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1

16p

A

Angelman syndromeAsperger syndrome

B

Baby sibsBiological motionBiomarkers

C

CHD8ChromatinChromosome 7Copy number variation

D

DNA sequencingDendritic spinesDysmorphology

E

EndophenotypesEpigeneticsEpilepsyExomeEye tracking

F

FeverFragile X syndrome

M

MacrocephalyMicrobiomeMitochondria

N

Neurotransmitters

P

Prevalence

R

Repetitive behaviorRett syndrome

S

SCN2ASHANK3Synapse

T

Theory of mindTuberous sclerosis complex

U

UBE3A

W

Williams syndrome

Biological motion

Biological motion is a term used in social and cognitive neuroscience to refer to the unique visual phenomenon of a moving, animate creature.

Point-light displays:

Biological motion is often represented solely by a set of small point-light dots or markers attached to the major joints of an actor’s body1. Within these point-light displays, the individual dots merely undergo translational and/or elliptical motions and only the global integration of these motion signals evokes the perception of biological motion.

Even though point-light displays lack visual features such as color, shading, and contours, they contain sufficient information to identify the gender of the actor2, the kind of action in which he or she is engaged, and even the emotional state of the actor3.

Overall, females have been shown to be faster than males in recognizing biological motion or emotional states depicted by point lights4.

Human infants as young as 2 days5 or 3 months of age6 show spontaneous preferences for attending biological vs. non-biological point-light animations, indicating an inborn predisposition to attend to biological motion.

Neuroimaging:

An area in the temporal lobe of the brain, namely the posterior part of the superior temporal sulcus is most consistently reported to be active during biological motion perception7,8,9,10.

Some studies also indicate that frontal areas in part of the brain’s action perception system (such as the premotor cortex) are important to point-light biological motion perception 11,12.

The superior temporal sulcus and action perception system are suggested to contribute to ‘social perception’ and may subserve the understanding and predicting of the reactions and emotions of others in social settings.

Relevance to autism:

A number of studies have investigated biological motion perception in autism13.

Overall, people with autism are not blind to biological motion and can identify the kind of action that is displayed in point-light displays14. However, they have been shown to be less sensitive to higher-order information in these displays, such as identifying subjective states (e.g., tired, hurt, cold) or discerning emotional content (e.g., angry, sad, happy)15,16,17. Also discriminating biological from non-biological (scrambled) motion has been shown to be less accurate in children with autism than in controls18. Moreover, spontaneous preferences for attending biological vs. non-biological point-light animations have been shown to be absent in two-year-olds with autism19.

To date, two studies scanned adults with autism and controls during point-light biological motion perception and both found hypo-activation in the superior temporal sulcus, an area consistently associated with biological motion processing20,21.

Overall, dysfunction of the superior temporal sulcus region — also a key processing area for language and social context — has been suggested to contribute substantially to the social problems associated with autism. A recent study examining the neural signatures of autism supports this view22.

References:
  1. Johansson G. Percept. Psychophys. 14, 201-211 (1973)
  2. Cutting J.E. and L.T. Kozlowski Bull. Psychon. Soc. 9, 353-356 (1977)
  3. Brownlow S. et al. Psychol. Rec. 47, 411-421 (1997)
  4. Alaerts K. et al. PLoS One 6, e20989 (2011)
  5. Simion F. et al. Proc. Natl. Acad. Sci. USA 105, 809-813 (2008)
  6. Fox R. and C. McDaniel Science 218, 486-487 (1982)
  7. Grossman E. et al. J. Cogn. Neurosci. 12, 711-720 (2000)
  8. Grezes J. et al. Neuroimage 13, 775-785 (2001)
  9. Grossman E.D. and R. Blake Neuron 35, 1167-1175 (2002)
  10. Jastorff J. and G.A. Orban J. Neurosci. 29, 7315-7329 (2009)
  11. Saygin A.P. et al. J. Neurosci. 24, 6181-6188 (2004)
  12. Saygin A.P. Brain 130, 2452-2461 (2007)
  13. Kaiser M.D. and M. Shiffrar Psychon. Bull. Rev. 16, 761-777 (2009)
  14. Moore D.G. et al. Brit. J. Dev. Psych. 15, 401-423 (1997)
  15. Parron C. et al. Autism 12, 261-274 (2008)
  16. Hubert B. et al. J. Aut. Dev. Disord. 37, 1386-1392 (2007)
  17. Atkinson A.P. Neuropsychologia 47, 3023-3029 (2009)
  18. Blake R. et al. Psych. Sci. 14, 151-157 (2003)
  19. Klin A. et al. Nature 459, 257-261 (2009)
  20. Freitag C.M. et al. Neuropsychologia 46, 1480-1494 (2008)
  21. Herrington J.D. et al. Res. Aut. Spect. Disord. 1, 14-27 (2007)
  22. Kaiser M.E. et al. Proc. Natl. Acad. Sci. USA 107, 21223-21228 (2010)