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See detailPrimary vision and facial emotion recognition in early Parkinson's disease
Hipp, Géraldine; Diederich, Nico UL; Pieria, Viannina et al

in Journal of the Neurological Sciences (2014), 338

Background: In early stages of idiopathic Parkinson's disease (IPD), lower order vision (LOV) deficits including reduced colour and contrast discrimination have been consistently reported. Data are less ... [more ▼]

Background: In early stages of idiopathic Parkinson's disease (IPD), lower order vision (LOV) deficits including reduced colour and contrast discrimination have been consistently reported. Data are less conclusive concerning higher order vision (HOV) deficits, especially for facial emotion recognition (FER). However, a link between both visual levels has been hypothesized. Objective: To screen for both levels of visual impairment in early IPD. Methods: We prospectively recruited 28 IPD patients with disease duration of 1.4 +/− 0.8 years and 25 healthy controls. LOV was evaluated by Farnsworth-Munsell 100 Hue Test, Vis-Tech and Pelli-Robson test. HOV was examined by the Ekman 60 Faces Test and part A of the Visual Object and Space recognition test. Results: IPD patients performed worse than controls on almost all LOV tests. The most prominent difference was seen for contrast perception at the lowest spatial frequency (p = 0.0002). Concerning FER IPD patients showed reduced recognition of “sadness” (p = 0.01). “Fear” perception was correlated with perception of low contrast sensitivity in IPD patients within the lowest performance quartile. Controls showed a much stronger link between “fear” perception” and low contrast detection. Conclusion: At the early IPD stage there are marked deficits of LOV performances, while HOV performances are still intact, with the exception of reduced recognition of “sadness”. At this stage, IPD patients seem still to compensate the deficient input of low contrast sensitivity, known to be pivotal for appreciation of negative facial emotions and confirmed as such for healthy controls in this study. [less ▲]

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See detailParkinson's disease: Acquired frailty of archaic neural networks?
Diederich, Nico UL; Parent, A.

in Journal of the Neurological Sciences (2012), 314(1-2), 143-51

In Parkinson's disease (PD) many motor and non-motor symptoms are difficult to explain in terms of a purely ascending degeneration process as described by Braak. This essay proposes phylogenetic ... [more ▼]

In Parkinson's disease (PD) many motor and non-motor symptoms are difficult to explain in terms of a purely ascending degeneration process as described by Braak. This essay proposes phylogenetic considerations for consolidating the multidimensional elements of PD. Subtle clinical analysis paired with ethological comparisons as well as patho-anatomical data suggests that disrupted automatic gait control, olfactory deficits, selected visual deficits, impaired emotional face recognition, and REM sleep behavior disorder could be due to dysfunction of phylogenetically ancient networks. Neuroanatomical and behavioral findings lead to a reconsideration of the basal ganglia, to be viewed as the nuclear core of a widely distributed neural network that arborizes throughout the primordial core of the neuraxis, including the brainstem. Fragility of the resulting multiple, closed, ancillary loops that link brainstem and forebrain components of the basal ganglia may be a nodal point, pivotal to the pathogenesis of PD. Other primitive neural networks, such as those located at cardiac or gastro-intestinal levels, may share the same vulnerability. Such a network-based hypothesis overrides the need of a fixed temporal ordering of symptoms based on putative caudal–cephalic propagation patterns of pathological lesions. It also creates testable, secondary hypotheses such as differential gene expression in different neural networks, potential early epigenetic influences, concepts of “overuse” or maladaptation of primitive networks to the constraints of adult life, and system frailty due to irreparable mitochondrial “exhaustion” in highly energy consuming postmitotic cells [less ▲]

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See detailSleep disorders in Parkinson's disease: many causes, few therapeutic options
Diederich, Nico UL; McIntyre, Deborah J.

in Journal of the Neurological Sciences (2012), 314(1-2), 12-9

Sleep symptoms in Parkinson's disease (PD) are frequent and have multifactorial and multilayered causes. Primary involvement of sleep/wake regulating centers in the brainstem, sleep problems caused by the ... [more ▼]

Sleep symptoms in Parkinson's disease (PD) are frequent and have multifactorial and multilayered causes. Primary involvement of sleep/wake regulating centers in the brainstem, sleep problems caused by the nocturnal manifestation of motor and dysautonomic signs and medication-induced sleep problems are often impossible to disentangle in the individual patient. Two syndromes, hypersomnia and REM sleep behavior disorder (RBD), are increasingly recognized as harbingers of the core PD motor syndrome. RBD, associated with a panoply of other nonmotor symptoms, may predispose to a specific PD phenotype. Long-acting dopaminergic stimulation, when abating nocturnal akinesia, also improves subjective sleep quantity. While this strategy is backed up by several randomized controlled trials (RCT), other treatment recommendations are mostly based on case series or expert opinion. Thus we identified only two other RCT, one treating insomnia with eszopiclone, the other nocturnal behavioral abnormalities in demented PD patients with memantine. While the causal complexity of sleep problems in PD certainly hampers the design of therapeutic studies, multiple general treatment strategies against sleep disorders can however be applied efficiently in PD patients as well. [less ▲]

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See detailConverging environmental and genetic pathways in the pathogenesis of Parkinson's disease.
Burbulla, Lena F.; Krüger, Rejko UL

in Journal of the neurological sciences (2011), 306(1-2), 1-8

As a prototypic neurodegenerative disorder Parkinson's disease (PD) is characterized by the progressive loss of specific neuronal subpopulations leading to a late-onset movement disorder. Based on ... [more ▼]

As a prototypic neurodegenerative disorder Parkinson's disease (PD) is characterized by the progressive loss of specific neuronal subpopulations leading to a late-onset movement disorder. Based on familial forms of PD, to date a significant number of genes were identified that allowed first insight into the molecular pathogenesis of this common movement disorder. These pathways include impaired protein degradation and subsequent aggregation within neuronal cells and impaired mitochondrial function followed by energy depletion due to oxidative stress leading to cell death. The respective disease models were supported by pathoanatomical and biochemical findings in brains of sporadic PD patients without apparent genetic contribution to pathogenesis. Indeed recent genetic and epidemiological studies hint to a complex interplay of genetic susceptibility factors and environmental risk factors to converge to processes of pathological protein accumulation and mitochondrial damage that trigger neurodegeneration in PD. Therefore large-scale geneticoepidemiological studies combining genetic whole genome approaches with a detailed ascertainment of environmental exposures are expected to provide important clues to decipher the complexity of neurodegeneration of this most frequent neurodegenerative movement disorder. [less ▲]

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See detailIpsilateral hyperschematia without spatial neglect after right frontal lesion
Saj, Arnaud; Chiuvé, Sabina C.; Brugger, Camille et al

in Journal of the Neurological Sciences (2011), 308(1-2), 142-3

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