16 research outputs found
Vergence-mediated modulation of the human horizontal angular VOR provides evidence of pathway-specific changes in VOR dynamics
The horizontal vestibulo-ocular reflex (VOR) evoked by passive, high-acceleration, head-on-body rotations (head thrusts) while viewing a far (124-cm) or near (15-cm) target was recorded (scleral search coil) In four subjects with normal vestibular function and in one subject with unilateral vestibular hypofunction. For responses in the subjects with normal vestibular function, the latency of responses relative to the onset of head movement was 7.5 +/- 1.5 ms for the VOR and 21.6 +/- 1.2 ms for the vergence-mediated increase in VOR gain. The gain of the VOR at the peak of the velocity response while viewing a far target was 1.01 +/- 0.06; while viewing a near target, it was 1.25 +/- 0.08 (p <0.003). The responses were modeled with two pathways based on the different latencies. The "far-viewing" pathway was represented by a constant gain term. The "near-viewing" pathway was represented by a first-order lead term, a gain that was dependent on viewing distance, and a delay. Analysis of the responses revealed that the lead term was greater for the adducting than the abducting eye. In the subject with unilateral vestibular hypofunction, ipsilesional responses showed no change in VOR gain with respect to viewing distance. Contralesional responses retained the vergence-dependent increase in gain. A bilateral model was developed based on the data from the subjects with normal vestibular function. Simulations of this model when inputs were eliminated from one side predict the changes observed in the subject with unilateral vestibular hypofunction. The response asymmetries arise because the near-viewing pathway is more susceptible to inhibitory cutoff than is the far-viewing pathway
Superior Canal Dehiscence Syndrome and VEMPs: Detection of Hypersensitivity of the Vestibular System to Sound
Gentamicin Injections for Ménière Disease: Comparison of Subjective and Objective end Points
Current Treatment of Vestibular, Ocular Motor Disorders and Nystagmus
Vertigo and dizziness are among the most common complaints with a lifetime
prevalence of about 30%. The various forms of vestibular disorders can be
treated with pharmacological therapy, physical therapy, psychotherapeutic
measures or, rarely, surgery. In this review, the current pharmacological
treatment options for peripheral and central vestibular, cerebellar and ocular
motor disorders will be described. They are as follows for peripheral vestibular
disorders. In vestibular neuritis recovery of the peripheral vestibular function
can be improved by treatment with oral corticosteroids. In
Menière's disease a recent study showed long-term
high-dose treatment with betahistine has a significant effect on the frequency
of the attacks. The use of aminopyridines introduced a new therapeutic principle
in the treatment of downbeat and upbeat nystagmus and episodic ataxia type 2 (EA
2). These potassium channel blockers presumably increase the activity and
excitability of cerebellar Purkinje cells, thereby augmenting the inhibitory
influence of these cells on vestibular and cerebellar nuclei. A few studies
showed that baclofen improves periodic alternating nystagmus, and gabapentin and
memantine, pendular nystagmus. However, many other eye movement disorders such
as ocular flutter opsoclonus, central positioning, or see-saw nystagmus are
still difficult to treat. Although progress has been made in the treatment of
vestibular neuritis, downbeat and upbeat nystagmus, as well as EA 2,
state-of-the-art trials must still be performed on many vestibular and ocular
motor disorders, namely Menière's disease, bilateral
vestibular failure, vestibular paroxysmia, vestibular migraine, and many forms
of central eye movement disorders