Track topics on Twitter Track topics that are important to you
Published on BioPortfolio: 2018-02-21T19:15:13-0500
By creating a neurogenebank from Parkinson's disease patients' blood donations we will ultimately be able to define genes for Parkinson's disease and other neurological conditions.
Upper-limb disorders in patients with Parkinson's disease include decreased speed and amplitude of movements, difficulty in sequential tasks, and disrupted execution of fine manipulative h...
The purpose of this study is to examine the feasibility and potential effectiveness of a cognitive training program among persons with Parkinson's disease. It is hypothesized that individu...
The purpose of this dual phase cross-sectional, controlled and prospective, open label, exploratory study is to determine the general characteristics of visuospatial exploration and its ne...
Patients with Parkinson's Disease frequently present impaired postural control that leads to loss of stability and increased risk of falls.Core system, includes passive structures of the t...
To investigate whether diabetes mellitus is associated with Parkinson-like pathology in people without Parkinson disease and to evaluate the effect of diabetes mellitus on markers of Parkinson patholo...
Identifying patients with early stages of Parkinson's disease (PD) in a home environment is an important area of neurological disorder research, because it is of therapeutic and economic benefits to o...
Visual hallucinations (VHs) are common in Parkinson's disease (PD), with prevalence ranging from 27-50% in cross-sectional cohorts of patients with well-established disease. However, minor hallucinati...
Neuroimaging in Parkinson's disease is an evolving field, providing in-vivo insights into the structural and biochemical changes of the condition, although its diagnosis remains clinical. Here, we aim...
To determine the effects of a high-intensity exercise therapy using sensorimotor and visual stimuli on non-demented Parkinson's disease (PD) patients' clinical symptoms, mobility, and standing balance...
Proteins associated with sporadic or familial cases of PARKINSON DISEASE.
A condition caused by the neurotoxin MPTP which causes selective destruction of nigrostriatal dopaminergic neurons. Clinical features include irreversible parkinsonian signs including rigidity and bradykinesia (PARKINSON DISEASE, SECONDARY). MPTP toxicity is also used as an animal model for the study of PARKINSON DISEASE. (Adams et al., Principles of Neurology, 6th ed, p1072; Neurology 1986 Feb;36(2):250-8)
A group of disorders which feature impaired motor control characterized by bradykinesia, MUSCLE RIGIDITY; TREMOR; and postural instability. Parkinsonian diseases are generally divided into primary parkinsonism (see PARKINSON DISEASE), secondary parkinsonism (see PARKINSON DISEASE, SECONDARY) and inherited forms. These conditions are associated with dysfunction of dopaminergic or closely related motor integration neuronal pathways in the BASAL GANGLIA.
Parkinsonism following encephalitis, historically seen as a sequella of encephalitis lethargica (Von Economo Encephalitis). The early age of onset, the rapid progression of symptoms followed by stabilization, and the presence of a variety of other neurological disorders (e.g., sociopathic behavior; TICS; MUSCLE SPASMS; oculogyric crises; hyperphagia; and bizarre movements) distinguish this condition from primary PARKINSON DISEASE. Pathologic features include neuronal loss and gliosis concentrated in the MESENCEPHALON; SUBTHALAMUS; and HYPOTHALAMUS. (From Adams et al., Principles of Neurology, 6th ed, p754)
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)