- •Contents
- •List of Contributors
- •Preface
- •Anatomy of the Oculomotor System
- •Abstract
- •Properties of Extraocular Muscles
- •Sensory Receptors in Extraocular Muscles
- •Muscle Spindles
- •Palisade Endings
- •Golgi Tendon Organs
- •Central Pathways
- •Motor and Premotor Pathways Controlling Eye Muscles
- •Premotor Circuits
- •A Proprioceptive Hypothesis
- •Conclusions
- •References
- •Abstract
- •History of Eye Movement Recording
- •The Electro-Oculogram
- •Infrared Reflection Devices
- •Search Coil
- •Video-Oculography
- •References
- •Web Links
- •Vestibulo-Ocular Reflex
- •Abstract
- •Central Processing of Vestibular Signals
- •Practical Aspects for Bedside Clinical Evaluation
- •Static Imbalance
- •Dynamic Disturbances
- •Positional Testing
- •Laboratory Evaluation: Electro-Oculography and Rotational Testing
- •Conventional Rotational Testing
- •Modern Vestibular Testing
- •Semicircular Canal Function
- •Otolith Function
- •Subjective Visual Vertical
- •Click-Evoked Myogenic Potentials
- •Conclusions
- •References
- •Neural Control of Saccadic Eye Movements
- •Abstract
- •The Brainstem Saccadic Generator
- •The Excitatory and Inhibitory Burst Neurons
- •The Omnipause Neurons
- •The Tonic Neurons
- •The Superior Colliculus
- •The Basal Ganglia
- •The Pontine Nuclei
- •The Nucleus Reticularis Tegmenti Pontis
- •The Oculomotor Cerebellum
- •References
- •Abstract
- •General Characteristics
- •Smooth Pursuit Eye Movements
- •Optokinetic Response
- •Ocular Following Response
- •Anatomy and Physiology
- •Smooth Pursuit Eye Movements
- •Optokinetic Nystagmus
- •Ocular Following Response
- •Disorders
- •Smooth Pursuit Eye Movements
- •Cortex
- •Pontine Structures
- •Cerebellum
- •Medulla
- •Optokinetic Nystagmus
- •References
- •Disconjugate Eye Movements
- •Abstract
- •Horizontal Vergence Movements
- •Vertical Vergence Movements
- •Cyclovergence
- •Saccade-Associated Vergence Movements
- •Binocular Adaptation
- •Phoria Adaptation
- •Adaptation of Listing’s Plane
- •Binocular Saccade Adaptation
- •Disconjugate Eye Movements Evoked by Vestibular Stimulation
- •Disconjugate Eye Movements and Blinks
- •Pathological Disconjugate Eye Movements
- •References
- •Abstract
- •Neural Control of the Eyelid
- •Lid-Eye Coordination
- •Physiology of the Interaction between Eyelid and Eye Movements
- •Visual Consequences of Blinks
- •Blink-Associated Eye Movements
- •Effect of Blinks on Eye Movements
- •Blinks and Saccades
- •Blinks and Vergence Eye Movements
- •Blinks and Saccade-Vergence Interaction
- •Blinks and Smooth Pursuit Eye Movements
- •Clinical Disorders of the Eyelid and Its Interaction with Saccades
- •Disorders of Blink Frequency
- •Disorders of Tonic Eyelid Position
- •Disorders of Eyelid-Eye Coordination
- •Clinical Application of Lid Movements
- •Blinks and the Initiation of Eye Movements
- •Blinks Unmasking Vestibular Imbalance
- •References
- •Mechanics of the Orbita
- •Abstract
- •Classical Anatomy
- •EOM Layers
- •Gross Structure of EOMs
- •Structure of Pulleys
- •Functional Anatomy of Pulleys
- •Kinematics of Pulleys
- •Controversy Concerning Pulleys
- •Implications for Neural Control
- •Implications for Strabismus
- •Surgical Treatment of Pulley Pathology
- •Pulley Heterotopy
- •Pulley Instability
- •Pulley Hindrance
- •Conclusion
- •Acknowledgement
- •References
- •Abstract
- •Eye Plant
- •The Neural Velocity-to-Position Integrator
- •Saccadic Eye Movements
- •A Modeling Example: A 3-D Model of the Angular VOR
- •Smooth Pursuit Eye Movements
- •Combined Eye-Head Movements
- •Conclusions
- •References
- •Therapeutic Considerations for Eye Movement Disorders
- •Abstract
- •Peripheral and Central Vestibular Disorders
- •Pathophysiology
- •Vestibular Neuritis
- •Clinical Aspects
- •Etiology
- •Treatment
- •Menière’s Disease
- •Clinical Aspects
- •Etiology
- •Treatment
- •Superior Canal Dehiscence Syndrome
- •Clinical Aspects
- •Etiology
- •Treatment
- •Vestibular Paroxysmia
- •Clinical Aspects
- •Etiology
- •Treatment
- •Downbeat Nystagmus
- •Clinical Aspects
- •Etiology
- •Treatment
- •Upbeat Nystagmus
- •Clinical Aspects
- •Etiology
- •Treatment
- •Seesaw Nystagmus
- •Clinical Aspects
- •Etiology
- •Therapeutic Recommendations
- •Periodic Alternating Nystagmus
- •Clinical Aspects
- •Etiology
- •Therapeutic Recommendations
- •Other Supranuclear Oculomotor Disorders
- •Acquired Pendular Nystagmus
- •Clinical Aspects
- •Etiology
- •Treatment
- •Opsoclonus and Ocular Flutter
- •Clinical Aspects
- •Etiology
- •Treatment
- •Infranuclear Oculomotor Disorders
- •Superior Oblique Myokymia
- •Clinical Aspects
- •Etiology
- •Treatment
- •Benign Paroxysmal Positional Vertigo
- •Clinical Aspects
- •Etiology
- •Treatment
- •References
- •Subject Index
the axes of the involved canals. Using this premise, one can stimulate the vestibular system in numerous ways (lowand high-velocity head movements in 3-D, 3-D calorics, and diverse methods of inducing positional nystagmus) and relate the resulting eye movements to the function or dysfunction of single SCCs [44–46].
Obviously, in humans one cannot stimulate with electrodes the vestibular nerve and record the resulting eye movements. We therefore tested patients in whom nature produced a situation where just one SCC is stimulated. These patients suffered from benign paroxysmal positioning nystagmus. When the nystagmus induced by positioning the subject in the offending position is measured in 3-D and the average axis of eye rotation is reconstructed and plotted into a head-fixed reference system together with the anatomical on-directions of the SCCs it can be shown that the elicited eye movements are closely aligned with the direction of the offending canal. With this proof that also in humans eye movements are produced in the plane of the stimulated SCC, it is possible to deduct which canals are responsible for the direction of eye movements found during vestibular stimulation when parts of the vestibular sensors are defective [44, 47, 48].
Otolith Function
Subjective Visual Vertical
The subjective visual vertical (SVV) is a sensitive measure of otolith and especially utricular function. The bilateral graviceptive input from the otoliths dominates our perception of verticality. To test for SVV, the subjects sit with their heads fixed in the upright position and look at an illuminated line (on computer display or projected with a laser galvanometer system) in complete darkness. They then have to adjust 10 times separately for each eye the line from different starting positions to their SVV. In acute peripheral vestibular lesions, including the utricles, there is an ipsiversive deviation of the SVV of about 10–15 . Likewise, most patients with acute unilateral brainstem infarctions exhibit pathological tilts of static SVV from the true vertical [49].
Click-Evoked Myogenic Potentials
Electromyograms can be recorded from surface electrodes over the sternomastoid muscles and averaged in response to brief (0.1-ms) clicks played through headphones. In normal subjects, clicks 85–100 dB above 45 dB SPL (perceptual threshold for normal subjects) evoke reproducible changes in the
Fetter |
48 |
