References of "Diederich, Nico 50001696"
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See detailImproved Parkinson’s disease classification from diffusion MRI data by Fisher vector descriptors
Salamanca Mino, Luis UL; Vlassis, Nikos UL; Diederich, Nico UL et al

in Improved Parkinson’s disease classification from diffusion MRI data by Fisher vector descriptors (2015, October)

Due to the complex clinical picture of Parkinson’s disease (PD), the reliable diagnosis of patients is still challenging. A promising approach is the structural characterization of brain areas affected in ... [more ▼]

Due to the complex clinical picture of Parkinson’s disease (PD), the reliable diagnosis of patients is still challenging. A promising approach is the structural characterization of brain areas affected in PD by diffusion magnetic resonance imaging (dMRI). Standard classification methods depend on an accurate non-linear alignment of all images to a common reference template, and are challenged by the resulting huge dimensionality of the extracted feature space. Here, we propose a novel diagnosis pipeline based on the Fisher vector algorithm. This technique allows for a precise encoding into a high-level descriptor of standard diffusion measures like the fractional anisotropy and the mean diffusivity, extracted from the regions of interest (ROIs) typically involved in PD. The obtained low dimensional, fixed-length descriptors are independent of the image alignment and boost the linear separability of the problem in the description space, leading to more efficient and accurate diagnosis. In a test cohort of 50 PD patients and 50 controls, the implemented methodology outperforms previous methods when using a logistic linear regressor for classification of each ROI independently, which are subsequently combined into a single classification decision. [less ▲]

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See detailStaining for unphosphorylated alpha-synuclein in the colon mucosa. No difference between patients with Parkinson's disease and healthy controls
Antony, Paul UL; Antunes, L; Frasquilho, S et al

Scientific Conference (2015, June)

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See detailFailing as Doorman and Disc Jockey at the Same Time: Amygdalar Dysfunction in Parkinson’s Disease
Diederich, Nico UL; Goldman, Jennifer; Stebbins, Glenn et al

in Movement Disorders : Official Journal of the Movement Disorder Society (2015), 00(00),

In Braak’s model of ascending degeneration in Parkinson’s disease (PD), involvement of the amygdala occurs simultaneously with substantia nigra degeneration. However, the clinical manifestations of ... [more ▼]

In Braak’s model of ascending degeneration in Parkinson’s disease (PD), involvement of the amygdala occurs simultaneously with substantia nigra degeneration. However, the clinical manifestations of amygdalar involvement in PD have not been fully delineated. Considered a multitask manager, the amygdala is a densely connected “hub,” coordinating and integrating tasks ranging from prompt, multisensorial emotion recognition to adequate emotional responses and emotional tuning of memories. Although phylogenetically predisposed to handle fear, the amygdala handles both aversive and positive emotional inputs. In PD, neuropathological and in vivo studies suggest primarily amygdalar hypofunction. However, as dopamine acts as an inverted U-shaped amygdalar modulator, medicationinduced hyperactivity of the amygdala can occur.We propose that amygdalar (network) dysfunction contributes to reduced recognition of negative emotional face expressions, impaired theory of mind, reactive hypomimia, and impaired decision making. Similarly, impulse control disorders in predisposed individuals, hallucinations, anxiety, and panic attacks may be related to amygdalar dysfunction. When available, we discuss amygdala-independent trigger mechanisms of these symptoms. Although dopaminergic agents have mostly an activation effect on amygdalar function, adaptive and compensatory network changes may occur as well, but these have not been sufficiently explored. In conclusion, our model of amygdalar involvement brings together several elements of Parkinson’s disease phenomenology heretofore left unexplained and provides a framework for testable hypotheses in patients during life and in autopsy analyses. VC 2015 International Parkinson and Movement Disorder Society [less ▲]

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See detailAre patients with Parkinson’s disease blind to blindsight?
Diederich, Nico UL; Stebbins, Glenn; Schiltz, Christine UL et al

in Brain : A Journal of Neurology (2014)

In Parkinson’s disease, visual dysfunction is prominent. Visual hallucinations can be a major hallmark of late stage disease, but numerous visual deficits also occur in early stage Parkinson’s disease ... [more ▼]

In Parkinson’s disease, visual dysfunction is prominent. Visual hallucinations can be a major hallmark of late stage disease, but numerous visual deficits also occur in early stage Parkinson’s disease. Specific retinopathy, deficits in the primary visual pathway and the secondary ventral and dorsal pathways, as well as dysfunction of the attention pathways have all been posited as causes of hallucinations in Parkinson’s disease. We present data from patients with Parkinson’s disease that contrast with a known neuro-ophthalmological syndrome, termed ‘blindsight’. In this syndrome, there is an absence of conscious object identification, but preserved ‘guess’ of the location of a stimulus, preserved reflexive saccades and motion perception and preserved autonomical and expressive reactions to negative emotional facial expressions. We propose that patients with Parkinson’s disease have the converse of blindsight, being ‘blind to blindsight’. As such they preserve conscious vision, but show erroneous ‘guess’ localization of visual stimuli, poor saccades and motion perception, and poor emotional face perception with blunted autonomic reaction. Although a large data set on these deficits in Parkinson’s disease has been accumulated, consolidation into one specific syndrome has not been proposed. Focusing on neuropathological and physiological data from two phylogenetically old and subconscious pathways, the retino-colliculo-thalamo-amygdala and the retino-geniculo-extrastriate pathways, we propose that aberrant function of these systems, including pathologically inhibited superior colliculus activity, deficient corollary discharges to the frontal eye fields, dysfunctional pulvinar, claustrum and amygdaloid subnuclei of the amygdala, the latter progressively burdened with Lewy bodies, underlie this syndrome. These network impairments are further corroborated by the concept of the ‘silent amygdala’. Functionally being ‘blind to blindsight’ may facilitate the highly distinctive ‘presence’ or ‘passage’ hallucinations of Parkinson’s disease and can help to explain handicaps in driving capacities and dysfunctional ‘theory of mind’. We propose this synthesis to prompt refined neuropathological and neuroimaging studies on the pivotal nuclei in these pathways in order to better understand the networks underpinning this newly conceptualized syndrome in Parkinson’s disease. [less ▲]

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See detailThe pathology of hallucinations: one or several points of processing breakdown?
Diederich, Nico UL; Goetz, Christopher G.; Stebbins, Glenn T.

in Collerton, Daniel; Mosimann, Urs Peter; Perry, Elaine (Eds.) The Neuroscience of Visual Hallucinations (2014)

This chapter describes neuropathological findings, earlier unimodal models and finally, multidimensional models concerning the pathogenesis of hallucinations. Because of the primary interest in Parkinson ... [more ▼]

This chapter describes neuropathological findings, earlier unimodal models and finally, multidimensional models concerning the pathogenesis of hallucinations. Because of the primary interest in Parkinson's disease (PD) and Lewy Body Dementia (LBD), the chapter focuses on these disorders. In PD and LBD, features of repetitive and emotionally neutral visual hallucinations are a frequent, disabling and progressive phenomenon. Multi-sensory hallucinations in which visual hallucinations are accompanied later by auditory, tactile, and olfactory hallucinations can occur, but the classic syndrome involves visual hallucinations. More recent models have attempted to integrate findings obtained in various domains and have proposed that recurrent complex visual hallucinations (RCVH) are the result of a multidimensional interactional process, the contributing factors being visual input, degree of alertness and internally or pharmacologically driven biochemical modulation. The Perception and Attention deficit model (PAD) and Hobson's Activation-Input-Modulation (AIM) model applied to RCVH definitely have extended the pathogenetic concept of RCVH. [less ▲]

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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 detailIntegrating Pathways of Parkinson's Disease in a Molecular Interaction Map
Fujita, Kazuhiro A.; Ostaszewski, Marek UL; Matsuoka, Yukiko et al

in Molecular Neurobiology (2014)

Parkinson's disease (PD) is a major neurodegenerative chronic disease, most likely caused by a complex interplay of genetic and environmental factors. Information on various aspects of PD pathogenesis is ... [more ▼]

Parkinson's disease (PD) is a major neurodegenerative chronic disease, most likely caused by a complex interplay of genetic and environmental factors. Information on various aspects of PD pathogenesis is rapidly increasing and needs to be efficiently organized, so that the resulting data is available for exploration and analysis. Here we introduce a computationally tractable, comprehensive molecular interaction map of PD. This map integrates pathways implicated in PD pathogenesis such as synaptic and mitochondrial dysfunction, impaired protein degradation, alpha-synuclein pathobiology and neuroinflammation. We also present bioinformatics tools for the analysis, enrichment and annotation of the map, allowing the research community to open new avenues in PD research. The PD map is accessible at http://minerva.uni.lu/pd_map . [less ▲]

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See detailThe hallmarks of Parkinson's disease.
Antony, Paul UL; Diederich, Nico UL; Krüger, Rejko UL et al

in FEBS Journal (2013)

Since the discovery of dopamine as a neurotransmitter in the 1950s, Parkinson's disease (PD) research has generated a rich and complex body of knowledge, revealing PD to be an age-related multifactorial ... [more ▼]

Since the discovery of dopamine as a neurotransmitter in the 1950s, Parkinson's disease (PD) research has generated a rich and complex body of knowledge, revealing PD to be an age-related multifactorial disease, influenced by both genetic and environmental factors. The tremendous complexity of the disease is increased by a non-linear progression of the pathogenesis between molecular, cellular, and organic systems. In this mini-review, we explore the complexity of PD and propose a systems-based approach, organizing the available information around cellular disease hallmarks. We encourage our peers to adopt this cell-based view with the aim of improving communication in interdisciplinary research endeavors targeting the molecular events, modulatory cell-to-cell signaling pathways, and emerging clinical phenotypes related to PD. This article is protected by copyright. All rights reserved. [less ▲]

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See detailThe Parkinson's Disease Map: A Framework for Integration, Curation and Exploration of Disease-related Pathways
Ostaszewski, Marek UL; Fujita, Kazuhiro; Matsuoka, Yukiko et al

Poster (2013, March 09)

Objectives: The pathogenesis of Parkinson's Disease (PD) is multi-factorial and age-related, implicating various genetic and environmental factors. It becomes increasingly important to develop new ... [more ▼]

Objectives: The pathogenesis of Parkinson's Disease (PD) is multi-factorial and age-related, implicating various genetic and environmental factors. It becomes increasingly important to develop new approaches to organize and explore the exploding knowledge of this field. Methods: The published knowledge on pathways implicated in PD, such as synaptic and mitochondrial dysfunction, alpha-synuclein pathobiology, failure of protein degradation systems and neuroinflammation has been organized and represented using CellDesigner. This repository has been linked to a framework of bioinformatics tools including text mining, database annotation, large-scale data integration and network analysis. The interface for online curation of the repository has been established using Payao tool. Results: We present the PD map, a computer-based knowledge repository, which includes molecular mechanisms of PD in a visually structured and standardized way. A bioinformatics framework that facilitates in-depth knowledge exploration, extraction and curation supports the map. We discuss the insights gained from PD map-driven text mining of a corpus of over 50 thousands full text PD-related papers, integration and visualization of gene expression in post mortem brain tissue of PD patients with the map, as well as results of network analysis. Conclusions: The knowledge repository of disease-related mechanisms provides a global insight into relationships between different pathways and allows considering a given pathology in a broad context. Enrichment with available text and bioinformatics databases as well as integration of experimental data supports better understanding of complex mechanisms of PD and formulation of novel research hypotheses. [less ▲]

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See detailLack of Polysomnographic Non-REM Sleep Changes in Early Parkinson’s Disease
Diederich, Nico UL; Rufra, Olivier; Pieri, Vannina et al

in Movement Disorders : Official Journal of the Movement Disorder Society (2013)

Background: Polysomnography (PSG) data are rare in patients who have early stage idiopathic Parkinson’s disease (IPD). Methods: Thirty-three patients who had IPD with a disease duration 3 years and 37 age ... [more ▼]

Background: Polysomnography (PSG) data are rare in patients who have early stage idiopathic Parkinson’s disease (IPD). Methods: Thirty-three patients who had IPD with a disease duration 3 years and 37 age-matched controls were recruited. PSG analysis was performed on current medication. Results: Patients with IPD had a reduced mean percentage of muscle atonia during rapid eye movement (REM) sleep (80% vs 93%; P < 0.05). Total sleep time, sleep efficiency, indices/hour of arousals, awakenings, apnea/hypopnea, and periodic leg movements were similar in both groups. Age, but not dopaminergic medication, had a negative impact on sleep architecture in patients with IPD. There was no correlation between sleep efficiency assessed by PSG and sleep quality assessed by questionnaire. Conclusions: The results confirmed a reduction in muscle atonia during REM sleep as a characteristic finding in early IPD. However, there were no further disease-inherent or medication-induced changes in sleep architecture. Although sleep disturbances are considered to be an integral part of IPD, PSG cannot yet identify them objectively at an early stage. VC 2013 International Parkinson and Movement Disorder Society [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 detailParkinson’s disease mouse models in translational research
Antony, Paul UL; Diederich, Nico UL; Balling, Rudi UL

in Mammalian Genome : Official Journal of the International Mammalian Genome Society (2011), 22(7-8), 401-19

Animal models with high predictive power are a prerequisite for translational research. The closer the similarity of a model to Parkinson's disease (PD), the higher is the predictive value for clinical ... [more ▼]

Animal models with high predictive power are a prerequisite for translational research. The closer the similarity of a model to Parkinson's disease (PD), the higher is the predictive value for clinical trials. An ideal PD model should present behavioral signs and pathology that resemble the human disease. The increasing understanding of PD stratification and etiology, however, complicates the choice of adequate animal models for preclinical studies. An ultimate mouse model, relevant to address all PD-related questions, is yet to be developed. However, many of the existing models are useful in answering specific questions. An appropriate model should be chosen after considering both the context of the research and the model properties. This review addresses the validity, strengths, and limitations of current PD mouse models for translational research. [less ▲]

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See detailDiscriminative power of different nonmotor signs in early Parkinson's disease. A case-control study
Diederich, Nico UL; Pieri, Vannina; Hipp, Geraldine et al

in Movement Disorders : Official Journal of the Movement Disorder Society (2010), 25(7), 882-887

The objective of this study was to evaluate the discriminative power of different nonmotor signs for early diagnosis of Parkinson's disease (PD). Thirty patients with PD with <or=3 years of disease ... [more ▼]

The objective of this study was to evaluate the discriminative power of different nonmotor signs for early diagnosis of Parkinson's disease (PD). Thirty patients with PD with <or=3 years of disease duration were compared with 30 healthy controls. Six deficit domains (DD) were defined: hyposmia, sleep abnormalities, dysautonomia, visual deficits, executive dysfunction, and depression. Plotting of Receiver operating characteristic (ROC) curves and exact conditional logistic modeling, followed by manual stepwise descending procedure were used to identify a model for nonmotor signs that detects early PD. Patients with PD and controls did not differ in terms of age, gender, and educational level. Several DD discriminated patients with PD from healthy controls. Visual deficits showed the largest area under the ROC curve (0.83), followed by hyposmia (0.81) and dysautonomia (0.80). When combining the DD visual deficits and dysautonomia, the best residual model was obtained; it maximized both sensitivity and specificity for PD at a level of 0.77. At an early disease stage, several nonmotor domains were already able to discriminate patients with PD from healthy controls. Visual deficits had the best discriminatory power. Being brief and inexpensive, visual tests should be further investigated in larger cohorts as potential screening tool for early PD. [less ▲]

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See detailThe placebo treatments in neurosciences: New insights from clinical and neuroimaging studies
Diederich, Nico UL; Goetz, Christopher G.

in Neurology (2008), 71(9), 677-684

Placebo (PL) treatment is a method utilized as a control condition in clinical trials. A positive placebo response is seen in up to 50% of patients with Parkinson disease (PD), pain syndromes, and ... [more ▼]

Placebo (PL) treatment is a method utilized as a control condition in clinical trials. A positive placebo response is seen in up to 50% of patients with Parkinson disease (PD), pain syndromes, and depression. The response is more pronounced with invasive procedures or advanced disease. Physiologic and biochemical changes have been studied in an effort to understand the mechanisms underlying placebo-related clinical improvement. In PD, objective clinical improvements in parkinsonism correlate with dopaminergic activation of the striatum, documented by PET and with changes in cell firings of the subthalamic nucleus documented by single cell recordings. Dopaminergic pathways mediating reward may underlie PL-mediated improvement in PD. In pain syndromes, endogenous opioid release triggered by cortical activation, especially the rostral anterior cingulated cortex, is associated with PL-related analgesia and can be reversed by opioid antagonists. Covert treatment of an analgesic is less effective than overt treatment, suggesting an expectation component to clinical response. In depression, PL partially imitates selective serotonin reuptake inhibitor-mediated brain activation. Diseases lacking major "top-down" or cortically based regulation may be less prone to PL-related improvement. [less ▲]

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See detailProgressive sleep 'destructuring' in Parkinson's disease. A polysomnographic study in 46 patients.
Diederich, Nico UL; Vaillant, Michel; Mancuso, Giovanna UL et al

in Sleep medicine (2005), 6(4), 313-8

BACKGROUND: Sleep abnormalities in Parkinson's disease (PD) are frequent, but it is unknown whether or not there is progressive loss of physiological sleep architecture or what the causes could be ... [more ▼]

BACKGROUND: Sleep abnormalities in Parkinson's disease (PD) are frequent, but it is unknown whether or not there is progressive loss of physiological sleep architecture or what the causes could be. METHODS: Retrospective review of medical records and polysomnographic data from 46 non-demented PD patients. RESULTS: Sleep latency was correlated with disease duration (F1,44=4.87, P=0.03). Total sleep time (F1,44=8.54, P=0.005), deep sleep time (F1,44=4.06, P=0.05), REM sleep time (F1,44=9.15, P=0.004) and sleep efficiency (SE) (F1,44=10.20, P=0.003) were inversely correlated with disease duration. The same sleep parameters were independent from the degree of motor impairment, dosage of the dopaminergic medications, and age. Subjective sleep complaints could only partially predict abnormalities in polysomnographic (PSG) studies. CONCLUSION: In PD nocturnal sleep 'destructuring' is linked to disease duration and evolves independently from other major disease parameters. [less ▲]

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See detailSleep apnea syndrome in Parkinson's disease. A case-control study in 49 patients.
Diederich, Nico UL; Vaillant, Michel; Leischen, Mike et al

in Movement disorders : official journal of the Movement Disorder Society (2005), 20(11), 1413-8

In PD, the impact of nocturnal respiration on sleep continuity and architecture has not been systematically investigated by polysomnography (PSG). We performed a case-control study with retrospective ... [more ▼]

In PD, the impact of nocturnal respiration on sleep continuity and architecture has not been systematically investigated by polysomnography (PSG). We performed a case-control study with retrospective analysis of PSG data of 49 PD patients. After classifying the PD patients according to their apnea/hypopnea index (AHI), they were matched with 49 controls in terms of age, gender, and AHI. There were 21 PD patients (43%) who had sleep apnea syndrome (SAS), classified as mild (AHI, 5-15) in 10 patients, moderate (AHI, >15-30) in 4 patients, and severe (AHI, > 30) in 7 patients. PD patients had more deep sleep (P = 0.02) and more nocturnal awakenings (P < 0.001) than the controls. Their body mass index (BMI) was lower (P = 0.04), and they maintained a more favorable respiratory profile, with higher mean and minimal oxygen saturation values (P = 0.006 and 0.01, respectively). These differences were preserved when only considering PD patients with AHI > 15. PD patients had less obstructive sleep apneas (P = 0.035), independently from the factor AHI. Only the respiratory changes of 4 PD patients with BMI > 27 and AHI > 15 (8%) approximated those seen in the controls. At an early or middle stage of the disease, non-obese PD patients frequently have AHI values suggesting SAS, however, without the oxygen desaturation profile of SAS. Longitudinal studies of patients with such "abortive" SAS are warranted to establish if this finding reflects benign nocturnal respiratory muscle dyskinesia or constitutes a precursor sign of dysautonomia in PD. [less ▲]

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