Parkinson's disease and parkinsonism.

Abstract

Parkinsonism and Parkinson' s disease are not synonymous. Parkinsonism refers classically to a triad of motor symptoms (bradykinesia, rigidity, and tremor), but gait instability is also considered a sign of parkinsonism. By contrast, Parkinson's disease (PD) is a specific disease entity (despite muted debate about whether PD represents a single disorder or many; Espay et al., 2020), including parkinsonism and nonmotor features such as cognitive, psychiatric, and autonomic disturbances.PD afflicts about 10 million persons worldwide (Elbaz et al., 2016), and its median standardized incidence in developed countries was estimated to be 14 per 100,000 person-years. Among parkinsonian disorders are the neurodegenerative mimics of PD often referred to as atypical parkinsonism: progressive supranuclear palsy (PSP), multiple system atrophy (MSA), and corticobasal degeneration (CBD). Atypical parkinsonisms are quite rare. CBD has an estimated incidence of 0.62 to 0.92 per 100,000 and prevalence of 5 to 7 per 100,000. Prevalence estimates of PSP range from 1.4 to 6.4 per 100,000, whereas those for MSA range from 1.9 to 4.4 per 100,000. Pathology and PathophysiologyRapid advances have been made especially in regard to an understanding of basal ganglia physiology, its derangement in various movement disorders, and differences in neuropathology among various movement disorders. Here we discuss especially the changing views about pathology and pathophysiology underlying PD.Parkinson's disease. At the root of the majority of neurodegenerative conditions is an either intra-or extracellular aggregation of misfolded proteins. PD and atypical parkinsonisms are no exception: PD and MSA involve the aggregation of alpha synuclein (and are referred to as synucleinopathies), whereas CBD and PSP are tauopathies involving aggregation of tau proteins. In the past decade, much has been made of the apparent ability of alpha synuclein and tau to "seed," that is, to recruit similar proteins and instigate their conversion into pathological forms, and to propagate from cell to cell in prionlike manner. Importantly, the proteins involved in PD and atypical parkinsonism lack the full suite of properties of abnormal prion proteins (including the core feature of infectivity) and self-propagate via seeding less efficiently than prion proteins. Nonetheless, studies of alpha synuclein-seeding characteristics and activity in brain homogenates extracted from persons with PD, dementia with Lewy bodies (DLB), and MSA were useful in supporting the notion that these conditions might be caused by different strains of alpha synuclein (Jaunmuktane & Brandner, 2020).

Movement disorders.

“…Test selection should consider the patient's condition, the differential diagnosis, the referral question(s), patient and caregiver concerns, the normative and psychometric properties of the tests (e.g., availability of alternate forms, test-retest reliability, validity for use in movement disorders and dementia), and the patient's ability to tolerate and cooperate with the tests. A recent summary of effect sizes associated with differences in mean scores obtained by persons with PD and those with intact cognition is available (Tröster, 2023) as is a summary of the impact of psychiatric features on cognition in PD (Tröster et al, 2013). Additionally, the choice of tests one might include in the evaluation of HD depends on the purpose of the evaluation (Snowden, 2017).…”

“…It may also be easier to distinguish tauopathies from alphasynucleinopathies than among conditions within each of these pathology-defined categories (Tröster, 2023). Although the differential diagnostic utility of patterns of test performance has not been empirically scrutinized, performances on individual tests may be helpful in differential diagnostic hypothesis generation (W. Lee et al, 2012;Y.-E. C. Lee et al, 2016).…”

Parkinson’s Disease Detection From Online Handwriting Based on Beta-Elliptical Approach and Fuzzy Perceptual Detector

“…It's common for the symptoms of PD to go undetected or be mistaken for other issues until the disease has progressed to a point where they become more noticeable. This delay in detection is one of the challenges in diagnosing PD accurately in its early stages [13]. Indeed, the timely detection of PD in its initial phases holds pivotal importance, enabling the implementation of appropriate interventions to mitigate morbidity and alleviate the healthcare load among the elderly.…”