Abstract
ObjectiveThe aim of our study was to investigate abnormal changes in brain activity in patients with persistent postural-perceptual dizziness (PPPD) using magnetoencephalography (MEG).MethodsMagnetoencephalography recordings from 18 PPPD patients and 18 healthy controls were analyzed to determine the source of brain activity in seven frequency ranges using accumulated source imaging (ASI).ResultsOur study showed that significant changes in the patterns of localization in the temporal-parietal junction (TPJ) were observed at 1–4, 4–8, and 12–30 Hz in PPPD patients compared with healthy controls, and changes in the frontal cortex were found at 1–4, 80–250, and 250–500 Hz in PPPD patients compared with controls. The neuromagnetic activity in TPJ was observed increased significantly in 1–4 and 4–8 Hz, while the neuromagnetic activity in frontal cortex was found increased significantly in 1–4 Hz. In addition, the localized source strength in TPJ in 1–4 Hz was positively correlated with DHI score (r = 0.7085, p < 0.05), while the localized source strength in frontal cortex in 1–4 Hz was positively correlated with HAMA score (r = 0.5542, p < 0.05).ConclusionOur results demonstrated that alterations in the TPJ and frontal cortex may play a critical role in the pathophysiological mechanism of PPPD. The neuromagnetic activity in TPJ may be related to dizziness symptom of PPPD patients, while the neuromagnetic activity in frontal lobe may be related to emotional symptoms of PPPD patients. In addition, frequency-dependent changes in neuromagnetic activity, especially neuromagnetic activity in low frequency bands, were involved in the pathophysiology of PPPD.
Highlights
Persistent postural-perceptual dizziness (PPPD) is considered a chronic functional vestibular disorder with clinical symptoms and has been defined by the World Health Organization (WHO) and the Bárány Society (Staab et al, 2017)
Our results found that the abnormal neuromagnetic source localization in patients with PPPD was more likely to be located in the temporal-parietal junction (TPJ) than in healthy controls, indicating that the function of this brain region was disordered in patients with PPPD
Our results indicated that emotional symptoms of PPPD patients, such as anxiety, may be resulted from a potential pathological basis in the frontal lobe, not just emotional feedback caused by dizziness symptoms of PPPD patients
Summary
Persistent postural-perceptual dizziness (PPPD) is considered a chronic functional vestibular disorder with clinical symptoms and has been defined by the World Health Organization (WHO) and the Bárány Society (Staab et al, 2017). The clinical characteristics of PPPD were persistent dizziness and/or unsteadiness for more than 3 months. Patients with PPPD adopt a stiffened postural control strategy in response to dizzying trigger events and persistently maintain this adaptation even if the trigger factors disappear (Cao et al, 2021). Researchers found that the ability to control posture through multisensory information inputs was impaired in patients with PPPD (Sohsten et al, 2016). PPPD patients were more dependent on visual or somatosensory inputs than vestibular inputs to control their body posture (Staab et al, 2017). Cortical integration dysfunction involving multisensory inputs may be suggested as a potential pathophysiological mechanism of PPPD
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