Brain volume analyses and somatosensory evoked potentials in multiple system atrophy

Miyatake, Satoko; Mochizuki, Hitoshi; Naka, Tetsuji; Ugawa, Yoshikazu; Tanabe, Hajime; Kuzume, Daisuke; Suzuki, Mikiya; Ogata, Katsuhisa; Kawai, Mitsuru

doi:10.1007/s00415-009-5338-5

Cited by 6 publications

(4 citation statements)

References 21 publications

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“…A previous SEP study reported that the central sensory conduction time was progressively prolonged in parallel with disease duration in MSA [39]. In this study, since the peak N20 latencies were not prolonged in either PD or MSA-P, the timing of TMS over the M1 appears to be appropriate for inducing cortical plasticity in the M1.…”

Section: Discussionsupporting

confidence: 49%

Differences in Dopaminergic Modulation to Motor Cortical Plasticity between Parkinson's Disease and Multiple System Atrophy

et al. 2013

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Dopamine modulates the synaptic plasticity in the primary motor cortex (M1). To evaluate whether the functioning of the cortico-striatal circuit is necessary for this modulation, we applied a paired associative stimulation (PAS) protocol that comprised an electric stimulus to the right median nerve at the wrist and subsequent transcranial magnetic stimulation of the left M1, to 10 patients with Parkinson's disease (PD) and 10 with multiple system atrophy of the parkinsonian type (MSA-P) with and without dopamine replacement therapy (-on/off). To investigate the M1 function, motor-evoked potentials (MEPs) were measured before and after the PAS. In both patient groups without medication, the PAS protocol failed to increase the averaged amplitude of MEPs. The dopamine replacement therapy in PD, but not in MSA-P effectively restored the PAS-induced MEP increase. This suggests that not the existence of dopamine itself but the activation of cortico-striatal circuit might play an important role for cortical plasticity in the human M1.

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Section: Discussionsupporting

confidence: 49%

Differences in Dopaminergic Modulation to Motor Cortical Plasticity between Parkinson's Disease and Multiple System Atrophy

et al. 2013

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“…For this reason, the usefulness of brain CT in MSA is limited, and should only be used in patients with contraindications to magnetic resonance (MR) imaging (i.e., pacemaker, metal implants). Brain volumetric analysis obtained from 3-dimensional CT scans, however, could be useful to monitor disease progression in MSA (Miyatake et al, 2010). …”

Section: Brain and Cardiac Neuroimagingmentioning

confidence: 99%

Diagnosis of multiple system atrophy

Palma

Norcliffe‐Kaufmann

Kaufmann

2018

Autonomic Neuroscience

126

114

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Multiple system atrophy (MSA) may be difficult to distinguish clinically from other disorders, particularly in the early stages of the disease. An autonomic-only presentation can be indistinguishable from pure autonomic failure. Patients presenting with parkinsonism may be misdiagnosed as having Parkinson disease. Patients presenting with the cerebellar phenotype of MSA can mimic other adult-onset ataxias due to alcohol, chemotherapeutic agents, lead, lithium, and toluene, or vitamin E deficiency, as well as paraneoplastic, autoimmune, or genetic ataxias. A careful medical history and meticulous neurological examination remain the cornerstone for the accurate diagnosis of MSA. Ancillary investigations are helpful to support the diagnosis, rule out potential mimics, and define therapeutic strategies. This review summarizes diagnostic investigations useful in the differential diagnosis of patients with suspected MSA. Currently used techniques include structural and functional brain imaging, cardiac sympathetic imaging, cardiovascular autonomic testing, olfactory testing, sleep study, urological evaluation, and dysphagia and cognitive assessments. Despite advances in the diagnostic tools for MSA in recent years and the availability of consensus criteria for clinical diagnosis, the diagnostic accuracy of MSA remains sub-optimal. As other diagnostic tools emerge, including skin biopsy, retinal biomarkers, blood and cerebrospinal fluid biomarkers, and advanced genetic testing, a more accurate and earlier recognition of MSA should be possible, even in the prodromal stages. This has important implications as misdiagnosis can result in inappropriate treatment, patient and family distress, and erroneous eligibility for clinical trials of disease-modifying drugs.

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“…In patients with MSA-C, for example, structural imaging data indicate that cerebellar volume is reduced in even early stages of MSA (Dash et al, 2018), and the related gray matter (GM) loss bears a significant association with cognitive profiles (Kim et al, 2015). Based on a three-dimensional gyrification index, Miyatake et al (Miyatake et al, 2010) have further demonstrated that patients with the MSA-C variant show GM losses primarily in upper lobules and anterior lobes of cerebellum, determining a negative correlation between hemispheric volume and cerebellar ataxia scores. Cerebellar abnormalities are also common in the MSA-P variant, which is typically considered a basal ganglia disorder.…”

Section: Introductionmentioning

confidence: 99%

Cerebellar atrophy and its contribution to motor and cognitive performance in multiple system atrophy

Yang

Wang

Luo

et al. 2019

NeuroImage: Clinical

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Objective Neuroanatomical differences in the cerebellum are among the most consistent findings in multiple system atrophy (MSA) patients. This study performed a detailed cerebellar morphology in MSA patients and its two subtypes: MSA-P (parkinson's symptoms predominate) and MSA-C (cerebellar symptoms predominant), and their relations to profiles of motor and cognitive deficits. Materials and methods Structure MRI data were acquired from 63 healthy controls and 61 MSA patients; voxel-based morphometry and the Spatially Unbiased Infratentorial Toolbox cerebellar atlas were performed to identify the cerebellar gray volume changes in MSA and its subtypes. Further, the gray matter changes were correlated with the clinical motor/cognitive scores. Results Patients with MSA exhibited widespread loss of cerebellar volume bilaterally, relative to healthy controls. In those with MSA-C, gray matter loss was detected from anterior (bilateral lobule IV-V) to posterior (bilateral crus I/II, bilateral lobule IX, left lobule VIII) cerebellar lobes. Lower anterior cerebellar volume negatively correlated with disease duration and motor performance, whereas posterior lobe integrity positively correlated with cognitive assessment. In patients with MSA-P, atrophy of anterior lobe (bilateral lobules IV-V) and posterior lobe in part (left lobule VI, bilateral IX) was evident; and in left cerebellar lobule IX, gray matter loss negatively correlated with motor scores. Direct comparison of MSA-P and MSA-C group outcomes showed divergence in right cerebellar crus II only. Conclusions Our data suggest that volumetric abnormalities of cerebellum contribute substantially to motor and cognitive performance in patients with MSA. In patients with MSA-P and MSA-C, affected regions of cerebellum differed.

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Brain volume analyses and somatosensory evoked potentials in multiple system atrophy

Cited by 6 publications

References 21 publications

Differences in Dopaminergic Modulation to Motor Cortical Plasticity between Parkinson's Disease and Multiple System Atrophy

Differences in Dopaminergic Modulation to Motor Cortical Plasticity between Parkinson's Disease and Multiple System Atrophy

Diagnosis of multiple system atrophy

Cerebellar atrophy and its contribution to motor and cognitive performance in multiple system atrophy

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