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Saccadic eye movement abnormalities in autism spectrum disorder indicate dysfunctions in cerebellum and brainstem.

Schmitt LM, Cook EH, Sweeney JA, Mosconi MW - Mol Autism (2014)

Bottom Line: Age-related changes did not differ across groups.Deficits precisely and consistently directing eye movements suggest impairment in the error-reducing function of the cerebellum in ASD.Atypical increases in the duration of movement acceleration combined with lower peak saccade velocities implicate pontine nuclei, specifically suggesting reduced excitatory activity in burst cells that drive saccades relative to inhibitory activity in omnipause cells that maintain stable fixation.

View Article: PubMed Central - PubMed

Affiliation: Center for Autism and Developmental Disabilities, University of Texas Southwestern, 5323 Harry Hines Blvd, Dallas, TX 75390-9086 USA.

ABSTRACT

Background: Individuals with autism spectrum disorder (ASD) show atypical scan paths during social interaction and when viewing faces, and recent evidence suggests that they also show abnormal saccadic eye movement dynamics and accuracy when viewing less complex and non-social stimuli. Eye movements are a uniquely promising target for studies of ASD as their spatial and temporal characteristics can be measured precisely and the brain circuits supporting them are well-defined. Control of saccade metrics is supported by discrete circuits within the cerebellum and brainstem - two brain regions implicated in magnetic resonance (MR) morphometry and histopathological studies of ASD. The functional integrity of these distinct brain systems can be examined by evaluating different parameters of visually-guided saccades.

Methods: A total of 65 participants with ASD and 43 healthy controls, matched on age (between 6 and 44-years-old), gender and nonverbal IQ made saccades to peripheral targets. To examine the influence of attentional processes, blocked gap and overlap trials were presented. We examined saccade latency, accuracy and dynamics, as well as the trial-to-trial variability of participants' performance.

Results: Saccades of individuals with ASD were characterized by reduced accuracy, elevated variability in accuracy across trials, and reduced peak velocity and prolonged duration. In addition, their saccades took longer to accelerate to peak velocity, with no alteration in the duration of saccade deceleration. Gap/overlap effects on saccade latencies were similar across groups, suggesting that visual orienting and attention systems are relatively spared in ASD. Age-related changes did not differ across groups.

Conclusions: Deficits precisely and consistently directing eye movements suggest impairment in the error-reducing function of the cerebellum in ASD. Atypical increases in the duration of movement acceleration combined with lower peak saccade velocities implicate pontine nuclei, specifically suggesting reduced excitatory activity in burst cells that drive saccades relative to inhibitory activity in omnipause cells that maintain stable fixation. Thus, our findings suggest that both cerebellar and brainstem abnormalities contribute to altered sensorimotor control in ASD.

No MeSH data available.


Related in: MedlinePlus

Cumulative frequency plot of gap and overlap saccade latencies for participants with ASD and healthy controls. Saccade latencies for overlap trials were significantly greater across participants. The extent to which latencies increased did not differ between groups, but latency variability was increased in ASD. ASD, autism spectrum disorder; Con, control.
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Fig2: Cumulative frequency plot of gap and overlap saccade latencies for participants with ASD and healthy controls. Saccade latencies for overlap trials were significantly greater across participants. The extent to which latencies increased did not differ between groups, but latency variability was increased in ASD. ASD, autism spectrum disorder; Con, control.

Mentions: As expected, the latencies of saccades during overlap trials were longer than those during gap trials (Table 2; F(1,104) = 297.81; P <0.001). The extent to which overlap trial saccades were delayed relative to gap trial saccades did not differ between groups (F(1,104) = 2.63; P = 0.108). No differences in mean saccade latencies were seen between participants with ASD and healthy controls (F(1,104) = 0.57; P = 0.454), however participants with ASD showed greater trial-to-trial variability in their saccade latencies (Figure 2; F(1,103) = 9.90; P = 0.002).Table 2


Saccadic eye movement abnormalities in autism spectrum disorder indicate dysfunctions in cerebellum and brainstem.

Schmitt LM, Cook EH, Sweeney JA, Mosconi MW - Mol Autism (2014)

Cumulative frequency plot of gap and overlap saccade latencies for participants with ASD and healthy controls. Saccade latencies for overlap trials were significantly greater across participants. The extent to which latencies increased did not differ between groups, but latency variability was increased in ASD. ASD, autism spectrum disorder; Con, control.
© Copyright Policy - open-access
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4233053&req=5

Fig2: Cumulative frequency plot of gap and overlap saccade latencies for participants with ASD and healthy controls. Saccade latencies for overlap trials were significantly greater across participants. The extent to which latencies increased did not differ between groups, but latency variability was increased in ASD. ASD, autism spectrum disorder; Con, control.
Mentions: As expected, the latencies of saccades during overlap trials were longer than those during gap trials (Table 2; F(1,104) = 297.81; P <0.001). The extent to which overlap trial saccades were delayed relative to gap trial saccades did not differ between groups (F(1,104) = 2.63; P = 0.108). No differences in mean saccade latencies were seen between participants with ASD and healthy controls (F(1,104) = 0.57; P = 0.454), however participants with ASD showed greater trial-to-trial variability in their saccade latencies (Figure 2; F(1,103) = 9.90; P = 0.002).Table 2

Bottom Line: Age-related changes did not differ across groups.Deficits precisely and consistently directing eye movements suggest impairment in the error-reducing function of the cerebellum in ASD.Atypical increases in the duration of movement acceleration combined with lower peak saccade velocities implicate pontine nuclei, specifically suggesting reduced excitatory activity in burst cells that drive saccades relative to inhibitory activity in omnipause cells that maintain stable fixation.

View Article: PubMed Central - PubMed

Affiliation: Center for Autism and Developmental Disabilities, University of Texas Southwestern, 5323 Harry Hines Blvd, Dallas, TX 75390-9086 USA.

ABSTRACT

Background: Individuals with autism spectrum disorder (ASD) show atypical scan paths during social interaction and when viewing faces, and recent evidence suggests that they also show abnormal saccadic eye movement dynamics and accuracy when viewing less complex and non-social stimuli. Eye movements are a uniquely promising target for studies of ASD as their spatial and temporal characteristics can be measured precisely and the brain circuits supporting them are well-defined. Control of saccade metrics is supported by discrete circuits within the cerebellum and brainstem - two brain regions implicated in magnetic resonance (MR) morphometry and histopathological studies of ASD. The functional integrity of these distinct brain systems can be examined by evaluating different parameters of visually-guided saccades.

Methods: A total of 65 participants with ASD and 43 healthy controls, matched on age (between 6 and 44-years-old), gender and nonverbal IQ made saccades to peripheral targets. To examine the influence of attentional processes, blocked gap and overlap trials were presented. We examined saccade latency, accuracy and dynamics, as well as the trial-to-trial variability of participants' performance.

Results: Saccades of individuals with ASD were characterized by reduced accuracy, elevated variability in accuracy across trials, and reduced peak velocity and prolonged duration. In addition, their saccades took longer to accelerate to peak velocity, with no alteration in the duration of saccade deceleration. Gap/overlap effects on saccade latencies were similar across groups, suggesting that visual orienting and attention systems are relatively spared in ASD. Age-related changes did not differ across groups.

Conclusions: Deficits precisely and consistently directing eye movements suggest impairment in the error-reducing function of the cerebellum in ASD. Atypical increases in the duration of movement acceleration combined with lower peak saccade velocities implicate pontine nuclei, specifically suggesting reduced excitatory activity in burst cells that drive saccades relative to inhibitory activity in omnipause cells that maintain stable fixation. Thus, our findings suggest that both cerebellar and brainstem abnormalities contribute to altered sensorimotor control in ASD.

No MeSH data available.


Related in: MedlinePlus