Abstract

Despite extensive research, the functions of the basal ganglia (BG) in movement control have not been fully understood. Eye movements, particularly saccades, are convenient indicators of BG function. Here, we review the main oculomotor findings reported in Parkinson’s disease (PD) and genetic parkinsonian syndromes. PD is a progressive, neurodegenerative disorder caused by dopaminergic cell loss within the substantia nigra pars compacta, resulting in depletion of striatal dopamine and subsequent increased inhibitory BG output from the internal globus pallidus and the substantia nigra pars reticulata. Eye movement abnormalities are common in PD: anomalies are more evident in voluntary than reflexive saccades in the initial stages, but visually guided saccades may also be involved at later stages. Saccadic hypometria (including abnormally fragmented saccades), reduced accuracy, and increased latency are among the most prominent deficits. PD patients show also unusually frequent and large square wave jerks and impaired inhibition of reflexive saccades when voluntary mirror saccades are required. Poor convergence ability and altered pursuit are common. Inherited parkinsonisms are a heterogeneous group of rare syndromes due to gene mutations causing symptoms resembling those of PD. Eye movement characteristics of some parkinsonisms have been studied. While sharing some PD features, each syndrome has a distinctive profile that could contribute to better define the clinical phenotype of parkinsonian disorders. Moreover, because the pathogenesis and the underlying neural circuit failure of inherited parkinsonisms are often well defined, they might offer a better prospect than idiopathic PD to understand the BG function.

Highlights

  • The basal ganglia (BG) are subcortical nuclei located at the base of the forebrain and extensively connected directly and indirectly with all cortical and subcortical structures

  • Studies of eye movements in inherited parkinsonian syndromes are often limited by small sample sizes and by inconsistent exam­ination techniques and paradigms

  • Some characteristics tend to recur across syndromes and could be more informative about BG functions: saccades with increased latency but normal velocity suggest a role of BG in motor initiation rather than execution, so that bradykinesia in parkinsonism should be interpreted more as a delayed motor onset than a slow movement

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Summary

INTRODUCTION

The basal ganglia (BG) are subcortical nuclei located at the base of the forebrain and extensively connected directly and indirectly with all cortical and subcortical structures. The saccadic system, allow to test a distributed network involving cortical (mainly frontal and parietal) and subcortical (BG, midbrain, brain stem, thalamus, and cerebellum) structures. The dorsolateral prefrontal cortex is supposed to be involved in the suppression of the unwanted reflexive movement and, with the posterior-parietal cortex, in the generation of the correct mirror movement, while the frontal eye field (FEF) is associated with antisaccade latency [4]. Ocular motor abnormalities of idiopathic neurodegenerative parkinsonisms such as progressive supranuclear palsy, multisystem atrophy, corticobasal syndrome, and dementia with Lewy bodies, have been extensively studied and are well known by clinicians [2, 6]. Parkinson’s disease motor manifestations are caused by dopaminergic cell loss within the substantia nigra pars compacta (SNc), resulting in dysfunction of the BG. Dopaminergic projections from the SNc target striatal neurons expressing D1 receptors; D1 neurons send direct inhibitory projections to the BG output nuclei: the

Latency Errors Corrections
Neurodegeneration with Brain Iron Accumulation
Gaucher Disease
Findings
CONCLUSION
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