We studied dynamic properties of horizontal, vertical, and oblique eye movements in 23 patients with the following parkinsonian syndromes: idiopathic parkinsonism (PD), multiple system atrophy (MSA), pure akinesia (PA), progressive supranuclear palsy (PSP), and cortical-basal ganglionic degeneration (CBGD). Compared with age-matched controls, only PSP patients showed slowing of saccades. Patients in all groups showed saccadic hypometria that was most marked vertically. The trajectories of saccades made to diagonal target jumps were deviated toward the horizontal plane, due to the vertical hypometria; this was most marked in PA and PSP groups. Saccade latency was only increased in the CBGD group. Sinusoidal smooth pursuit did not differentiate between controls and patients; however, with step-ramp stimuli, pursuit eye acceleration was impaired in all patient groups compared with controls. The vestibulo-ocular reflex, with or without visual enhancement, was similar in patients and controls. These findings indicate that (1) in parkinsonian syndromes apart from PSP, the saccade-generating brainstem burst neurons are probably spared, but the signals that they receive, specifying the size and direction of saccades, are flawed; and (2) measurements of the gain and trajectory of oblique saccades, and initiation of smooth pursuit, may aid in diagnosing these different types of parkinsonism.
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NPJ Parkinsons Dis
January 2025
Department of Neuroscience & Experimental Therapeutics, Texas A&M University College of Medicine, 8447 John Sharp Pkwy, Bryan, TX, 77807-3260, USA.
The smoking cessation drug cytisine exerts neuroprotection in substantia nigra pars compacta (SNc) dopaminergic (DA) neurons of female but not male 6-hydroxydopamine (6-OHDA) lesioned parkinsonian mice. To address the important question of whether circulating 17β-estradiol mediates this effect, we employ two mouse models aimed at depleting systemically circulating 17β-estradiol: (i) bilateral ovariectomy (OVX), and (ii) aromatase inhibition with systemically administered letrozole. In both models, depleting systemically circulating 17β-estradiol in female 6-OHDA lesioned parkinsonian mice results in the loss of cytisine-mediated neuroprotection as measured using apomorphine-induced contralateral rotations and SNc DA neurodegeneration.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Medicine, Faculty of Medicine, Universiti Malaya, Kuala Lumpur, Malaysia.
Aging Clin Exp Res
January 2025
Instituto de Neurociencias del Principado de Asturias (INEUROPA), University of Oviedo, Oviedo, 33003, Spain.
Background: The presence of frailty is common in people with Parkinson's disease, as is cognitive dysfunction. Previous research on frailty has focused on the physical aspects of the pathology.
Aims: To analyze the relationship between frailty and cognitive impairment in patients with Parkinson's disease and to know which disease characteristics are associated with frailty.
J Neurol
January 2025
Department of Neurology, LMU University Hospital, Ludwig-Maximilians-Universität (LMU) München, Munich, Germany.
Background And Objective: Non-motor symptoms frequently develop throughout the disease course of Parkinson's disease (PD), and pose affected individuals at risk of complications, more rapid disease progression and poorer quality of life. Addressing such symptom burden, the 2023 revised "Parkinson's disease" guideline of the German Society of Neurology aimed at providing evidence-based recommendations for managing PD non-motor symptoms, including autonomic failure, pain and sleep disturbances.
Methods: Key PICO (Patient, Intervention, Comparison, Outcome) questions were formulated by the steering committee and refined by the assigned authors.
Alzheimers Dement
December 2024
University of Exeter, Exeter, Devon, United Kingdom.
Background: Huntington's disease (HD) is an autosomal dominant condition causing severe neurodegeneration in the striatum and the entorhinal cortex (EC). An epigenome wide association study of DNA methylation in HD by our group, identified potential hypomethylation at the PTGDS gene in the striatum. We aimed to validate this result through pyrosequencing, examining the locus in fine detail, and to assess the signal specificity by profiling multiple neurodegenerative diseases.
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