Jill Boucher

Language in Autism and Specific Language Impairment: Where Are the Links?

It has been suggested that language impairment in autism is behaviorally, neurobiologically, and etiologically related to specific language impairment (SLI). In this article, the authors review evidence at each level and argue that the vast majority of data does not support the view that language impairment in autism can be explained in terms of comorbid SLI. The authors make recommendations for how this debate might be resolved and suggest a shift in research focus. They recommend that researchers concentrate on those aspects of language impairment that predominate in each disorder rather than on those comparatively small areas of potential overlap.

Memory in autistic spectrum disorder.

Behavioral evidence concerning memory in forms of high-functioning autism (HFA) and in moderately low-functioning autism (M-LFA) is reviewed and compared. Findings on M-LFA are sparse. However, it is provisionally concluded that memory profiles in HFA and M-LFA (relative to ability-matched controls) are similar but that declarative memory impairments are more extensive in M-LFA than in HFA. Specifically, both groups have diminished memory for emotion- or person-related stimuli. Regarding memory for nonsocial stimuli, both groups probably have mental-age-appropriate nondeclarative memory, and within declarative memory, both groups have mental-age-appropriate immediate free recall of within-span or supraspan lists of unrelated items, as well as cued recall and paired associate learning. By contrast, recognition is largely unimpaired in HFA but moderately impaired in M-LFA, and free recall of meaningful or structured stimuli is moderately impaired in HFA but more severely impaired in M-LFA. Theoretical explanations of data on declarative memory in HFA identify problems in the integrative processing, or the consolidation and storage, of complex stimuli or a specific problem of recollection. Proposed neural substrates include the following: disconnectivity of primary sensory and association areas; dysfunctions of medial prefrontal cortex, hippocampus, or posterior parietal lobe; or combinations of these associated with neural disconnectivity. Hypothetically, perirhinal dysfunction might explain the more extensive declarative memory impairments in M-LFA. Foreseeable consequences of uneven memory abilities in HFA and M-LFA are outlined, including possible effects on language and learning in M-LFA. Finally, priorities for future research are identified, highlighting the urgent need for research on memory in lower functioning individuals.

Putting theory of mind in its place: psychological explanations of the socio-emotional-communicative impairments in autistic spectrum disorder:

In this review, the history of the theory of mind (ToM) theory of autistic spectrum disorder (ASD) is outlined (in which ToM is indexed by success on false belief tasks), and the explanatory power and psychological causes of impaired ToM in ASD are critically discussed. It is concluded that impaired ToM by itself has only limited explanatory power, but that explorations of the psychological precursors of impaired ToM have been fruitful in increasing understanding of mindreading impairments in ASD (where ‘mindreading’ refers those abilities that underlie triadic interaction as well as ToM). It is argued that early explanations of impaired mindreading are untenable for various reasons, but that impairments of dyadic interaction in ASD that could lead to impaired ability to represent others’ mental states may be the critical psychological cause, or causes, of impaired ToM. The complexity of causal routes to impaired ToM is emphasized.

How do individuals with Williams syndrome learn a route in a real-world environment?

Individuals with Williams syndrome (WS) show a specific deficit in visuo-spatial abilities. This finding, however, derives mainly from performance on small-scale laboratory-based tasks. This study investigated large-scale route learning in individuals with WS and two matched control groups (moderate learning difficulty group [MLD], typically developing group [TD]). In a non-labelling and a labelling (verbal information provided along the route) condition, participants were guided along one of two unfamiliar 1-km routes with 20 junctions, and then retraced the route themselves (two trials). The WS participants performed less well than the other groups, but given verbal information and repeated experience they learnt nearly all of the turns along the route. The extent of improvement in route knowledge (correct turns) in WS was comparable to that of the control groups. Relational knowledge (correctly identifying spatial relationships between landmarks), compared with the TD group, remained poor for both the WS and the MLD group. Assessment of the relationship between performance on the large-scale route-learning task and that on three small-scale tasks (maze learning, perspective taking, map use) showed no relationship for the TD controls, and only a few non-specific associations in the MLD and WS groups.

Assessing recollection and familiarity in autistic spectrum disorders: methods and findings.

We hypothesise that of the two processes underlying declarative memory, recollection is impaired in high-functioning autism (HFA) whereas recollection and familiarity are impaired in low-functioning autism (LFA). Testing these hypotheses necessitates assessing recollection and familiarity separately. However, this is difficult, because both processes contribute to performance on standard memory tests. Moreover, tests must be suitable for use with young or intellectually disabled participants. This study aimed to develop tests of recollection and familiarity separately, and to make preliminary tests of our hypotheses. We developed a temporal source memory task to assess recollection in LFA, and a shape recognition task to assess familiarity and an action recall task assessing recollection in HFA. The methods and implications of the results are discussed.

Time-based and event-based prospective memory in autism spectrum disorder: The roles of executive function and theory of mind, and time estimation

Prospective memory (remembering to carry out an action in the future) has been studied relatively little in ASD. We explored time-based (carry out an action at a pre-specified time) and event-based (carry out an action upon the occurrence of a pre-specified event) prospective memory, as well as possible cognitive correlates, among 21 intellectually high-functioning children with ASD, and 21 age- and IQ-matched neurotypical comparison children. We found impaired time-based, but undiminished event-based, prospective memory among children with ASD. In the ASD group, time-based prospective memory performance was associated significantly with diminished theory of mind, but not with diminished cognitive flexibility. There was no evidence that time-estimation ability contributed to time-based prospective memory impairment in ASD.

Memory in ASD: have we been barking up the wrong tree?:

In this theoretical note, possible neural causes of episodic memory impairment in individuals with ASD and currently normal intellectual and linguistic function are considered. The neural causes most commonly argued for are hippocampal or prefrontal cortex dysfunction, associated with impaired neural connectivity. It is argued here that a hippocampal dysfunction hypothesis is weakened by differences in cued recall and paired associate learning in individuals with ASD compared with individuals with developmental or acquired hippocampus-related amnesia, and that recent findings on patients with posterior parietal lesions (PPC) offer a better fit with the dissociation between free and cued recall observed in ASD. The PPC forms part of the default system subserving mindreading, among other functions, and an association between PPC dysfunction and memory impairment in ASD is consistent with recent suggestions that neural disconnectivity within the default system underlies behaviours diagnostic of ASD.

A quantitative measure of JS’s memory

JS is a highly able, well-educated 37 year old man with Asperger syndrome. A recent qualitative paper (Boucher, 2007) described his self-report of verbal and visual memory difficulties. The present paper used the WMS-III to compare the memory profile of JS to that of the adults with HFA in the Williams et al. (2005) WMS-III paper. Results show that JS’s self-report of his memory difficulties can by and large be supported, that JS’s memory performance is at the lower end of the group examined in the Williams et al. (2005) paper, and that, unlike the group profile in Williams et al. (2005), JS shows reduced performance on both verbal and visual measures of memory. A qualitative analysis of JS’s performance raises the possibility that JS is using language to retain details he can generalize over, as a compensatory strategy for some reductions in episodic memory.

Memory, learning and language in autism spectrum disorder:

Background and aims The ‘dual-systems’ model of language acquisition has been used by Ullman et al. to explain patterns of strength and weakness in the language of higher-functioning people with autism spectrum disorder. Specifically, intact declarative/explicit learning is argued to compensate for a deficit in non-declarative/implicit procedural learning, constituting an example of the so-called see-saw effect. Ullman and Pullman extended their argument concerning a see-saw effect on language in autism spectrum disorder to cover other perceived anomalies of behaviour, including impaired acquisition of social skills. The aim of this paper is to present a critique of Ullman et al.’s claims and to propose an alternative model of links between memory systems and language in autism spectrum disorder. Main contribution We argue that a four-system model of learning, in which intact semantic and procedural memory are used to compensate for weaknesses in episodic memory and perceptual learning, can better explain patterns of language ability across the autistic spectrum. We also argue that attempts to generalise the ‘impaired implicit learning/spared declarative learning’ theory to other behaviours in autism spectrum disorder are unsustainable. Conclusions Clinically significant language impairments in autism spectrum disorder are under-researched, despite their impact on everyday functioning and quality of life. The relative paucity of research findings in this area lays it open to speculative interpretation which may be misleading. Implications More research is needed into links between memory/learning systems and language impairments across the spectrum. Improved understanding should inform therapeutic intervention and contribute to investigation of the causes of language impairment in autism spectrum disorder with potential implications for prevention.