- •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
way from the treatment. The patients in whom the influence of the gravity-depen- dent component is more pronounced also seem to benefit more from a supine head position [41]. In isolated patients with a craniocervical anomaly, a surgical decompression involving the removal of part of the occipital bone in the region of the foramen magnum was beneficial [42, 43].
As a practical rule, treatment should be started by trying clonazepam. If this option does not improve the nystagmus satisfactorily, 4-aminopyridine (10 mg three times daily) should be tried.
Upbeat Nystagmus
Clinical Aspects
Upbeat nystagmus occurs when the eyes are close to the central position and usually increases during upgaze [44]. The nystagmus usually disrupts vertical smooth pursuit. In some patients, the upbeat nystagmus changes to downbeat nystagmus during convergence. An upbeat nystagmus has in general a better prognosis than a downbeat nystagmus and is often only a temporary problem [11].
Etiology
A central vestibular imbalance is involved in upbeat nystagmus as in downbeat nystagmus. The most frequently seen lesions are medullary lesions [44]. Probable causes of upbeat nystagmus are lesions in the ascending pathways from the anterior canals (and/or the otoliths) at the pontomesencephalic or pontomedullary junction, near the perihypoglossal nuclei [44, 45]. The main causes are multiple sclerosis, tumors of the brainstem, Wernicke’s encephalopathy, intoxication (e.g. nicotine), and seldom cerebellar degeneration.
Treatment
Treatment with baclofen (5–10 mg p.o. three times daily) caused an improvement in several patients [37]. Probably 4-aminopyridine will also improve the upbeat nystagmus in some patients [46].
Seesaw Nystagmus
Clinical Aspects
Seesaw nystagmus is a rare pendular or jerk oscillation around the line of gaze. A half-cycle consists of elevation and intorsion of one eye with synchronous
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