purpose of this
study. The data of two groups of control and dyslexic children in the age
range of 7 to 17 years could be compared. The analysis revealed developmental
deficits of the dyslexic group which becomes more evident with increasing age.
This article presents the data in a preliminary from. They will be further
analyzed and compared with other data describing the visual and optomotor
performance of control and dyslexic children.
Methods
Subjects: The children had normal educational opportunities and did not suffer
from neurological or psychiatric illnesses. Their visual acuity was normal or
corrected to normal.
A battery of standardized psychometric tests was used to classify the subjects
as dyslexic or control: an intelligence test (K-ABC), a reading test (Zuericher
Lesetest), and a spelling test (DRT). A discrepancy criterion was used:
his/her reading or spelling performance was at least 1 standard deviation
below his/her performance IQ level and either his/her reading or spelling
performance was under the 25 percentile (0.7 standard deviation from the
average 50%) of a standard population. 262 dyslexics and 99 controls were
selected in this way.
Eye movement recording: The horizontal movements of both eye were measured
simultaneously using an infrared-light reflection method. The analog signal of
the eye positions was digitized and stored on a computer with 1ms temporal and
about 0.1 spatial resolution. Because absolute eye position could be
determined not better than about 0.5 we used the velocity as a criterion for
stability (see below).
Eye movement tasks: Eye movements were recorded during an overlap prosaccade
task (the fixation point remains visible after target onset) and during a gap
antisaccade task (the fixation point was turned off 200ms before the stimulus
was presented). The stimuli were presented randomly at 4 degrees to the right
or left. The prosaccade task required saccades to the stimulus, the
antisaccade task required saccades in the opposite direction of the stimulus
side. Two-hundred trials (100 to each side) were presented in each task. The
tasks, the procedure, and the visual display of the stimuli followed the
protocol published elsewhere (5).
Eye-movement variables and data analysis: During the off-line analysis
saccades were detected by an eye velocity criterion of 30 /s. Trials
completely contaminated by blinks and/or head movements were discarded. The
percentage of intrusive saccades per trial detected during a 400ms period
before target onset was defined as a measure for fixation stability. Mean
values and standard deviation were calculated after separating the pool of
subjects into four different age groups (7- 8, 9-10, 11-13, 14-17 years)and
plotted as age curves.
Results
Fig. 1 shows the age curves for the number of intrusive saccades per trial
determined from the overlap prosaccade task, i. e. during periods, where the
subjects were supposed to look at the stationary fixation point. An age
development can be seen in both groups. The dyslexics generated more intrusive
saccades in each age group with the exception of the youngest group. The
developmental deficit increases with age.
When the same analysis was carried out with the data collected during the
antisaccade task high correlations exist between the values derived from the
overlap and the gap task. However, the performance was better in the
antisaccade as compared with the prosaccade task. In both groups the number of
intrusive saccades was smaller by a mean value of 0.1. Therefore, the
difference between the groups was about the same regardless of whether the
prosaccade or the antisaccade data were used.
Discussion
This study has shown that fixation stability measured by the number of
intrusive saccades per trial develops until adulthood. In addition to
previously reported deficits in eye movement control dyslexics exhibit a
systematic developmental deficit in the percentage of saccadic intrusions.
While other visual and oculomotor deficits in dyslexia have been attributed to
structural abnormalities in the magnocellular system the question is still
open, whether the present data can also be interpreted in the same way.
Support for this notion may be seen in the fact that the magnocellular stream
of visual information projects from the primary visual cortical areas dorsally
to the parietal and further onto the frontal and prefrontal cortex. Cells
involved in visual fixation are found in the colliculus superior (9). Deficits
in the low level visual functions attributed to the magnocellular system will
therefore have consequences for these higher level visuomotor functions. In
this way the present data may well be understood by the same magnocellular
hypothesis.
It remains to be seen whether fixation stability can be improved be daily
practice of corresponding visual tasks. While antisaccade performance improves
by training as indicated by smaller error rates and higher correction rates
the training not necessarily transfers to fixation stability, because
different neural systems are involved in these functions. For example, the
training effects observed for antisaccade performance were not reflected in
the reaction times of the prosaccades in an overlap prosaccade task (6).
Acknowledgements:
This work was supported by the DFG Fi 227/11-3.
References
Biscaldi M, Fischer B, Hartnegg K, Gutjahr G. Voluntary saccade control in
dyslexia. Perception 2000;
Demp JB, Boynton GM, and Heeger DJ. Psychophysical evidence for a
magnocellular pathway deficit in dyslexia. Vision Res 1998; 38: 1555-9.
Eden GF and Zeffiro TA. Looking Beyond The Reading Difficulties In Dyslexia, A
Vision Deficit. The Journal of NIH Research 1996; 831-5.
Fischer B, Biscaldi M, Gezeck S. On the development of voluntary and reflexive
components in human saccade generation. Brain-Res 1997; 754:285-97.
Fischer B, Gezeck S, Hartnegg K. The analysis of saccadic eye movements from
gap and overlap paradigms. Brain Research Brain Research Protocols 1997;
2:47-52.
Fischer B, Hartnegg K. Effects of visual training on saccade control in
dyslexia. Perception 2000;
Fischer B, Hartnegg K, and Mokler A. Dynamic visual perception of dyslexic
children. Perception 2000;
Lovegrove W. Weakness in the transient visual system: a causal factor in
dyslexia? Ann N Y Acad Sci 1993; 682:57-69.
Munoz DP, Wurtz RH. Role of the rostral superior colliculus in active visual
fixation and execution of express saccades. J-Neurophysiol 1992; 67:1000-2.
Stein J and Talcott J. Impaired neuronal timing in developmental dyslexia -
The magnocellular hypothesis. Dyslexia 1999; 559-77.
Stein JF, Fowler MS. Unstable binocular control in dyslexic children. J of
Research in Reading 1993; 16(1):30-45. Figure Caption
Fig. 1 The mean value of the number of intrusive saccades per trial are
plotted against age for each of the 2 groups. Vertical pars show the
confidence intervals for each age group.
--
Burkhart Fischer, Universitaet Freiburg, AG Hirnforschung
Hansastr. 9, 79104 Freiburg, Germany, Tel ++49 761 203 9535, Fax 9540
[log in to unmask] www.brain.uni-freiburg.de/fischer/
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