Reading Working Papers in Linguistics 4 (2000) - The University of ...

R. INGHAM
using the Wilcoxon ranked sums test showed that the [+GD] group performed
significantly worse on argument structure alternations than its LN matches,
while the [-GD] group was statistically non-distinct from its LN matches.
A-structure therefore seems to be a grammatical discriminator
identifying SLIs with a grammatical deficit, but not those without a GD. This
is interesting because a-structure is not encoded in English by grammatical
morphology. So the grammatical deficit in the GD children is seen to go
beyond morphological deficit, of the kind envisaged in e.g. Gopnik & Crago
(1991).
Let us now return to the issue posed by Locke of the relation between
grammatical deficit and lexical deficit, which was not upheld here. The
problem is that 4 of the 9 GD subjects show no lexical deficit. Therefore we
have no reason to believe their utterance acquisition mechanism was
defective. Yet they have a marked grammatical deficit. How can this be if a
GD is consequent upon a deficient utterance acquisition mechanism?
Conversely, five of the SLIs with NGD have a severe lexical deficit. How can
this not have led to a grammatical deficit if GD is consequent upon an
impaired utterance acquisition mechanism?
If we insist on linking lexical deficit and GD we might have to say that
the constant lag assumption made by Locke is simply too strong. The GD
subjects with no LD at the point of testing could have had a lexical deficit
years earlier, but accelerated their lexical acquisition at a faster rate than
normal so that they arrive with LN a.e. scores by the time they reached the
point of BPVS testing. Conversely the NGD subjects with a lexical deficit at
the point of testing could have had an age appropriate receptive lexicon in
time for Locke's structure analysis phase, phase 2, but thereafter their lexicon
grew at a much slower rate than normal, so that they arrive at the point of
BPVS testing with a major lexical deficit, which led to problems in Locke’s
Phase 3.
These explanations are logically possible. But if we adopt them we
have to give up the constant lag claim made by Bishop, which appears to have
been well-motivated, on the basis of a large sample (over 80) languagedelayed
children.
We might have to do that. But for now, while there are as yet no
detailed longitudinal studies of SLI children that would resolve this issue as
far as I am aware, I suggest that the cross-sectional data reported here indicate
a somewhat modified version of the constant lag assumption. In some SLI
children vocabulary development exhibits a persisting lag, while in others
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