會議議程

Executive Summary：
李薰華醫師長期深耕耳神經學，對前庭功能與眩暈相關疾病懷抱高度熱忱。早期英國倫敦大學參加短期訓練課程，於雙和醫院眩暈中心接受完整而紮實的臨床訓練，奠定了診斷與治療的專業基礎。其後更前往澳洲雪梨學理大學（University of Sydney）所屬的 Royal Prince Alfred Hospital，接受國際耳神經學權威 Miriam Welgampola 教授德指導，深入學習耳神經學的臨床評估與研究方法。為持續與國際前沿接軌，李醫師至今仍維持每年固定前往雪梨進行短期受訓，並與布拉格查理大學每年定期互訪及合作，精進專業、更新視野，致力將最新的耳神經學知識與臨床經驗帶回台灣，造福更多患者。

Lecture Abstract：
PPPD(persistent postural perceptual dizziness)，簡稱知覺性頭暈， 是一種常見但容易被忽略的功能性前庭疾病，特徵為長期、非旋轉性的頭暈或不穩感，通常持續三個月以上。症狀在以下情境中特別明顯：直立或行走時，主動或被動移動時，接觸複雜或動態的視覺刺激（如人多的地方、超市、滑動螢幕）。PPPD 常在急性前庭事件（如前庭神經炎、BPPV、偏頭痛性眩暈、驚恐發作或腦震盪）之後發展，屬於前庭系統在「恢復過程中產生不良適應」的結果，而非結構性病變。PPPD 是可治療的疾病，早期正確診斷與清楚衛教極為重要。最佳治療方式為，藥物治療 ，前庭復健 心理支持 / 認知行為治療。

醫病關係與持續追蹤，是治療成功的關鍵因素

Executive Summary：
Dr. Jung-Lung Hsu is a leading neurologist and dementia researcher currently serving as Director of the Department of Neurology at New Taipei Municipal TuCheng Hospital. He received his medical education at Taipei Medical University and completed his neurology residency at Shin Kong WHS Memorial Hospital. Dr. Hsu holds a PhD in Image Science from Utrecht University and was a visiting fellow at the Swartz Center for Computational Neuroscience at the University of California, San Diego.

Dr. Hsu’s clinical and academic expertise centers on dementia and advanced neuroimaging. His work emphasizes the application of state-of-the-art neuroimaging techniques to address critical clinical questions in dementia diagnosis, progression, and management. In addition to his clinical leadership, he holds teaching appointments at Taipei Medical University and Chang Gung Memorial Hospital, contributing to interdisciplinary education in medicine and neuroscience.

Dr. Hsu has played a pivotal role in advancing dementia research and advocacy in Taiwan. He is a founding member and current President of the Taiwan Dementia Society, actively promoting research collaboration, clinical innovation, and public awareness. He has published extensively in the field of neuroimaging and serves as a reviewer for international scientific journals, reflecting his standing in the global research community

Lecture Abstract：
Neurodegenerative diseases such as Alzheimer’s disease (AD) and Parkinson’s disease (PD) are characterized by progressive accumulation of misfolded proteins, reflecting a fundamental failure of cerebral proteostasis. Emerging evidence has reframed sleep—particularly deep non-rapid eye movement (NREM) stage N3 sleep—as a critical physiological state for neurotoxic waste clearance through the glymphatic system. During slow-wave sleep, suppression of noradrenergic tone from the locus coeruleus induces expansion of the interstitial space, markedly enhancing cerebrospinal fluid–interstitial fluid exchange and facilitating the removal of amyloid-β, tau, and other metabolic byproducts

Aging and sleep fragmentation significantly impair this clearance mechanism through reduced arterial pulsatility, vascular stiffening, and loss of aquaporin-4 (AQP4) polarization, creating a permissive environment for protein aggregation, neuroinflammation, and cognitive decline. Recent clinical and imaging studies demonstrate strong associations between glymphatic dysfunction, reduced gray matter volume, and poorer neuropsychological performance in older adults, underscoring the clinical relevance of sleep architecture beyond sleep duration alone

Therapeutic strategies are now shifting toward enhancement of slow-wave activity and glymphatic flow. Pharmacologic agents such as dexmedetomidine, which mimics N3 physiology via α2-adrenergic modulation, alongside orexin antagonists and melatonin, show promise in restoring glymphatic efficiency. Non-pharmacologic interventions—including acoustic slow-wave stimulation, neurostimulation, and lateral sleep positioning—offer additional avenues for clinical translation.

Together, these findings position deep sleep as a modifiable, disease-relevant target in preventive neurology. Optimizing slow-wave sleep represents a critical strategy for preserving cognitive reserve and protecting the aging brain from neurodegeneration.

Executive Summary：
陳彥中醫師現任職於中國醫藥大學附設醫院和臺中市立老人復健綜合醫院（委託中醫大經營）神經部主治醫師，專長於帕金森氏症.動作障礙疾病及神經免疫疾病診斷及照護。陳醫師畢業於高雄醫學大學醫學系，於彰化基督教醫院完成神經科專科訓練與動作障礙次專科研究，並曾任彰基巴金森氏症暨動作障礙中心執行長。

他於中山醫學大學取得公共衛生博士學位，研究主題聚焦於人類基因資料庫及甲基化分析。臨床興趣涵蓋深腦刺激術（DBS）、磁振導引聚焦超音波（MRgFUS）、超音波導引肉毒桿菌素治療及神經免疫疾病。陳醫師目前擔任彰化師範大學資訊統計研究所助理教授,台灣神經免疫學會副財務長和國際動作障礙暨巴金森學會實證醫學委員會委員。

Lecture Abstract：
Rapid eye movement sleep behavior disorder (RBD) represents one of the most specific prodromal manifestations of α-synucleinopathies, providing a unique window for early detection and disease modification in Lewy body disease (LBD). Longitudinal cohort studies indicate that up to 80–90% of idiopathic RBD patients convert to Parkinson’s disease (PD), dementia with Lewy bodies (DLB), or multiple system atrophy (MSA) within 10–15 years, underscoring its predictive value. The pathophysiological progression from RBD to LBD involves sequential spreading of α-synuclein pathology from pontomedullary structures regulating REM atonia to nigrostriatal and limbic networks, accompanied by neurochemical and immune alterations. Emerging biomarkers offer multidimensional insights into this conversion process. Neuroimaging markers such as nigrostriatal dopaminergic loss (DAT-SPECT), brainstem and limbic volumetric changes (MRI), and diffusion alterations (DTI) correlate with phenoconversion risk. Fluid biomarkers—including CSF α-synuclein seeding amplification assays (RT-QuIC), neurofilament light chain (NfL), and plasma exosomal α-synuclein—are increasingly validated as sensitive indicators of underlying pathology. Peripheral autonomic dysfunction, cardiac MIBG scintigraphy, and skin biopsy detecting phosphorylated α-synuclein further enhance diagnostic specificity. Recent interventional trials in prodromal cohorts are reshaping the therapeutic landscape. Studies such as NCT05696747 (prasinezumab), NCT05696760 (cinpanemab), and NCT05640364 (α-synuclein-targeted immunotherapies) have begun enrolling RBD participants based on biomarker-confirmed synucleinopathy, marking a paradigm shift toward preventive neuroprotection. Parallel trials targeting neuroinflammation, gut microbiome modulation, and circadian regulation are also underway. Integrating multimodal biomarkers, clinical staging, and digital actigraphy-based monitoring may enable a precision medicine framework for RBD, facilitating timely enrollment in disease-modifying trials. Understanding the mechanistic continuum from RBD to LBD is essential for redefining diagnostic criteria, prognostic counseling, and early therapeutic intervention in α-synuclein disorders. Keywords: REM sleep behavior disorder, Lewy body disease, α-synuclein, biomarkers, phenoconversion