Abstract
Chronic subjective dizziness (CSD) is a common vestibular disorder characterized by persistent non-vertiginous dizziness, unsteadiness, and heightened sensitivity to motion stimuli that may last for months to years after events that cause acute vestibular symptoms or disrupt balance. CSD is not associated with abnormalities of basic vestibular or oculomotor reflexes. Rather, it is thought to arise from persistent use of high-threat postural control strategies and greater reliance on visual cues for spatial orientation (i.e., visual dependence), long after triggering events resolve. Anxiety-related personality traits confer vulnerability to CSD. Anomalous interactions between the central vestibular system and neural structures related to anxiety may sustain it. Vestibular- and anxiety-related processes overlap in the brain, particularly in the insula and hippocampus. Alterations in activity and connectivity in these brain regions in response to vestibular stimuli may be the neural basis of CSD. We examined this hypothesis by comparing brain activity from 18 patients with CSD and 18 healthy controls measured by functional magnetic resonance imaging during loud short tone bursts, which are auditory stimuli that evoke robust vestibular responses. Relative to controls, patients with CSD showed reduced activations to sound-evoked vestibular stimulation in the parieto-insular vestibular cortex (PIVC) including the posterior insula, and in the anterior insula, inferior frontal gyrus, hippocampus, and anterior cingulate cortex. Patients with CSD also showed altered connectivity between the anterior insula and PIVC, anterior insula and middle occipital cortex, hippocampus and PIVC, and anterior cingulate cortex and PIVC. We conclude that reduced activation in PIVC, hippocampus, anterior insula, inferior frontal gyrus, and anterior cingulate cortex, as well as connectivity changes among these regions, may be linked to long-term vestibular symptoms in patients with CSD. Furthermore, altered connectivity between the anterior insula and middle occipital cortex may underlie the greater reliance on visual cues for spatial orientation in CSD patients relative to controls.
Highlights
Chronic subjective dizziness (CSD) or persistent posturalperceptual dizziness (PPPD), as it is defined in the beta draft version of the International Classification of Diseases, 11th edition (ICD-11, http://www.who.int/classifications/icd/en/), is a complex disorder encountered clinically at the interface of neurology, otology, and psychiatry
A recent functional magnetic resonance imaging study in healthy volunteers exposed to sound-evoked vestibular stimulation showed that high neuroticism and introversion scores were associated with changes in activity and connectivity in brain areas belonging to vestibular and anxiety circuits (Indovina et al, 2014)
parieto-insular vestibular cortex (PIVC) Localizer Results During sound-evoked vestibular stimulation (STB100 dB > STB65 dB exclusively masked for white noise), the group of healthy participants showed robust activations in the left and right PIVC independently of the stimulation side, with the local maxima in the superior temporal gyrus (STg, Montreal Neurological Institute (MNI) x, y, z = −44, −42, 12, Z-score = 4.71, p-Family Wise Error (FWE)-CL corrected = 0.046, 197 voxels; MNI x, y, z = 48, −22, 2, Z-score = 4.41, p-FWE-CL corrected = 0.007, 305 voxels)
Summary
Chronic subjective dizziness (CSD) or persistent posturalperceptual dizziness (PPPD), as it is defined in the beta draft version of the International Classification of Diseases, 11th edition (ICD-11, http://www.who.int/classifications/icd/en/), is a complex disorder encountered clinically at the interface of neurology, otology, and psychiatry. Relative to controls, patients with CSD would show altered functioning in brain regions that are thought to be important in CSD These include vestibular cortical areas, PIVC (Indovina et al, 2005; Lopez and Blanke, 2011; Lopez et al, 2012; zu Eulenburg et al, 2012), visual cortical areas (Cousins et al, 2014; Indovina et al, 2014), and regions of potential interaction between vestibular and anxiety systems, such as the hippocampus, anterior insula, inferior frontal gyrus, and anterior cingulate cortex (LeDoux, 2000; Grillon, 2002; Kalisch et al, 2006; Etkin and Wager, 2007; Alvarez et al, 2008; Craig, 2009; Shinder and Taube, 2010; Hüfner et al, 2011; Indovina et al, 2011; Lopez and Blanke, 2011; Lopez et al, 2012; Gu et al, 2013; Staab et al, 2013; Hitier et al, 2014; Dieterich and Brandt, 2015). To focus on core brain mechanisms of CSD and minimize confounds from psychological risk factors (i.e., anxiety-related personality traits) and comorbidity (i.e., anxiety and depressive disorders), we matched CSD patients and healthy controls on standardized measures of neuroticism, introversion, anxiety and depression, and repeated the analyses after excluding the participants with active psychiatric disorders
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