It is well established that the head and eye velocity axes do not always align during compensatory vestibular slow phases. It has been shown that the eye velocity axis systematically tilts away from the head velocity axis in a manner that is dependent on eye-in-head position. The mechanisms responsible for producing these axis tilts are unclear. In this model-based study, we aimed to determine whether muscle pulleys could be involved in bringing about these phenomena. The model presented incorporates semicircular canals, central vestibular pathways, and an ocular motor plant with pulleys. The pulleys were modeled so that they brought about a rotation of the torque axes of the extraocular muscles that was a fraction of the angle of eye deviation from primary position. The degree to which the pulleys rotated the torque axes was altered by means of a pulley coefficient. Model input was head velocity and initial eye position data from passive and active yaw head impulses with fixation at 0 degrees, 20 degrees up and 20 degrees down, obtained from a previous experiment. The optimal pulley coefficient required to fit the data was determined by calculating the mean square error between data and model predictions of torsional eye velocity. For active head impulses, the optimal pulley coefficient varied considerably between subjects. The median optimal pulley coefficient was found to be 0.5, the pulley coefficient required for producing saccades that perfectly obey Listing's law when using a two-dimensional saccadic pulse signal. The model predicted the direction of the axis tilts observed in response to passive head impulses from 50 ms after onset. During passive head impulses, the median optimal pulley coefficient was found to be 0.21, when roll gain was fixed at 0.7. The model did not accurately predict the alignment of the eye and head velocity axes that was observed early in the response to passive head impulses. We found that this alignment could be well predicted if the roll gain of the angular vestibuloocular reflex was modified during the initial period of the response, while pulley coefficient was maintained at 0.5. Hence a roll gain modification allows stabilization of the retinal image without requiring a change in the pulley effect. Our results therefore indicate that the eye position-dependent velocity axis tilts could arise due to the effects of the pulleys and that a roll gain modification in the central vestibular structures may be responsible for countering the pulley effect.

Neuro-Ophthalmology helps clinicians evaluate and manage patients with neuro-ophthalmic problems, and is divided into five sections: afferent (visual) disorders; efferent (eye movement) disorders; eyelid disorders; pupil disorders; and combination syndromes. It is based on the most current scholarly evidence and is filled with practical advice.

Idiopathic intracranial hypertension is a syndrome of raised intracranial pressure of unknown cause that most often occurs in obese young women. Bilateral papilledema is usually present and can cause severe, irreversible vision loss if left untreated. In this chapter, we review the symptoms, signs, evaluation, and management of idiopathic intracranial hypertension.

No abstract

Gaze-evoked nystagmus is the one of the most common types of nystagmus encountered in clinical practice, but it is poorly localizing. It is often confused with physiologic “end-point” nystagmus. In this chapter, we begin by discussing the pathogenesis of gaze-evoked nystagmus. We next describe its clinical features as well as features that help distinguish it from “end-point” nystagmus, which is physiologic and of no concern. We then review common causes of gaze-evoked nystagmus, which include drugs (especially anticonvulsants), cerebellar degenerations, multiple sclerosis, and episodic ataxias. Lastly, we discuss the diagnostic approach to the patient with gaze-evoked nystagmus and basic management strategies.