In this study, the authors demonstrated that a single dose of 3,4-DAP significantly improved DBN. In view of animal studies reporting that micromolar concentrations of 4-aminopyridine increased the excitability of Purkinje cells, it is suggested that the efficacy of 3,4-DAP may be due to an increase of the physiologic inhibitory influence of the vestibulocerebellum on the vestibular nuclei.
There is sound evidence from histopathological and magnetic resonance imaging (MRI) studies that focal ischemic brain lesions tend to increase in size over time. Considerable lesion growth was observed in models of animal stroke as well as in patients presenting with hemispheric stroke. In focal cerebral ischemia, lesions predominantly enlarge early within 12 hours after onset. Ischemic injury is caused by complete necrosis in most of the affected tissue. By contrast, in global cerebral ischemia as seen after cardiac arrest, lesions appear late (>12 h) in selectively vulnerable brain regions such as the hippocampus, and neurons are damaged by apoptotic cell death. The high and regionally distinct vulnerability of the brain explains why prolonged periods of global ischemia result in widespread loss of energy metabolites combined with diffuse brain edema and global damage. Postulated mechanisms involved in lesion growth include among others excitotoxicity, periinfarct depolarizations, lactacidosis, microcirculatory disturbances, and flow-metabolism uncoupling. Research in the field faces two main challenges. First,maturation phenomena of injury may require special imaging techniques to detect early ischemic changes. Second, the dynamic nature of the changes underlines the need to conduct longitudinal studies with a variety of imaging techniques (e. g., metabolic imaging, diffusion/perfusion MRI, positron emission tomography) that require a differentiated interpretation of the alterations observed.
The aim of this study was to investigate the possible interaction of vestibulo-ocular and vestibulo-spinal functions. Spontaneous eye movements and anterior-posterior and lateral body sway were recorded simultaneously in 10 patients with vestibular neuritis (Experiment 1) and in 11 healthy subjects (Experiment 2) while all subjects wore a mask that allowed fixation of a head-fixed target. For the healthy subjects, there was no significant difference in postural sway for the conditions of eyes open in darkness and fixation of the head-fixed target. For the patients, the question was whether transient suppression of the spontaneous nystagmus by fixating the target affected excessive body sway or whether modulation of nystagmus and postural sway were largely independent. The mean peak slow-phase velocity of the spontaneous nystagmus decreased from 13.5 +/- 5.6 to 4.3 +/- 2.4 degrees /s during fixation. The suppression of nystagmus also reduced postural sway while standing on foam rubber. Mean value decreased from 25.2 +/- 7.6 to 16.2 +/- 7.7 mm (right-left root mean square values; ANOVA, P = 0.003). Since a head-fixed target was used to suppress spontaneous eye movements, the data cannot be explained by any stabilizing effect of afferent visual cues. Instead, ocular motor efference copy signals or reafferences may have contributed to the postural instability of patients with vestibular neuritis, which would explain the reduction of postural sway during fixation suppression of the nystagmus. Thus, ocular motor signals rather than afferent visual cues about retinal slip are used for visual control of postural sway, at least in this experimental paradigm.
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