- •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
central structures (multiple sclerosis) may show hyperventilation-induced nystagmus [36].
Laboratory Evaluation: Electro-Oculography and Rotational Testing
Vestibular laboratory testing can aid in diagnosis, can be used to document an abnormality suspected at bedside evaluation, and can aid in devising a treatment plan. The ability to perform serial vestibular evaluations allows an assessment over time of patients who are undergoing treatment for their dizziness or who are undergoing treatment with a potentially ototoxic medication. Both electro-oculography (EOG) and rotational testing can provide information that is helpful for determining if a vestibular abnormality is present and, if so, whether it is located in the central or peripheral vestibular system. The choice of subtests that are preformed may vary according to the clinical suspicions of the physician ordering the test. When a peripheral vestibular abnormality is suspected caloric testing may be helpful, and when a central vestibular abnormality is suspected visual-vestibular interaction tests may prove useful.
Positional testing is performed as part of the EOG battery by placing the patient in the supine and head-hanging positions, head-right and right-lateral positions, and head-left and left-lateral positions. However, BPPV may be difficult to record in the vestibular laboratory because EOG is insensitive to torsional eye movements and vertical EOG is plagued by eyeblink and muscle artifacts and has a low signal/noise ratio. Despite these limitations, patients with positioning vertigo should have Dix-Hallpike testing, as many patients with BPPV produce a recordable eye movement whose temporal characteristics can be objectified. A paroxysmal nystagmus observed during the Dix-Hallpike maneuver that does not conform to the typical pattern seen with BPPV should be considered the result of a CNS abnormality until it is proved otherwise. Examples of such nystagmus include downbeating nystagmus in a head-hang- ing position and nystagmus that does not fatigue with repeated positioning.
Caloric testing is the mainstay of vestibular laboratory testing. The caloric response is primarily the result of the convection current caused by the combination of a thermal gradient across the horizontal SCC and placement of the lateral canal in a vertical plane. Although research from microgravity experiments has indicated that direct thermal effects generate a portion of the caloric response, the convection current theory still accounts for most of the caloric response [37]. Warm irrigation of the ear causes excitation of the lateral SCC and thus induces slow movement of the eyes away from the side of irrigation with subsequent beating toward the ear being irrigated. The irrigation of the left ear with cool water induces right-beating nystagmus. Many studies have shown
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that the maximum slow component velocity attained after each caloric irrigation is the best determinant of the response of a particular ear to a particular stimulus [38]. A reduced vestibular response typically indicates a peripheral vestibular injury. It may include damage to the labyrinth itself, the eighth cranial nerve, or the root entry zone of the vestibular nerve. When an ear is unresponsive to warm and cold irrigation, direct irrigation with ice water may be helpful. The chief advantage of caloric testing is its ability to stimulate each ear individually.
The types of rotational vestibular testing that are in common clinical use include earth-vertical axis rotation and visual-vestibular interaction. Rotational testing makes use of a natural stimulus to the labyrinth (i.e. rotational acceleration). Besides sinusoidal rotations, rotating a subject at a constant velocity for enough time for the perrotatory nystagmus to decay is widely used. The rotational chair is then stopped abruptly and the induced postrotatory nystagmus is measured. The main measures of the response to constant velocity rotation are gain and time constant. The gain is, by definition, the ratio of the magnitude of the response to the magnitude of the stimulus (maximum eye velocity divided by maximum head velocity). The time constant of the VOR is a measure of how rapidly vestibular nystagmus decays after an abrupt stop of the rotation chair [39].
Conventional Rotational Testing
The hallmark of unilateral peripheral vestibular loss is a reduced vestibular response on caloric testing. With acute peripheral vestibular lesions, a brisk spontaneous nystagmus may make interpretation of caloric testing difficult, especially if nystagmus in the same direction is seen regardless of the side or temperature of the irrigation during bithermal testing. In such cases, ice-water irrigation may be helpful. Ice-water irrigation of the normal ear should stop the nystagmus in the acute phase and reverse it in compensated states [40]. Acute unilateral peripheral vestibular lesions are usually associated with a normal ocular motor screening battery and an absence of gaze-evoked nystagmus. However, with a severe acute unilateral peripheral loss there may be asymmetrical pursuit and asymmetrical optokinetic nystagmus as a result of superposition of an intense spontaneous vestibular nystagmus with visual following. Also, with an acute unilateral peripheral vestibular lesion, there may be spontaneous nystagmus during fixation. Rotational testing shortly after an acute unilateral peripheral loss usually shows severe asymmetry and drastically reduced time constants [41].
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