Differentiating clinical examinations of Parkinson’s and parkisonisms

Introduction: The main symptoms of Parkinson are: tremors, movement resistance, postural instability and bradykinesia. However, other diseases such as Progressive Supranuclear Paralysis, Multiple System Atrophy and Corticobasal Degeneration have similar symptoms. This similarity generates a difficulty of diagnosis, for example, Corticobasal Degeneration is often diagnosed by autopsy. Objectives: To define the differentiating symptoms of Parkinson and the diseases mentioned and to find clinical tests that could aid in the diagnosis. Methodology: The integrative review utilized Scielo and Pubmed databases and the selected clinical examinations were obtained by the book Exame Clinico - 8° edition. Results: Multiple Systems Atrophy is distinguished from Parkinson by occurrence of cerebelar abnormalities, therefore Romberg Test can evidence modified coordination, which may be indicative of Multiple System Atrophy. Corticobasal Degeneration causes loss of ability to identify things by touch and impaired sensitivity on one side of the body, thereby the verification of stereognosia and the examination of superficial sensitivity are useful. Supranuclear Paralysis Progressive generates difficulty of performing vertical movements, thus the examination of ocular motility is necessary. Conclusion: Only clinical examinations aren’t sufficient to generate an accurate diagnosis and complementary exams are necessary for greater precision. However, knowledge about differentiating clinical examinations helps to generate a line of reasoning and examinations to be requested.

In situ architecture of neuronal α-Synuclein inclusions

Summaryα-Synuclein (α-Syn) aggregation is a hallmark of devastating neurodegenerative disorders including Parkinson’s disease (PD) and multiple systems atrophy (MSA)1,2. α-Syn aggregates spread throughout the brain during disease progression2, suggesting mechanisms of intercellular seeding. Formation of α-Syn amyloid fibrils is observed in vitro3,4 and fibrillar α-Syn has been purified from patient brains5,6, but recent reports questioned whether disease-relevant α-Syn aggregates are fibrillar in structure7-9. Here we use cryo-electron tomography (cryo-ET) to image neuronal Lewy body-like α-Syn inclusions in situ at molecular resolution. We show that the inclusions consist of α-Syn fibrils crisscrossing a variety of cellular organelles such as the endoplasmic reticulum (ER), mitochondria and autophagic structures, without interacting with membranes directly. Neuronal inclusions seeded by recombinant or MSA patient-derived α-Syn aggregates have overall similar architecture, although MSA-seeded fibrils show higher structural flexibility. Using gold-labeled seeds we find that aggregate nucleation is predominantly mediated by α-Syn oligomers, with fibrils growing unidirectionally from the seed. Our results conclusively demonstrate that neuronal α-Syn inclusions contain α-Syn fibrils intermixed with cellular membranes, and illuminate the mechanism of aggregate nucleation.

Movement Disorders 2: Parkinson’s Plus and Degenerative Diseases (DRAFT)

The video in this chapter explores movement disorders, and focuses on Parkinson’s Plus and degenerative diseases. It outlines the features and pathology of dementia with lewy bodies (DLB), progressive supranuclear palsy (PSP), multiple systems atrophy (MSA) and corticobasal degeneration (CBD), as well as genetic movement disorders, Wilson’s disease, and Huntington’s disease.