The findings of Experiment 1 and Experiment 2 provide
strong evidence that PAL deficits in dyslexia stem from the
verbal demands of the task, rather than difficulties in
crossmodal associative learning. However, despite demonstrating
the specificity of deficits to verbal output conditions,
they cannot speak to the locus of these difficulties.
For example, do deficits arise during the verbal learning
or associative stage of PAL? Evidence supports the notion
that the phonological and associative components of PAL
tasks are indeed dissociable. Importantly,
difficulties at either (or both) stages of learning
would lead to the verbal-output PAL deficits observed in
Experiments 1 and 2. Traditional nonword PAL paradigms
are confounded by the fact that verbal learning and associative
learning occur simultaneously, making it difficult
to estimate the effects of verbal learning and associative
learning on performance. Yet, locating the source of failure
is crucial for guiding our conceptualization of PAL deficits
in dyslexia. If deficits arise solely from demands on verbal
learning, PAL deficits should be viewed as a corollary of
verbal deficits, rather than a defining feature of dyslexia.
If, however deficits emerge in the associative learning
phase, a different explanation might be necessary, giving
special status to associative learning deficits in dyslexia, albeit
deficits specific to associations requiring verbal
output.
Experiment 3 was designed to address these confounds
by separating the learning procedure into a verbal learning
and associative learning phase. This was achieved by presenting
the children with verbal stimuli in a pre-exposure
phase, before requiring them to associate the verbal forms
with input stimuli. The primary question of interest was
whether verbal learning ability, as indexed by the preexposure
phase, would fully account for any observed difference
between dyslexic and control groups in a test of visual–
verbal PAL. We hypothesized that differences in
verbal learning in the pre-exposure phase would fully explain
deficits in visual–verbal PAL in the associative learning
phase. That is, we expected no difference between the dyslexic and control groups in visual–verbal PAL, after
accounting for verbal learning ability. If, however, children
with dyslexia have an additional difficulty binding verbal
information to a referent in memory, we would expect
PAL deficits to be additive, such that they are more severe
than would be predicted solely from underlying language
deficits.
The findings of Experiment 1 and Experiment 2 providestrong evidence that PAL deficits in dyslexia stem from theverbal demands of the task, rather than difficulties incrossmodal associative learning. However, despite demonstratingthe specificity of deficits to verbal output conditions,they cannot speak to the locus of these difficulties.For example, do deficits arise during the verbal learningor associative stage of PAL? Evidence supports the notionthat the phonological and associative components of PALtasks are indeed dissociable. Importantly,difficulties at either (or both) stages of learningwould lead to the verbal-output PAL deficits observed inExperiments 1 and 2. Traditional nonword PAL paradigmsare confounded by the fact that verbal learning and associativelearning occur simultaneously, making it difficultto estimate the effects of verbal learning and associativelearning on performance. Yet, locating the source of failureis crucial for guiding our conceptualization of PAL deficitsin dyslexia. If deficits arise solely from demands on verballearning, PAL deficits should be viewed as a corollary ofverbal deficits, rather than a defining feature of dyslexia.If, however deficits emerge in the associative learningphase, a different explanation might be necessary, givingspecial status to associative learning deficits in dyslexia, albeitdeficits specific to associations requiring verbaloutput.Experiment 3 was designed to address these confoundsby separating the learning procedure into a verbal learningand associative learning phase. This was achieved by presentingthe children with verbal stimuli in a pre-exposurephase, before requiring them to associate the verbal formswith input stimuli. The primary question of interest waswhether verbal learning ability, as indexed by the preexposurephase, would fully account for any observed differencebetween dyslexic and control groups in a test of visual–verbal PAL. We hypothesized that differences inverbal learning in the pre-exposure phase would fully explaindeficits in visual–verbal PAL in the associative learningphase. That is, we expected no difference between the dyslexic and control groups in visual–verbal PAL, afteraccounting for verbal learning ability. If, however, childrenwith dyslexia have an additional difficulty binding verbalinformation to a referent in memory, we would expectPAL deficits to be additive, such that they are more severethan would be predicted solely from underlying languagedeficits.
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