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Motion perception and autistic spectrum disorder

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Motion perception and autistic spectrum disorder: A review.

Elizabeth Milne CA

Department of Psychology, University of Sheffield

Western Bank, SHEFFIELD, S10 2TP, UK.

+44 (0) 114 2226558, Fax: + 44 (0) 114 2766515

[email protected]

John Swettenham & Ruth Campbell

Department of Human Communication Science, University College London

Chandler House, 2 Wakefield Street, LONDON, WC1N 1PF, UK.

[email protected] [email protected]

This is a reprint of an article printed in the February – April issue (2005) of Cahiers

de Psychologie Cognitive / Current Psychology of Cognition, volume 23 (1 – 2), pp 3

– 33.


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Abstract

Recent evidence has indicated that some children with autistic spectrum disorder

(ASD) show reduced ability to detect visual motion. The data suggest that this

impairment is present in children with a range of autistic spectrum diagnoses, but not

present in all children diagnosed with ASD. The occurrence of abnormal motion

perception in children with ASD has led to speculation regarding the root of this

impairment. Hypotheses regarding reduced sensitivity of the visual magnocellular

system / cortical dorsal stream (Milne et al., 2002; Spencer et al., 2000) and reduced

neuronal integration (Bertone et al., 2003), will be discussed in this review. Clinical

implications of the impairment, such as the degree to which motion perception may be

related to diagnostic criteria and /or symptom severity in ASD, and the relationship

between abnormal motion perception in autistic spectrum, and other, non-autistic

spectrum developmental disorders will also be discussed. The conclusion is drawn

that more research should be carried out including larger samples of participants, and

that in future studies researchers should provide details of the variability of

performance in their data, and investigate relationships between motion perception,

diagnostic criteria, symptom severity and other potential correlates which, it is hoped

will lead to further understanding of the implications of abnormal motion perception

in ASD.

Key words

Autistic spectrum disorder, motion perception, visual system, developmental

disorders.


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Autistic spectrum disorder (ASD) is a family of pervasive developmental

disorders, usually diagnosed in childhood. Within the autistic spectrum are autistic

disorder, diagnosed on the basis of impairments in social interaction, communication,

and repetitive, stereotyped patterns of behaviour (American Psychiatric Association,

1994); Asperger’s disorder, which is popularly characterised as a less severe form of

autistic disorder but in actuality is diagnosed on the basis of impairment of social

interaction, accompanied by repetitive, stereotyped behaviour, but without a

significant impairment in communication (American Psychiatric Association, 1994);

and pervasive developmental disorder not otherwise specified (PPD-NOS), which is

diagnosed on the basis of impairment in social interaction or communication skills, or

when stereotyped behaviours are present, but the full criteria for a specific pervasive

developmental disorder are not met. This category includes atypical autism which is

diagnosed when presentations do not meet the criteria for autistic disorder because of

late age of onset, atypical symptomatology, subthreshold symptomatology, or all of

these (American Psychiatric Association, 1994). ASD affects over 500,000 families

in the UK (National Autistic Society, 2004). A recent meta-analysis of 19 international

epidemiological surveys carried out since 1987 has indicated that the prevalence of

autistic disorder is 10 cases in every 10,000 (Fombonne, 2003). In the same study, the

prevalence of Asperger’s disorder and PDDNOS was estimated to be 2.5/10,000 and

15/10,000 respectively, giving a current estimate of the occurrence of ASD as

27.5/10,000. The origins of ASD are currently unknown, although evidence points to

a genetic link, which at some time during early development impacts on subsequent

brain development (for a review of genetic research on ASD see Muhle, Trentacoste,

& Rapin, 2004). In addition to the impairments of social interaction, communication

and repetitive behaviour, other symptoms are often present, such as abnormal

responses to sensory stimuli, hyper-sensitivity to sound or touch, and disturbances in

visual perception (Talay-Ongan & Wood, 2000; O'Neill & Jones, 1997; Rogers,

Hepburn, & Wehner, 2003). In particular, recent research suggests that the ability to

detect moving stimuli is abnormal in some individuals with ASD (Bertone, Mottron,

Jelenic, & Faubert, 2003; Blake, Turner, Smoski, Pozdol, & Stone, 2003; Gepner &

Mestre, 2002; Gepner, Mestre, Masson, & De-Schonen, 1995; Milne et al., 2002;

Milne et al., in press; Spencer et al., 2000). The aim of this paper is to review the

literature which has investigated motion perception in individuals with ASD and to


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discuss the implications arising from this research. The implications will be

considered from two angles;

1) What, if anything, can a motion perception impairment in ASD currently tell

us about the neuronal architecture of ASD?

2) What are the clinical implications of a motion perception impairment in ASD?

For example, how might motion perception impairment impact on other

perceptual / cognitive abilities? And what is the relationship between

abnormal motion perception in ASD and the impaired ability to detect

coherent motion which has been reported in other non autism spectrum

developmental disorders?

Finally, a summary of outstanding questions will be presented, and new areas of

research will be highlighted which may lead to further understanding of the neural

correlates of autistic spectrum and other developmental disorders.

Evidence of abnormal motion perception in individuals with ASD

Postural stability in response to optic flow

The first published study which suggested that children with autistic disorder

may perceive motion in a different way to typically developing children reported that

when standing on a force platform and presented with optic flow, children with

autistic disorder were less posturally reactive to visual motion than typically

developing controls (Gepner et al., 1995). The results of this study were extended in

2002, by additional data which demonstrated that in a different sample of participants,

three children with autistic disorder and developmental delay (mean age of 9 years, 5

months) showed less postural reactivity to visual motion than both a typically

developing control group (mean age 8 years, 2 months) and a group of three children

with Asperger’s syndrome and normal IQ (mean age 7 years and 5 months), who in

fact showed increased postural activity compared to the control group (Gepner &

Mestre, 2002). It remains to be seen whether postural hypo-reactivity in children with

autistic disorder arises as a result of reduced sensitivity to dynamic stimuli, abnormal

postural control, or both.

Sensitivity to coherent motion

Coherent motion is a global motion signal that is apparent from the integration

of locally moving elements. Sensitivity to coherent motion can be measured by


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manipulating the number of coherently moving local signals within an array of

dynamic noise presented in a random dot kinematogram, as shown in figure 1.

A high proportion of coherent elements renders global coherent motion easier to

detect than a lower proportion. Coherent motion sensitivity can thus be determined by

a threshold for detection of coherent motion, a low threshold (low proportion of

coherently moving dots needed to detect coherent motion) reflects good sensitivity

whereas a high threshold (high proportion of moving dots needed to detect coherent

motion) reflects poor sensitivity.

Insert figure 1 about here please

Two research groups have reported significantly increased motion coherence

thresholds in children with autistic disorder as compared to controls (Milne et al.,

2002; Spencer et al., 2000), suggesting reduced sensitivity to coherent motion in

children with autistic disorder. Spencer et al. (2002) found elevated motion coherence

thresholds in children with autistic disorder (verbal age range from 7 -11 years)

compared with those of verbal-age matched typically developing children, whereas

Milne et al. (2002) found elevated thresholds in children with autistic disorder and

normal intelligence (mean age 11 years, 8 months) as compared to typically

developing children matched for chronological age and non-verbal ability (mean age

11 years and 7 months). Spencer et al. (2000) further demonstrated that the

participants with autistic disorder in their sample were not impaired at detecting

coherent form in a control task (see figure 2) which was similar in application to the

coherent motion detection task but which recruited a visual sub-system that is unlikely

to be involved in the detection of coherent motion. That is, reduced sensitivity to

coherent motion in children with autistic disorder did not occur as a result of a general

visual impairment or other task factors such as a lack of task attention or motivation.

Additionally, because the form control task also involves integrating local elements

(static lines) into a global percept (of a circle), it is unlikely that the high motion

coherence thresholds shown by the individuals with autistic disorder were due to a

failure to integrate local elements into a global percept, as may be suggested by a

model which attempts to explain the data in terms of the reduced integration of

perceptual information, or “weak central coherence” (cf Frith, 2003).


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Sensitivity to biological motion

Biological motion is the term used to characterise any perceived animate

movement, such as gait (posture and movements of walking), sitting, cycling,

jumping etc. The human visual system is extremely sensitive to biological motion.

This is shown by the fact that even when visual information is reduced to a point-light

display, tracking movement at the joints of limbs (see figure 3), people can reliably

identify and discriminate complex stimulus sequences (Johansson, 1973), as well as

subtle social information such as the gender and emotional state of the actor (Cutting

& Kozlowski, 1977).

Insert figure three about here please

Infants of 3 months can distinguish between biological and non-biological

motion portrayed in point-light displays (Fox & McDaniel, 1982), and children as

young as 3 years can reliably recognise different types of biological motion, such as

human and non human (animal) forms (Pavlova, Krageloh-Mann, Sokolov, &

Birbaumer, 2001). To date, there have been two published studies investigating the

perception of biological motion in autistic disorder (Blake et al., 2003; Moore,

Hobson, & Lee, 1997). Moore et al. (1997) presented children with autistic disorder

and below average ability (as measured by the British Picture Vocabulary Scale, mean

chronological age of the sample 14 years, 10 months) and non-autistic learning

disabled children (mean chronological age 14 years, 2 months) with brief video

sequences of point-light displays depicting a human actor walking across the screen,

or the movement of an object such as a chair being rotated or a ball bouncing. The

participants were asked to identify the stimulus by answering the question “What are

the dots stuck to?” The dependent variable reported was the length of time needed to

view the stimulus before correctly identifying the person depicted in the point light

display. The results indicated that while there was a trend towards poorer

performance among children with autistic disorder compared to the non-autistic

controls when the images were presented at short (<1000 msec) exposure duration

and with only 5 point lights in the display, overall the children with autistic disorder

were not impaired at detecting the person from the array of moving point-lights.


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Additionally with a 10 light display, both the children with and without autistic

disorder recognised the person at a similar time duration to that of normal adults –

approximately 200 msec (Johansson, 1973). However, Blake et al. (2003) have

reported that children with autistic disorder are less able than typically developing

children to detect biological motion from point light displays. Blake et al. also tested

children with autistic disorder and developmental delay (aged between 8 and 10

years) – and a group of typically developing children who were chronologically

younger (aged between 5 and 10 years), but matched in terms of mental age. This

study differed from Moore et al.’s study as the participants were not required to

identify the object depicted in point lights, but to simply detect whether a point-light

stimulus showed a person or not (i.e. a two alternative forced-choice). 50% of the

stimuli depicted a human actor engaged in activity such as running, kicking, climbing,

throwing or jumping, whereas the remaining half of the stimuli were phase-scrambled

sequences containing the same amount of absolute motion as the target stimuli but

without producing a recognisable percept. Under these conditions children with

autistic disorder had significantly lower d’ scores than the typically developing group,

indicating reduced sensitivity to biological motion in the children with autistic

disorder. Again, in line with Spencer et al. (2000), despite having reduced sensitivity

to biological motion, the children with autistic disorder showed no differences

compared to controls in their ability to accurately detect coherent form in a control

task. One caveat about this study should be noted however; the children with autistic

disorder in the sample were developmentally delayed and were matched to a group of

typically developing younger children. Therefore it could be possible that the children

with autistic disorder showed less sensitivity to biological motion because of general

developmental delay rather than being specifically related to autism.

Sensitivity to second order motion

As Mather & Murdoch have described; “First order stimuli contain stable and

coherent spatio-temporal energy corresponding to the velocity of motion. Second-

order stimuli do not contain coherent energy but, instead, motion information is

conveyed by contours with dynamically changing and/or incoherent Fourier energy

(texture borders, for instance)” (Mather & Murdoch, 1997 p 605). Thus, first-order

refers to motion which is perceived on the basis of luminance change over time, and

second-order refers to motion which is perceived on the basis of changes in


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characteristics other than luminance (such as contrast) over time (Clifford & Vaina,

1999). In order to investigate the perception of first- and second- order motion in

autism, Bertone et al. (2003) devised a task in which the perception of motion in

radiating, rotating and translating patterns was mediated by either first- or second-

order motion cues (luminance and contrast respectively). A schematic illustration of

these stimuli is presented in figure 4.


Bertone et al. found that the participants with autistic disorder and normal IQ

(mean chronological age 12.18 years) showed no deficit in their ability to detect the

direction of motion from these patterns when the stimuli were mediated by first order

characteristics (luminance), but when motion was defined by second order

characteristics (contrast), participants with autistic disorder were significantly

impaired compared to a chronological age matched control group (mean

chronological age 13.13 years). Bertone et al. suggested that individuals with autism

do not show abnormal perception of motion per se, but that the reported reduction in

their ability to detect motion could be related to the complexity of the stimulus. They

further suggested that the results of their study may reflect an impairment of

integrating complex stimuli in autism. They point out that to discriminate global

motion patterns, such as coherent motion, the visual system must first integrate local

motion signals, therefore reduced performance on these tasks could be explained by a

deficit of integrating complex information at a perceptual level.

Summary

Considering all the data regarding motion perception in ASD, it appears that

some children with autistic spectrum diagnoses are less able to detect motion stimuli

than matched controls. What, if anything, does this suggest about the neuronal

architecture of ASD? This issue will be considered below. However, in order to

consider the implications of reduced sensitivity to motion in ASD, it is necessary to

briefly review the anatomical architecture which underlies intact motion perception.

The functional anatomy of motion perception in the human visual system.


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The human visual system has been broadly defined as consisting of two

parallel but interconnected streams of cortical areas; the dorsal and the ventral stream

(Ungerleider & Mishkin, 1982). It is thought that motion perception is governed by

structures of the dorsal stream, whereas the ventral stream is specialised for form and

colour perception. Specialisation for motion perception occurs very early in the visual

system, as specific retinal neurons (known as α cells and β cells) channel information

into two parallel pathways; the magnocellular and parvocellular pathways which are

thought to be specialised for motion and form perception respectively. The axons

from retinal α and β cells form separate streams within the optic nerve and innervate

different layers of the lateral geniculate nucleus (LGN). The LGN consists of 6-layers,

layers 1 and 2 receive input from only α ganglion cells and layers 3 – 6 receive input

from the β ganglion cells. Layers 1 and 2 contain large cell bodies, known as

magnocells, whereas layers 3 – 6 contain smaller, parvo, cells. The magnocellular and

parvocellular pathways are separated not only anatomically, but also functionally.

Magnocellular neurons respond preferentially to low-spatial and high-temporal

frequency stimuli, e.g. motion and flicker, whereas parvocellular neurons respond

preferentially to high-spatial and low-temporal frequency stimuli, e.g. static stimuli

(Derrington & Lennie, 1984). Cortical motion perception is therefore thought to be

dominated by inputs from the magnocellular pathway. This has been demonstrated

experimentally by studies which selectively lesion either the magnocellular or

parvocellular layers of the monkey LGN; lesioning the magnocellular layers leaves

the monkey motion blind, whereas lesioning the parvocellular layers leaves motion

perception intact (Schiller, Logothetis, & Charles, 1990).

To some extent the segregation of magnocellular and parvocellular channels is

preserved into the cortex, with axons from the two streams innervating different

layers of cortical area V1 (Nealy & Maunsell, 1994), however, via the blobs and

interblobs of V1 and the thick and thin stripes of V2 (Wong-Riley et al., 1993),

neuronal intermixing occurs, and the ventral stream receives input from both the

magnocellular and parvocellular layers of the LGN, whereas the dorsal stream

receives input mainly from the magnocellular layers (Nealy & Maunsell, 1994). The

ventral stream includes area V1, extra-striate areas V2, V4, and areas of the infero-

temporal cortex, the dorsal stream includes area V1, extra-striate areasV2, V5 (or

medial temporal area MT), and areas of the posterior parietal cortex (Milner &

Goodale, 1995). Functional imaging has shown that several cortical areas, mainly


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defined as forming part of the dorsal stream, are active during the presentation of

moving stimuli. V1 is activated by many classes of moving stimuli, including flicker

and dynamic noise, suggesting that this area responds to general spatiotemporal

luminance modulations (Smith, Greenlee, Singh, Kraemer, & Hennig, 1998). Area

V5, which lies at the juncture of the temporal, parietal and occipital lobes (Sunaert,

Van Hecke, Marchal, & Orban, 1999) is perhaps the most well defined area in terms

of motion perception. Converging data from single cell recording (Britten, Shalden,

Newsome, & Movshon, 1992), lesion studies (Newsome & Pare, 1988, Zihl, Von

Cramon, Mai, & Schmid, 1983) and fMRI (Zeki et al., 1991) all report an essential

role of area V5 in motion perception. Specifically, cells in area V5 are particularly

sensitive to coherent motion. This has been demonstrated by monkey single cell

recording (Britten et al., 1992) and human fMRI, which has also elucidated other

areas, such as area V3, V3a and discrete foci in the intraparietal sulcus which are also

activated by coherent motion (Braddick et al., 2001).

A double dissociation of motion impaired patients suggests that perception of

first- and second- order motion may also be cortically segregated. A patient with a

brain lesion close to the surface of the occipital lobe, probably encompassing areas V2

and V3, has been reported to show a selective impairment of first-order motion

perception (Vaina, Makris, Kennedy, & Cowey, 1998), whereas a patient with a

cortical lesion close to area MT appears to have a selective impairment of second-

order motion perception (Vaina & Cowey, 1996).

Biological motion also appears to activate discrete cortical areas, notably the

superior temporal sulcus (STS), quite distinct from those activated by coherent motion

or specific first or second order motion signals (Battelli, Cavanagh, & Thornton,

2003). Functional imaging has revealed increased activation in the STS region during

perception of hand action, mouth movement, lip-reading, body movement and eye

gaze (Calvert, Campbell, & Brammer, 2000; Puce, Allison, Bentin, Gore, &

McCarthy, 1998.Grezes et al., 2001; Howard et al., 1996, for a review see Puce and

Perrett 2003). Cells in the STS region of the monkey cortex have been found which

are responsive to the sight of a hand purposefully manipulating an object, but are

unresponsive to the sight of tools manipulating the same object (Jellema, Baker,

Wicker, & Perrett, 2000). Similarly, Oram and Perrett have reported cells in the upper

bank of the monkey STS which fire in response to moving hands and faces but not to

movement elicited by inanimate objects (Oram & Perrett, 1994). In humans, areas of


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the STS, particularly the posterior STS (Bonda, Petrides, Ostry, & Evans, 1996;

Grossman et al., 2000) and the superior temporal polysensory area (STP) (Vaina &

Gross, 2004) are particularly sensitive to point-light displays of biological motion,

therefore this area is thought to be important both in the extraction of form from

motion, and may also be implicated in the detection and recognition of the behaviour

of others (Puce & Perrett, 2003). Recent data using the technique of

magnetoencephalography (MEG) suggests changes in neuromagnetic gamma activity

correlate with ability to extract structure from motion, and coincide with task-related

cortical activity as measured by fMRI (Singh, Barnes, Hillebrand, Forde, & Williams,

2002). By measuring oscillatory gamma brain activity using MEG, Pavlova et al. have

demonstrated that the brain can dissociate coherent structure conveyed by biological

motion as early as 100 ms after stimulus onset. By 130 ms, activity over the parietal

lobes indicates that the brain can distinguish between a regular point light walker and

a scrambled one, suggesting that the detection of biological motion is achieved at

relatively early stages of cortical processing (Pavlova, Lutzenberger, Sokolov, &

Birbaumer, 2004).

What is the aetiology of impaired motion perception in ASD?

Findings of reduced sensitivity to motion in individuals with ASD have led to

differing suggestions as to the possible aetiology of this impairment. At present, no

firm conclusions can be drawn. However two main suggestions run through the

literature. Some researchers have suggested that impaired motion perception in ASD

could arise from an abnormality in the particular area of the visual system implicated

in visual motion perception, namely the (sub-cortical) magnocellular system or the

(cortical) dorsal stream (Milne et al., 2002; Spencer et al., 2000). Other researchers

(Bertone et al., 2003), reporting that individuals with ASD have reduced sensitivity to

second- but not first-order motion, have suggested that the structural architecture

which underpins motion perception is intact and that impaired motion perception may

indicate reduced ability to integrate complex perceptual information. However, as yet

there is no direct evidence to support either one of these positions. Structural

abnormalities of dorsal stream structures are not usually identified in MRI studies of

ASD, although until recently, researchers have not directly investigated these cortical

areas as the majority of ASD MRI studies have focussed on the cerebellum and / or

the hippocampus / amygdala / limbic structures (Brambilla et al., 2003). However,


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neuromagnetic data demonstrated that a group of 4 adults with Asperger’s syndrome

and 1 adult with autistic disorder, showed the same degree of oscillatory brain activity

in the primary motor cortex when viewing human action (Avikainen, Kulomäki, &

Hari, 1999). A functional MRI study of different types of motion perception in

individuals with ASD would help to clarify whether abnormalities in specific areas of

the dorsal stream underlie reduced motion perception in ASD. Similarly, the

magnocellular system has not been investigated directly in ASD. Within the literature

it is unclear to what extent high motion coherence thresholds implicate impairments

of the magnocellular system. Some researchers, drawing from psychophsyiological

evidence that lesions of the magnocellular pathway in monkeys impair coherent

motion detection (Schiller et al., 1990) claim that coherent motion detection

represents a reliable, albeit putative, indicator of the magnocellular pathway

(Cornelissen, Hansen, Hutton, Evangelinou, & Stein, 1998; Milne et al., 2002; Talcott

et al., 1998), whereas others, drawing on further psychophsyiological evidence that

direction discrimination can be retained even after magnocellular lesions (Merigan,

Byrne, & Maunsell, 1991), suggest that coherent motion detection is not a reliable

indication of magnocellular integrity (Skottun, 2000). Further psychophysical tests,

which provide a more direct indication of the integrity of the magnocellular /

parvocellular systems need to be carried out to establish whether high motion

coherence thresholds in children with ASD represent magnocellular impairment. For

example, contrast sensitivity of static and flickering gratings of low and high spatial

frequencies can provide a clearer separation of the sensitivity of the magnocellular

and parvocellular systems, and EEG investigation of visual evoked potentials elicited

by moving / static / coloured stimuli (see Neville & Bavelier, 2000, cf Boeschoten,

Kemner, Kenemans, & van Engeland, 2004) can provide direct data on both the

latency and amplitude of brain responses generated by the specific processing

streams. In addition future post-mortem and histological studies which directly

measure magno- and parvo-cell density in the LGN will be essential if this claim is to

be supported.

As described above, Bertone et al. (2003) have shown that participants with

ASD are just as sensitive to simple first order motion stimuli as matched controls, but

significantly less sensitive than controls to second-order motion stimuli. However,

other studies have shown that when a more complex first-order stimulus is presented

(e.g. a random dot kinematogram), participants with ASD are less able to detect


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coherent motion than controls (Milne et al., 2002; Spencer et al., 2000). To examine

this point it is necessary to clarify exactly what is meant by the terms first- and

second- order motion. As we have stated earlier, first-order motion refers to motion

defined by changes in luminance, and second order motion refers to motion defined

by changes other than luminance. Less straightforward however, is the distinction

between first- and second- order motion detectors, and it remains to be seen whether

the visual system employs separate, independent populations of neurons for the

perception of first- and second- order motion, or whether a single system resolves

both classes of motion. To clearly understand the implications of sensitivity to first-

and second- order motion in individuals with ASD, it is important to bear in mind the

distinction between the physical properties of first- and second- order motion stimuli,

and the psychophysical properties of the motion detectors (see Mather & Murdoch,

1997). The perception of coherent motion from a random dot kinematogram of the

type used by Milne et al., 2002 and Spencer et al., 2000 investigates the global

processing of first order motion. In order to detect coherent motion within this

stimulus participants must integrate the local, first order signals to derive a global

directional signal, i.e. the stimulus is a first-order stimulus (motion within the

stimulus is generated purely by changes of luminance over time), but the operation of

perceiving coherent motion requires additional processing of these first order signals.

This explanation illustrates that the question of abnormal motion perception in

individuals with ASD cannot be reduced simply to a division between the physical

characteristics of first and second order motion stimuli, but that, as Bertone et al.

(2003) suggested, abnormality may occur at the stage at which local motion signals

are integrated. However, contrary to Bertone et al.’s suggestion that impaired

detection of complex motion in ASD can be explained by a “decreased capacity to

integrate complex perceptual information rather than a specific inability to efficiently

process motion information as such” (Bertone et al., 2003 pg 4), the finding that

individuals with autistic disorder who are impaired at detecting coherent and

biological motion show no equivalent impairment in detecting coherent form (Blake

et al., 2003; Spencer et al., 2000) suggests that impairments in the ability to integrate

perceptual information occur in the perception of motion, but not in integrating all

perceptual information.

Clearly individuals with ASD are not motion blind, neither their behaviour not

any test suggests this, what is apparent in the data however is that individuals with


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ASD (or at least, some individuals with ASD as will be discussed below) have

reduced sensitivity to visual motion. Using random dot kinematograms establishes a

threshold for coherent motion detection; every participant is tested until they reach the

level at which they can no longer detect the coherent signal, that is, they are tested to

the limits of their perception. Results arising from these studies show, not that the

participants with ASD cannot perceive motion (either in the noise dots or even the

coherent motion signal), but that some participants with ASD require a denser

coherent signal in order to be able to detect coherent motion. This becomes apparent

only by presenting trials until each participant can no longer perceive the coherent

signal. Similarly, in Bertone et al.’s (2003) data, both the participants with ASD and

the controls were much more sensitive to first- than second-order motion (with log

motion sensitivity dropping from approximately 2.5 in both groups for first order

motion to less than 1 in both groups for second-order motion), indicating that

detection of second order motion in this paradigm is a more difficult task. Task

difficulty could therefore predict whether or not individuals with ASD have impaired

motion perception compared with controls, with only relatively complex tasks being

sensitive enough to measure such an impairment.

When searching for a cause of impaired motion perception in ASD, it is

important to note that reduced sensitivity to certain types of motion stimuli does not

necessarily predict reduced sensitivity to other types of motion stimuli. There may be

systems specialised for perceiving different motion stimuli. For example, case studies

in the literature discuss brain-damaged patients who are impaired at detecting

coherent motion but show no deficit in detecting biological motion (Vaina, LeMay,

Bienfang, Choi, & Nakayama, 1990), and conversely, from patients who are impaired

at detecting biological motion but have no deficit in detecting coherent motion

(Schenk & Zihl, 1997). In addition, as highlighted above, different cortical areas

appear, from fMRI data, to be specialised for the perception of different motion

classes, suggesting that motion perception is not a unitary phenomenon. However, it

is worth noting that whilst there is strong evidence for a dissociation between

performance on motion coherence perception tasks and biological motion perception

tasks in normal (Grossman & Blake, 1999) and brain damaged adults (Battelli et al.,

2003; Viana, Lemay, Bienfang, Choi, & Nakayama, 1990), this does not necessarily

imply that there is no developmental relationship between the two (Bishop, 1997;

Karmiloff-Smith, 1998). Data from adult neuropsychological studies don’t take into


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account the notion that perceptual ability can develop with experience, which could

be akin to specialisation of that ability. It appears that learning, and environmental

factors may affect the developmental trajectory of motion perception. For example,

participants can be trained to discriminate biological motion embedded in dense noise

dots from scrambled motion as (Grossman, Blake, & Kim, 2004), and both

behavioural and neurophysiological studies indicate that sensitivity to visual

movement in the peripheral visual field is greater in deaf than in hearing people, and

may be modified by early exposure to a signed language (Bavelier et al., 2001;

Neville & Lawson, 1987). It has also been shown that individuals with autistic

disorder and learning difficulties can improve their ability to recognise form-from-

motion with training (Carlin, Hobbs, Bud, & Soraci, 1999). It would be interesting to

know whether the visual environment experienced by children with autism influences

the development of motion perception.

Theoretical implications of impaired motion perception in ASD.

Each of the theories highlighted above could lead to further testable

hypotheses about visual perception in ASD. For example it has been hypothesised that

if an impairment of the magnocellular system gives rise to reduced motion perception

in autism, then other perceptual functions which are heavily supported by this system

may also be abnormal in ASD (Milne, 2004). As reviewed above, the magnocellular

system is functionally specialised for the perception of moving and flickering stimuli,

and is thought to transmit lower spatial frequencies to the cortex than the

parvocellular system (Livingstone & Hubel, 1988). A recent report has indicated that

children with autism rely more on high spatial frequency cues when processing faces,

in contrast to typically developing children who rely more on low spatial frequency

cues (Deruelle, Rondan, Gepner, & Tardif, 2004). This finding supports the

suggestion that low spatial frequency information processing may be abnormal in

individuals with ASD. Additionally, recent work has investigated visual evoked

potentials in response to high and low spatial frequency gratings in autism. The results

suggest that both high and low spatial frequencies are analysed differently in children

with autism than controls (Boeschoten et al., 2004). It has been suggested in the

psychophysical literature that low spatial frequencies mediate the perceptual global

bias which is seen in hierarchical stimuli such as Navon-type figures (Badcock,

Whitworth, Badcock, & Lovegrove, 1990; Hughes, Nozawa, & Kitterle, 1996;


16

LaGasse, 1993 cf Navon, 1977). Children with ASD have been reported to show

abnormal perception of hierarchical figures (Mottron & Belleville, 1993; Plaisted,

Swettenham, & Rees, 1999; Rinehart, Bradshaw, Moss, Brereton, & Tonge, 2000),

and the degree of global or local bias exhibited in this task is related to motion

coherent threshold such that those children with a local bias had high motion

coherence thresholds (reduced motion sensitivity), whereas those with a global bias

had normal motion coherence thresholds (Milne, Swettenham, Campbell, & Coleman,

2004). This suggests that, if coherent motion detection acts as a reliable indicator of

magnocellular integrity, which, as has been discussed above, it still open for

discussion, then abnormal magnocellular processing may impact on the so-called

unusual cognitive style of reduced global bias / enhanced local bias (cf Mottron,

Burack, Iarocci, Belleville, & Enns, 2003; O'Riordan & Plaisted, 2001) which has

been reported in ASD.

Clearly the implications of impaired motion perception are only just beginning

to be discussed, and the above summary represents a tentative hypothesis. However, it

is presented as an example of new hypotheses which may help to explain cognitive

phenomena of autism based in low-level perceptual aspects of the disorder as opposed

to less clearly defined higher-level models.

Clinical implications of motion perception impairment in ASD.

In addition to investigating what abnormal motion perception may suggest

about the neuronal architecture of ASD, it is important to consider the clinical

implications of abnormal motion perception in ASD. For example, it is important to

ascertain whether abnormal motion perception occurs in all diagnoses within the

autism spectrum. As can be seen from the review of the literature above, the majority

of studies which have investigated motion perception in ASD have recruited children

who have been diagnosed with autistic disorder and who have varying degrees of

developmental delay. Few studies have investigated motion perception in children

diagnosed with other disorders on the autistic spectrum. An exception is Gepner et al.

(2002) who reported that children diagnosed with autistic disorder showed postural

hypo-responsivity in response to visual motion, whereas children diagnosed with

Asperger’s syndrome showed visual hyper-responsivity. This suggests that the exact

nature of autistic spectrum disorder may predict sensitivity to visual motion. However

a recent account of coherent motion detection in children diagnosed with disorders


17

that encompass the range of ASDs, has found increased motion thresholds in children

diagnosed with autistic disorder, Asperger’s syndrome and PDDNOS (Milne et al. in

press), suggesting, contrary to Gepner et al (2002) that abnormalities in motion

perception do not occur only in autistic disorder. Blake et al. (2003) reported a

significant relationship between sensitivity to biological motion and severity of autism

as measured by the Autism Diagnostic Observation Schedule, (ADOS, Lord et al.,

2000) and the Childhood Autism Rating Scale, (CARS, Schopler, Reichler, &

Renner, 1988). However, the total number of children in this sample was only 12,

which is a small number for drawing conclusions from correlation data.

It has been reported that individuals with non-specific mental retardation show

impairments in the perception of some types of biological motion (depictions of

throwing rather than depictions of walking) (Sparrow, Shinkfield, Day, & Zerman,

1999), and in the detection of motion defined form (Fox & Oross, 1990). It could be

suggested therefore that learning difficulties associated with ASD may contribute to

poor performance on motion perception tasks. The data appear to contradict this claim

however, as high functioning participants with ASD and without developmental delay

have been reported to show motion impairments when compared to matched controls

(Milne et al. 2002, Bertone et al. 2003). In addition, Milne et al. (in press) did not find

a relationship between coherent motion detection and non-verbal IQ in individuals

with ASD.

Does abnormal motion perception have a causal role in autistic spectrum

disorder? This seems unlikely as not all participants with ASD have impairments in

detecting motion. Milne et al., (2002) highlighted the fact that not all children with

autistic spectrum disorder in their sample showed elevated motion coherence

thresholds, despite an overall mean difference between the groups, and a subsequent

study has reported abnormally high thresholds in only 22% of the ASD group (Milne

et al., in press). Again, the children who showed the largest impairment in detecting

coherent motion had diagnoses which spanned the autistic spectrum and were

unremarkable in terms of non-verbal IQ or chronological age, however no information

regarding symptomatology was available for these children. The reason why some

children with ASD and not others, show elevated motion coherence thresholds

compared to typically developing controls remains to be seen, however, it is

interesting to note that elevated motion coherence thresholds have been recorded in


18

individuals with other (non-autistic spectrum) developmental disorders. These data

are reviewed below.

Motion perception impairments in other developmental disorders.

Reduced sensitivity to motion stimuli, at least to coherent motion, has been

reported in other developmental disorders, including dyslexia (Hansen, Stein, Orde,

Winter, & Talcott, 2001; Talcott et al., 1998), William’s syndrome (Atkinson et al.,

1997), and Fragile X syndrome (Kogan et al., 2004). The genetic bases of dyslexia are

still contentious, but both Williams’ and Fragile X syndromes are known to arise as a

result of either a genetic deletion or mutation. Williams’ syndrome results from a

deletion on chromosome 7q11.23, and is characterised by moderate mental retardation

and impaired spatial cognition. Fragile X syndrome arises from a mutation of the

FMR1 gene, leading to a lack of fragile X mental retardation protein (FMRP), and is

characterised by intellectual disability, attention deficit disorders, autistic behaviours

(such as hand-flapping, poor eye contact) and an aversion to touch and noise. Despite

the diverse range of symptoms across the four developmental disorders (ASD,

dyslexia, William’s syndrome and Fragile X syndrome), it is interesting to note that

reduced sensitivity to coherent motion has been documented in all of them. Given that

reduced sensitivity to coherent motion has frequently been interpreted as indicating

abnormalities of the magnocellular system (Cornelissen et al., 1998; Demb, Boynton,

Best, & Heeger, 1998; Hansen et al., 2001; Talcott et al., 1998, however see Skottun,

2000 for a review of contrasting evidence), it is possible that the magnocellular

system could be a common area of deficit in a range of developmental disorders. This

claim has been supported by anatomical evidence of reduced magno-cell size in the

lateral geniculate nucleus of people who have had dyslexia (Livingstone, Rosen,

Drislane, & Galaburda, 1991) and Fragile X syndrome (Kogan et al., 2004). In

addition, it has been reported that the expression of FMRP is higher in magnocellular

neurons than in parvocellular neurons (found in both non-human primate and human

LGNs), suggesting that reduced FMRP associated with Fragile X syndrome may

impact specifically on the development of magnocellular neurons (Kogan et al.,

2004).

Evidence of impaired motion detection in these different developmental

disorders suggests a vulnerability of the magnocellular system / dorsal stream

(Braddick et al. 2003), both in acquired brain damage (Gunn et al., 2002) and


19

developmental disorders. A number of speculative suggestions regarding the origin of

such a vulnerability have been put forward including; the physical position of

magnocellular neurons, which makes them more susceptible to compression than

parvocellular neurons (Tassinari, Marzi, Lee, Di Lollo, & Campara, 1999); focal

cortical anomalies which, under certain hormonal conditions, give rise to secondary

disruption in sensory pathways (Ramus, 2004); or a non-specific physical

vulnerability (Gunn et al., 2002). However it is clear from the literature that reduced

sensitivity to coherent motion is not specific to one particular developmental disorder,

neither is it a universal finding in all individuals who have developmental disorders.

As reviewed above, only a proportion of individuals with ASD have abnormally high

motion coherence thresholds (Milne et al., 2002; in press). This appears to be

mirrored in data from children with Williams’ Syndrome (Atkinson et al., 2001), and

also in dyslexia. A meta-analysis of sensitivity to coherent motion revealed that in a

selection of published studies, only 29% of dyslexics had elevated motion coherence

thresholds (Ramus, 2003). An important key to understanding developmental

disorders will be to establish why only sub-groups of individuals with these disorders

have reduced sensitivity to coherent motion, and whether the cause of poor coherent

motion detection is the same in each of the disorders. The normal trajectory of the

development of motion sensitivity may reflect a range of developmental

contingencies, which highlights the possibility that motion perception impairment

may follow rather than precede other cognitive impairments.

There is evidence of abnormal perception of different kinds of motion

amongst individuals with ASD, however in other developmental disorders only

coherent motion detection has been reported as abnormal. This could be because

researchers have not investigated other types of motion perception in other

developmental disorders, although there has been a report of intact biological motion

perception in Williams’ syndrome (Jordan, Reiss, Hoffman, & Landau, 2002), or it

could be that in the other developmental disorders, only coherent motion detection is

impaired and other types of motion stimuli are spared. This suggests that if reduced

sensitivity to coherent motion in ASD shares an underlying aetiology with other

developmental disorders, a further explanation must be sought for the cause of

reduced sensitivity to other types of motion (e.g. biological motion) in ASD. This

work would be enlightened by further investigation of different types of motion


20

perception in a range of developmental disorders, and a comprehensive investigation

of different types of motion perception in individuals who have ASD.

A similar issue is the degree to which reduced sensitivity to coherent motion

relates to the varying cognitive profiles of other developmental disorders.

Abnormalities in the magnocellular system have been suggested as causal to poor

reading in individuals with dyslexia, via their input to sub-cortical structures which

control eye-movement (Stein & Walsh, 1997), and a relationship has been found

between sensitivity to coherent motion and reading ability (Cornelissen et al., 1998).

Does this mean that individuals with other developmental disorders who have reduced

sensitivity to coherent motion, will also show reading impairment? A logical

extension of this argument would expect this to be the case. However, recent data

suggests otherwise, as a double dissociation has been found between children with

ASD who have reduced sensitivity to coherent motion but normal reading age and

those who have normal sensitivity to coherent motion and a lower than would be

expected reading age (White et al., in preparation).

Similarly, if it is the case that coherent motion detection is related to global /

local perception via low-spatial frequency processing, then it would be expected that

individuals with dyslexia, Williams’ syndrome and Fragile X syndrome who have

been identified as having high motion coherence thresholds would also show a less

globally biased perceptual style. Given that dyslexics show no abnormality in their

processing of global and local stimuli as indexed by the Navon hierarchical figure

task (Keen & Lovegrove, 2000), this appears not to be the case. However, individuals

with Williams’ syndrome do appear to have a locally biased visuo-motor style which

is shown by their tendency to focus on the local level when asked to reproduce

hierarchical stimuli (Pani, Mervis, & Robinson, 1999).

Conclusions

In conclusion, some individuals with ASD and other developmental disorders

(dyslexia, Williams’ syndrome and Fragile X syndrome) have reduced sensitivity to

visual motion. In ASD this impairment appears to be generalised across many types of

motion (coherent motion, biological motion, response to optic flow and detection of

second-order translational, rotational and radial motion). In other developmental

disorders the impairment appears to be restricted to the detection of coherent motion.

It is not clear whether this reflects a common aetiology across several developmental


21

disorders or whether perception of coherent motion is a vulnerable ability which is

diminished in some individuals with developmental disorders. A parallel could be

drawn to IQ, which is generally lower in individuals with developmental disorders,

but is not pin-pointed to a specific aetiology. Available evidence does not yet allow

reliable conclusions regarding the aetiology of impaired motion perception in ASD,

however arguments posited so far have focussed on impairment in a specific area of

the visual system (magnocellular / dorsal stream) and reduced neuronal integration

required for processing complex stimuli.

It remains unclear whether there is a relationship between reduced motion

sensitivity and specific ASD diagnosis. While children with autistic disorder and

Apserger’s syndrome can be differentiated on their postural stability in response to

optic flow (Gepner & Mestre, 2002), high motion coherence thresholds have been

reported in children diagnosed with autistic disorder, Asperger’s Disorder and PDD-

NOS (Milne et al., in press). In addition, a positive relationship between autistic

severity and ability to detect biological motion has been reported by Blake et al.

(2003). It is important for future studies on motion perception in ASD to report the

range of individual differences in the data, and to explicitly illustrate how many

participants with ASD in the sample showed motion perception impairment and how

many showed no impairment. With this approach to the work it is hoped that a clearer

picture will emerge regarding the extent of motion perception impairment in ASD and

the degree to which this is related to other cognitive and / or diagnostic features.

Future Directions

Further understanding the nature of reduced motion sensitivity in individuals

with ASD and other developmental disorders appears to suggest a promising inroad to

a greater understanding not only of the biological architecture and the heterogeneous

nature of ASD, but also of the relationship and over-lap between different

developmental disorders. The phenomenon of motion perception has been studied for

over 50 years, and scientists have made great progress in understanding the functional

anatomy, the psychophysical and also cognitive factors involved in the perception of

motion. Therefore it represents a well-defined model from which to investigate visual

perception in developmental disorders. However, the study of motion perception in

individuals with ASD is a relatively new area in the field and one which will benefit


22

from more inclusive, thorough investigation. A number of key issues and further

questions remain outstanding including, but not restricted to:

1) Is reduced sensitivity to motion a general impairment in some individuals with

ASD, that is, are the individuals with ASD who show reduced sensitivity to

coherent motion also the participants who show reduced sensitivity to other

types of motion, e.g. second order motion and/or biological motion?

2) Is there a relationship between reduced sensitivity to motion and ASD

diagnosis and / or between motion perception and symptom severity?

3) Do individuals with developmental disorders other than ASD who show

reduced sensitivity to coherent motion also show deficits in the perception of

other types of motion?

4) Is there direct evidence of abnormal magnocellular neurons in individuals with

ASD?

5) Will functional MRI investigation reveal abnormality in dorsal stream

structures, specifically area V5 during motion perception in individuals with

ASD?

6) Is there direct evidence for reduced neuronal integration across visual motion

areas in individuals with ASD?

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Figure one. Schematic Illustration of a random dot kinematogram used to investigate

coherent motion detection.

The stimulus consists of two patches of moving dots. Dots with no arrow indicators

represent dots which move randomly. Dots with arrow indicators represent dots which

move coherently from right to left and left to right. The task is a 2-alternative forced

choice where the participant must detect the patch which contains coherent motion (in

this example, on the left).


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Figure two. Schematic illustration of form detection stimuli.

The stimulus consists of two patches of white lines. In the patch on the right all the

lines are oriented randomly, in the patch on the left some of the lines are oriented to

make a circle. The task is a 2-alternative forced choice where the participant must

detect the coherent form (circle).


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Figure 3. A schematic illustration of a biological motion stimulus (right).

The biological motion display on the right of the figure is composed of point lights

positioned at the joints of the actor. When played as a movie, a strong perception of

walking is apparent solely from the point light display (figure reproduced from Puce

and Perrett, 2003, an adaptation of Johansson, 1973).


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Figure 4. A schematic representation of first and second order translation, radial and

rotational motion (reproduced from Bertone et al, 2003).

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