Disrupted saccade control in chronic cerebral injury

Upper motor neuron-like disinhibition in the ocular motor system

John Ross Rizzo, Todd E. Hudson, Andrew Abdou, Yvonne W. Lui, Janet C. Rucker, Preeti Raghavan, Michael Landy

Research output: Contribution to journalArticle

Abstract

Saccades rapidly direct the line of sight to targets of interest to make use of the high acuity foveal region of the retina. These fast eye movements are instrumental for scanning visual scenes, foveating targets, and, ultimately, serve to guide manual motor control, including eye-hand coordination. Cerebral injury has long been known to impair ocular motor control. Recently, it has been suggested that alterations in control may be useful as a marker for recovery. We measured eye movement control in a saccade task in subjects with chronic middle cerebral artery stroke with both cortical and substantial basal ganglia involvement and in healthy controls. Saccade latency distributions were bimodal, with an early peak at 60 ms (anticipatory saccades) and a later peak at 250 ms (regular saccades). Although the latencies corresponding to these peaks were the same in the two groups, there were clear differences in the size of the peaks. Classifying saccade latencies relative to the saccade "go signal" into anticipatory (latencies up to 80 ms), "early" (latencies between 80 and 160 ms), and "regular" types (latencies longer than 160 ms), stroke subjects displayed a disproportionate number of anticipatory saccades, whereas control subjects produced the majority of their saccades in the regular range. We suggest that this increase in the number of anticipatory saccade events may result from a disinhibition phenomenon that manifests as an impairment in the endogenous control of ocular motor events (saccades) and interleaved fixations. These preliminary findings may help shed light on the ocular motor deficits of neurodegenerative conditions, results that may be subclinical to an examiner, but clinically significant secondary to their functional implications.

Original languageEnglish (US)
Article number12
JournalFrontiers in Neurology
Volume8
Issue numberJAN
DOIs
StatePublished - Jan 26 2017

Fingerprint

Saccades
Motor Neurons
Wounds and Injuries
Eye Movements
Middle Cerebral Artery Infarction
Basal Ganglia
Retina
Hand
Stroke

Keywords

  • Cortex
  • Disinhibition
  • Latency
  • Saccades
  • Stroke

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Cite this

Disrupted saccade control in chronic cerebral injury : Upper motor neuron-like disinhibition in the ocular motor system. / Rizzo, John Ross; Hudson, Todd E.; Abdou, Andrew; Lui, Yvonne W.; Rucker, Janet C.; Raghavan, Preeti; Landy, Michael.

In: Frontiers in Neurology, Vol. 8, No. JAN, 12, 26.01.2017.

Research output: Contribution to journalArticle

Rizzo, John Ross ; Hudson, Todd E. ; Abdou, Andrew ; Lui, Yvonne W. ; Rucker, Janet C. ; Raghavan, Preeti ; Landy, Michael. / Disrupted saccade control in chronic cerebral injury : Upper motor neuron-like disinhibition in the ocular motor system. In: Frontiers in Neurology. 2017 ; Vol. 8, No. JAN.
@article{a6f72ca4c3e7449b8b130d8a38d0fbca,
title = "Disrupted saccade control in chronic cerebral injury: Upper motor neuron-like disinhibition in the ocular motor system",
abstract = "Saccades rapidly direct the line of sight to targets of interest to make use of the high acuity foveal region of the retina. These fast eye movements are instrumental for scanning visual scenes, foveating targets, and, ultimately, serve to guide manual motor control, including eye-hand coordination. Cerebral injury has long been known to impair ocular motor control. Recently, it has been suggested that alterations in control may be useful as a marker for recovery. We measured eye movement control in a saccade task in subjects with chronic middle cerebral artery stroke with both cortical and substantial basal ganglia involvement and in healthy controls. Saccade latency distributions were bimodal, with an early peak at 60 ms (anticipatory saccades) and a later peak at 250 ms (regular saccades). Although the latencies corresponding to these peaks were the same in the two groups, there were clear differences in the size of the peaks. Classifying saccade latencies relative to the saccade {"}go signal{"} into anticipatory (latencies up to 80 ms), {"}early{"} (latencies between 80 and 160 ms), and {"}regular{"} types (latencies longer than 160 ms), stroke subjects displayed a disproportionate number of anticipatory saccades, whereas control subjects produced the majority of their saccades in the regular range. We suggest that this increase in the number of anticipatory saccade events may result from a disinhibition phenomenon that manifests as an impairment in the endogenous control of ocular motor events (saccades) and interleaved fixations. These preliminary findings may help shed light on the ocular motor deficits of neurodegenerative conditions, results that may be subclinical to an examiner, but clinically significant secondary to their functional implications.",
keywords = "Cortex, Disinhibition, Latency, Saccades, Stroke",
author = "Rizzo, {John Ross} and Hudson, {Todd E.} and Andrew Abdou and Lui, {Yvonne W.} and Rucker, {Janet C.} and Preeti Raghavan and Michael Landy",
year = "2017",
month = "1",
day = "26",
doi = "10.3389/fneur.2017.00012",
language = "English (US)",
volume = "8",
journal = "Frontiers in Neurology",
issn = "1664-2295",
publisher = "Frontiers Research Foundation",
number = "JAN",

}

TY - JOUR

T1 - Disrupted saccade control in chronic cerebral injury

T2 - Upper motor neuron-like disinhibition in the ocular motor system

AU - Rizzo, John Ross

AU - Hudson, Todd E.

AU - Abdou, Andrew

AU - Lui, Yvonne W.

AU - Rucker, Janet C.

AU - Raghavan, Preeti

AU - Landy, Michael

PY - 2017/1/26

Y1 - 2017/1/26

N2 - Saccades rapidly direct the line of sight to targets of interest to make use of the high acuity foveal region of the retina. These fast eye movements are instrumental for scanning visual scenes, foveating targets, and, ultimately, serve to guide manual motor control, including eye-hand coordination. Cerebral injury has long been known to impair ocular motor control. Recently, it has been suggested that alterations in control may be useful as a marker for recovery. We measured eye movement control in a saccade task in subjects with chronic middle cerebral artery stroke with both cortical and substantial basal ganglia involvement and in healthy controls. Saccade latency distributions were bimodal, with an early peak at 60 ms (anticipatory saccades) and a later peak at 250 ms (regular saccades). Although the latencies corresponding to these peaks were the same in the two groups, there were clear differences in the size of the peaks. Classifying saccade latencies relative to the saccade "go signal" into anticipatory (latencies up to 80 ms), "early" (latencies between 80 and 160 ms), and "regular" types (latencies longer than 160 ms), stroke subjects displayed a disproportionate number of anticipatory saccades, whereas control subjects produced the majority of their saccades in the regular range. We suggest that this increase in the number of anticipatory saccade events may result from a disinhibition phenomenon that manifests as an impairment in the endogenous control of ocular motor events (saccades) and interleaved fixations. These preliminary findings may help shed light on the ocular motor deficits of neurodegenerative conditions, results that may be subclinical to an examiner, but clinically significant secondary to their functional implications.

AB - Saccades rapidly direct the line of sight to targets of interest to make use of the high acuity foveal region of the retina. These fast eye movements are instrumental for scanning visual scenes, foveating targets, and, ultimately, serve to guide manual motor control, including eye-hand coordination. Cerebral injury has long been known to impair ocular motor control. Recently, it has been suggested that alterations in control may be useful as a marker for recovery. We measured eye movement control in a saccade task in subjects with chronic middle cerebral artery stroke with both cortical and substantial basal ganglia involvement and in healthy controls. Saccade latency distributions were bimodal, with an early peak at 60 ms (anticipatory saccades) and a later peak at 250 ms (regular saccades). Although the latencies corresponding to these peaks were the same in the two groups, there were clear differences in the size of the peaks. Classifying saccade latencies relative to the saccade "go signal" into anticipatory (latencies up to 80 ms), "early" (latencies between 80 and 160 ms), and "regular" types (latencies longer than 160 ms), stroke subjects displayed a disproportionate number of anticipatory saccades, whereas control subjects produced the majority of their saccades in the regular range. We suggest that this increase in the number of anticipatory saccade events may result from a disinhibition phenomenon that manifests as an impairment in the endogenous control of ocular motor events (saccades) and interleaved fixations. These preliminary findings may help shed light on the ocular motor deficits of neurodegenerative conditions, results that may be subclinical to an examiner, but clinically significant secondary to their functional implications.

KW - Cortex

KW - Disinhibition

KW - Latency

KW - Saccades

KW - Stroke

UR - http://www.scopus.com/inward/record.url?scp=85012045866&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85012045866&partnerID=8YFLogxK

U2 - 10.3389/fneur.2017.00012

DO - 10.3389/fneur.2017.00012

M3 - Article

VL - 8

JO - Frontiers in Neurology

JF - Frontiers in Neurology

SN - 1664-2295

IS - JAN

M1 - 12

ER -