Publications by authors named "Pauline Dodet"

21 Publications

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Functional brain imaging using 18F-fluorodeoxyglucose positron emission tomography/computerized tomography in 138 patients with Kleine-Levin syndrome: an early marker?

Brain Commun 2021 17;3(2):fcab130. Epub 2021 Jun 17.

Sorbonne University, Paris Brain Institute (ICM), Inserm UMR-S975, CNRS UMR7225, Paris 75013, France.

Kleine-Levin syndrome is a rare disorder characterized by relapsing-remitting episodes of severe hypersomnia, cognitive impairment, apathy, derealization and behavioural disturbances. Between episodes, most patients experience normal sleep, mood and behaviour, but they may have some residual abnormalities in brain functional imaging; however, the frequency, localization and significance of abnormal imaging are unknown, as brain functional imaging have been scarce and heterogenous [including scintigraphy 18F-fluorodeoxyglucose positron emission tomography/computerized tomography (FDG-PET/CT) and functional MRI during resting state and cognitive effort] and based on case reports or on group analysis in small groups. Using visual individual analysis of 18F-fluorodeoxyglucose positron emission tomography/computerized tomography at the time of Kleine-Levin syndrome diagnosis, we examined the frequency, localization and clinical determinants of hypo- and hypermetabolism in a cross-sectional study. Among 179 patients with Kleine-Levin syndrome who underwent 18F-fluorodeoxyglucose positron emission tomography/computerized tomography, the visual analysis was restricted to the 138 untreated patients studied during asymptomatic periods. As many as 70% of patients had hypometabolism, mostly affecting the posterior associative cortex and the hippocampus. Hypometabolism was associated with younger age, recent (<3years) disease course and a higher number of episodes during the preceding year. The hypometabolism was more extensive (from the left temporo-occipital junction to the entire homolateral and then the bilateral posterior associative cortex) at the beginning of the disorder. In contrast, there was hypermetabolism in the prefrontal dorsolateral cortex in half of the patients (almost all having concomitant hypometabolism in the posterior areas), which was also associated with younger age and shorter disease course. The cognitive performances (including episodic memory) were similar in patients with versus without hippocampus hypometabolism. In conclusion, hypometabolism is frequently observed upon individual visual analysis of 18F-fluorodeoxyglucose positron emission tomography/computerized tomography during asymptomatic Kleine-Levin syndrome periods; it is mostly affecting the posterior associative cortex and the hippocampus and is mostly in young patients with recent-onset disease. Hypometabolism provides a trait marker during the first years of Kleine-Levin syndrome, which could help clinicians during the diagnosis process.
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http://dx.doi.org/10.1093/braincomms/fcab130DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8226192PMC
June 2021

Sweet or Bland Dreams? Taste Loss in Isolated REM-Sleep Behavior Disorder and Parkinson's Disease.

Mov Disord 2021 Jun 12. Epub 2021 Jun 12.

Sleep Disorders Unit, University Hospital Pitié-Salpêtrière, APHP-Sorbonne, Paris, France.

Background: Hyposmia and isolated REM sleep behavior disorder are well-established features of prodromal Parkinson's disease (PD).

Objectives: The objective of the present study was to evaluate whether taste loss (reported in PD and possibly suggesting brain stem involvement) is present at the isolated REM sleep behavior disorder stage.

Methods: We assessed taste function using the Taste Strip Test (evaluating 4 concentrations of bitter, sweet, sour, and salty) in 44 participants with isolated REM sleep behavior disorder, 19 with PD, and 29 controls. All participants underwent video-polysomnography, standardized questionnaires, and clinical examination, including olfactory assessment.

Results: Participants with isolated REM sleep behavior disorder and PD had lower taste scores than controls. There was no difference between isolated REM sleep behavior disorder and PD cohorts, nor was there any correlation between taste and olfaction, age, disease duration, cognition, or autonomic function.

Conclusion: This study demonstrates for the first time the presence of taste impairment in isolated REM sleep behavior disorder that is independent of olfactory dysfunction and comparable to participants with PD. © 2021 International Parkinson and Movement Disorder Society.
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http://dx.doi.org/10.1002/mds.28692DOI Listing
June 2021

Long-term effect of apomorphine infusion in advanced Parkinson's disease: a real-life study.

NPJ Parkinsons Dis 2021 Jun 11;7(1):50. Epub 2021 Jun 11.

Neurology Department, Pitié-Salpêtrière Hospital, AP-HP, Paris, France.

Long-term effects of continuous subcutaneous apomorphine infusion (CSAI) on health-related quality of life (HRQoL) and predictors of CSAI discontinuation are poorly known. Data from consecutive advanced Parkinson's disease patients treated in routine care were retrospectively collected over 24 months after CSAI initiation, with a focus on the 39-item Parkinson's disease questionnaire (PDQ-39). We determined predictors of CSAI discontinuation and HRQoL improvement using multiple regression analysis. Of the 110 subjects evaluated over a 2-year period, 35% discontinued CSAI. Of those who continued treatment, HRQoL remained stable with a sustained reduction in motor fluctuations. The observed effect on dyskinesias was mild and transient. Of note, patients with preexisting impulse control disorders showed an overall good tolerability. PDQ-39 was the only baseline predictor of HRQoL improvement after 2 years of treatment. The presence of dyskinesias, poorer psychological status, shorter disease duration, male sex, and worse OFF state were predictors of discontinuation. Best candidates for CSAI are patients with: (i) poor baseline HRQoL and (ii) marked motor fluctuations.
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http://dx.doi.org/10.1038/s41531-021-00194-7DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8196159PMC
June 2021

The spatiotemporal changes in dopamine, neuromelanin and iron characterizing Parkinson's disease.

Brain 2021 May 12. Epub 2021 May 12.

Sorbonne Université, Institut du Cerveau - Paris Brain Institute - ICM, INSERM, CNRS, 75013 Paris, France.

In Parkinson's disease, there is a progressive reduction in striatal dopaminergic function, and loss of neuromelanin-containing dopaminergic neurons and increased iron deposition in the substantia nigra. We tested the hypothesis of a relationship between impairment of the dopaminergic system and changes in the iron metabolism. Based on imaging data of patients with prodromal and early clinical Parkinson's disease, we assessed the spatiotemporal ordering of such changes and relationships in the sensorimotor, associative and limbic territories of the nigrostriatal system. Patients with Parkinson's disease (disease duration < 4 years) or idiopathic REM sleep behaviour disorder (a prodromal form of Parkinson's disease) and healthy controls underwent longitudinal examination (baseline and 2-year follow-up). Neuromelanin and iron sensitive MRI and dopamine transporter single-photon emission tomography were performed to assess nigrostriatal levels of neuromelanin, iron, and dopamine. For all three functional territories of the nigrostriatal system, in the clinically most and least affected hemispheres separately, the following was performed: cross-sectional and longitudinal inter-group difference analysis of striatal dopamine and iron, and nigral neuromelanin and iron; in Parkinson's disease patients, exponential fitting analysis to assess the duration of the prodromal phase and the temporal ordering of changes in dopamine, neuromelanin or iron relative to controls; voxel-wise correlation analysis to investigate concomitant spatial changes in dopamine-iron, dopamine-neuromelanin and neuromelanin-iron in the substantia nigra pars compacta. The temporal ordering of dopaminergic changes followed the known spatial pattern of progression involving first the sensorimotor, then the associative and limbic striatal and nigral regions. Striatal dopaminergic denervation occurred first followed by abnormal iron metabolism and finally neuromelanin changes in the substantia nigra pars compacta, which followed the same spatial and temporal gradient observed in the striatum but shifted in time. In conclusion, dopaminergic striatal dysfunction and cell loss in the substantia nigra pars compacta are interrelated with increased nigral iron content.
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http://dx.doi.org/10.1093/brain/awab191DOI Listing
May 2021

Kleine-Levin syndrome is associated with birth difficulties and genetic variants in the gene loci.

Proc Natl Acad Sci U S A 2021 Mar;118(12)

Histocompatibility Department, Blood Center of the Community of Madrid, 28032 Madrid, Spain.

Kleine-Levin syndrome (KLS) is a rare disorder characterized by severe episodic hypersomnia, with cognitive impairment accompanied by apathy or disinhibition. Pathophysiology is unknown, although imaging studies indicate decreased activity in hypothalamic/thalamic areas during episodes. Familial occurrence is increased, and risk is associated with reports of a difficult birth. We conducted a worldwide case-control genome-wide association study in 673 KLS cases collected over 14 y, and ethnically matched 15,341 control individuals. We found a strong genome-wide significant association (rs71947865, Odds Ratio [OR] = 1.48, = 8.6 × 10) within the 3'region of gene locus, previously associated with bipolar disorder and schizophrenia. Strikingly, KLS cases with rs71947865 variant had significantly increased reports of a difficult birth. As perinatal outcomes have dramatically improved over the last 40 y, we further stratified our sample by birth years and found that recent cases had a significantly reduced rs71947865 association. While the rs71947865 association did not replicate in the entire follow-up sample of 171 KLS cases, rs71947865 was significantly associated with KLS in the subset follow-up sample of 59 KLS cases who reported birth difficulties (OR = 1.54, = 0.01). Genetic liability of KLS as explained by polygenic risk scores was increased (pseudo = 0.15; < 2.0 × 10 at = 0.5 threshold) in the follow-up sample. Pathway analysis of genetic associations identified enrichment of circadian regulation pathway genes in KLS cases. Our results suggest links between KLS, circadian regulation, and bipolar disorder, and indicate that the polymorphisms in conjunction with reported birth difficulties may predispose to KLS.
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http://dx.doi.org/10.1073/pnas.2005753118DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7999876PMC
March 2021

Speculating on Kleine-Levin Syndrome mechanisms.

J Clin Sleep Med 2021 03;17(3):611-612

National Reference Center for Kleine-Levin Syndrome, Sleep Disorders Unit, Pitie-Salpetriere Hospital, APHP-Sorbonne, Paris, France.

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http://dx.doi.org/10.5664/jcsm.9104DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7927329PMC
March 2021

Are sleep paralysis and false awakenings different from REM sleep and from lucid REM sleep? A spectral EEG analysis.

J Clin Sleep Med 2021 04;17(4):719-727

Sleep Disorder Unit, Pitié-Salpêtrière University Hospital, AP-HP, Paris, France.

Study Objectives: To determine the polysomnography characteristics during sleep paralysis, false awakenings, and lucid dreaming (which are states intermediate to rapid eye movement [REM] sleep and wake but exceptionally observed in sleep laboratory).

Methods: In 5 participants, we captured 5 episodes of sleep paralysis (2 time marked with the ocular left-right-left-right code normally used to signal lucid dreaming, 1 time marked by an external noise, and 2 retrospectively reported) and 2 episodes of false awakening. The sleep coding (using 3-second mini-epochs) and spectral electroencephalography analysis were compared during these episodes and normal REM sleep as well as wakefulness in the same 4 of 5 participants and vs lucid REM sleep in 4 other patients with narcolepsy.

Results: During episodes of sleep paralysis, 70.8% of mini-epochs contained theta electroencephalography rhythm (vs 89.7% in REM sleep and 21.2% in wakefulness), 93.8% contained chin muscle atonia (vs 89.7% in REM sleep and 33.3% in wakefulness), and 6.9% contained rapid eye movements (vs 11.9% in REM sleep and 8.1% in wakefulness). The electroencephalography spectrum during sleep paralysis was intermediate between wakefulness and REM sleep in the alpha, theta, and delta frequencies, whereas the beta frequencies were not different between sleep paralysis and normal REM sleep. The power spectrum during false awakening followed the same profile as in sleep paralysis.

Conclusions: The predominant theta electroencephalography rhythm during sleep paralysis and false awakenings (with rare and lower alpha rhythm) suggests that the brain during sleep paralysis is not in an awake but in a dreaming state.
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http://dx.doi.org/10.5664/jcsm.9056DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8020694PMC
April 2021

Blackout of my nights: Contentless, timeless and selfless report from the night in patients with central hypersomnias.

Conscious Cogn 2020 05 24;81:102931. Epub 2020 Apr 24.

Sorbonne University, Paris, France; Paris Brain Institute ([email protected]; Inserm UMR_S 975; CNRS UMR 7225), Paris, France; Sleep Disorders Unit, Pitié-Salpêtrière University Hospital, Assistance Publique - Hôpitaux de Paris, Paris, France; National Reference Center on Narcolepsy and Rare Hypersomnias, France. Electronic address:

At the extreme spectrum of consciousness during sleep, some patients with rare hypersomnias reported experiencing a specific night 'blackout' when sleeping, i.e., an absence of experiences or recall of them from sleep onset to offset. Thus, we explored through questionnaires the conscious experiences (dreaming experience, mind, self) during the night in 133 patients with idiopathic hypersomnia, 108 patients with narcolepsy, and 128 healthy controls. The night blackout was more frequent in idiopathic hypersomnia than in narcolepsy and control groups. Patients with idiopathic hypersomnia and frequent night amnesia had lower dream recall frequencies, and felt more often sleep as deep and mind as blank during the night. They had a higher proportion of slow wave sleep on their (retrospectively collected) sleep recordings than those without night blackout. This night blackout provides a new model for studying loss of consciousness during sleep, here as a contentless, selfless and timeless feeling upon awakening.
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http://dx.doi.org/10.1016/j.concog.2020.102931DOI Listing
May 2020

Simple behavioral criteria for the diagnosis of disorders of arousal.

J Clin Sleep Med 2020 01 4;16(1):121-128. Epub 2019 Dec 4.

AP-HP, Pitié -Salpêtrière Hospital, Sleep Disorders Unit, Paris, France.

Study Objectives: This case-control study aimed to identify and validate behavioral markers supporting the diagnosis of disorders of arousal (DOA) with video polysomnography.

Methods: All behaviors associated with 1,335 episodes of N3 interruptions were compared in 52 adult patients with DOA versus 52 participants without DOA (healthy control patients and patients with insomnia, hypersomnia, or sleep apnea syndrome).

Results: Patients with DOA had more frequent (5.1 ± 2.4 versus 3.4 ± 1.9 interruptions/N3 time) and longer (35.8 ± 33 versus 23.1 ± 21.4 sec) arousals and awakenings from N3 than control patients. In the DOA group, the onset of behaviors was more abrupt, and behaviors including eye opening (69% versus 16%), head raising (41% versus 9%), visually exploring the environment (27% versus 1%), expression of fear/surprise (21% versus zero), speaking (18% versus 0.3%), trunk raising (13% versus 0.3%), and interacting with the environment (13% versus 0.5%), were (unlike quiet, comfort behaviors) more frequent than in control patients. A cutoff of two or more N3 interruptions containing eye opening yielded a sensitivity of 94.2% and a specificity of 76.9% for a DOA diagnosis. This accuracy was confirmed in a second set of data (second night of monitoring). Behaviors including an expression of fear/surprise (67.3%), sitting (32.7%), screaming, and standing up were specific to patients with DOA.

Conclusions: A simple, behavioral video marker of behavioral reactions during N3 interruption (ie, opening the eyes at least two times in the same night) was sensitive, specific, and reproducible for discriminating patients with DOA from sleep laboratory control patients.

Clinical Trial Registration: This study is a surrogate study of NCT02648568 and NCT03074578 on ClinicalTrials.gov.
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http://dx.doi.org/10.5664/jcsm.8136DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7053005PMC
January 2020

Sleep in -Related Dyskinesia: Prolonged Awakenings Caused by Abnormal Movements.

J Clin Sleep Med 2019 07 15;15(7):1021-1029. Epub 2019 Jul 15.

Sleep Disorders (Department "R3S"), Pitié-Salpêtrière Hospital, Sorbonne University, Paris, France.

Study Objectives: mutations cause early-onset hyperkinetic movement disorders comprising diurnal and nocturnal paroxysmal dyskinesia, and patient-reported sleep fragmentation. We aimed to characterize all movements occurring during sleep and in the transition from sleep to awakening, to ascertain if there is a primary sleep disorder, or if the sleep disturbance is rather a consequence of the dyskinesia.

Methods: Using video polysomnography, we evaluated the nocturnal motor events and abnormal movements in 7 patients with -related dyskinesia and compared their sleep measures with those of 14 age- and sex-matched healthy controls.

Results: We observed an increased occurrence of abnormal movements during wake periods compared to sleep in patients with -related dyskinesia. While asleep, abnormal movements occurred more frequently during stage N2 and REM sleep, in contrast with stage N3 sleep. Abnormal movements were also more frequent during morning awakenings compared to wake periods before falling asleep. The pattern of the nocturnal abnormal movements mirrored those observed during waking hours. Compared to controls, patients with -related dyskinesia had lower sleep efficiencies due to prolonged awakenings secondary to the abnormal movements, but no other differences in sleep measures. Notably, sleep onset latency was short and devoid of violent abnormal movements.

Conclusions: In this series of patients with -related dyskinesia, nocturnal paroxysmal dyskinesia were not associated with drowsiness or delayed sleep onset, but emerged during nighttime awakenings with subsequent delayed sleep, whereas sleep architecture was normal.
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http://dx.doi.org/10.5664/jcsm.7886DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6622513PMC
July 2019

Precision Medicine for Idiopathic Hypersomnia.

Sleep Med Clin 2019 Sep;14(3):333-350

National Reference Center for Rare Hypersomnias, Pitie-Salpetriere University Hospital, APHP, and Sorbonne University, 47-83 Boulevard de l'Hôpital, Paris 75013, France.

Idiopathic hypersomnia (IH) is characterized by excessive daytime sleepiness despite normal or prolonged sleep. IH is distinguished from narcolepsy by the female predominance, severe morning inertia, continuous drowsiness (rather than sleep attacks), unrefreshing naps, absence of cataplexy, sleep onset in REM periods, and hypocretin deficiency. In IH, the multiple sleep latency test demonstrates low sensitivity, specificity, and reproducibility, compared with prolonged sleep monitoring. In some IH cases, an endogenous hypnotic peptide stimulating GABA receptors during wakefulness is suspected, which are improved by anti-GABA drugs. The benefits of modafinil, sodium oxybate, mazindol, and pitolisant were found in mostly retrospective studies.
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http://dx.doi.org/10.1016/j.jsmc.2019.05.007DOI Listing
September 2019

Transthyretin amyloid polyneuropathies mimicking a demyelinating polyneuropathy.

Neurology 2018 07 15;91(2):e143-e152. Epub 2018 Jun 15.

From Service de Physiologie Clinique-Explorations Fonctionnelles (P.L.), AP-HP, Hôpital Lariboisière, Paris; INSERM UMR965 (P.L.), Paris; Université Paris Diderot Sorbonne Paris Cité (P.L., B.A.), Paris; French National Reference Center for FAP (NNERF) (L.-L.M., P.D., G.B., M.T., C.A., D.A.), Le Kremlin-Bicêtre; Service de Neurologie (L.-L.M., P.D., M.T., D.A.) and Service d'anatomopathologie (C.A.), APHP, Hôpital Bicêtre, Le Kremlin-Bicêtre; Unité de Neurophysiologie Clinique et d'épileptologie (G.B.), Hôpital Bicêtre, Le Kremlin-Bicêtre; Immuno-Hematology Department (B.A.), Saint-Louis Hospital, Paris; Université Paris 11 (D.A.); and INSERM UMR1195 (D.A.), Le Kremlin-Bicêtre, France.

Objective: To clearly define transthyretin familial amyloid polyneuropathies (TTR-FAPs) fulfilling definite clinical and electrophysiologic European Federation of Neurological Societies/Peripheral Nerve Society criteria for chronic inflammatory demyelinating polyneuropathy (CIDP).

Methods: From a cohort of 194 patients with FAP, 13 of 84 patients (15%) of French ancestry had late-onset demyelinating TTR-FAP. We compared clinical presentation and electrophysiology to a cohort with CIDP and POEMS (polyneuropathy, organomegaly, endocrinopathy, monoclonal protein, and skin changes) syndrome. We assessed nerve histology and the correlation between motor/sensory amplitudes/velocities. Predictors of demyelinating TTR-FAP were identified from clinical and electrophysiologic data.

Results: Pain, dysautonomia, small fiber sensory loss above the wrists, upper limb weakness, and absence of ataxia were predictors of demyelinating TTR-FAP ( < 0.01). The most frequent demyelinating features were prolonged distal motor latency of the median nerve and reduced sensory conduction velocity of the median and ulnar nerves. Motor axonal loss was severe and frequent in the median, ulnar, and tibial nerves ( < 0.05) in demyelinating FAP. Ulnar nerve motor amplitude <5.4 mV and sural nerve amplitude <3.95 μV were distinguishing characteristics of demyelinating TTR-FAP. Nerve biopsy showed severe axonal loss and occasional segmental demyelination-remyelination.

Conclusion: Misleading features of TTR-FAP fulfilling criteria for CIDP are not uncommon in sporadic late-onset TTR-FAP, which highlights the limits of European Federation of Neurological Societies/Peripheral Nerve Society criteria. Specific clinical aspects and marked electrophysiologic axonal loss are red flag symptoms that should alert to this diagnosis and prompt gene sequencing.
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http://dx.doi.org/10.1212/WNL.0000000000005777DOI Listing
July 2018

Author Correction: REM sleep respiratory behaviours match mental content in narcoleptic lucid dreamers.

Sci Rep 2018 Apr 12;8(1):6128. Epub 2018 Apr 12.

Sorbonne Université, [email protected], INSERM, CNRS UMR7225, équipe MOV'IT, F-75013, Paris, France.

A correction to this article has been published and is linked from the HTML and PDF versions of this paper. The error has been fixed in the paper.
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http://dx.doi.org/10.1038/s41598-018-24179-4DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5897333PMC
April 2018

Stridor combined with other sleep breathing disorders in multiple system atrophy: a tailored treatment?

Sleep Med 2018 02 8;42:53-60. Epub 2018 Jan 8.

Sleep Disorder Unit, Pitie-Salpetriere Hospital, AP-HP, Paris, France(1); Sorbonne University, Paris, France. Electronic address:

Objectives: To determine the frequency of sleep breathing disorders in multiple systemic atrophy (MSA, combining Parkinsonism, cerebellar syndrome, and dysautonomia) and evaluate the benefit/tolerance of various modes of ventilation.

Methods: We retrospectively analyzed 45 patients with MSA having undergone a videopolysomnography. Their sleep characteristics were compared to those of 45 patients with Parkinson's disease and 45 healthy controls, matched for age and sex. Patients with MSA received fixed continuous positive airway pressure (CPAP) when stridor was isolated, auto-adjusting CPAP when it was combined with obstructive sleep apnea, and adaptive servo-ventilation (ASV) when combined with central sleep apnea.

Results: Higher periodic leg movements index and more frequent REM sleep behavior disorder were observed in MSA patients, compared to patients with Parkinson's disease and healthy controls. In MSA, 28/45 (62.2%) patients had sleep breathing disorders, including (overlapping samples) stridor (n = 17, 38%), obstructive sleep apnea (n = 14, 31%), central sleep apnea (n = 4, 9%), and ataxic breathing (n = 1). Except for three initial refusals and two yet untreated patients, fixed CPAP (n = 9), auto-adjusting CPAP (n = 8) and ASV (n = 2) were well-tolerated (limited leaks and good compliance) and successfully controlled stridor plus sleep apnea. Treated patients had survival times similar to those of patients without any sleep breathing disorder.

Conclusion: In this small group, tailored management of stridor in MSA as an independent issue or combined with obstructive and central sleep apnea, yields a survival similar to survival in patients without sleep breathing disorders.
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http://dx.doi.org/10.1016/j.sleep.2017.12.008DOI Listing
February 2018

REM sleep respiratory behaviours mental content in narcoleptic lucid dreamers.

Sci Rep 2018 02 8;8(1):2636. Epub 2018 Feb 8.

Sorbonne Université, [email protected], INSERM, CNRS UMR7225, équipe MOV'IT, F-75013 Paris, France.

Breathing is irregular during rapid eye-movement (REM) sleep, whereas it is stable during non-REM sleep. Why this is so remains a mystery. We propose that irregular breathing has a cortical origin and reflects the mental content of dreams, which often accompany REM sleep. We tested 21 patients with narcolepsy who had the exceptional ability to lucid dream in REM sleep, a condition in which one is conscious of dreaming during the dream and can signal lucidity with an ocular code. Sleep and respiration were monitored during multiple naps. Participants were instructed to modify their dream scenario so that it involved vocalizations or an apnoea, -two behaviours that require a cortical control of ventilation when executed during wakefulness. Most participants (86%) were able to signal lucidity in at least one nap. In 50% of the lucid naps, we found a clear congruence between the dream report (e.g., diving under water) and the observed respiratory behaviour (e.g., central apnoea) and, in several cases, a preparatory breath before the respiratory behaviour. This suggests that the cortico-subcortical networks involved in voluntary respiratory movements are preserved during REM sleep and that breathing irregularities during this stage have a cortical/subcortical origin that reflects dream content.
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http://dx.doi.org/10.1038/s41598-018-21067-9DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5805737PMC
February 2018

Spinal Koebner phenomenon: Medullar sarcoidosis facing a discal hernia.

Joint Bone Spine 2017 07 29;84(4):497-498. Epub 2016 Jun 29.

Neurology Department, Pitié-Salpêtrière Hospital, Assistance publique-Hôpitaux de Paris, 75013 Paris, France.

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http://dx.doi.org/10.1016/j.jbspin.2016.05.009DOI Listing
July 2017

Paroxysmal Exercise-induced Dyskinesias Caused by GLUT1 Deficiency Syndrome.

Tremor Other Hyperkinet Mov (N Y) 2016 4;6:371. Epub 2016 Mar 4.

Institut du Cerveau et de la Moelle épinière, ICM, Paris, France; Département de Neurologie, Assistance Publique - Hôpitaux de Paris, Hôpital de la Pitié Salpêtrière, Paris, France; Sorbonne Universités, Université Pierre et Marie Curie (Paris VI), Paris, France; Institut National de la Santé et de la Recherche Médicale (Inserm), Unité 1127, Paris, France; Centre National de la Recherche Scientifique (CNRS), Unité 7225, Paris, France.

Background: Glucose transporter type 1 deficiency syndrome is due to de novo mutations in the SLC2A1 gene encoding the glucose transporter type 1.

Phenomenology Shown: Paroxysmal motor manifestations induced by exercise or fasting may be the main manifestations of glucose transporter type 1 deficiency syndrome.

Educational Value: Proper identification of the paroxysmal events and early diagnosis is important since the disease is potentially treatable.
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http://dx.doi.org/10.7916/D89W0F96DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4790204PMC
June 2016

Lucid dreaming in narcolepsy.

Sleep 2015 Mar 1;38(3):487-97. Epub 2015 Mar 1.

Sorbonne Universites, UPMC Univ Paris 06, Paris, France.

Objective: To evaluate the frequency, determinants and sleep characteristics of lucid dreaming in narcolepsy.

Settings: University hospital sleep disorder unit.

Design: Case-control study.

Participants: Consecutive patients with narcolepsy and healthy controls.

Methods: Participants were interviewed regarding the frequency and determinants of lucid dreaming. Twelve narcolepsy patients and 5 controls who self-identified as frequent lucid dreamers underwent nighttime and daytime sleep monitoring after being given instructions regarding how to give an eye signal when lucid.

Results: Compared to 53 healthy controls, the 53 narcolepsy patients reported more frequent dream recall, nightmares and recurrent dreams. Lucid dreaming was achieved by 77.4% of narcoleptic patients and 49.1% of controls (P < 0.05), with an average of 7.6±11 vs. 0.3±0.8 lucid dreams/ month (P < 0.0001). The frequency of cataplexy, hallucinations, sleep paralysis, dyssomnia, HLA positivity, and the severity of sleepiness were similar in narcolepsy with and without lucid dreaming. Seven of 12 narcoleptic (and 0 non-narcoleptic) lucid dreamers achieved lucid REM sleep across a total of 33 naps, including 14 episodes with eye signal. The delta power in the electrode average, in delta, theta, and alpha powers in C4, and coherences between frontal electrodes were lower in lucid than non-lucid REM sleep in spectral EEG analysis. The duration of REM sleep was longer, the REM sleep onset latency tended to be shorter, and the percentage of atonia tended to be higher in lucid vs. non-lucid REM sleep; the arousal index and REM density and amplitude were unchanged.

Conclusion: Narcolepsy is a novel, easy model for studying lucid dreaming.
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http://dx.doi.org/10.5665/sleep.4516DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4335518PMC
March 2015

Sleep-related declarative memory consolidation and verbal replay during sleep talking in patients with REM sleep behavior disorder.

PLoS One 2013 13;8(12):e83352. Epub 2013 Dec 13.

Sleep Disorder Unit, Pitié-Salpêtrière University Hospital, Assistance Publique-Hôpitaux de Paris, Paris, France ; Centre de Recherche de l'Institut Cerveau-Moelle épinière, Institut national de la santé et de la recherche médicale Unité 975, Pierre and Marie Curie University ; Institut national de la santé et de la recherche médicale Unités mixtes de recherches 975, Centre national de la recherche scientifique Unités mixtes de recherche 7225, Paris, France ; Institut National de la Santé et de la Recherché Médicale, Unité 975, Paris, France.

Objective: To determine if sleep talkers with REM sleep behavior disorder (RBD) would utter during REM sleep sentences learned before sleep, and to evaluate their verbal memory consolidation during sleep.

Methods: Eighteen patients with RBD and 10 controls performed two verbal memory tasks (16 words from the Free and Cued Selective Reminding Test and a 220-263 word long modified Story Recall Test) in the evening, followed by nocturnal video-polysomnography and morning recall (night-time consolidation). In 9 patients with RBD, daytime consolidation (morning learning/recall, evening recall) was also evaluated with the modified Story Recall Test in a cross-over order. Two RBD patients with dementia were studied separately. Sleep talking was recorded using video-polysomnography, and the utterances were compared to the studied texts by two external judges.

Results: Sleep-related verbal memory consolidation was maintained in patients with RBD (+24±36% words) as in controls (+9±18%, p=0.3). The two demented patients with RBD also exhibited excellent nighttime consolidation. The post-sleep performance was unrelated to the sleep measures (including continuity, stages, fragmentation and apnea-hypopnea index). Daytime consolidation (-9±19%) was worse than night-time consolidation (+29±45%, p=0.03) in the subgroup of 9 patients with RBD. Eleven patients with RBD spoke during REM sleep and pronounced a median of 20 words, which represented 0.0003% of sleep with spoken language. A single patient uttered a sentence that was judged to be semantically (but not literally) related to the text learned before sleep.

Conclusion: Verbal declarative memory normally consolidates during sleep in patients with RBD. The incorporation of learned material within REM sleep-associated sleep talking in one patient (unbeknownst to himself) at the semantic level suggests a replay at a highly cognitive creative level.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0083352PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3862769PMC
September 2014

Sensory impairment in obese patients? Sensitivity and pain detection thresholds for electrical stimulation after surgery-induced weight loss, and comparison with a nonobese population.

Clin J Pain 2013 Jan;29(1):43-9

Department of Internal Medicine, Assistance Publique-Hôpitaux de Paris, Hôpital Lariboisière, Unit of Therapeutic Research, Paris, France.

Introduction: Obese patients have a high prevalence of painful musculoskeletal disorders that may decrease after massive weight loss. Pain thresholds may be different in obese participants.

Objectives: To assess the sensitivity and pain detection thresholds, through the application of an electrical sensitivity, before and after massive weight loss, and to compare the thresholds obtained with those in a control population.

Methods: The sensitivity and pain detection thresholds obtained in participants subjected to electrical stimulation were determined in 31 obese individuals (age: 40.3 ± 10.5 y) before (body mass index: 45.7 ± 6.8 kg/m) and 6 months after a mean weight loss of 32 kg induced by gastric bypass. The results obtained were compared with those for 49 nonobese control participants (38.5 ± 11.2 y; body mass index: 22.6 ± 2.6 kg/m). Body composition and metabolic biomarkers, such as leptin, adiponectin, insulin, and interleukin 6, were assessed and single-nucleotide polymorphisms of the mu opioid receptor [OPRM1 (c.118A > G) and COMT (p.Val158Met)] were genotyped in obese patients.

Results: Sensitivity and pain detection thresholds (3.9 ± 1.1; 11.6 ± 6.0) were significantly higher in obese than in nonobese participants (3.1 ± 1.1; 6.0 ± 3.0), respectively (P < 0.0001), and were not affected by drastic weight loss (mean change: 32 kg). Pain thresholds in obese participants were not correlated with any of the clinical and biological variables studied. The obese participants in the highest quartile for both sensitivity and pain detection thresholds were significantly older than those in the lowest quartile.

Conclusions: Further studies are required to explore sensory dysfunction in obese individuals and to investigate the implications of this dysfunction for pain management.
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http://dx.doi.org/10.1097/AJP.0b013e31824786adDOI Listing
January 2013
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