10 research outputs found
Visuomotor Cerebellum in Human and Nonhuman Primates
In this paper, we will review the anatomical components of the visuomotor cerebellum in human and, where possible, in non-human primates and discuss their function in relation to those of extracerebellar visuomotor regions with which they are connected. The floccular lobe, the dorsal paraflocculus, the oculomotor vermis, the uvula–nodulus, and the ansiform lobule are more or less independent components of the visuomotor cerebellum that are involved in different corticocerebellar and/or brain stem olivocerebellar loops. The floccular lobe and the oculomotor vermis share different mossy fiber inputs from the brain stem; the dorsal paraflocculus and the ansiform lobule receive corticopontine mossy fibers from postrolandic visual areas and the frontal eye fields, respectively. Of the visuomotor functions of the cerebellum, the vestibulo-ocular reflex is controlled by the floccular lobe; saccadic eye movements are controlled by the oculomotor vermis and ansiform lobule, while control of smooth pursuit involves all these cerebellar visuomotor regions. Functional imaging studies in humans further emphasize cerebellar involvement in visual reflexive eye movements and are discussed
P78 The phenotype, survival, distribution, and integration of autologous chondrocytes used to treat articular cartilage defects in a rabbit model.
Challenges in the evaluation of safety and efficacy of human tissue and cell based products
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
Muscimol inactivation caudal to the interstitial nucleus of Cajal induces hemi-seesaw nystagmus
A model-based theory on the origin of downbeat nystagmus
The pathomechanism of downbeat nystagmus (DBN), an ocular motor sign typical for vestibulo-cerebellar lesions, remains unclear. Previous hypotheses conjectured various deficits such as an imbalance of central vertical vestibular or smooth pursuit pathways to be causative for the generation of spontaneous upward drift. However, none of the previous theories explains the full range of ocular motor deficits associated with DBN, i.e., impaired vertical smooth pursuit (SP), gaze evoked nystagmus, and gravity dependence of the upward drift. We propose a new hypothesis, which explains the ocular motor signs of DBN by damage of the inhibitory vertical gaze-velocity sensitive Purkinje cells (PCs) in the cerebellar flocculus (FL). These PCs show spontaneous activity and a physiological asymmetry in that most of them exhibit downward on-directions. Accordingly, a loss of vertical floccular PCs will lead to disinhibition of their brainstem target neurons and, consequently, to spontaneous upward drift, i.e., DBN. Since the FL is involved in generation and control of SP and gaze holding, a single lesion, e.g., damage to vertical floccular PCs, may also explain the associated ocular motor deficits. To test our hypothesis, we developed a computational model of vertical eye movements based on known ocular motor anatomy and physiology, which illustrates how cortical, cerebellar, and brainstem regions interact to generate the range of vertical eye movements seen in healthy subjects. Model simulation of the effect of extensive loss of floccular PCs resulted in ocular motor features typically associated with cerebellar DBN: (1) spontaneous upward drift due to decreased spontaneous PC activity, (2) gaze evoked nystagmus corresponding to failure of the cerebellar loop supporting neural integrator function, (3) asymmetric vertical SP deficit due to low gain and asymmetric attenuation of PC firing, and (4) gravity-dependence of DBN caused by an interaction of otolith-ocular pathways with impaired neural integrator function