View clinical trials related to Shy-Drager Syndrome.
Filter by:Transcranial magnetic stimulation (TMS) is a procedure that has been shown to improve fatigue in chronic sufferers. It uses a plastic covered coil that sends a magnetic pulse through the skull into the brain and by targeting particular areas in the brain it can be used to help modulate the perception of fatigue. The study intends to use this technique to treat such a disabling symptom in patients who suffer from Multiple System Atrophy (MSA). Initially the aim is to study this technique in 22 MSA patients who are suffering from fatigue . These patients would require an resting-state funtional MRI before and after the stimulation. The stimulation would be performed ten sessions and the patients would be assessed by a clinician using well recognized clinical tools. It is anticipated that there will be a meaningful improvement in fatigue. It is also anticipated that TMS is a safety technique to use in MSA patients . Our findings will revealed that fatigue may be associated with an altered default mode network and sensorimotor network connectivity in MSA patients. We hypothesize that these divergent motor and cognitive networks connectivity changes and their adaptive or maladaptive functional outcome may play a prominent role in the pathophysiology of fatigue in MSA.
The purpose of this study is; compare respiratory function parameters and respiratory muscle strength in patients with MSA compare to healthy controls, and to evaluate the results of SNIP and PImax in measuring inspiratory muscle strength in MSA patients.
Multiple system atrophy (MSA) is a rare and fatal neurodegenerative disorder. The pathologic hallmark is the accumulation of aggregated alpha-synuclein in oligodendrocytes forming glial cytoplasmic inclusions. Some symptomatic treatments are available while disease-modification remains an unmet treatment need. Post-mortem findings suggest insulin resistance, i.e. reduced insulin signaling, in the brains of MSA patients. The aim of this study is to complete the target validation of insulin resistance for future treatment trials.
Alpha-synucleinopathies refer to age-related neurodegenerative and dementing disorders, characterized by the accumulation of alpha-synuclein in neurons and/or glia. The anatomical location of alpha-synuclein inclusions (Lewy Bodies) and the pattern of progressive neuronal death (e.g. caudal to rostral brainstem) give rise to distinct neurological phenotypes, including Parkinson's disease (PD), Multiple System Atrophy (MSA), Dementia with Lewy Bodies (DLB). Common to these disorders are the involvement of the central and peripheral autonomic nervous system, where Pure Autonomic Failure (PAF) is thought (a) to be restricted to the peripheral autonomic system, and (b) a clinical risk factor for the development of a central synucleinopathy, and (c) an ideal model to assess biomarkers that predict phenoconversion to PD, MSA, or DLB. Such biomarkers would aid in clinical trial inclusion criteria to ensure assessments of disease- modifying strategies to, delay, or halt, the neurodegenerative process. One of these biomarkers may be related to the neurotransmitter dopamine (DA) and related changes in the substantia nigra (SN) and brainstem. [18F]F-DOPA is a radiolabeled substrate for aromatic amino acid decarboxylase (AAADC), an enzyme involved in the production of dopamine. Use of this radiolabeled substrate in positron emission tomography (PET) may provide insight to changes in monoamine production and how they relate to specific phenoconversions in PAF patients. Overall, this study aims to identify changes in dopamine production in key regions including the SN, locus coeruleus, and brainstem to distinguish between patients with PD, MSA, and DLB, which may provide vital information to predict conversion from peripheral to central nervous system disease.
Multiple system atrophy (MSA) is a rare and fatal neurodegenerative disease characterised by a variable combination of parkinsonism, cerebellar impairment and autonomic dysfunction. The neuropathological hallmark is the accumulation of alpha-synuclein in oligodendrocytes. While some symptomatic treatments exist, neuroprotective treatments for MSA remain an urgent, unmet need. Moreover, at present there is not a single surrogate biomarker of MSA which could be used to inform clinical trials. This study seeks to characterise the natural history of MSA on a panel of candidate biomarkers, pre-selected for being putative surrogates of the underlying neurodegenerative process
This is a multicenter, open-label, non-controlled, non-randomized, phase 3 clinical study to compare the SPECT findings after a single IV administration of DaTSCAN™ ioflupane (123I) injection for patients with a clinical diagnosis of Parkinsonian syndrome (PS) involving striatal dopaminergic deficit (SDD; specifically, Parkinson's disease [PD] [SDD], multiple system atrophy [MSA] [SDD] or or progressive supranuclear palsy [PSP] [SDD]) as compared with patients with a clinical diagnosis of essential tremor (ET) (no SDD) and age-matched healthy controls.
In total 20 subjects will be enrolled at one participating site -UMC Ljubljana. The 20 subjects will be treated with placebo and NBMI 300 mg in a cross-over design. In case of subject drop-outs, additional subjects may be enrolled as decided by the Sponsor, to allow for expected number of evaluable subjects in each group.
The primary objectives are to evaluate the safety and tolerability of multiple doses of ION464 administered via intrathecal (IT) injection (Part 1) and to evaluate the long-term safety and tolerability of ION464 (Part 2) in participants with multiple system atrophy (MSA). The secondary objectives are to evaluate the pharmacodynamic (PD) effect of ION464 on the level of a potential biomarker of target engagement (Parts 1 and 2) and to evaluate the pharmacokinetic (PK) profile of ION464 in serum (Part 1).
Neurodegenerative cerebellar ataxias represent a group of disabling disorders which currently lack effective therapies. Cerebellar transcranial direct current stimulation (tDCS) is a non-invasive technique, which has been demonstrated to modulate cerebellar excitability and improve symptoms in patients with cerebellar ataxias. In this randomized, double-blind, sham-controlled study followed by an open-label phase, the investigators will evaluate whether a repetition of two-weeks' treatment with cerebellar anodal tDCS and spinal cathodal tDCS, after a three months interval, may further outlast clinical improvement in patients with neurodegenerative cerebellar ataxia and can modulate cerebello-motor connectivity, at short and long term.
The aim of study is to investigate most effective site for control the motor coordination using transcranial direct current stimulation in multiple system atrophy with cerebellar feature