25 research outputs found
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Sudden Onset of Oromandibular Dystonia after Cerebellar Stroke
Background: We present the case of a 65-year-old female with sudden-onset involuntary mouth opening, deviation of the jaw, facial grimacing, and tongue movements that started 6 months prior to her admission.
Case Report: She was diagnosed with oromandibular dystonia. Differential diagnosis of oromandibular dystonia and various etiologies were investigated. Neuroimaging studies revealed a left cerebellar infarction.
Discussion: To our knowledge, this case is the first oromandibular dystonia presenting with cerebellar ischemic stroke. Possible roles of the cerebellum for the pathophysiology of oromandibular dystonia are discussed.
Keywords: Dystonia, oromandibular dystonia, cerebrovascular disease
Citation: Akin A, Yilmaz R, Selcuk F, et al. Sudden onset of oromandibular dystonia after cerebellar stroke. Tremor Other Hyperkinet Mov. 2014; 4. doi: 10.7916/D8C24TN
Serum Inflammatory Profile for the Discrimination of Clinical Subtypes in Parkinson's Disease
Background: Blood levels of immune markers have been proposed to discriminate patients with Parkinson's disease (PD) from controls. However, differences between clinical PD subgroups regarding these markers still need to be identified. Objective: To investigate whether clinical phenotypes can be predicted by the assessment of immune marker profiles in the serum of PD patients. Methods: Phenotypes of clinical PD from Tübingen, Germany (n = 145) and Toronto, Canada (n = 90) were defined regarding clinical subtype, disease onset, severity, and progression as well as presence of cognitive and/or autonomic dysfunction. A panel of serum immune markers was assessed using principal component analysis (PCA) and regression models to define the marker(s) that were associated with clinical phenotypes after adjusting for potential confounders. Findings of both centers were compared for validation. Further, a [18F] FEPPA-PET was performed in a group of patients with high and low values of candidate markers for the assessment of in vivo brain microglial activation. Results: Overall, serum immune markers did not cluster to define a pro/anti-inflammatory profile in PCA. Out of 25 markers only IL-12p40 showed a trend to discriminate between PD subgroups in both cohorts which could not be replicated by [18F] FEPPA-PET. Conclusions: Assessment of cytokines in serum does not reliably differentiate clinical PD subtypes. Accompanying subtype-irrelevant inflammation in PD, dual activity, and lack of specificity of the immune markers, the complex function of microglia, probable effects of treatment, disease stage, and progression on inflammation as well as current technical limitations may limit the usefulness of serum immune markers for the differentiation of subtypes
Serum Inflammatory Profile for the Discrimination of Clinical Subtypes in Parkinson's Disease
Background: Blood levels of immune markers have been proposed to discriminate patients with Parkinson's disease (PD) from controls. However, differences between clinical PD subgroups regarding these markers still need to be identified.Objective: To investigate whether clinical phenotypes can be predicted by the assessment of immune marker profiles in the serum of PD patients.Methods: Phenotypes of clinical PD from Tübingen, Germany (n = 145) and Toronto, Canada (n = 90) were defined regarding clinical subtype, disease onset, severity, and progression as well as presence of cognitive and/or autonomic dysfunction. A panel of serum immune markers was assessed using principal component analysis (PCA) and regression models to define the marker(s) that were associated with clinical phenotypes after adjusting for potential confounders. Findings of both centers were compared for validation. Further, a [18F] FEPPA-PET was performed in a group of patients with high and low values of candidate markers for the assessment of in vivo brain microglial activation.Results: Overall, serum immune markers did not cluster to define a pro/anti-inflammatory profile in PCA. Out of 25 markers only IL-12p40 showed a trend to discriminate between PD subgroups in both cohorts which could not be replicated by [18F] FEPPA-PET.Conclusions: Assessment of cytokines in serum does not reliably differentiate clinical PD subtypes. Accompanying subtype-irrelevant inflammation in PD, dual activity, and lack of specificity of the immune markers, the complex function of microglia, probable effects of treatment, disease stage, and progression on inflammation as well as current technical limitations may limit the usefulness of serum immune markers for the differentiation of subtypes
Developments in the Role of Transcranial Sonography for the Differential Diagnosis of Parkinsonism
Screen Fast, Screen Faster: A Pilot Study to Screen for Depressive Symptoms Using the Beck Depression Inventory Fast Screen in Parkinson's Disease With Mild Cognitive Impairment
Sudden Onset of Oromandibular Dystonia after Cerebellar Stroke
Background: We present the case of a 65-year-old female with sudden-onset involuntary mouth opening, deviation of the jaw, facial grimacing, and tongue movements that started 6 months prior to her admission. Case Report: She was diagnosed with oromandibular dystonia. Differential diagnosis of oromandibular dystonia and various etiologies were investigated. Neuroimaging studies revealed a left cerebellar infarction.Discussion: To our knowledge, this case is the first oromandibular dystonia presenting with cerebellar ischemic stroke. Possible roles of the cerebellum for the pathophysiology of oromandibular dystonia are discussed.</p
Continuous infusion of apomorphine in a series of thirty patients with parkinson's disease
Biomarkers of Parkinson's disease: 20years later
Despite intensive effort, biomarker research for the detection of prodromal stage, diagnosis and progression of Parkinson's disease (PD) falls short of expectations. This article reviews the attempts in the last 20years to find a biomarker, addresses challenges along the biomarker search and suggests the steps that should be taken to overcome these challenges. Although several biomarkers are currently available, none of them is specific enough for diagnosis, prediction of future PD or disease progression. The main reason for the failure finding a strong biomarker seems to be drastic heterogeneity of PD, which exhibits itself in all domains; from the clinic to pathophysiology or genetics. The diversity in patient selection, assessment methods or outcomes in biomarker studies also limit the interpretation and generalizability of the data. In search of a reliable biomarker, consideration of novel approaches encompassing individual demographic, clinical, genetic, epigenetic and environmental differences, employment of strategies enabling marker combinations, designing multicenter studies with compatible assessment methods, integration of data from preclinical domains and utilization of novel technology-based assessments are necessary