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. 2017;12(6):457-473.
doi: 10.1080/17469899.2017.1395695. Epub 2017 Nov 28.

Basic and Translational Neuro-Ophthalmology of Visually Guided Saccades: Disorders of Velocity

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Free PMC article

Basic and Translational Neuro-Ophthalmology of Visually Guided Saccades: Disorders of Velocity

Sushant Puri et al. Expert Rev Ophthalmol. .
Free PMC article

Abstract

Introduction: Saccades are rapid, yoked eye movements in an effort to direct a target over fovea. The complex circuitry of saccadic eye movements has been exhaustively described. As a result clinicians can elegantly localize the pathology if it falls on the neuraxis responsible for saccades. Traditionally saccades are studied with their quantitative characteristics such as amplitude, velocity, duration, direction, latency and accuracy.

Areas covered: Amongst all subtypes, the physiology of the visually guided saccades is most extensively studied. Here we will review the basic and pertinent neuro-anatomy and physiology of visually guided saccade and then discuss common or classic disorders affecting the velocity of visually guided saccades. We will then discuss the basic mechanism for saccade slowing in these disorders.

Expert commentary: Prompt appreciation of disorders of saccade velocity is critical to reach appropriate diagnosis. Disorders of midbrain, cerebellum, or basal ganglia can lead to prolonged transition time during gaze shift and decreased saccade velocity.

Keywords: eye movements; saccade; saccade velocity.

Conflict of interest statement

Declaration of interest The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Figures

Fig 1
Fig 1
A schematic figure of the neural structures that project to the brainstem saccade generator (premotor burst neurons in the PPRF and riMLF). Instructions for saccades originate from frontal and parietal cortex through parallel direct or indirect pathways, via caudate nucleus, onto superior colliculus and omnipause neurons. The caudate nucleus inhibits the substantia nigra pars reticulata (SNpr), which itself tonically inhibits the SC. Caudate nucleus excitation, therefore disinhibits superior colliculus and triggers voluntary saccades. Frontal eye fields also send projections to cerebellum via pontine nuclei which calibrates the amplitude of saccadic eye movements. The kinetics of saccadic eye movement are under control of distinct neuronal populations in the brainstem (Scudder, Kaneko et al. 2002) and the cerebellum (Robinson and Fuchs 2001). STN = subthalamic nucleus, SNpr = Substantia Nigra pars reticulata, PPRF = Paramedian Pontine Reticular Formation, riMLF = rostral interstitial nucleus of Medial Longitudinal Fasciculus Red: Excitatory Blue: Inhibitory The thickness of the line corresponds with the degree of influence of the projections from a structure to its downstream components
Fig 2
Fig 2
A Block diagram of the macro circuits of basal ganglia network in saccadic eye movements and interaction with cortical eye fields. Striatum and STN are the principal input nuclei of basal ganglia. Substantia nigra pars compacta (SNpc) send inhibitory (blue) and excitatory (red) projections to the striatum. The striatum projects via direct and indirect pathways to the output nuclei of the basal ganglia. The excitatory inputs to the striatum continue, via direct pathway as inhibitory projection to Globus Pallidus pars interna (GPi) and Substantia Nigra pars reticulata (SNpr). Parallel to these, the inhibitory inputs to the striatum continue, via indirect pathway as inhibitory projection to Globus Pallidus pars externa (GPe) and Subthalamic Nucleus (STN). B A schematic figure of the midbrain network involved in saccadic eye movements. Inhibitory projections (blue) from the omnipause neurons present in the pontine nucleus raphe interpositus (RIP) on to the burst neurons inhibit saccadic eye movements. Burst neurons located in the midbrain are disinhibited when the initial trigger for saccade turns off the omnipause neurons. Burst neurons in the Paramedian Pontine Reticular Formation (PPRF) project to nuclei of Abducens nerve (Cranial Nerve VI) and Oculomotor Nerve (Cranial Nerve III) which innervate the medial and lateral recti to generate horizontal saccades. Burst neurons in the rostral interstitial nucleus of the Medial Longitudinal Fasciculus (riMLF) project to nuclei of Abducens nerve (Cranial Nerve VI) and Oculomotor Nerve (Cranial Nerve III) which innervate the superior and inferior recti to generate vertical saccades. Red: Excitatory Blue: Inhibitory The thickness of the line corresponds with the degree of influence of the projections from a structure to its downstream components
Fig 3
Fig 3
A Degeneration of dopaminergic SNpc in Parkinson’s Disease produce a cascade of changes in the basal ganglia, which ultimately results in reduced inhibition of GPi and SNr. The net effect is an increased output from GPi and SNr leading to inhibition of Superior Colliculus. B Vertical gaze impairment manifesting as slow, hypometric saccades is characteristic of Progressive Supranuclear Palsy (PSP). Early involvement of brainstem reticular formation containing riMLF is responsible for the vertical motion abnormalities. With disease progression, complete vertical gaze palsy develops. C The characteristic pathoanatomy of Huntington ‘s disease includes caudate nucleus degeneration and frontal lobe atrophy. It leads to decreased inhibitory projection to SNpr resulting in excessive inhibition of the Superior Colliculus. Frontal lobe atrophy decreases the excitatory projections to the Superior Colliculus. Collectively, decreased outflow from the Superior Colliculus results in impaired gaze in both horizontal and vertical directions. Red: Excitatory Blue: Inhibitory The thickness of the line corresponds with the degree of influence of the projections from a structure to its downstream components. Dotted line indicates pathologically decreased outputs.
Fig 4
Fig 4
Hypometric saccades with slowing and occasional abrupt cessation in Late-Onset Tay Sachs disease presumably due to premature activation of omnipause neurons. Red: Excitatory Blue: Inhibitory The thickness of the line corresponds with the degree of influence of the projections from a structure to its downstream components. Dotted line indicates pathologically decreased outputs.
Fig 5
Fig 5
Slowing of saccades and dysmetria in patients with Spinocerebellar Ataxia correlates with cerebellar atrophy and pontine nuclei degeneration. Red: Excitatory Blue: Inhibitory The thickness of the line corresponds with the degree of influence of the projections from a structure to its downstream components. Dotted line indicates pathologically decreased outputs.

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