The aim of this study was to determine the specificity and sensitivity of transcranial sonography (TCS) and the Pocket Smell Test (PST) in differing Parkinson's disease from essential tremor. The results were compared with the dopamin transporter scan (DaTSCAN) findings. Based on the DaTSCAN finding we formed a group of patients with essential tremor (51 patients) and a group with the Parkinson's disease (59 patients). The control group consisted of 26 healthy one. To evaluate the olfactory dysfunction the PST was used, whereas by TCS the substantia nigra hyperechogenicity was marked. The sensitivity and specificity of each diagnostic method was statistically calculated. In confirming Parkinson's disease the specificity of TCS was 88.2 % and the sensitivity 94.9 %. The specificity of PST was 80.4 % whereas the sensitivity was 74.6 %. TCS and PST should be performed to evaluate which patients need to be examined by DaTSCAN.
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http://dx.doi.org/10.1007/s10072-015-2152-y | DOI Listing |
Rev Neurol (Paris)
December 2024
Department of Neurology, Inselspital, University Hospital Bern, University of Bern, Bern, Switzerland.
Introduction: Neuropsychiatric symptoms are highly prevalent in Parkinson's disease (PD) and significantly affect the quality of life of patients and their significant others. The aim of this work is to describe typical neuropsychiatric symptoms and their treatment.
Methods: This is a narrative opinion paper, illustrated by a fictional case report.
Neurobiol Dis
December 2024
Department of Pharmacology, Toxicology, and Pharmacy, University of Veterinary Medicine Hannover, Bünteweg 17, 30559 Hannover, Germany. Electronic address:
Increasing evidence points to infectious diseases as contributor to the pathogenesis of neurodegeneration in Parkinson's disease (PD), probably driven by a peripheral and CNS inflammatory response together with alpha-synuclein (aSyn) pathology. Pro-inflammatory lipopolysaccharide (LPS) endotoxin is suggested as a risk factor, and LPS shedding gram-negative bacteria are more prevalent in the gut-microbiome of PD patients. Here, we investigated whether LPS could contribute to the neurodegenerative disease progression via neuroinflammation, especially under conditions of aSyn pathology.
View Article and Find Full Text PDFBrain Res
December 2024
Department of Pharmacology, Escola Paulista de Medicina, Universidade Federal de São Paulo, São Paulo, São Paulo, Brazil.
Numerous studies have explored the role of cannabinoids in neurological conditions, chronic pain and neurodegenerative diseases. Restoring autophagy has been proposed as a potential target for the treatment of neurodegenerative diseases. In our study, we used a neuroblastoma cell line that overexpresses wild-type α-synuclein to investigate the effects of cannabidiol on autophagy modulation and reduction in the level of cytosolic α-synuclein.
View Article and Find Full Text PDFComput Biol Med
December 2024
School of Engineering, RMIT University, Victoria, Australia. Electronic address:
Background: Changes in voice are a symptom of Parkinson's disease and used to assess the progression of the condition. However, natural differences in the voices of people can make this challenging. Computerized binary speech classification can identify people with PD (PwPD), but its multiclass application to detect the severity of the disease remains difficult.
View Article and Find Full Text PDFActa Neuropathol Commun
December 2024
Department of Physiology & Biophysics, Case Western Reserve University School of Medicine, Cleveland, OH, 44106, USA.
Mitochondrial dysfunction and α-synuclein (αSyn) aggregation are key contributors to Parkinson's Disease (PD). While genetic and environmental risk factors, including mutations in mitochondrial-associated genes, are implicated in PD, the precise mechanisms linking mitochondrial defects to αSyn pathology remain incompletely understood, hindering the development of effective therapeutic interventions. Here, we identify the loss of branched chain ketoacid dehydrogenase kinase (BCKDK) as a mitochondrial risk factor that exacerbates αSyn pathology by disrupting Complex I function.
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