Loss of dorsolateral nigral hyperintensity on 3.0 tesla susceptibility‐weighted imaging in idiopathic rapid eye movement sleep behavior disorder

Marzi, Roberto De; Seppi, Klaus; Högl, Birgit; Müller, Christoph; Scherfler, Christoph; Stefani, Ambra; Iranzo, Álex; Tolosa, Eduardo; Santamaría, Joan; Gizewski, Elke R.; Schocke, Michael; Skalla, Elisabeth; Kremser, Christian; Poewe, Werner

doi:10.1002/ana.24646

Cited by 99 publications

(74 citation statements)

References 11 publications

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“…Neuroimaging has shown altered neuromelanin signal intensity in the locus coeruleus/subcoeruleus nucleus region, 29,57,112–115 and functional imaging studies, including dopamine transporter uptake, have found decreased nigrostriatal putamenal dopaminergic uptake in patients with idiopathic RBD 95,116–120 as well as decreased cortical thickness and diffuse resting state metabolic network dysfunction with similar patterns to PD. 121–123 Lastly, autopsy series of patients with RBD have found underlying synucleinopathy in 94% of patients, 25,97,124,125 and tissues from living patients with idiopathic RBD have exhibited abnormal α-synuclein immunoreactivity in peripheral tissues such as the submandibular gland 126 and colonic submucosal nerve fibers or ganglia.…”

Section: Clinical Implications Of Rbdmentioning

confidence: 99%

REM Sleep Behavior Disorder: Diagnosis, Clinical Implications, and Future Directions

Louis

Boeve

2017

Mayo Clinic Proceedings

161

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Rapid eye movement sleep behavior disorder (RBD) is diagnosed by a clinical history of dream enactment accompanied by polysomnographic rapid eye movement sleep atonia loss (rapid eye movement sleep without atonia). Rapid eye movement sleep behavior disorder is strongly associated with neurodegenerative disease, especially synucleinopathies such as Parkinson disease, dementia with Lewy bodies, and multiple system atrophy. A history of RBD may begin several years to decades before onset of any clear daytime symptoms of motor, cognitive, or autonomic impairments, suggesting that RBD is the presenting manifestation of a neurodegenerative process. Evidence that RBD is a synlucleinopathy includes the frequent presence of subtle prodromal neurodegenerative abnormalities including hyposmia, constipation, and orthostatic hypotension, as well as abnormalities on various neuroimaging, neurophysiological, and autonomic tests. Up to 90.9% of patients with idiopathic RBD ultimately develop a defined neurodegenerative disease over longitudinal follow-up, although the prognosis for younger patients and antidepressant-associated RBD is less clear. Patients with RBD should be treated with either melatonin 3 to 12 mg or clonazepam 0.5 to 2.0 mg to reduce injury potential. Prospective outcome and treatment studies of RBD are necessary to enable accurate prognosis and better evidence for symptomatic therapy and future neuroprotective strategies.

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Section: Clinical Implications Of Rbdmentioning

confidence: 99%

REM Sleep Behavior Disorder: Diagnosis, Clinical Implications, and Future Directions

Louis

Boeve

2017

Mayo Clinic Proceedings

161

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“…Because therapeutic interventions should ideally target the triggering pathogenic events as early as possible to achieve not only slowing of disease progression but also forestalling of disease onset, early diagnosis is a key priority and creates an urgent need for valid PD biomarkers with predictive validity for PD diagnosis (Mahlknecht et al 2015; Poewe et al 2017). Indeed, there is preliminary evidence that novel MR markers seems to identify prodromal degenerative parkinsonism as loss of DNH was found in at least two-thirds of subjects with idiopathic REM sleep behaviour disorder (iRBD) (De Marzi et al 2016) and in clinically asymptomatic LRKK2 carriers (Ceravolo et al 2015). Moreover, a study including patients with PD as well as symptomatic and asymptomatic LRRK2 and Parkin mutation carriers found that R2* values in the SN were increased in PD and mutation-carrying patients as compared with controls and in mutation-carrying patients as compared with PD, while asymptomatic mutation carriers showed higher R2* values than controls and did not differ from PD patients, suggesting that iron deposition occurs early during the preclinical phase of the disease and that R2* measurements may be used as markers for investigating nigrostriatal damage in preclinical mutation-carrying patients (Pyatigorskaya et al 2015).…”

Section: Conclusion and Future Developmentmentioning

confidence: 99%

Magnetic resonance imaging for the diagnosis of Parkinson’s disease

et al. 2017

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The differential diagnosis of parkinsonian syndromes is considered one of the most challenging in neurology and error rates in the clinical diagnosis can be high even at specialized centres. Despite several limitations, magnetic resonance imaging (MRI) has undoubtedly enhanced the diagnostic accuracy in the differential diagnosis of neurodegenerative parkinsonism over the last three decades. This review aims to summarize research findings regarding the value of the different MRI techniques, including advanced sequences at high- and ultra-high-field MRI and modern image analysis algorithms, in the diagnostic work-up of Parkinson’s disease. This includes not only the exclusion of alternative diagnoses for Parkinson’s disease such as symptomatic parkinsonism and atypical parkinsonism, but also the diagnosis of early, new onset, and even prodromal Parkinson’s disease.

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“…Only one study has investigated this sign in pre-clinical disease (de Marzi et al, 2016). De Marzi and colleagues performed SWI sequences in 15 RBD subjects, 104 Parkinson's patients and 42 healthy controls.…”

Section: Neuroimaging In Pre-motor Parkinson'smentioning

confidence: 99%

Neuroimaging in pre-motor Parkinson's disease

Barber

Klein

Mackay

et al. 2017

NeuroImage: Clinical

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The process of neurodegeneration in Parkinson's disease begins long before the onset of clinical motor symptoms, resulting in substantial cell loss by the time a diagnosis can be made. The period between the onset of neurodegeneration and the development of motoric disease would be the ideal time to intervene with disease modifying therapies. This pre-motor phase can last many years, but the lack of a specific clinical phenotype means that objective biomarkers are needed to reliably detect prodromal disease. In recent years, recognition that patients with REM sleep behaviour disorder (RBD) are at particularly high risk of future parkinsonism has enabled the development of large prodromal cohorts in which to investigate novel biomarkers, and neuroimaging has generated some of the most promising results to date. Here we review investigations undertaken in RBD and other pre-clinical cohorts, including modalities that are well established in clinical Parkinson's as well as novel imaging methods. Techniques such as high resolution MRI of the substantia nigra and functional imaging of Parkinsonian brain networks have great potential to facilitate early diagnosis. Further longitudinal studies will establish their true value in quantifying prodromal neurodegeneration and predicting future Parkinson's.

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Loss of dorsolateral nigral hyperintensity on 3.0 tesla susceptibility‐weighted imaging in idiopathic rapid eye movement sleep behavior disorder

Cited by 99 publications

References 11 publications

REM Sleep Behavior Disorder: Diagnosis, Clinical Implications, and Future Directions

REM Sleep Behavior Disorder: Diagnosis, Clinical Implications, and Future Directions

Magnetic resonance imaging for the diagnosis of Parkinson’s disease

Neuroimaging in pre-motor Parkinson's disease

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