Central Ocular Motor Disorders: Clinical and Topographic Anatomical Diagnosis, Syndromes and Underlying Diseases

2021 ◽  
Vol 238 (11) ◽  
pp. 1197-1211
Author(s):  
Michael Leo Strupp ◽  
Dominik Straumann ◽  
Christoph Helmchen
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Time Course ◽  
Metabolic Diseases ◽  
Spontaneous Nystagmus ◽  
Medial Longitudinal Fasciculus ◽  
Motor Disorders ◽  
Ocular Motor ◽  
Ocular Motor Disorders ◽  
Underlying Diseases

AbstractThe key to the diagnosis of ocular motor disorders is a systematic clinical examination of the different types of eye movements, including eye position, spontaneous nystagmus, range of eye movements, smooth pursuit, saccades, gaze-holding function, vergence, optokinetic nystagmus, as well as testing of the function of the vestibulo-ocular reflex (VOR) and visual fixation suppression of the VOR. This is like a window which allows you to look into the brain stem and cerebellum even if imaging is normal. Relevant anatomical structures are the midbrain, pons, medulla, cerebellum and rarely the cortex. There is a simple clinical rule: vertical and torsional eye movements are generated in the midbrain, horizontal eye movements in the pons. For example, isolated dysfunction of vertical eye movements is due to a midbrain lesion affecting the rostral interstitial nucleus of the medial longitudinal fasciculus (riMLF), with impaired vertical saccades only or vertical gaze-evoked nystagmus due to dysfunction of the Interstitial nucleus of Cajal (INC). Lesions of the lateral medulla oblongata (Wallenberg syndrome) lead to typical findings: ocular tilt reaction, central fixation nystagmus and dysmetric saccades. The cerebellum is relevant for almost all types of eye movements; typical pathological findings are saccadic smooth pursuit, gaze-evoked nystagmus or dysmetric saccades. The time course of the development of symptoms and signs is important for the diagnosis of underlying diseases: acute: most likely stroke; subacute: inflammatory diseases, metabolic diseases like thiamine deficiencies; chronic progressive: inherited diseases like Niemann-Pick type C with typically initially vertical and then horizontal saccade palsy or degenerative diseases like progressive supranuclear palsy. Treatment depends on the underlying disease. In this article, we deal with central ocular motor disorders. In a second article, we focus on clinically relevant types of nystagmus such as downbeat, upbeat, fixation pendular, gaze-evoked, infantile or periodic alternating nystagmus. Therefore, these types of nystagmus will not be described here in detail.

Ocular motor disorders

2014 ◽  
Vol 27 (1) ◽  
pp. 75-82 ◽  
Author(s):  
Anna Willard ◽  
Christian J. Lueck
Keyword(s):  
Motor Disorders ◽  
Ocular Motor ◽  
Ocular Motor Disorders

Lidocaine-induced unilateral internuclear ophthalmoplegia: effects on convergence and conjugate eye movements

1989 ◽  
Vol 62 (1) ◽  
pp. 82-95 ◽  
Author(s):  
P. D. Gamlin ◽  
J. W. Gnadt ◽  
L. E. Mays
Keyword(s):  
Eye Movements ◽  
Smooth Pursuit ◽  
Open Loop ◽  
Medial Longitudinal Fasciculus ◽  
Slow Phase ◽  
Internuclear Ophthalmoplegia ◽  
Unaffected Side ◽  
Affected Side ◽  
Position Signal ◽  
Slow Drift

1. To characterize the vergence signal carried by the medial longitudinal fasciculus (MLF), it was subjected to reversible blockade by small injections of 10% lidocaine hydrochloride. The effects of these blockades on both conjugate and vergence eye movements were studied. 2. With this procedure, experimentally induced internuclear ophthalmoplegia (INO) and its effects on conjugate eye movements could be studied acutely, without possible contamination from long-term oculomotor adaptation. In the eye contralateral to the MLF blockade, saccadic and horizontal smooth-pursuit eye movements were normal. Horizontal abducting nystagmus, often seen in patients with INO, was not observed in this eye. 3. As previously reported for INO, profound oculomotor deficits were seen in the eye ipsilateral to the MLF blockade. During maximal blockade, adducting saccades and horizontal smooth-pursuit movements in this eye did not cross the midline. Adducting saccades were reduced in amplitude and peak velocity and showed significantly increased durations. Abducting saccades, which were slightly hypometric, displayed a marked postsaccadic centripetal drift. 4. The eye ipsilateral to the blockade displayed a pronounced, upward, slow drift, whereas the eye contralateral to the blockade showed virtually no drift. Furthermore, although vertical saccades to visual targets remained essentially conjugate, the size of the resetting quick phases in each eye was related to the amplitude of the slow phase movement in that eye. Thus the eye on the affected side displayed large quick phases, whereas the eye on the unaffected side showed only slight movements. On occasion, unilateral downbeating nystagmus was seen. This strongly suggests that the vertical saccade generators for the two eyes can act independently. 5. The effect of MLF blockade on the vergence gain of the eye on the affected side was investigated. As a measure of open-loop vergence gain, the relationship of accommodative convergence to accommodation (AC/A) was measured before, during, and after reversible lidocaine block of the MLF. After taking conjugate deficits into account, the net vergence signal to the eye ipsilateral to the injection was found to increase significantly during the reversible blockade. 6. The most parsimonious explanation for this increased vergence signal is suggested by the accompanying single-unit study. This study showed that abducens internuclear neurons, whose axons course in the MLF, provide medial rectus motoneurons with an appropriate horizontal conjugate eye position signal but an inappropriate vergence signal. Ordinarily, this incorrect vergence signal is overcome by another, more potent, v

Anti-GAD antibody ocular flutter: expanding the spectrum of autoimmune ocular motor disorders

2013 ◽  
Vol 260 (10) ◽  
pp. 2675-2677 ◽  
Author(s):  
Raffaele Dubbioso ◽  
Vincenzo Marcelli ◽  
Fiore Manganelli ◽  
Rosa Iodice ◽  
Marcello Esposito ◽  
...  
Keyword(s):  
Motor Disorders ◽  
Ocular Motor ◽  
Ocular Flutter ◽  
Ocular Motor Disorders

Ocular motor disorders

2011 ◽  
Author(s):  
Christopher Kennard
Keyword(s):  
Eye Movement ◽  
Movement Disorders ◽  
Motor Disorder ◽  
Motor Disorders ◽  
Ocular Motor ◽  
Idiopathic Orbital Inflammation ◽  
Pupillary Light ◽  
Ocular Motor Disorders ◽  
The Central Nervous System ◽  
Eye Movement Disorders

This chapter discusses motor disorders of the eye. The first part of the chapter describes the proper examination of eye movements to facilitate identification of ocular motor disorder pathology. The effects of nerve palsies on ocular motor function are then described.Eye movement disorders can also have their cause in the central nervous system; both the brainstem, and cerebellum have been implicated as causal factors in some eye movement disorders. Disorders of the pupil, which affect the pupillary light reflex, can be caused by lesions to central, afferent and efferent pupillary pathways as well as sympathetic pathways lesions.Finally, this chapter describes diseases of the eye orbits, including dysthyroid eye disease, idiopathic orbital inflammation, orbital tumours, vascular disorders and orbital infections.

scholarly journals Bedside Tested Ocular Motor Disorders in Multiple Sclerosis Patients

2014 ◽  
Vol 2014 ◽  
pp. 1-4 ◽  
Author(s):  
G. Servillo ◽  
D. Renard ◽  
G. Taieb ◽  
P. Labauge ◽  
S. Bastide ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Disease Duration ◽  
Clinically Isolated Syndrome ◽  
Motor Disorders ◽  
Ocular Motor ◽  
Mri Findings ◽  
Substantial Impact ◽  
Ocular Motor Disorders ◽  
Definition Of ◽  
Multiple Sclerosis Patients

Background/Aims. Ocular motor disorders (OMDs) are a common feature of multiple sclerosis (MS). In clinical practice, if not reported by patients, OMDs are often underdiagnosed and their prevalence is underestimated.Methods. We studied 163 patients (125 women, 76.7%, 38 men, 23.3%; median age 45.0 years; median disease duration 10 years; median EDSS 3.5) with definite MS (n=150, 92%) or clinically isolated syndrome (n=13, 8%) who underwent a thorough clinical examination of eye movements. Data on localization of previous relapses, MS subtype, and MRI findings were collected and analyzed.Results. Overall, 111/163 (68.1%) patients showed at least one abnormality of eye movement. Most frequent OMDs were impaired smooth pursuit (42.3%), saccadic dysmetria (41.7%), unilateral internuclear ophthalmoplegia (14.7%), slowing of saccades (14.7%), skew deviation (13.5%), and gaze evoked nystagmus (13.5%). Patients with OMDs had more severe disability(P=0.0005)and showed more frequently infratentorial MRI lesions(P=0.004). Localization of previous relapses was not associated with presence of OMDs.Conclusion. OMDs are frequent in patients with stable (no relapses) MS. A precise bedside examination of eye motility can disclose abnormalities that imply the presence of subclinical MS lesions and may have a substantial impact on definition of the diagnosis and on management of MS patients.

scholarly journals Central ocular motor disorders, including gaze palsy and nystagmus

2014 ◽  
Vol 261 (S2) ◽  
pp. 542-558 ◽  
Author(s):  
M. Strupp ◽  
O. Kremmyda ◽  
C. Adamczyk ◽  
N. Böttcher ◽  
C. Muth ◽  
...  
Keyword(s):  
Motor Disorders ◽  
Ocular Motor ◽  
Ocular Motor Disorders ◽  
Gaze Palsy

Ocular motor disorders

2001 ◽  
Vol 14 (1) ◽  
pp. 5-10 ◽  
Author(s):  
Dominik Straumann ◽  
T. Haslwanter
Keyword(s):  
Motor Disorders ◽  
Ocular Motor ◽  
Ocular Motor Disorders

Disconjugate Eye Movements during Electronystagmographic Testing in Patients with Known Central Nervous System Lesions

1975 ◽  
Vol 84 (3) ◽  
pp. 368-373
Author(s):  
Joseph Kimm ◽  
James B. MacLean
Keyword(s):  
Central Nervous System ◽  
Eye Movements ◽  
Eye Movement ◽  
Motor System ◽  
Treatment Plan ◽  
Medial Longitudinal Fasciculus ◽  
Ocular Motor ◽  
Measuring Techniques ◽  
Ocular Motor System ◽  
Cns Lesions

A tacit assumption underlying current ENG testing is that the eyes move conjugately. However, considering the intricate neuroanatomical pathways within the ocular motor system in addition to the elaborate vestibulo-ocular connections, we think it reasonable that disconjugate eye movements may result with certain CNS lesions. Recently we have employed independent eye movement measuring techniques in order to assess the movement of each eye separately during our ENG valuations. The preliminary work has revealed that disconjugate eye movements occurred even with extra-axial lesions which spared the medial longitudinal fasciculus. These data may be valuable for the neurotologist with regard to differential diagnosis and prescription of a treatment plan for the patient. The eye movement patterns of patients with confirmed CNS lesions and other interesting findings are presented.

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