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(Introduction to) Language History and Use
Specific Language Impairment
Rachael-Anne Knight ([email protected])
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Specific Language Impairment
1 Introduction
Specific Language Impairment is the name given to a condition in which children
have a severe limitation in language ability despite any obvious cause. Although we
are often told that language acquisition is rapid and effortless, for some children this
is not the case.
1.1 The incidence of SLI
Conservative estimates suggest that SLI affects about 7% of the population. It has
long been observed to be slightly more common in males than females and seems to
run in families.
1.2 The diagnosis of SLI
SLI is described as a significant limitation in language ability despite the absence of
other problems in intelligence, hearing, oral motor function, neurology etc. Thus, the
criteria for SLI are mostly exclusionary. It is normally easy to tell that a child has
some sort of language problem but for it to be specific language impairment, it is
important to establish that there are not other additional problems, which may be
contributing to the language difficulties. Many tests are now available which allow
children to be screened in various areas.
Factor
Language Ability
Nonverbal IQ
Hearing
Otitis media with effusion
Neurological dysfunction
Oral structure
Oral Motor Function
Physical and social interactions
Criterion for SLI
Scores of –1.5 standard deviations or
lower
IQ of 85 or higher
Pass normal screening tests
No recent episodes
No evidence of seizure, cerebral palsy or
brain lesions
No anomalies
Pass screening tests
No symptoms of impaired interactions
1.3 Studying SLI
1.3.1 Control groups
We know that children with SLI have impaired language ability but to characterise the
deficit more accurately we have to compare them to normally developing children. It
is important to decide what kind of group the SLI group will be compared to.
1.3.1.1 Age-matched controls
Normally developing children of the same age as those in the SLI group are used as
age-match controls. This allows researchers to say if SLI children really are impaired
for their age.
(Introduction to) Language History and Use
Specific Language Impairment
Rachael-Anne Knight ([email protected])
1.3.1.2 IQ matched controls
It would be possible to find a group of age-matched controls that have a higher IQ
than the SLI group. This could mean that any effects found would be to due to
differences in IQ rather than language ability. In order to overcome this problem it is
sometimes necessary to use a control group matched on IQ.
1.3.1.3 Language matched controls
A comparison to children matched on age or IQ will allow us to see if SLI children
are impaired but will not tell us in what way they are impaired. If they cannot do
something that the matched children can do, it might mean that they are just at an
earlier stage of development. In order to test this possibility a control group matched
on language can be used. Several different matching variables can be used depending
on the factor under consideration.
1.3.2 Delay or deviance?
An important question in the study of SLI is whether the language problems are best
described as a delayed normal language development or deviant development which
is unlike anything that normally developing children do. Traditionally this debate is
represented by a dichotomy between delay and deviance but it is now recognised that
these descriptions are too simple. Leonard (1998) suggests that there are 5 ways that
SLI children can differ from normally developing children,
1.3.2.1 Delay
Delayed language development may imply only that children with SLI start learning
later than their peers but then develop at the same speed. This is true for many
children who have caught up by the age of about three but these children are not
usually diagnosed with SLI. More common is for children who start developing later
to also proceed at a slower rate of development so that the gap between them and their
peers widens over time.
1.3.2.2 Plateau
Some children not only suffer from delayed and protracted development but may
never achieve full mastery of certain aspects of the language even in adulthood. This
pattern is described as a plateau in development.
1.3.2.3 Profile difference
The pattern of delay suggests that a child with SLI may be identical to a younger child
in their linguistic abilities. However, it is also important to consider the relationship
between different abilities. For example, SLI children may look the same as a
younger normally developing child on one feature but may be different on another.
1.3.2.4 Abnormal frequency of error
This is type of quantitative difference. Children with SLI may produce the same types
of errors as (younger) normally developing children but with a much greater
frequency than is ever seen in the normal population.
1.3.2.5 Qualitative difference
This is closest to the traditional ‘deviance’ description. It suggests that children with
SLI may produce patterns that are never seen in normally developing children.
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(Introduction to) Language History and Use
Specific Language Impairment
Rachael-Anne Knight ([email protected])
2 SLI in English
2.1 Lexicon
First words and word combinations occur later than age-controls but otherwise mirror
the patterns of normally developing children. For example 55% of early words are
nominals. They may have some word finding difficulties indicated by pauses, nonspecific words (‘stuff’, ‘thing’) and phonological and semantic word substitutions.
2.2 Argument structure
SLI children use most argument structures although there is a lack of consistency in
their use. Generally by school age though, SLI children infrequently omit obligatory
arguments and perform much like MLU controls on other measures.
2.3 Morphosyntax
SLI children use certain syntactic structures less frequently than age controls. They
also perform worse than MLU controls on measures that concern syntactic complexity
and on many measures of syntactic comprehension (e.g. reversible passives).
There is a relative weakness in the area of grammatical morphology. The sequence of
acquisition is the same as for normally developing children but percentage use of
most grammatical morphemes is lower and mastery is attained at a higher MLU.
2.4 Phonology
The sequence of acquisition is the same are for normally developing children but the
acquisition of the first phonemes (/n/, /m/, /b/, /w/) is later. Segments acquired later in
normal development (/s/, /v/) may continue to be problematic for SLI children for a
long time. They seem to be better at +voice than normal children but make unusual
errors (such as inserting nasals or non-native sounds) more often.
2.5 Pragmatics
Problems with pragmatics are not exclusively caused by problems with the lexicon
and morphosyntax. Some SLI children fail to enter into multiparty conversations or
use situation-specific phrases in inappropriate contexts. On many other measures
though they interact appropriately often matching the performance of MLU controls.
2.6 Conclusion
Children with SLI have weakness in all areas of language ability. Development is
usually delayed and protracted but it is not equally disrupted in every area. It seems
that lexical and pragmatic skills are relatively intact, with phonology and argument
structure abilities being slightly worse with morphosyntax (particularly grammatical
morphemes) being the most impaired. SLI children do not seem to be qualitatively
different that normally developing children but may make more unusual errors. These
findings suggest that SLI children language problems are best described in terms of a
profile difference.
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(Introduction to) Language History and Use
Specific Language Impairment
Rachael-Anne Knight ([email protected])
3 Explanations of SLI
3.1 Deficits in Linguistic Knowledge
These are accounts that generally focus on SLI children’s weaknesses in grammar.
They suggests that the patterns seen are due to a lack of knowledge of a rule, principle
or constraint.
3.1.1 Functional Category Deficit
Many researchers have suggested that normally developing children can’t
accommodate function words or other grammatical elements in their grammars until
they are about 2 years old. They suggest that even elements that seem to be function
words are in fact misanalysed lexical items. SLI children are considered to be stuck at
this stage, never being able to represent function words or bound morphemes.
However, cross-linguistic research shows that in many languages function words do
not present a particular problem for normally developing or SLI children.
3.1.2 Extended Optional Infinitive (primarily Rice and colleagues)
Normal children appear to go through a stage of only marking tense sometimes in
main clauses. When they do mark tense however, they generally get it right. So, they
may produce a bare stem e.g. ‘She see me’ but would rarely produce a wrong
inflection e.g. ‘They sees me’. It is proposed that SLI children are stuck at this stage
as they do not know that it is obligatory to mark tense. It has been shown however
that SLI children in Hebrew and Italian match controls in this respect.
3.1.3 Implicit Grammatical Rule Deficit (primarily Gopnik and
colleagues)
These researchers see grammatical deficits in SLI as the inability to acquire rules to
mark tense, number and person. Therefore, people with SLI can compensate in two
different ways. One is rote-learning in which every regular inflected form must be
learned like irregular forms (so ‘cats’ would be learned in the same way as
‘cherubim’). Another strategy is to explicitly remember rules of the language such as
‘add an –s if there’s more than one’. These strategies were both observed in the KE
family but it seems that most SLI sufferers can in fact learn at least some implicit
rules and may even over extend them.
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(Introduction to) Language History and Use
Specific Language Impairment
Rachael-Anne Knight ([email protected])
3.2 General Processing Limitations
Accounts which posit limitations in general processing capacity suggest that it is not
the specific nature of the material that is important but rather how it is processed and
manipulated in the brain. Therefore, problems may occur because memory is limited,
or because there is insufficient energy to complete operations or if information is not
processed quickly enough.
3.2.1 Generalised Slowing Hypothesis (Kail)
It has been found that SLI sufferers’ reaction times are slower than MLU controls on
a wide variety of tasks such as picture naming.
Kail suggests that SLI sufferer’s RTs are slower by a common factor than the RTs of
the normally developing controls. Experimental tests of this hypothesis have
suggested that SLI RTs are about 33% slower on each of 5 different tasks. This
finding lends support to the hypothesis as the factor held regardless of the number of
separate tasks needed for each operation. However, a generalised slowing hypothesis
can’t explain why some areas of language are weaker than others.
3.2.2 The Surface Hypothesis (Leonard and Colleagues)
The surface hypothesis aims to explain why grammatical morphemes are so badly
affected in SLI sufferers. Leonard proposes that SLI sufferers do have a general
processing deficit and that this especially affects acquisition of grammatical
morphemes because of their short duration in English. It is suggested that the child
can perceive them but because they are morphological they require more processing.
Combined with their short duration and the limitations on processing speed, the
analysis is not always completed. Thus SLI children need to hear these morphemes
more often before they are acquired.
There is support from Hebrew and Italian where morphemes are usually
syllabic and SLI children are generally no worse than MLU controls. However, brief
morphemes are not equally affected in every language.
3.2.3 Morphological Richness Account
The observation that brief morphemes are not equally affected in every language lead
to the proposal of the morphological richness account. Although SLI children
acquiring German perform worse than MLU controls, they still perform better than
English children with SLI on comparable morphemes. This suggests that additional
characteristics about the language have to be taken into account. Morphological
richness accounts suggest that as SLI children have limited processing resources they
will have to be selective about what to pay attention to. If the language they’re
acquiring is very dependant on morphology (e.g. German), they will pay more
attention to this than to other aspects. If the language is not morphologically rich (e.g.
English), less processing capacity will be devoted to this aspect and more to other
aspects such as word order.
Thus it seems that general processing deficits can account for much of the SLI
data. However these deficits cannot explain everything on their own. In order to
explain why some areas of language are weaker than others and why differences exist
between languages, it is necessary to consider the acoustic and typological properties
of the language in question.
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(Introduction to) Language History and Use
Specific Language Impairment
Rachael-Anne Knight ([email protected])
3.3 Processing Deficits in Specific Mechanisms
These accounts suggest that processing is deficient but in these cases it is specific
mechanisms that are affected rather than general processing
3.3.1 Phonological Memory Deficits (Gathercole and Baddely)
It is proposed that new lexical material is stored in a phonological store in working
memory. The phonological representations fade quickly from this store if they are not
reinforced. After a certain time in the store the information will enter long-term
memory. Proponents of this idea suggest that for SLI children, segmental analysis
poor is therefore representations are well-formed when retrieved. Alternatively the
representations may decay more quickly or there may be less capacity in the store so
that fewer items (or less well represented items) can be stored. This helps to explain
why children with SLI find it more difficult to repeat nonsense words or recall lists of
real words than controls. However, SLI sufferers have many problems that don’t
seem to be connected to phonological memory.
3.3.2 Deficit in temporal processing (Tallal and colleagues)
In a collection of papers starting in the 70’s Tallal and her colleagues demonstrated
that children with SLI are poor at processing rapid or brief auditory stimuli. Subjects
were trained on two different stimuli and then asked to press a button if they heard the
stimuli in a set of random noise. The control group performed well regardless of the
speed of presentation. The SLI group only performed above chance when ISIs were
above 300ms. However, performance at short ISIs improves if the stimuli are longer.
The effect was also demonstrated for non-speech sounds. For example SLI subjects
could distinguish between [ε] and [æ] but not between [ba] and [da] where the
difference is only one of a 43ms formant transition.
In addition a training package is now on the market that trains sufferers on
obvious contrasts through use of computer games and then gradually reduces the
duration and amplitude of these contrasts. The training package has been very
successful.
However, many of the differences in the stimuli are spectral rather than
temporal and many of the experiments have a large memory component. Finally the
origin of the deficit is unknown.
3.3.3 Grammatical analysis by unsuitable mechanisms (Locke)
Locke assumes that SLI begins as part of a general maturational delay that leads to
later acquisition of vocabulary. He suggests that there is a specific grammatical
analysis mechanism that only functions optimally between 20 and 36 months of age.
This analysis mechanism is switched on by the acquisition of a certain amount of
lexical material. As SLI children are delayed in this respect the grammatical analysis
mechanism doesn’t have enough time to complete a grammatical analysis of the
language and therefore the job is taken over by less efficient mechanisms.
Although tests prove that SLI children in the single word stage have worse
vocabulary comprehension abilities than age-controls, this is not the case once
grammatical analysis has begun (in the word-combination) stage. Lock’s theory
cannot account for this unless it states that lexical development is faster than normal
in SLI children after activation of the mechanism.
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(Introduction to) Language History and Use
Specific Language Impairment
Rachael-Anne Knight ([email protected])
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4 Genetics and SLI
It has often been suggested that SLI may have a genetic component. Initial findings
have suggested that SLI tends to run in families.
4.1 Family studies and the KE family
A family called the KE family have been extensively studied, as it appears that half of
them are affected by SLI.
Female
Male
Shading = Language
Impaired
Figure 1 Pedigree of the KE family
4.1.1 Genetics Basics
 The genotype is the genetic make-up of an individual
 The phenotype is the observable physical and behavioural manifestations of
that make-up
 Humans have 23 pairs of chromosomes. In each pair one is inherited from
the mother and one from the father
 Every chromosome contains hundreds of genes
 Genes can come in different forms called alleles
 For any particular gene a person might have 2 copies of the same allele or two
different alleles
 Dominant alleles have their characteristics expressed in the phenotype
regardless of the allele on the other chromosome
 Recessive alleles are expressed in the phenotype only if they occur on both
chromosomes.
(Introduction to) Language History and Use
Specific Language Impairment
Rachael-Anne Knight ([email protected])
4.1.2 Interpretation of the phenotype
These facts allow us to observe phenotypes to see how a trait might be inherited. The
pattern we see in the KE family suggests that their SLI is caused by a dominant allele
in a single autosomal gene. Several distinct patterns of autosomal dominant
inheritance are as follows.
 If a member has one abnormal and one normal allele, they will be affected and
the odds their children will inherit the abnormal allele are 50:50
 If a member is phenotypically normal (shows no evidence of the condition)
then they must have 2 normal alleles, as a (dominant) abnormal allele would
always be expressed in the phenotype. Therefore the members’ children
should never be affected.
 As the gene is autosomal (not on a sex chromosome) it should affect all sexes
equally
4.1.3 Molecular Studies
Molecular studies linked the KE’s disorder to a part of chromosome 7 labelled
SPCH1. Recently the exact gene has been identified as FOXP2. All the affected
members of the KE family (and one unrelated person) have a point mutation in this
region where a guanine (G) nucleotide is replaced by and adenine (A) nucleotide.
None of the unaffected family members have this mutation. Researchers postulate
that this nucleotide replacement leads to a different amino acid in the gene’s protein
product. This presumably changes the function of the protein. In other animals
FOXP2 controls other genes that affect embryonic neurological development.
4.1.4 Conclusion
It certainly seems as though a genetic cause is highly implicated in explaining the
problems of the KE family. However, there are have been some suggestions that the
KE family may not be typical of people with SLI. In addition, although SLI tends to
run in families it is very rare that the pedigree is so clear-cut and SLI sufferers may
often be the only affected members of their families. It seems therefore that this
dominant gene explanation will not work for all SLI sufferers.
4.2 Twin Studies
Family studies cannot prove that a factor is genetic. The communicative environment
or other factors such as diet or disease can also influence behaviour. Twin studies are
a common way of teasing apart the factors of a condition that are environmental and
that are genetic.
4.2.1 Twin Biology
 Monozygotic (MZ) twins are commonly known as identical twins and are
formed from a single egg. The twins have identical genotypes.
 Dizygotic twins are commonly known as non-identical twins and a formed
from two separate eggs. They are no more alike than any other siblings and
therefore only share half their genes
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(Introduction to) Language History and Use
Specific Language Impairment
Rachael-Anne Knight ([email protected])
4.2.2 The rational behind twin studies
If MZ twins are more similar than DZ twins this suggests that at least part of that
similarity is due to genetic rather than environmental factors. For SLI, researchers
look at whether one or both twins have SLI.
4.2.3 The Results
Studies indicate that the concordance of SLI (the proportion of pairs where both twins
are affected) is significantly higher in MZ than DZ twins.
4.2.4 Conclusions
There is a strong genetic component to SLI, however it seems that different genes
may be implicated in different people with SLI. It is not yet clear how the genetic
factors fit with other causal explanations of SLI. However, the genetic findings open
up the hope of possible drug treatment for sufferers and may also open up lines of
research concerning the evolution and species specificity of language.
Reading
Leonard, L. (1998) Children with Specific Language Impairment, Massachusetts:
MIT Press
Bishop, D. (2002) “The role of genes in the etiology of specific language
impairment”, Journal of Communication Disorders, 35, 4, 311-328
Pinker, S. (2001) “Talk of genetics and vice versa”, Nature 413, 465-566
Lai, C. Fisher, S., Hurst, J., Vargha-Khadem, F. and Monaco, A. (2001) “A forkheaddomain gene is mutated in a severe speech and language disorder”, Nature 413, 519523
Ors, M. (2002) “Time to drop “specific” in “specific language impairment”, Acta
Paediatr, 91, 1025-1026
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