Analysis of Cortisol and Other Stress-Related Hormones in Patients with M??ni??re??s Disease

Cruijsen, Nynke van; Dullaart, Robin; Wit, H. P.; Albers, F. W. J.

doi:10.1097/01.mao.0000179528.24909.ba

Cited by 39 publications

(15 citation statements)

References 16 publications

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“…One obvious explanation for hippocampal atrophy in humans with BVD is that chronic stress from the disability leads to high circulating levels of cortisol. Short-term increases in cortisol have been reported in patients with vestibular disorders (Horii et al, 2007); however, long-term increases have been reported only in the case of Meniere’s disease and acoustic neuroma (Horner and Cazals, 2005; van Cruijsen et al, 2005). To date, every rat or guinea pig study that has examined corticosterone or cortisol levels (respectively) following unilateral or BVD has found no significant difference compared to sham controls up 5 months post-op.…”

Section: Discussionmentioning

confidence: 99%

The Effects of Bilateral Vestibular Loss on Hippocampal Volume, Neuronal Number, and Cell Proliferation in Rats

Zheng¹,

Balabhadrapatruni²,

Baek³

et al. 2012

Front. Neur.

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Previous studies in humans have shown that bilateral loss of vestibular function is associated with a significant bilateral atrophy of the hippocampus, which correlated with the patients’ spatial memory deficits. More recently, patients who had recovered from unilateral vestibular neuritis have been reported to exhibit a significant atrophy of the left posterior hippocampus. Therefore, we investigated whether bilateral vestibular deafferentation (BVD) would result in a decrease in neuronal number or volume in the rat hippocampus, using stereological methods. At 16 months post-BVD, we found no significant differences in hippocampal neuronal number or volume compared to sham controls, despite the fact that these animals exhibited severe spatial memory deficits. By contrast, using bromodeoxyuridine (BrdU) as a marker of cell proliferation, we found that the number of BrdU-labeled cells significantly increased in the dentate gyrus of the hippocampus between 48 h and 1 week following BVD. Although a substantial proportion of these cells survived for up to 1 month, the survival rate was significantly lower in BVD animals when compared with that in sham animals. These results suggest a dissociation between the effects of BVD on spatial memory and hippocampal structure in rats and humans, which cannot be explained by an injury-induced increase in cell proliferation.

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Section: Discussionmentioning

confidence: 99%

The Effects of Bilateral Vestibular Loss on Hippocampal Volume, Neuronal Number, and Cell Proliferation in Rats

Zheng¹,

Balabhadrapatruni²,

Baek³

et al. 2012

Front. Neur.

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show abstract

“…Short-term elevations of cortisol and arginine vasopressin have been reported in patients with vestibular disorders (Horii et al, 2007); however, longer term elevations have been reported only in Meniere's disease and acoustic neuroma (Horner and Cazals, 2005;van Cruijsen et al, 2005), in the former case possibly because of its paroxysmal nature. No longterm studies have been carried out in patients with chronic bilateral vestibular loss.…”

Section: Why Should Manipulation Of the Vestibular System Have Effectmentioning

confidence: 94%

Move it or lose it—Is stimulation of the vestibular system necessary for normal spatial memory?

2009

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Studies in both experimental animals and human patients have demonstrated that peripheral vestibular lesions, especially bilateral lesions, are associated with spatial memory impairment that is long-lasting and may even be permanent. Electrophysiological evidence from animals indicates that bilateral vestibular loss causes place cells and theta activity to become dysfunctional; the most recent human evidence suggests that the hippocampus may cause atrophy in patients with bilateral vestibular lesions. Taken together, these studies suggest that self-motion information provided by the vestibular system is important for the development of spatial memory by areas of the brain such as the hippocampus, and when it is lost, spatial memory is impaired. This naturally suggests the converse possibility that activation of the vestibular system may enhance memory. Surprisingly, there is some human evidence that this may be the case. This review considers the relationship between the vestibular system and memory and suggests that the evolutionary age of this primitive sensory system as well as how it detects self-motion (i.e., detection of acceleration vs. velocity) may be the reasons for its unique contribution to spatial memory.

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“…The changes in the limbic system are particularly interesting with respect to the hippocampal atrophy and related spatial memory deficits seen in patients with BVF [1]: Vestibular failure is known to be associated with an increase in the level of glucocorticoids [40], [41] and a reductive effect of these hormones on hippocampal volume was shown in various neuropsychiatric diseases [42]. Balance trained individuals have also shown a decrease in the anterior portion of the hippocampus [11], which is often related to emotional and chemical processing.…”

Section: Discussionmentioning

confidence: 99%

Vestibular Loss and Balance Training Cause Similar Changes in Human Cerebral White Matter Fractional Anisotropy

et al. 2014

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Patients with bilateral vestibular loss suffer from severe balance deficits during normal everyday movements. Ballet dancers, figure skaters, or slackliners, in contrast, are extraordinarily well trained in maintaining balance for the extreme balance situations that they are exposed to. Both training and disease can lead to changes in the diffusion properties of white matter that are related to skill level or disease progression respectively. In this study, we used diffusion tensor imaging (DTI) to compare white matter diffusivity between these two study groups and their age- and sex-matched controls. We found that vestibular patients and balance-trained subjects show a reduction of fractional anisotropy in similar white matter tracts, due to a relative increase in radial diffusivity (perpendicular to the main diffusion direction). Reduced fractional anisotropy was not only found in sensory and motor areas, but in a widespread network including long-range connections, limbic and association pathways. The reduced fractional anisotropy did not correlate with any cognitive, disease-related or skill-related factors. The similarity in FA between the two study groups, together with the absence of a relationship between skill or disease factors and white matter changes, suggests a common mechanism for these white matter differences. We propose that both study groups must exert increased effort to meet their respective usual balance requirements. Since balance training has been shown to effectively reduce the symptoms of vestibular failure, the changes in white matter shown here may represent a neuronal mechanism for rehabilitation.

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Analysis of Cortisol and Other Stress-Related Hormones in Patients with M??ni??re??s Disease

Cited by 39 publications

References 16 publications

The Effects of Bilateral Vestibular Loss on Hippocampal Volume, Neuronal Number, and Cell Proliferation in Rats

The Effects of Bilateral Vestibular Loss on Hippocampal Volume, Neuronal Number, and Cell Proliferation in Rats

Move it or lose it—Is stimulation of the vestibular system necessary for normal spatial memory?

Vestibular Loss and Balance Training Cause Similar Changes in Human Cerebral White Matter Fractional Anisotropy

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