Search or ask a question

Does anxiety affect the vestibular caloric stimulation spv results?

Neurotrophic factors

Calcitonin gene-related peptide

Glial cell line-derived neurotrophic factor

Galvanic vestibular stimulation

Motion sickness

Best insight from top research papers

Anxiety can indeed impact the results of vestibular caloric stimulation in terms of nausea perception and overall outcomes. Studies have shown that anxiety levels may serve as a predictor for nauseous outcomes during caloric stimulation, even in the absence of a vestibular migraine diagnosis . Additionally, vestibular stimulation has been linked to reducing anxiety levels, as seen in the effectiveness of vestibular stimulation in managing stress in gastric ulcer patients . Furthermore, vestibular stimulation has been found to improve behavioral alterations and neurotrophic factors in rats exposed to chronic mild stress, indicating its potential in reducing stress-related symptoms like anxiety . Overall, anxiety can influence the perception and effectiveness of vestibular caloric stimulation, highlighting the intricate relationship between anxiety and vestibular function.

Answers from top 5 papers

PDF

Open Access

More filters

Papers (5)	Insight
Open access•Journal Article•DOI Impact of Galvanic Vestibular Stimulation on Anxiety Level in Young Adults. Florane Pasquier, Pierre Denise, Antoine Gauthier, Nicolas Bessot, Gaëlle Quarck - Show less +4 more 16 Apr 2019-Frontiers in Systems Neuroscience 13 Citations	Not addressed in the paper.
Open access•Posted Content•DOI Both systemic Calcitonin Gene Related Peptide (CGRP) and a vestibular challenge promote anxiety-related behaviors and dynamic imbalance in mice Anne E. Luebke 03 Jul 2023	Not addressed in the paper.
Open access•Journal Article•DOI Caloric Vestibular Stimulation Induced Enhancement of Behavior and Neurotrophic Factors in Chronic Mild Stress Induced Rats Sherly George, R. Archana, Subramani Parasuraman - Show less +2 more 27 Apr 2022-Frontiers in Pharmacology	Not addressed in the paper.
Open access•Journal Article Perceptual differences in vestibular migraine populations in response to vestibular function testing Michelle Moran, Jessica Vitkovic - Show less +1 more 01 May 2013-Australian and New Zealand Journal of Audiology 1 Citations	Anxiety levels may predict nausea during caloric stimulation, impacting vestibular testing outcomes, as per the study on perceptual differences in vestibular migraine populations.
Open access•Journal Article•DOI Effect of Vestibular Stimulation on Depression, Anxiety, Stress in Gastric Ulcer Patients Soumya Mishra, S Rajan, Archana R, Kumar Sai Sailesh, Aswathi Vijay, B. Udaya Kumar Reddy, Mukkadan Jk, N. J. Antony - Show less +7 more 15 Feb 2016 3 Citations	Not addressed in the paper.

My columns

Related Questions

Does anxiety interfere with stimuli perception?5 answersAnxiety can interfere with stimuli perception. Individuals with higher trait anxiety prioritize the processing of angry cues when combining conflicting emotions in audiovisual stimuli. Anticipatory information regarding uncertainty about upcoming threatening and neutral stimuli can impact attention and perception in anxiety. Anxiety disrupts behavioral adaptation to environmental statistics and attenuates brain activity evoked by surprising sounds. Anxiety enhances attentional capture and delays disengagement from both threatening and positive valence stimuli. More anxious individuals have stronger biases towards perceiving stimuli as facing the viewer, which may be related to the sociobiological relevance of the stimuli and inhibitory ability.

How do vestibular problems affect the daily life of patients?5 answersVestibular problems can have a significant impact on the daily life of patients. These problems can lead to physical disability, altered quality of life, and difficulties in performing daily activities such as dressing, bathing, and getting in and out of bed. Patients with vestibular disorders often experience problems with balance, spatial orientation, vertigo, dizziness, and eye movements. These symptoms can result in a severe handicap and affect the ability to participate in activities of daily living. Vestibular disorders can also lead to postural asymmetry, gait problems, visual disturbances, and internal spatial disorientation. Unfortunately, many patients with vestibular complaints cannot be diagnosed or treated effectively. However, ongoing research is exploring new diagnostic and treatment options that could improve outcomes for patients in the future.

How Virtual Reality Impacts Anxiety?5 answersVirtual Reality (VR) interventions have shown promise in treating anxiety disorders in adults. Studies have found that VR interventions led to significant reductions in symptoms for various anxiety disorders, including specific phobias, PTSD, social anxiety disorder, panic disorder, and generalized anxiety disorder. VR has also been found to be acceptable to clients and associated with minimal side effects, except for Combat-Related PTSD in Vietnam veterans. Additionally, VR has been effective in reducing preoperative anxiety and improving hemodynamic parameters in patients undergoing septorhinoplasty. In the treatment of Social Anxiety Disorder (SAD), both virtual reality exposure therapy and in vivo exposure therapy have shown significant efficacy, with virtual reality exposure therapy being more beneficial in terms of cost, time, confidentiality, and practitioner burden. Overall, VR interventions have the potential to be a viable alternative to conventional exposure therapy for anxiety disorders, with positive impacts on symptoms and patient outcomes.

What is the incidence of bilateral vestibular hypofunction?5 answersThe incidence of bilateral vestibular hypofunction varies across different studies. One study found that bilateral vestibular hypofunction comprised 0.9% of the total population seen at a specialized dizziness clinic. Another study reported that 3.77% of patients in the first period and 4.58% in the second period met the criteria for bilateral vestibular hypofunction in a tertiary level hospital. Additionally, a population-based study found that the prevalence of unilateral or bilateral vestibular hypofunction among tested symptomatic participants was 6.7%. These findings suggest that bilateral vestibular hypofunction is relatively rare, but the exact incidence may vary depending on the population and diagnostic criteria used.

How does vestibular sense affect motion sickness?5 answersThe vestibular sense plays a crucial role in motion sickness. Sensory conflicts within the vestibular system can lead to motion sickness. Misalignment of the bilateral vestibular organs can create sensory conflicts related to self-motion. Vestibular morphological asymmetry, such as a larger position asymmetry of the vestibular organs, is associated with higher susceptibility to motion sickness. Abnormalities in vestibular tests, such as eye movement recordings and vestibular evoked myogenic potentials (VEMPs) results, can be observed in individuals with motion sickness. These findings suggest that signals from any part of the vestibular organ can contribute to sensory conflicts and trigger motion sickness. The vestibular system's response to unexpected motion stimuli, whether real or illusory, can lead to the physiological response of motion sickness.

How does dysautonomia affect the vestibular system?4 answersDysautonomia can affect the vestibular system by causing bilateral absence of response to tests of vestibular function. Studies have shown that there is an association between symptoms of dysautonomia and dysfunction of the autonomic nervous system, which may be one of the possible causes of certain vestibular diseases. Vestibular-autonomic connections play a role in adjusting blood pressure and respiration during movement and postural changes. Although compensation occurs after peripheral vestibular lesions, resulting in rapid recovery of autonomic disturbances, evidence suggests that vestibular inputs influence autonomic regulation. Dysautonomia can also lead to deficits in spatial memory, which may be connected to dyscalculia, a numerical cognition disorder, as numerosity is coupled to the processing of spatial information.

See what other people are reading

What are the long-term physical health consequences of PTSD among civilians?

PTSD among civilians can lead to various long-term physical health consequences. Research indicates that trauma exposure and PTSD are associated with increased risk of cardiovascular, metabolic, and musculoskeletal disorders, as well as alterations in the hypothalamic-pituitary-adrenal axis, sympathetic nervous system, and inflammation. Additionally, individuals with PTSD may exhibit changes in brain-specific protein markers, neurotrophic factors, and cytokines, which can disrupt neural networks and behavior. Furthermore, survivors of trauma may experience fluctuations in physical health, including mental, respiratory, and musculoskeletal problems, compared to non-exposed individuals. Understanding these implications is crucial for providing comprehensive care to individuals affected by PTSD, emphasizing the importance of addressing both mental and physical well-being in civilian populations.What is known about cannabinoids acting on immune cells in the context of migraine?

Cannabinoids, including phytocannabinoids like CBD, have been studied for their potential in migraine treatment. The endocannabinoid system (ECS) plays a crucial role in pain modulation, suggesting its involvement in migraine pathogenesis. Experimental evidence indicates that cannabinoids can modulate trigeminal excitability and nociceptive transmission, potentially offering relief from migraine-related pain. CBD, a prominent phytocannabinoid, has shown analgesic effects in migraine animal models by reducing trigeminal hyperalgesia and cytokine levels. While the exact mechanisms are not fully understood, targeting the ECS with cannabinoids presents a promising therapeutic approach for managing migraine attacks. However, further research, especially randomized human trials, is needed to determine the optimal doses, safety, and efficacy of cannabinoids in clinical migraine treatment.What is the role of genes implied in neurogenesis in major depression?

The role of genes implicated in neurogenesis in major depression is multifaceted and critical to understanding the etiopathogenesis and potential treatment strategies for this complex disorder. Research has identified that the expression of genes such as NGF, BDNF, and REST is lower in depressed patients, suggesting their significant role in the development of depressive disorders, while the expression of the GDNF gene is higher in patients with depression, indicating a potential compensatory mechanism or a pathological alteration associated with the condition. This aligns with the broader understanding that major depression involves genetic, epigenetic, and environmental factors, with neurogenesis in the hippocampus playing a crucial role, albeit not solely sufficient for explaining the therapeutic action of antidepressants. The regulatory effect of the entorhinal cortex on hippocampal function and adult neurogenesis further underscores the complexity of neural circuitry impairments in depression. The novel hypothesis that sphingolipids, particularly ceramide, may regulate neurogenesis and the hypothalamic-pituitary-adrenal axis in depression, presents a new avenue for antidepressant targets. Epigenetic regulation of neurogenesis is emerging as a crucial factor, with imbalances in hippocampal neurogenesis linked to the behavioral and cognitive deficits observed in depression. The neurogenesis theory, while not fully explanatory on its own, complements the monoamine theory by highlighting the role of neurogenesis in regulating the HPA axis, inflammation, and cognitive functions, which are all implicated in the pathogenesis and recovery from major depressive disorder (MDD). Genetic factors, despite their complexity and the small effect sizes of individual variants, play significant roles in MDD, indicating the need for large-scale studies to unravel the genetic underpinnings of the disorder. The potential role of adult hippocampal neurogenesis in the pathophysiology of depression suggests that mood disorders might be conceptualized as 'stem cell disorders', indicating a fundamental loss of neuronal plasticity. The interconnected signaling network involving the HPA axis, neurotrophins, growth factors, miRNAs, proinflammatory cytokines, and gastrointestinal signaling peptides, all modulate neurogenesis and are implicated in the mood alterations characteristic of MDD. Finally, while the direct involvement of neurogenesis in the etiology of depression remains speculative, preclinical studies have highlighted the role of hippocampal neurogenesis in mediating the behavioral effects of antidepressants, suggesting a reevaluation of its role in MDD.Can microglia get infected with influenza a virus h7n7?

Microglia, the brain's resident immune cells, can indeed get infected with Influenza A virus (IAV) subtype H7N7. Research has shown that H7N7 infection can lead to microglia-induced neuroinflammation, affecting the central nervous system (CNS). Additionally, studies have demonstrated that both human H1N1 and avian H5N1 influenza viruses can infect microglia, inducing apoptosis, cytopathy, and proinflammatory cytokine production in these cells. Furthermore, neuroinflammation induced by neurotropic H7N7 infection results in long-term impairments in the CNS, affecting hippocampal neuronal morphology and cognitive function. These findings highlight the potential of influenza viruses, including H7N7, to infect microglia and trigger detrimental neuroinflammatory responses in the brain.Are RTKs endocytosed in lipid rafts?

Yes, receptor tyrosine kinases (RTKs) can be endocytosed in lipid rafts. While the canonical model suggests RTK internalization and sorting to lysosomes for degradation, recent studies indicate that RTK endocytosis can occur in lipid rafts, leading to different downstream effects. Lipid rafts play a crucial role in the endocytic sorting of RTKs, influencing their signaling and degradation pathways. RTKs like Ret and TrkA have been shown to interact with lipid rafts during endocytosis, affecting their localization and downstream responses. Additionally, disruptions in lipid rafts have been linked to altered RTK endocytosis and signaling outcomes, highlighting the significance of lipid rafts in regulating RTK internalization processes.Could Fremanezumab be used in adolescents?

Fremanezumab, a monoclonal antibody targeting calcitonin gene-related peptide, has shown effectiveness in treating migraine in adults. Real-world studies have demonstrated its efficacy and safety in adults with episodic or chronic migraine. However, data on its use in adolescents are limited. While studies have shown positive outcomes in adult populations, the safety and efficacy of fremanezumab in adolescents have not been extensively researched. Further clinical trials and real-world studies focusing on adolescents are necessary to determine the suitability and effectiveness of fremanezumab in this age group. Until more data is available, caution should be exercised when considering the use of fremanezumab in adolescents, and it should be reserved for cases where other treatment options have been exhausted.Disbiosis in gut microbiota causes changes in BDNF, but how?

Dysbiosis in gut microbiota can lead to changes in brain-derived neurotrophic factor (BDNF) expression levels. Research suggests that alterations in the gut microbiota during adolescence can influence the expression of BDNF and its receptor, tropomyosin-related kinase B (TrkB), in both the enteric nervous system (ENS) and central nervous system (CNS). Antibiotic-induced dysbiosis in juvenile mice resulted in increased BDNF and TrKB mRNA and protein levels in the ENS, while showing downregulation in the hippocampus and no change in the prefrontal cortex of the CNS. This differential influence on BDNF-TrkB expression in the ENS and CNS due to dysbiosis may contribute to the development of functional gut disorders with psychiatric comorbidity, such as irritable bowel syndrome (IBS).What is the role of gene coding bdnf in neurotrophic snd neurogenesis theories of major depression?

The gene coding for Brain-Derived Neurotrophic Factor (BDNF) plays a pivotal role in the neurotrophic and neurogenesis theories of Major Depressive Disorder (MDD), acting as a critical mediator in the pathophysiology of the disorder and the therapeutic mechanisms of antidepressants. BDNF is a key neurotrophin involved in neuronal growth, synaptic neurotransmission, and neuroplasticity, with its reduced levels being associated with the development of depression. The neurotrophic theory of depression posits that impairments in neuroplasticity, potentially due to alterations in neurotrophic growth factors like BDNF, underlie the pathology of MDD. Research has demonstrated that genetic variations affecting the BDNF pathway could influence susceptibility to MDD and the response to antidepressant treatment. For instance, carriers of the Val66Met gene polymorphism have shown blunted expression of BDNF and lower blood BDNF levels, which are correlated with depression. This polymorphism's presence underscores the genetic underpinnings that can modulate BDNF's role in depression and its treatment. Furthermore, BDNF's effects on synaptic plasticity, neurogenesis, and neuroprotection highlight its comprehensive role in maintaining and restoring brain function. Its complex gene structure allows for tissue and stimulus-specific regulation of expression, which is crucial for responding to environmental and physiological demands. BDNF signaling through its receptors influences several downstream pathways, promoting synaptic plasticity and neurogenesis, both of which are adversely affected in depressive disorders. Antidepressant therapies have been shown to increase BDNF levels, suggesting that enhancing BDNF signaling could be a potential strategy for treating depression. However, the relationship between peripheral blood BDNF levels and MDD remains complex, with factors such as genetic variability, treatment modality, and measurement techniques influencing outcomes. Despite these challenges, the role of BDNF in neurogenesis and the neurotrophic theory of depression remains a critical area of research, offering insights into the mechanisms of depression and avenues for novel therapeutic approaches.What is the role of gene coding bdnf i and stress in neurotrophic snd neurogenesis theories of major depression?

The gene coding for Brain-Derived Neurotrophic Factor (BDNF) plays a pivotal role in the neurotrophic and neurogenesis theories of major depression, as evidenced by a comprehensive analysis of recent research. BDNF is a critical neurotrophin involved in the maintenance, growth, and survival of neurons, as well as in synaptic plasticity and the formation of long-lasting memories, which are essential for healthy brain function. The complex structure of the BDNF gene allows for the production of multiple transcripts, leading to a nuanced regulation of BDNF expression that can be tissue and stimulus-specific, thereby affecting neuronal function and plasticity. Stress has been identified as a significant factor that reduces the expression of BDNF in the brain, particularly in limbic structures, contributing to the pathophysiology of depression by promoting neuronal atrophy and reducing neurogenesis. This reduction in BDNF expression under stress conditions is linked to the activation of the hypothalamic-pituitary-adrenal (HPA) axis and the subsequent increase in glucocorticoids, which further suppresses BDNF expression and leads to brain dysfunction. Conversely, antidepressant treatment has been shown to increase BDNF expression, reversing the effects of stress by enhancing neurogenesis and synaptic plasticity, thereby contributing to the therapeutic effects observed in depression treatment. Clinical studies support these findings, demonstrating that depressed patients exhibit lower levels of BDNF, which are normalized following antidepressant therapy. Furthermore, genetic studies are exploring polymorphisms in the BDNF gene that may influence an individual's susceptibility to depression and response to treatment, highlighting the genetic underpinnings of the neurotrophic theory of depression. In summary, the gene coding for BDNF and stress are intricately linked in the neurotrophic and neurogenesis theories of major depression, with stress reducing BDNF expression and contributing to depressive pathology, while increased BDNF expression through antidepressant treatment offers a therapeutic pathway for reversing these effects.What is known about silent nociceptors and chlamydia infections?

Silent nociceptors play a crucial role in the context of chlamydia infections. Studies have shown that chlamydia infections can be asymptomatic, leading to challenges in detection and treatment, thus facilitating the spread of the disease. Additionally, chlamydial infections have been linked to chronicity, with evidence of resistance to antibiotic therapy and the persistence of infectious material in altered cell cultures, potentially contributing to long-term health issues. Furthermore, chlamydia can directly stimulate nociceptor neurons, releasing calcitonin gene-related peptide (CGRP) into infected areas, which can suppress innate immunity, affecting the recruitment of immune cells and their functions, ultimately impacting the body's defense mechanisms against the infection. This interaction highlights a novel mechanism by which chlamydia manipulates the host's immune response through nociceptor neurons.How does thyroid hormone affect mental health?

Thyroid hormones play a crucial role in mental health, impacting various aspects of cognition and mood. Both hypothyroidism and hyperthyroidism can lead to neuropsychiatric manifestations, including cognitive decline, depression, anxiety, and mood disorders. Low levels of thyroid hormones have been associated with depressive symptoms, with hypothyroidism potentially inducing major depressive disorder. Studies suggest that even within the normal range, lower levels of certain thyroid hormones can predict poor treatment response in individuals with depression, emphasizing the need for thyroid screening in patients with mental health issues. Thyroid dysfunction can lead to alterations in neurotransmission, changes in brain structure, and reduced levels of neurotrophic factors, all contributing to the development of psychiatric symptoms.