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Related Experiment Videos

Spasm of fixation: a quantitative study.

J L Johnston1, J A Sharpe, M J Morrow

  • 1Neuro-Ophthalmology Unit, Toronto Hospital, University of Toronto, Ont., Canada.

Journal of the Neurological Sciences
|February 1, 1992
PubMed
Summary
This summary is machine-generated.

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Cerebral hemispheric damage impairs saccade initiation when a fixation target is present, causing prolonged latencies. Removing the target normalizes saccadic latency, suggesting a disinhibition mechanism in visual fixation control.

Area of Science:

  • Neuroscience
  • Ophthalmology
  • Neurology

Background:

  • Spasm of fixation is characterized by impaired saccade initiation with a fixation target present.
  • This condition was studied in a patient with cerebral hemispheric damage.

Observation:

  • Horizontal saccades to a new target showed prolonged latencies (369 ms) with a central fixation target.
  • Saccadic latency normalized (197 ms) when the central fixation target was absent.
  • Target extinction during a gap interval elicited express saccades (122 ms).
  • Self-paced refixation saccades were prolonged with head immobile, but shorter with head free.

Findings:

  • Cerebral hemispheric damage can lead to spasm of fixation, affecting saccadic eye movements.
  • The findings suggest a disruption in the neural pathways controlling visual fixation and saccade initiation.

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Implications:

  • The study postulates that damage disinhibits the substantia nigra pars reticulata, subsequently inhibiting the superior colliculus.
  • Understanding these mechanisms is crucial for diagnosing and treating visual fixation disorders.