Lecture Summary

Multiple system atrophy (MSA) is a rare, progressive neurodegenerative disorder marked by alpha-synuclein accumulation in oligodendrocytes, forming glial cytoplasmic inclusions that drive neuronal loss in key brain regions. Neuroanatomically, MSA manifests mainly as striatonigral degeneration (causing parkinsonism, MSA-P subtype) or olivopontocerebellar atrophy (leading to cerebellar ataxia, MSA-C subtype) with autonomic failure (orthostatic hypotension, urinary dysfunction). Regional variations exist: MSA-P dominates in Western countries, while MSA-C prevails in Japan. This lecture explores MSA, focusing on its pathological distributions and its clinical manifestations.

Lecture Summary

Discover the earliest footprints of Multiple System Atrophy (MSA) in “Unveiling Prodromal and Early MSA: From Mono‐System Signs to Biomarker‐Based Insights.” Drawing on the latest longitudinal data, such as pontine volume trajectories (Mov Disord, 2025 Apr 2; doi:10.1002/mds.30182), we explore how subtle clinical manifestations in the mono‐system phase evolve into overt multisystem degeneration. Participants will gain an integrated perspective on cutting‐edge molecular imaging—including α‐synuclein PET and serotonin transporter studies—alongside emerging evidence of kynurenine‐pathway metabolic dysregulation. By linking prodromal clinical features with quantifiable biomarker changes, we’ll unpack new opportunities for early diagnosis and patient stratification. Finally, we discuss how these insights are shaping innovative drug‐development strategies aimed at halting or slowing MSA progression. Join us to chart the path from first‐sign recognition to targeted therapeutic design, and help redefine the frontier of MSA diagnosis, intervention, and patient support.

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The lecture will cover recent insights into the disease mechanisms of MSA with special focus on glial pathology.

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Freezing of Gait (FOG) presents a complex and multifaceted challenge for both patients and healthcare providers. This lecture focuses on the heterogeneity of FOG, exploring its various subtypes and the implications for clinical practice, while deliberately steering clear of topics related to prediction, detection, and practical management strategies.FOG manifests as sudden, temporary episodes where an individual is unable to move forward despite the intention to walk. This phenomenon can be dissected into different subtypes: motor, cognitive, and mixed, each with its unique underlying neural disruptions. Understanding these subtypes is essential because they affect how FOG presents and responds to treatment.By examining these subtypes, we gain insight into the complex interplay of neurological, psychological, and environmental factors that contribute to FOG. This understanding is crucial for clinicians as it influences the assessment and development of individualized therapeutic approaches. Acknowledging the heterogeneity of FOG can lead to more effective and targeted interventions, ultimately enhancing patient care.In this lecture, we aim to deepen the understanding of FOG’s diverse nature, emphasizing the importance of recognizing its complexity to foster a more holistic approach in clinical settings. This exploration is intended to spark further research and innovation in addressing the multifaceted challenges posed by FOG.

Lecture Summary

Freezing of gait (FOG) is one of the most disabling and enigmatic symptoms of Parkinson’s disease (PD). Its sudden, unpredictable onset poses major challenges for patients, caregivers, and clinicians alike—often leading to falls, reduced independence, and diminished quality of life. This presentation explores current and emerging approaches to both assessing and predicting FOG. For patients who already experience FOG, we review assessment methods ranging from traditional self-report and standardized clinical tests to state-of-the-art tools such as wearable sensors and computer vision for automated, real-world monitoring. For patients with PD who do not yet exhibit FOG, we summarize new evidence from a large-scale meta-analysis (35 studies, nearly 9,000 participants) identifying key risk factors—including motor severity, cognition, mood, and medication use—that may predict future onset, sometimes more than a decade in advance. By combining rigorous clinical observation with innovative technologies and longitudinal insights, this work highlights opportunities to move beyond reactive care toward proactive strategies. Importantly, several identified risk factors appear to be modifiable, raising the possibility of delaying or even preventing the development of FOG in at-risk patients.

Lecture Summary

Freezing of gait (FoG) is one of the most challenging and disabling motor symptoms in Parkinson's disease and related disorders. Despite its prevalence, effective management remains complex due to its heterogeneous clinical presentations and underlying mechanisms. This lecture offers a practical phenotype-based approach to FoG treatment. We will review key clinical patterns and provide guidance on tailored interventions, including medication adjustments, cueing techniques, and rehabilitative strategies. Join us to enhance your diagnostic precision and therapeutic effectiveness in managing this complex and often treatment-resistant symptom.

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This lecture explores the evidence of inflammation & neuroinflammation in Parkinson's disease, discusses the immune biomarkers that indicate such inflammation from central and peripheral system, and explains how these biomarkers are related to the pathophysiology of the disease.

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In this talk, I will discuss whether neuroimaging can be a promising biomarker for early detection of cognitive decline and prediction of its progression in Parkinson's disease.

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Cardoso et al. propose a biological definition and classification system for Parkinson's Disease (PD), emphasizing the need for an objective staging system similar to those used in cancer models. They highlight the significance of α-synuclein aggregates in diagnosing PD and related synucleinopathies, such as Dementia with Lewy Bodies and Multiple System Atrophy. Recently, two classification systems have been proposed: SynNeurGe, which focuses on molecular characteristics, and NSD-ISS, based on biological markers and functional impairment. Both systems aim to enhance early diagnosis and treatment strategies. Additionally, it calls for integrating Alzheimer's disease markers into PD classification to refine precision medicine approaches. Our team confirmed that the RT-QuIC method can be used to diagnose the RBD group, a high-risk cohort. Moving forward, blood markers are expected to prove highly effective in identifying such risk cohorts. In my lecture, In my presentation, I would like to explain the importance of liquid biomarkers and their achievements.

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Dystonia is defined as a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive, movements or postures, or both. Dystonic movements and postures are typically patterned and repetitive and may be tremulous and jerky. The clinical features of dystonia belong to a varied phenomenological spectrum. This clinical complexity comes in parallel with marked heterogeneity of etiologies and biological mechanisms. This heterogeneity has led to different classification approaches over the years. In 2013, an innovative classification system divided dystonia into two axes: axis 1 - clinical characteristics, including age at onset, body distribution, temporal pattern and associated features; and axis 2 – etiology, which includes nervous system pathology and inheritance. Although this two-axis plan has solved many issues related to prior classifications, some areas where varied interpretations lead to inconsistent applications still exists. Here this session reviews the change of concepts related to dystonia classification based on historical background, and discusses emerging controversies related to current concept and classification of dystonia.

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Dystonia is a clinically and genetically highly heterogeneous neurological disorder. A number of groundbreaking genetic and molecular insights have recently been gained, especially with the advent of new sequencing technologies. While these discoveries improve genetic testing and counseling, their translation into new (molecular) therapies is still limited. However, we are beginning to understand shared pathophysiological pathways and molecular mechanisms. It has become clear that dystonia results from a dysfunctional network involving the basal ganglia, cerebellum, thalamus, and cortex. On the molecular level, more than a handful of, often intertwined, pathways have been linked to pathogenic variants in dystonia genes, including gene transcription during neurodevelopment, calcium homeostasis, striatal dopamine signaling, endoplasmic reticulum stress response, autophagy, and others. Thus, different forms of dystonia can be molecularly grouped, which may facilitate treatment development in the future.

Lecture Summary

Task-specific and non-task-specific focal dystonias share many clinical features, yet it remains an important and unresolved question whether they originate from common pathophysiological substrates or from distinct neural mechanisms. This lecture will review current evidence from clinical observations, neurophysiological studies, and neuroimaging research to shed light on this issue.

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Visal dysfunction is a specific nonmotor symptom that characterizes Parkinson's disease. Afferent visual dysfunctions relating to the retinal dopamine loss appear from the very early stage of PD and visual perceptual dysfunction is a key cognitive feature of PD patients. Minor illusion or hallucinatory symptoms are frequent throughout the disease course, which evolve into florrid visual hallucinations and psychosis affecting individuals drastically in advanced stages. This talk will cover clinical and pathophysiological aspects of visual dysfunction and present how to approch this disabling symptom in PD patients.

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This presentation will provide an overview of the current understanding of psychiatric symptoms in Parkinson’s disease.

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The importance of nonmotor fluctuation and treatment options will be discussed in this lecture

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This lecture will focus on current real world use of digital technology in clinical practice of movement disorders patients.

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This lecture will provide a comprehensive review of recent applications of digital technology in Parkinson’s disease and movement disorders, with a particular focus on motor aspects. Advances in sensors, video-based assessments, and smartphone applications have enabled more detailed evaluation of motor symptoms. These technologies facilitate early detection and assessment in the prodromal and early stages of disease, as well as longitudinal monitoring of symptom changes in real-world settings. Furthermore, they are increasingly being adopted as outcome measures in clinical trials. This presentation will highlight these developments and discuss their implications for both clinical practice and research.

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Non-motor symptoms of Parkinson's disease, including sleep disorders and autonomic dysfunction, significantly impact quality of life but remain challenging to assess objectively. This lecture will present cutting-edge research on digital bkiomarkers using wearble sensors and mobile applications for monitoring of these symptoms.

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We had initiated a cohort study of residents in Takahata Town and Sagae City, Yamagata Prefecture, in 2000. From the cohort, the prevalence of iNPH was 0.5% for residents aged 61 years and older, and 7.7% for those aged 86, 27.4% in aged 92, with the prevalence increasing with age, and the incidence was 15 times higher (Iseki et al. 2015) than previous hospital-based study in Netherland. We also found that there are cases suspected to be complicated with Alzheimer's disease and other forms of dementia. It is challenging to differentiate iNPH from age-related changes, other diseases, especially in those over 80. We were also the first familial normal pressure hydrocephalus (fNPH), which was indistinguishable from iNPH both in symptoms and brain imaging (Takahashi et al. 2011). Furthermore, genetic analysis found that a copy number loss in the SFMBT1 gene was identified as a risk gene for iNPH (Sato et al. 2016). It was hoped that the pathogenesis of iNPH, which has been "pathogenesis unknown," could be elucidated by the combination and accumulation of multifactorial risks.

Lecture Summary

Normal pressure hydrocephalus (NPH) is a disorder with wide clinical spectrum from multiple system based on heterogeneous pathophysiologies. On the other hand, various disorders can share common clinical features, including cognitive decline or movement disorders, with NPH. Considering NPH can respond to shunt surgery, understanding the clinical features of NPH and differentiation are important and clinically meaningful. In this talk, we will address various movement disorders seen in NPH and focus on differential values and clinical meanings.

Lecture Summary

"Idiopathic normal pressure hydrocephalus (INPH) is characterized by non-obstructive enlargement of the cerebral ventricles, accompanied by gait disturbance, cognitive impairment, and urinary dysfunction. Although INPH is a treatable condition, its diagnosis can be challenging due to variability in clinical presentation and overlapping features with other common neurodegenerative disorders such as Parkinson’s disease (PD) and Alzheimer’s disease (AD).Fluorinated N-3-fluoropropyl-2β-carbomethoxy-3β-(4-iodophenyl)-nortropane (F-18 FP-CIT) positron emission tomography (PET) is widely used to evaluate parkinsonian syndromes by assessing dopaminergic function. Amyloid PET also offers high sensitivity and specificity for detecting amyloid deposition, particularly neuritic plaques, in INPH patients. Some patients with INPH may demonstrate abnormal findings on F-18 FP-CIT or amyloid PET imaging.While many researchers believe that shunt surgery is unlikely to be effective in INPH patients with AD comorbidity, we suggest that this perspective warrants re-evaluation. Clinicians should recognize the possibility of comorbid INPH and PD. In elderly patients with abnormal dopamine transporter (DAT) scans, INPH should be considered as a differential diagnosis following comprehensive clinical and radiological evaluation. If shunt-responsive INPH is supported by additional diagnostic tests, shunt surgery should be considered as a viable treatment option."

Lecture Summary

Neuropalliative care is increasingly recognized as an essential aspect of managing Parkinson’s disease and related parkinsonian disorders. Moving beyond its traditional association with end-of-life settings, it emphasizes early, integrated interventions to address diverse patient and caregiver needs, including motor and non-motor symptoms, pain, psychiatric and autonomic disturbances, communication challenges, and functional decline. Evidence demonstrates that early application of palliative principles improves quality of life, enhances symptom control, facilitates advance care planning, and reduces caregiver burden. Effective delivery relies on interdisciplinary collaboration among neurologists, palliative specialists, rehabilitation teams, and psychosocial support services.

Globally, neuropalliative care models have been introduced in movement disorder clinics, yet their integration varies according to healthcare structures, workforce readiness, and cultural perspectives. In Korea, awareness is growing, but clinical adoption remains limited by fragmented services, lack of standardized pathways, and insufficient reimbursement.

This lecture will outline the current status of neuropalliative care for Parkinsonism, present international best practices, and discuss opportunities for integration in Korea through multidisciplinary training, coordinated care networks, and culturally adapted guidelines.

Lecture Summary

Parkinsonism remains a progressive neurodegenerative disorder with no definitive disease-modifying treatment currently available. As a result, patients and their caregivers face increasing physical, psychological, and socio-economic burdens throughout the course of the disease. Despite growing recognition of the importance of palliative and supportive care in chronic neurological conditions, neuropalliative-supportive care for PD patients remains limited and underutilized in Korea.
To explore the unmet needs in this area, we conducted a nationwide survey involving PD patients, caregivers, and neurologists. The survey assessed levels of awareness, current utilization, and perceived unmet needs related to neuropalliative-supportive care.

Lecture Summary

Home-Based Care for Advanced Parkinsonism

With an aging population and advancements in medical technology, the number of people living with mobility impairments from neurodegenerative diseases, such as Parkinson's disease, is increasing. Patients with advanced neurodegenerative diseases spend a significant portion of their illness trajectory at home, facing numerous challenges including high symptom burden, functional decline, and limited access to timely medical service. These difficulties can lead to increased suffering for patients and their caregivers, as well as increased preventable hospital visits due to condition exacerbation.

To address the growing population of patients with mobility impairments, various home-based medical care (HBMC) models are emerging. In South Korea, a Home-Based Primary Care pilot program for patients with chronic conditions treating in primary care clinic as launched in 2018, followed by the Long-Term Care Home Medical Center pilot program in 2023. However, services specifically for advanced neurodegenerative diseases remain insufficient.

Patients with advanced neurodegenerative diseases require a HBMC model that can provide not only appropriate symptom management but also timely advance care planning for patients and caregivers as the disease progresses. A targeted HBMC model for patients with advanced neurodegenerative diseases should aim to provide individualized care through close collaboration with a medical team, enhance continuity of care, reduce avoidable hospital utilization, and improve the experience of both patients and caregivers. In this lecture, based on our experience with a hospital-based HBMC model at a tertiary hospital in Korea, we aim to explore an HBMC model that can provide appropriate neuropalliative care for patients with advanced neurodegenerative diseases.

Lecture Summary

Transcranial focused ultrasound (tFUS) has recently gained attention as a non-invasive neuromodulation technique with superior spatial precision and depth penetration. Unlike traditional approaches such as transcranial magnetic or electrical stimulation, tFUS can target deep brain structures while maintaining millimeter-level accuracy. This talk introduces key advances in tFUS applications for neurodegenerative disorders, highlighting preclinical and clinical findings. We present evidence from multimodal studies—functional MRI, PET, EEG, and behavioral assays—demonstrating region-specific neuromodulation in both animals and humans. In particular, we showcase our recent work at KIST using tFUS for modulating pathological brain circuits related to neurodegenerative disorders.

Lecture Summary

Transcranial magnetic stimulation (TMS) is a noninvasive brain stimulation technique extensively used in neuroscience and neuropsychiatry. Here I would like to update TMS research focusing on dementing disorders.Short-latency afferent inhibition (SAI), which can evaluate the central cholinergic function, decreases in Alzheimer’s disease (AD) and dementia with Lewy bodies (DLB). Short-interval intracortical inhibition and intracortical facilitation measured by paired-pulse paradigms, which show the functions of central GABAAergic and glutamatergic neuronal circuits respectively, are reduced in patients with frontotemporal dementia and DLB. Combination of these parameters can successfully differentiate dementing disorders. A novel technique combining TMS with electroencephalogram allows the evaluation of functional brain networks. Neural activity propagation from precuneus to frontal lobe is disrupted in patients with AD. The long-term potentiation (LTP)-like synaptic plasticity induced by repetitive TMS mode is impaired in patients having AD pathology, and its severity correlates with degrees of cognitive declines, AD-related biomarkers including amyloid-beta 42 in the cerebrospinal fluid and amyloid accumulation in precuneus detected by amyloid positron emission tomography.In conclusion, TMS holds significant promise as a tool for understanding the pathophysiology of dementia.

Lecture Summary

Transcranial direct current stimulation (tDCS) has recently emerged as a safe and convenient neuromodulation tool, and a growing body of research has explored its applications. In this lecture, we will examine how tDCS induces changes in the brain and discuss recent research trends in the field

Lecture Summary

Essential tremor (ET) is a disease entity with various etiologies. Despite the complexity of pathogenesis, all ET patients share a common symptom: an action tremor, defined by involuntary rhythmic movement. Specifically, tremor can be mathematically described by two features, tremor amplitudes and tremor frequencies. In this talk, we will apply state-of-the-art neural dynamic approaches in awake behaving mice to illustrate how tremor frequencies and amplitudes are ensembled in the brain. We will further describe how different patterns of neuronal synchrony can affect the circuitry dynamics of tremor, therefore leading to differential responses to ET medications. Finally, we will come back to patients and show how these frequency and amplitude coding mechanisms can facilitate novel drug design and therapies in ET.

Lecture Summary

Currently, the MDS Tremor Expert Panels have categorized the movements accompanying dystonia into two types: (1) regular, sinusoidal movements consistent with “tremors in dystonia”, and (2) irregular, jerky, non-oscillatory movements, known as “jerky dystonia”. Tremor in dystonia is a regular oscillatory movement that occurs in either dystonic or non-dystonic body parts. The term “dystonic tremor”, characterized by irregular tremor in the dystonic body regions, and “tremor associated with dystonia”, where tremor exhibits in the non-dystonic part, have been discouraged due to a lack of clarity. The pathophysiology of tremor in dystonia is widespread, involving the cerebello-thalamo-cortical pathway (CTC) and the basal ganglia-thalamo-cortical (BG-TH-C) networks. The CTC may be the primary involvement, and the BG-TH-C networks may interact to contribute to tremor genesis in dystonia.