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Published on: July 14, 2016
Disconnections in infantile-onset saccade initiation delay: a hypothesis
Michael S Salman1, Kristin M Ikeda
1Section of Pediatric Neurology, Children's Hospital, University of Manitoba, Winnipeg, Manitoba, Canada.
Summary
Infantile-onset saccade initiation delay (ISID) involves difficulty initiating voluntary eye movements. This condition may stem from disrupted brain connections or damage in regions controlling saccades.
Area of Science:
- Neuroscience
- Ophthalmology
- Developmental Pediatrics
Background:
- Infantile-onset saccade initiation delay (ISID), or congenital ocular motor apraxia, is a condition affecting voluntary eye movement control.
- It is characterized by difficulty initiating horizontal saccades and often presents with compensatory head thrusts in infancy.
- ISID is frequently associated with broader developmental delays and observed brain abnormalities.
Purpose of the Study:
- To propose a unifying hypothesis for the underlying neurobiological cause of ISID.
- To elucidate the potential brain mechanisms responsible for saccade initiation deficits in infants.
Main Methods:
- Review of existing literature on ISID and related neurological conditions.
- Analysis of reported brain imaging findings in patients with ISID.
- Hypothesizing based on known pathways for saccade generation and interhemispheric communication.
Main Results:
- ISID is linked to abnormalities in the corpus callosum, brainstem, and cerebellum.
- The condition involves impaired horizontal volitional saccade initiation.
- Associated symptoms include head thrusting and developmental delays.
Conclusions:
- ISID may result from disrupted axonal connections between homologous brain regions responsible for saccade processing.
- Alternatively, bilateral damage to these critical saccade-related brain areas could be the cause.
- Further research is needed to confirm these proposed mechanisms.

