Outcome of deep brain stimulation in slowly progressive multiple system atrophy: A clinico-pathological series and review of the literature

Meissner, Wassilios G.; Laurencin, Chloé; Tranchant, C.; Witjas, Tatiana; Viallet, François; Guehl, Dominique; Damier, Philippe; Houeto, Jean‐Luc; Tison, François; Eusebio, Alexandre; Vital, Anne; Streichenberger, Nathalie; Lannes, Béatrice; Paula, André Maues De; Thobois, Stéphane

doi:10.1016/j.parkreldis.2016.01.005

Cited by 47 publications

(38 citation statements)

References 26 publications

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“…Of these, orofacial dyskinesia was more common in YOMSA than YOPD. The prevalence of dyskinesia varies with progression and has been reported in up to 50% of MSA cases later in the course . Another study suggested that YOMSA with predominant parkinsonism may closely resemble YOPD at onset, also owing to the development of motor fluctuations and levodopa‐induced dyskinesias .…”

Section: Discussionmentioning

confidence: 99%

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Young‐onset multiple system atrophy: Clinical and pathological features

et al. 2018

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Section: Discussionmentioning

confidence: 99%

“…The prevalence of dyskinesia varies with progression and has been reported in up to 50% of MSA cases later in the course. 23 Another study suggested that YOMSA with…”

Section: Levodopa Responsivenessmentioning

confidence: 99%

Young‐onset multiple system atrophy: Clinical and pathological features

et al. 2018

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“…Available data on interventional therapies in APSs are sparse: small case series highlight the risk of clinical worsening after deep-brain stimulation in histologically proven MSA patients and strongly discourage its use (26). In line with this finding, another case report revealed rapid post-thalamotomy deterioration in a patient who received a postmortem diagnosis of CBD (27).…”

Section: Treatment and Prognosismentioning

confidence: 99%

¹⁸F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment

et al. 2017

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Learning Objectives: On successful completion of this activity, participants should be able to (1) describe the clinical demand and rationale for differential diagnosis in parkinsonism, (2) recognize and differentiate the disease-specific patterns of regional glucose metabolism associated with Parkinson disease and the different atypical parkinsonian syndromes, and (3) identify regional metabolic changes that predict cognitive decline in Parkinson disease.Financial Disclosure: Dr. Meyer receives support from GE and Piramal for a research study outside the present topic. The authors of this article have indicated no other relevant relationships that could be perceived as a real or apparent conflict of interest. CME Credit: SNMMI is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to sponsor continuing education for physicians. SNMMI designates each JNM continuing education article for a maximum of 2.0 AMA PRA category 1 credits. Physicians should claim only credit commensurate with the extent of their participation in the activity. For CE credit, SAM, and other credit types, participants can access this activity through the SNMMI website (http://www.snmmilearningcenter.org) through December 2020.Accurate differential diagnosis of parkinsonism is of paramount therapeutic and prognostic importance. In addition, with the development of invasive therapies and novel disease-specific therapies, strategies for patient enrichment in trial populations are of growing importance. Imaging disease-specific patterns of regional glucose metabolism with PET and 18 F-FDG allows for a highly accurate distinction between Parkinson disease (PD) and atypical parkinsonian syndromes, including multiple-system atrophy, progressive supranuclear palsy, and corticobasal degeneration. On the basis of a preliminary metaanalysis of currently available studies with inclusion of multiple disease groups, we estimated that the diagnostic sensitivity and specificity for visual PET readings supported by voxel-based statistical analyses for diagnosis of atypical parkinsonian syndromes are 91.4% and 90.6%, respectively. The diagnostic specificity of 18 F-FDG PET for diagnosing multiple-system atrophy, progressive supranuclear palsy, and corticobasal degeneration was consistently shown to be high (.90%), whereas sensitivity was more variable (.75%). It is increasingly acknowledged that cognitive impairment represents a major challenge in PD, with mild cognitive impairment being a prodromal stage of PD with dementia (PDD). In line with clinical and neuropsychologic studies, recent PET studies demonstrated that posterior cortical dysfunction in nondemented PD patients precedes cognitive decline and the development of PDD by several years. Taken together, the current literature underscores the utility of 18 F-FDG PET for diagnostic evaluation of parkinsonism and the promising role of 18 F-FDG PET for assessment and risk stratification of cognitive impairment in PD.

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“…This was recently underscored in series of neuropathologically confirmed cases with benign, slowly progressive MSA, who underwent STN-DBS. Only a subset of these patients showed a short-term benefit from DBS that was rapidly counteracted by severely disabling symptoms related to MSA (Meissner et al 2016). …”

Section: Strategies To Define Diseases Stagesmentioning

confidence: 99%

Classification of advanced stages of Parkinson’s disease: translation into stratified treatments

Krüger

Klucken²,

Weiß

et al. 2017

J Neural Transm

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Advanced stages of Parkinson’s disease (advPD) still impose a challenge in terms of classification and related stage-adapted treatment recommendations. Previous concepts that define advPD by certain milestones of motor disability apparently fall short in addressing the increasingly recognized complexity of motor and non-motor symptoms and do not allow to account for the clinical heterogeneity that require more personalized approaches. Therefore, deep phenotyping approaches are required to characterize the broad-scaled, continuous and multidimensional spectrum of disease-related motor and non-motor symptoms and their progression under real-life conditions. This will also facilitate the reasoning for clinical care and therapeutic decisions, as neurologists currently have to refer to clinical trials that provide guidance on a group level; however, this does not always account for the individual needs of patients. Here, we provide an overview on different classifications for advPD that translate into critical phenotypic patterns requiring the differential therapeutic adjustments. New concepts refer to precision medicine approaches also in PD and first studies on genetic stratification for therapeutic outcomes provide a potential for more objective treatment recommendations. We define novel treatment targets that align with this concept and make use of emerging device-based assessments of real-life information on PD symptoms. As these approaches require empowerment of patients and integration into treatment decisions, we present communication strategies and decision support based on new technologies to adjust treatment of advPD according to patient demands and safety.

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Outcome of deep brain stimulation in slowly progressive multiple system atrophy: A clinico-pathological series and review of the literature

Cited by 47 publications

References 26 publications

Young‐onset multiple system atrophy: Clinical and pathological features

Young‐onset multiple system atrophy: Clinical and pathological features

¹⁸F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment

Classification of advanced stages of Parkinson’s disease: translation into stratified treatments

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Outcome of deep brain stimulation in slowly progressive multiple system atrophy: A clinico-pathological series and review of the literature

Cited by 47 publications

References 26 publications

Young‐onset multiple system atrophy: Clinical and pathological features

Young‐onset multiple system atrophy: Clinical and pathological features

18F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment

Classification of advanced stages of Parkinson’s disease: translation into stratified treatments

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Product

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¹⁸F-FDG PET in Parkinsonism: Differential Diagnosis and Evaluation of Cognitive Impairment