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Background. Delirium disorder is a frequent neurological complication of SARS-CoV-2 infection and associated with an increased disease severity and mortality. Cognitive impairment is a major risk factor for developing delirium disorder during Covid-19, which, in turn, increases the risk of subsequent neurological complications and cognitive decline. Summary. The bidirectional connection between delirium disorder and dementia likely resides at multiple levels, and its pathophysiological mechanisms during Covid-19 include endothelial damage, blood-brain barrier dysfunction and local inflammation, with activation of microglia and astrocytes. Here, we describe the putative pathogenic pathways underlying delirium disorder during Covid-19 and highlight how they cross with the ones leading to neurodegenerative dementia. Key messages. The analysis of the two-sided link can offer useful insights for confronting with long-term neurological consequences of Covid-19 and framing future prevention and early treatment strategies.

Impairments in speech and executive functions are both observed in Parkinson's disease (PD) and might be influenced by subthalamic nucleus deep brain stimulation (STN-DBS). We investigated the effects of STN-DBS on speech and executive functions and their mutual interference in PD.14 PD patients eligible for bilateral STN-DBS (PD-DBS), and 16 PD patients with best medical treatment (PD-BMT) were included. Global cognition, executive functions (inhibition and verbal fluency), speech tasks with acoustic measures, and a dual-task (DT) combining a speech task with a Go or Go/NoGo task were performed at baseline and 12 months follow-up. A normative group of matched healthy participants was included at baseline for the evaluation of speech and DT performance.In both patient groups, global cognition mildly decreased after 12 months (p .001). PD-DBS showed decreased inhibition (p = .016) whereas PD-BMT deteriorated in vowel articulation (p = .011). Using the DT paradigm, PD-DBS showed a slowing of speech rate after 12 months (p = .009) in contrast to PD-BMT (p = .203).STN-DBS does not seem to impair speech and global cognition but might affect certain executive functions (notably inhibition). Speech-cognition interference is relatively preserved in PD patients, even though PD-DBS present larger DT cost on speech rate at 12 months post-DBS compared to PD-BMT. An evaluation with a longer follow-up using a larger sample is needed to confirm long-term effects.

IntroductionRisk factors (e.g., motor symptom asymmetry) for short- and long-term cognitive and neuropsychiatric symptoms following deep brain stimulation (DBS) of the subthalamic nucleus (STN) in patients with Parkinson’s disease have yet to be fully identified. The objectives of the present study were to determine whether motor symptom asymmetry in Parkinson’s disease is one such risk factor and to identify predictors of subnormal cognitive decline.MethodsA total of 26 patients receiving STN-DBS (13 with left-sided motor symptoms and 13 with right-sided ones) underwent follow-up neuropsychological, depression and apathy assessments over a 5-year period. Nonparametric intergroup comparisons were performed on raw scores, as well as Cox regression analyses on standardized Mattis Dementia Rating Scale scores.ResultsCompared with patients who had predominantly left-sided symptoms, right-sided patients scored higher on both apathy (at 3 months and 36 months) and depressive symptoms (at 6 months and 12 months) and scored lower on global cognitive efficiency (at 36 months and 60 months). Survival analyses revealed that only right-sided patients had subnormal standardized dementia scores, which were negatively associated with the number of perseverations in the Wisconsin Card Scoring Test.ConclusionRight-sided motor symptoms are a risk factor for more severe short- and long-term cognitive and neuropsychiatric symptoms following STN-DBS, confirming literature findings on left hemispheric vulnerability.

Vocal emotion recognition, a key determinant to analyzing a speaker’s emotional state, is known to be impaired following cerebellar dysfunctions. Nevertheless, its possible functional integration in the large-scale brain network subtending emotional prosody recognition has yet to be explored. We administered an emotional prosody recognition task to patients with right versus left-hemispheric cerebellar lesions and a group of matched controls. We explored the lesional correlates of vocal emotion recognition in patients through a network-based analysis by combining a neuropsychological approach for lesion mapping with normative brain connectome data. Results revealed impaired recognition among patients for neutral or negative prosody, with poorer sadness recognition performances by patients with right cerebellar lesion. Network-based lesion-symptom mapping revealed that sadness recognition performances were linked to a network connecting the cerebellum with left frontal, temporal, and parietal cortices. Moreover, when focusing solely on a subgroup of patients with right cerebellar damage, sadness recognition performances were associated with a more restricted network connecting the cerebellum to the left parietal lobe. As the left hemisphere is known to be crucial for the processing of short segmental information, these results suggest that a corticocerebellar network operates on a fine temporal scale during vocal emotion decoding.

Lifelong bilingualism is associated with delayed dementia onset, suggesting a protective effect on the brain. Here, we aim to study the effects of lifelong bilingualism as a dichotomous and continuous phenomenon, on brain metabolism and connectivity in individuals with Alzheimer's dementia. Ninety‐eight patients with Alzheimer's dementia (56 monolinguals; 42 bilinguals) from three centers entered the study. All underwent an [18F]‐fluorodeoxyglucose positron emission tomography (PET) imaging session. A language background questionnaire measured the level of language use for conversation and reading. Severity of brain hypometabolism and strength of connectivity of the major neurocognitive networks was compared across monolingual and bilingual individuals, and tested against the frequency of second language life‐long usage. Age, years of education, and MMSE score were included in all above mentioned analyses as nuisance covariates. Cerebral hypometabolism was more severe in bilingual compared to monolingual patients; severity of hypometabolism positively correlated with the degree of second language use. The metabolic connectivity analyses showed increased connectivity in the executive, language, and anterior default mode networks in bilingual compared to monolingual patients. The change in neuronal connectivity was stronger in subjects with higher second language use. All effects were most pronounced in the left cerebral hemisphere. The neuroprotective effects of lifelong bilingualism act both against neurodegenerative processes and through the modulation of brain networks connectivity. These findings highlight the relevance of lifelong bilingualism in brain reserve and compensation, supporting bilingual education and social interventions aimed at usage, and maintenance of two or more languages, including dialects, especially crucial in the elderly people., We investigated the neural mechanisms underlying the ability of bilingual senior individuals to better cope with pathology and symptoms of Alzheimer dementia, as compared to matched monolingual individuals with Alzheimer dementia. By using FDG‐PET to measure brain glucose metabolism and connectivity, we found evidence of neural reserve on brain hypometabolism and compensatory effects on brain metabolic connectivity, predominantly in the left hemisphere. In both cases, effects of lifelong bilingualism on the brain were linearly associated with the degree of second language use, that is, the higher the second language use, the higher the neural reserve/compensatory effect on brain metabolism and connectivity, respectively.

Purpose: The clinical diagnosis of motor speech disorders (MSDs) is mainly based on perceptual approaches. However, studies on perceptual classification of MSDs often indicate low classification accuracy. The aim of this study was to determine in a forced-choice dichotomous decision-making task (a) how accuracy of speech-language pathologists (SLPs) in perceptually classifying apraxia of speech (AoS) and dysarthria is impacted by speech task, severity of MSD, and listener's expertise and (b) which perceptual features they use to classify. Method: Speech samples from 29 neurotypical speakers, 14 with hypokinetic dysarthria associated with Parkinson's disease (HD), 10 with poststroke AoS, and six with mixed dysarthria associated with amyotrophic lateral sclerosis (MD-FlSp [combining flaccid and spastic dysarthria]), were classified by 20 expert SLPs and 20 student SLPs. Speech samples were elicited in spontaneous speech, text reading, oral diadochokinetic (DDK) tasks, and a sample concatenating text reading and DDK. For each recorded speech sample, SLPs answered three dichotomic questions following a diagnostic approach, (a) neurotypical versus pathological speaker, (b) AoS versus dysarthria, and (c) MD-FlSp versus HD, and a multiple-choice question on the features their decision was based on. Results: Overall classification accuracy was 72% with good interrater reliability, varying with SLP expertise, speech task, and MSD severity. Correct classification of speech samples was higher for speakers with dysarthria than for AoS and higher for HD than for MD-FlSp. Samples elicited with continuous speech reached the best classification rates. An average number of three perceptual features were used for correct classifications, and their type and combination differed between the three MSDs. Conclusions: The auditory-perceptual classification of MSDs in a diagnostic approach reaches substantial performance only in expert SLPs with continuous speech samples, albeit with lower accuracy for AoS. Specific training associated with objective classification tools seems necessary to improve recognition of neurotypical speech and distinction between AoS and dysarthria.

Idiopathic Normal Pressure Hydrocephalus (iNPH)—the leading cause of reversible dementia in aging—is characterized by ventriculomegaly and gait, cognitive and urinary impairments. Despite its high prevalence estimated at 6% among the elderlies, iNPH remains underdiagnosed and undertreated due to the lack of iNPH‐specific diagnostic markers and limited understanding of pathophysiological mechanisms. INPH diagnosis is also complicated by the frequent occurrence of comorbidities, the most common one being Alzheimer's disease (AD). Here we investigate the resting‐state functional magnetic resonance imaging dynamics of 26 iNPH patients before and after a CSF tap test, and of 48 normal older adults. Alzheimer's pathology was evaluated by CSF biomarkers. We show that the interactions between the default mode, and the executive‐control, salience and attention networks are impaired in iNPH, explain gait and executive disturbances in patients, and are not driven by AD‐pathology. In particular, AD molecular biomarkers are associated with functional changes distinct from iNPH functional alterations. Finally, we demonstrate a partial normalization of brain dynamics 24 hr after a CSF tap test, indicating functional plasticity mechanisms. We conclude that functional changes involving the default mode cross‐network interactions reflect iNPH pathophysiological mechanisms and track treatment response, possibly contributing to iNPH differential diagnosis and better clinical management., Idiopathic normal pressure hydrocephalus (iNPH), the leading cause of reversible dementia in ageing, is a prevalent neurological disorder characterised by gait, urinary, and cognitive impairments with ventriculomegaly. We show that iNPH patients have changes of brain functional dynamics which explain gait and executive deficits, are partially reverted by a CSF tap test, and are not driven by Alzheimer's disease or cerebrovascular comorbidities. Our results shed new light on the neurobiological substrates of iNPH and functional plasticity mechanisms following an invasive intervention, with possible implications for iNPH differential diagnosis and better clinical management.

We conducted a cross-sectional pilot study to explore the biological substrate of the Motoric Cognitive Risk (MCR) syndrome in a Memory Clinic cohort, using a multimodal imaging approach. Twenty participants were recruited and classified as MCR+/−. Amyloid- and tau-PET uptakes, temporal atrophy, white matter hyperintensities, lateral ventricular volume (LVV), and diffusion tensor parameters were compared between groups. No significant differences were found in imaging features related to Alzheimer’s disease or gross vascular damage. MCR+ patients had increased LVV and altered diffusion parameters in the superior corona radiata. Ventricular enlargement and microstructural damage of the surrounding white matter tracts could contribute to MCR pathophysiology.

There is growing evidence that both the basal ganglia and the cerebellum play functional roles in emotion processing, either directly or indirectly, through their connections with cortical and subcortical structures. However, the lateralization of this complex processing in emotion recognition remains unclear. To address this issue, we investigated emotional prosody recognition in individuals with Parkinson’s disease (model of basal ganglia dysfunction) or cerebellar stroke patients, as well as in matched healthy controls (n = 24 in each group). We analysed performances according to the lateralization of the predominant brain degeneration/lesion. Results showed that a right (basal ganglia and cerebellar) hemispheric dysfunction was likely to induce greater deficits than a left one. Moreover, deficits following left hemispheric dysfunction were only observed in cerebellar stroke patients, and these deficits resembled those observed after degeneration of the right basal ganglia. Additional analyses taking disease duration / time since stroke into consideration revealed a worsening of performances in patients with predominantly right-sided lesions over time. These results point to the differential, but complementary, involvement of the cerebellum and basal ganglia in emotional prosody decoding, with a probable hemispheric specialization according to the level of cognitive integration.

Objective To assess whether gait, neuropsychological, and multimodal MRI parameters predict short-term symptom reversal after cerebrospinal fluid (CSF) tap test in idiopathic normal pressure hydrocephalus (iNPH). Methods Thirty patients (79.3 ± 5.9 years, 12 women) with a diagnosis of probable iNPH and 46 healthy controls (74.7 ± 5.4 years, 35 women) underwent comprehensive neuropsychological, quantitative gait, and multimodal MRI assessments of brain morphology, periventricular white-matter microstructure, cortical and subcortical blood perfusion, default mode network function, and white-matter lesion load. Responders were defined as an improvement of at least 10% in walking speed or timed up and go test 24 h after tap test. Univariate and multivariable tap test outcome prediction models were evaluated with logistic regression and linear support vector machine classification. Results Sixteen patients (53%) respondedpositively to tap test. None of the gait, neuropsychological, or neuroimaging parameters considered separately predicted outcome. A multivariable classifier achieved modest out-of-sample outcome prediction accuracy of 70% (p = .028); gait parameters, white-matter lesion load and periventricular microstructure were the main contributors. Conclusions Our negative findings show that short-term symptom reversal after tap test cannot be predicted from single gait, neuropsychological, or MRI parameters, thus supporting the use of tap test as prognostic procedure. However, multivariable approaches integrating non-invasive multimodal data are informative of outcome and may be included in patient-screening procedures. Their value in predicting shunting outcome should be further explored, particularly in relation to gait and white-matter parameters.

The A/T/N model is a research framework proposed to investigate Alzheimer’s disease (AD) pathological bases (i.e., amyloidosis A, neurofibrillary tangles T, and neurodegeneration N). The application of this system on clinical populations is still limited. The aim of the study is to evaluate the topography of T distribution by 18F-flortaucipir PET in relation to A and N and to describe the A/T/N status through imaging biomarkers in memory clinic patients. Eighty-one patients with subjective and objective cognitive impairment were classified as A+/A− and N+/N− through amyloid PET and structural MRI. Tau deposition was compared across A/N subgroups at voxel level. T status was defined through a global cut point based on A/N subgroups and subjects were categorized following the A/T/N model. A+N+ and A+N− subgroups showed higher tau burden compared to A−N− group, with A+N− showing significant deposition limited to the medial and lateral temporal regions. Global cut point discriminated A+N+ and A+N− from A−N− subjects. On A/T/N classification, 23% of patients showed a negative biomarker profile, 58% fell within the Alzheimer’s continuum, and 19% of the sample was characterized by non-AD pathologic change. Medial and lateral temporal regions represent a site of significant tau accumulation in A+ subjects and possibly a useful marker of early clinical changes. This is the first study in which the A/T/N model is applied using 18F-flortaucipir PET in a memory clinic population. The majority of patients showed a profile consistent with the Alzheimer’s continuum, while a minor percentage showed a profile suggestive of possible other neurodegenerative diseases. These results support the applicability of the A/T/N model in clinical practice.

Lack of awareness of cognitive impairment (i.e. anosognosia) could be a key factor for distinguishing between neuropsychological post-COVID-19 condition phenotypes. In this context, the 2-fold aim of the present study was to (i) establish the prevalence of anosognosia for memory impairment, according to the severity of the infection in the acute phase and (ii) determine whether anosognosic patients with post-COVID syndrome have a different cognitive and psychiatric profile from nosognosic patients, with associated differences in brain functional connectivity. A battery of neuropsychological, psychiatric, olfactory, dyspnoea, fatigue and quality-of-life tests was administered 227.07 ± 42.69 days post-SARS-CoV-2 infection to 102 patients (mean age: 56.35 years, 65 men, no history of neurological, psychiatric, neuro-oncological or neurodevelopmental disorder prior to infection) who had experienced either a mild (not hospitalized; n = 45), moderate (conventional hospitalization; n = 34) or severe (hospitalization with intensive care unit stay and mechanical ventilation; n = 23) presentation in the acute phase. Patients were first divided into two groups according to the presence or absence of anosognosia for memory deficits (26 anosognosic patients and 76 nosognosic patients). Of these, 49 patients underwent an MRI. Structural images were visually analysed, and statistical intergroup analyses were then performed on behavioural and functional connectivity measures. Only 15.6% of patients who presented mild disease displayed anosognosia for memory dysfunction, compared with 32.4% of patients with moderate presentation and 34.8% of patients with severe disease. Compared with nosognosic patients, those with anosognosia for memory dysfunction performed significantly more poorly on objective cognitive and olfactory measures. By contrast, they gave significantly more positive subjective assessments of their quality of life, psychiatric status and fatigue. Interestingly, the proportion of patients exhibiting a lack of consciousness of olfactory deficits was significantly higher in the anosognosic group. Functional connectivity analyses revealed a significant decrease in connectivity, in the anosognosic group as compared with the nosognosic group, within and between the following networks: the left default mode, the bilateral somatosensory motor, the right executive control, the right salient ventral attention and the bilateral dorsal attention networks, as well as the right Lobules IV and V of the cerebellum. Lack of awareness of cognitive disorders and, to a broader extent, impairment of the self-monitoring brain system, may be a key factor for distinguishing between the clinical phenotypes of post-COVID syndrome with neuropsychological deficits.

Objective: The aim of this study was to examine neurocognitive course over time among people with well treated HIV. Design: The Neurocognitive Assessment in the Metabolic and Aging Cohort (NAMACO) study is an ongoing, prospective, longitudinal, multicenter and multilingual study within the Swiss HIV Cohort Study (SHCS). Participants undergo neuropsychological assessment at baseline and two-yearly follow-up. Setting: Seven SHCS centres. Participants: Patients aged at least 45 years enrolled in the SHCS with fluency in the local language (French, German or Italian) and agreeing to participate in the NAMACO study: 981 participants at baseline, 720 at 2-year follow-up of whom 644 had complete data sets. Intervention: Standardized neuropsychological assessment at baseline and 2-year follow-up. Main outcome measure: Neurocognitive performance using Frascati criteria and mean z-scores. Results: Four participants (of 644, 0.6%) had plasma HIV-1 RNA more than 50 copies/ml; median CD4+ cell count was 660 cells/μl. According to Frascati criteria, 204 participants (31.7%) had neurocognitive impairment (NCI) at baseline. NCI severity in these participants changed little over 2 years and comprehensive models based on Frascati criteria were not feasible. Examining mean z-scores, however, we observed neurocognitive stability or improvement over two years in five of seven neurocognitive domains assessed. Age at least 65 years (P = 0.02) and cognitive complaints (P = 0.004) were associated with neurocognitive decline, while black race (P = 0.01) and dolutegravir treatment (P = 0.002) were associated with improvement. Conclusion: Frascati criteria were less sensitive in measuring NCI change and therefore unsuitable for following neurocognitive course in our cohort of people with well treated HIV. Examining neurocognitive course by mean z-score change, we observed stability or improvement.

The posterior parietal cortex (PPC) is an anatomically heterogeneous brain region implicated in a wide range of cognitive operations, including egocentric spatial processing and both short- and long-term memory. Here, we report functional specificities of cytoarchitectonically defined subregions of PPC during the processing of scenes across changes in viewpoint. Participants (n = 16) saw photographs of familiar and unfamiliar places while undergoing functional magnetic resonance imaging (fMRI). On each trial, 4 viewpoints of the same place were presented, with either a plausible sequence of viewpoints (SEQ) or a scrambled order (SCRA). Distinct response profiles were observed within PPC. Area 7A showed increased activity for SEQ versus SCRA order, regardless of place familiarity, whereas the rostral inferior parietal lobule showed preferential increases for unfamiliar versus familiar places in SEQ series. In contrast, more posterior subregions in both superior and inferior PPC exhibited increases for familiar versus unfamiliar places at the end of the sequence, regardless of order. The data highlight the distinctive contribution of several subregions of PPC during the processing of scenes, with specific cortical areas involved in the progressive integration of spatial information across viewpoint changes, and others involved in the retrieval and maintenance of scene information in memory.

Encephalopathy is a neurological complication of COVID-19. The objective of this exploratory study is to investigate the link between systemic inflammation and brain microstructural changes (measured by diffusion-weighted imaging) in patients with COVID-19 encephalopathy. 20 patients with COVID-19 encephalopathy (age: 67.3 $$\pm$$ ± 10.0 years; 90% men) hospitalized in the Geneva University Hospitals for a SARS-CoV-2 infection between March and May 2020 were included in this retrospective cohort study. COVID-19 encephalopathy was diagnosed following a comprehensive neurobiological evaluation, excluding common causes of delirium, such as hypoxemic or metabolic encephalopathy. We investigated the correlation between systemic inflammation (measured by systemic C-reactive protein (CRP)) and brain microstructural changes in radiologically normal white matter (measured by apparent diffusion coefficient (ADC)) in nine spatially widespread regions of the white matter previously associated with delirium. Systemic inflammation (CRP = 60.8 ± 50.0 mg/L) was positively correlated with ADC values in the anterior corona radiata (p = 0.0089), genu of the corpus callosum (p = 0.0064) and external capsule (p = 0.0086) after adjusting for patients’ age. No statistically significant association between CRP and ADC was found in the other six white matter regions. Our findings indicate high risk of white matter abnormalities in COVID-19 encephalopathy patients with high peripheral inflammatory markers, suggesting aggressive imaging monitoring may be warranted in these patients. Future studies should clarify a possible specificity of the spatial patterns of CRP–white matter microstructure association in COVID-19 encephalopathy patients and disentangle the role of individual cytokines on brain inflammatory mechanisms.

Background. This study aims to investigate the clinical use of the main Alzheimer’s disease (AD) biomarkers in patients with mild cognitive impairment (MCI) by examining the beliefs and preferences of clinicians and biomarker experts of the European Alzheimer’s Disease Consortium (EADC).Methods. Out of 306 contacted EADC professionals, 150 (101 clinicians, 43 biomarker experts, and 6 falling into other categories) filled in an online survey from May to September 2020. The investigated biomarkers were: medial temporal lobe atrophy score (MTA) on structural MRI, typical AD (i.e. temporoparietal and posterior cingulate) hypometabolism on FDG-PET, CSF (Aβ42, p-tau, t-tau), amyloid-PET and tau-PET.Results. Despite the abnormal accumulation of amyloid rather than tau was deemed by the majority of responders as the initial cause of AD, responders did not show a clear preference for amyloid-PET. The most widely used biomarker is MTA (77% of responders reported to use it at least frequently), followed by Aβ42, p-tau, t-tau levels in CSF (45%), typical AD hypometabolism on FDG-PET (32%), amyloid-PET (8%), and tau-PET (2%). Imaging and CSF biomarkers were found to be widely used to support the etiological diagnostic process in MCI, while APOE genotyping was performed only in a minority of patients. CSF is considered the most valuable biomarker in terms of additional diagnostic value, followed by amyloid-PET, tau-PET, and typical AD hypometabolism on FDG-PET. The combination of amyloidosis and neuronal injury biomarkers is associated with the highest diagnostic confidence in an etiological diagnosis of AD in MCI, while MTA alone was perceived as the less reliable biomarker.Conclusions. Biomarkers are widely used across Europe for the diagnosis of MCI. Overall, we observed that CSF is currently considered as the most useful biomarker, followed by amyloid-PET. Moreover, the use of molecular imaging (i.e. amyloid-PET and tau-PET) in the diagnostic work-up of MCI patients is increasing over time.

Prism adaptation (PA) is one of the few rehabilitation techniques for spatial neglect that directly targets physiological mechanisms underlying space representation, but its efficacy and neural mechanisms remain unresolved. Using PA and fMRI in patients with spatial neglect after an acute right-hemispheric stroke, we previously observed post-PA increases in activity in bilateral parietal, frontal, and occipital cortex during specific visuo-spatial tasks (bisection and visual search). However, given a key role of parietal areas for PA in healthy individuals, we hypothesized that such activation might differ according to the site of brain damage. We studied a group of 10 patients with focal right hemisphere stroke and spatial neglect at baseline and after PA, who were divided in two groups (5 patients with frontal and 5 patients with parietal strokes). We compared their behavioural performance and brain activation patterns during fMRI. At the behavioural level, frontal and parietal patients showed similar neglect signs on visuo-spatial tasks before PA, but frontal patients showed larger benefit from PA. Differences were also observed in cortical activity, with enhanced recruitment of right parietal areas in frontal patients and less consistent patterns in parietal patients. Furthermore, fMRI analysis during PA itself (divided in 5 successive periods) showed differential activations between group in anatomically preserved pathways, including occipital areas and cerebellum, that preceded changes in parietal areas and were specific to frontal patients. These data accord with the hypothesis that intact cerebello-parietal connections may underpin improvement of spatial neglect after PA. Altogether, these results provide important insights on brain networks involved in spatial cognition and may allow an optimal selection of patients benefiting from PA after right hemispheric stroke.

Funder: University of Cambridge, Feeling of presence (FOP) refers to the vivid sensation of a person's presence near oneself and is common in Dementia with Lewy Bodies (DLB). Based on previous observations on epileptic subjects, we hypothesized that DLB subjects with FOP would harbour 18F-fluorodeoxyglucose PET hypometabolism in left parietal areas. 25 subjects (mean age 71.9 ± 6.7, disease duration at scan 1.7 ± 1.5 years) were included in the study, of whom nine (36%) experienced FOP. No significant between-group difference was observed regarding dopamine transporters striatal uptake (p = 0.64), daily dopaminergic treatment dosage (p = 0.88) and visual hallucinations (p = 0.83). Statistical parametric mapping showed that subjects with FOP had a significantly reduced glucose metabolism in several left frontoparietal areas (p < 0.001), including superior parietal lobule and precuneus. Interregional correlation analysis of these areas showed specific connectivity with right insula and putamen in the FOP subgroup and right orbitofrontal and superior frontal in subjects without FOP. This provides further evidence about the role of a left frontoparietal network and suggest a possible contribution of impaired orbitofrontal reality filtering associated with FOP.

Among the long-COVID symptoms, neuropsychological sequelae are frequent after an infection by SARS-CoV-2, whatever the severity of the respiratory disease in the acute phase. These deficits seem to result from a neurological disorder, but also from psychiatric symptoms. Not only inflammatory components, which can play a major role in the genesis of the neuropsychological sequelae, but also the hypotheses of vascular systemic lesions, the neurotropism of SARS-CoV-2, or the effect of the stress and the hypothalamic-pituitary-adrenal axis (HPA) are suggested. Psychiatric complications due to SSARS-CoV-2 infection would partly explain these neuropsychological sequelae.Parmi les symptômes de Covid long, les séquelles neuropsychologiques sont fréquentes dans les suites d’une infection par le SARS-CoV-2, et ce quel que soit le degré de sévérité de l’atteinte respiratoire en phase aiguë. Ces déficits semblent résulter d’une atteinte neurologique, mais aussi de l’installation de troubles psychiatriques. En plus de l’inflammation, qui joue un rôle majeur dans la genèse des séquelles neuropsychologiques, les hypothèses de lésions endothéliales systémiques, de l’existence d’un neurotropisme du SARS-CoV-2, de même que de celles de l’effet du stress et de la mise en jeu de l’axe hypothalamo-hypophysaire-surrénalien, sont proposées. Les complications psychiatriques de l’infection par le SARS-CoV-2 semblent, quant à elles, n’expliquer qu’une partie des séquelles neuropsychologiques.

BackgroundThere is growing awareness that severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection can include long-term neuropsychological deficits, even in its mild or moderate respiratory forms.MethodsStandardized neuropsychological, psychiatric, neurological and olfactory tests were administered to 45 patients (categorized according to the severity of their respiratory symptoms during the acute phase) 236.51 ± 22.54 days post-discharge following SARS-CoV-2 infection.ResultsDeficits were found in all the domains of cognition and the prevalence of psychiatric symptoms was also high in the three groups. The severe performed more poorly on long-term episodic memory and exhibited greater anosognosia. The moderate had poorer emotion recognition, which was positively correlated with persistent olfactory dysfunction. The mild were more stressed, anxious and depressed.ConclusionThe data support the hypothesis that the virus targets the central nervous system (and notably the limbic system), and support the notion of different neuropsychological phenotypes.

International audience; Abstract Study Objectives The COVID-19 pandemic has had dramatic effects on society and people’s daily habits. In this observational study, we recorded objective data on sleep macro- and microarchitecture repeatedly over several nights before and during the COVID-19 government-imposed lockdown. The main objective was to evaluate changes in patterns of sleep duration and architecture during home confinement using the pre-confinement period as a control. Methods Participants were regular users of a sleep-monitoring headband that records, stores, and automatically analyzes physiological data in real time, equivalent to polysomnography. We measured sleep onset duration, total sleep time, duration of sleep stages (N2, N3, and rapid eye movement [REM]), and sleep continuity. Via the user’s smartphone application, participants filled in questionnaires on how lockdown changed working hours, eating behavior, and daily life at home. They also filled in the Insomnia Severity Index, reduced Morningness–Eveningness Questionnaire, and Hospital Anxiety and Depression Scale questionnaires, allowing us to create selected subgroups. Results The 599 participants were mainly men (71%) of median age 47 (interquartile range: 36–59). Compared to before lockdown, during lockdown individuals slept more overall (mean +3·83 min; SD: ±1.3), had less deep sleep (N3), more light sleep (N2), and longer REM sleep (mean +3·74 min; SD: ±0.8). They exhibited less weekend-specific changes, suggesting less sleep restriction during the week. Changes were most pronounced in individuals reporting eveningness preferences, suggesting relative sleep deprivation in this population and exacerbated sensitivity to societal changes. Conclusion This unique dataset should help us understand the effects of lockdown on sleep architecture and on our health.

International audience; Identifying characteristics of articulatory impairment in speech motor disorders is complicated due to the timeconsuming nature of kinematic measures. The goal is to explore whether analysing the acoustic signal in terms of total squared changes of Mel-Frequency Cepstral Coefficients (TSC_MFCC) and its pattern over time provides sufficient spectral information to distinguish mild and moderate dysarthric French speakers with Amyotrophic Lateral Sclerosis (ALS) and Parkinson's Disease (PD) from each other and from healthy speakers. Participants produced the vowel-glide sequences /ajajaj/, /ujujuj/, and /wiwiwi/. From the time course of TSC_MFCCs, event-related and global measures were extracted to capture the degree of acoustic change and its variability. In addition, durational measures were obtained. For both mild and moderately impaired PD and ALS speakers, the degree of acoustic change and its variability, averaged over the complete contour, separated PD and ALS speakers from each other and from healthy speakers, especially when producing the sequences /ujujuj/ and /wiwiwi/. Durational measures separated the moderate ALS from healthy and moderate PD speakers. Using the approach on repetitive sequences targeting the lingual and labial articulators to characterize articulatory impairment in speech motor disorders is promising. Findings are discussed against prior findings of articulatory impairment in the populations studied.

Severe acute respiratory coronavirus 2 (SARS‐CoV‐2) has been associated with neurological complications, including acute encephalopathy. To better understand the neuropathogenesis of this acute encephalopathy, we describe a series of patients with coronavirus disease 2019 (COVID‐19) encephalopathy, highlighting its phenomenology and its neurobiological features. On May 10, 2020, 707 patients infected by SARS‐CoV‐2 were hospitalized at the Geneva University Hospitals; 31 (4.4%) consecutive patients with an acute encephalopathy (64.6 ± 12.1 years; 6.5% female) were included in this series, after exclusion of comorbid neurological conditions, such as stroke or meningitis. The severity of the COVID‐19 encephalopathy was divided into severe and mild based on the Richmond Agitation Sedation Scale (RASS): severe cases (n = 14, 45.2%) were defined on a RASS

Background Idiopathic normal pressure hydrocephalus (iNPH) presents typical radiological signs that have been summarised in a semi-quantitative scale named the iNPH Radscale. However, the iNPH Radscale's predictive value for response to cerebrospinal fluid (CSF) tap test has never been studied. This study aims to investigate if the iNPH Radscale can predict locomotion improvement after CSF tap test. Methods A total of 100 patients with iNPH (age: 76.3 ± 7.9, gender: 36% female) were included in this retrospective study. Two raters, blinded to the response of the CSF tap test, evaluated the iNPH Radscale and its seven subitems (Evan's index, callosal angle, size of temporal horns, narrow high-convexity sulci, dilated Sylvian fissures, focally dilated sulci, and periventricular hypodensities). Locomotion improvement was assessed by the Timed Up and Go (TUG) performed before, and 24 h after, the CSF tap test. Results The iNPH Radscale (total score) was similar between the CSF tap test responders and non-responders (responders: 8.31 ± 1.96, non-responders: 9.18 ± 2.51, p = 0.128). However, the temporal horns score was smaller in the responders group (1.66 ± 0.57 versus 1.94 ± 0.24, p = 0.045), even after adjusting for age, gender, education level, white matter changes, and global cognition (β: -0.250, C.I. 95%: [−3.185; −0.161], p = 0.031). Conclusion The iNPH Radscale (total score) does not predict locomotion improvement after CSF tap test, while a smaller temporal horns score at baseline is associated with a positive tap test responder status.

Purpose Assess the individual and combined diagnostic value of amyloid-PET and tau-PET in a memory clinic population. Methods Clinical reports of 136 patients were randomly assigned to two diagnostic pathways: AMY-TAU, amyloid-PET is presented before tau-PET; and TAU-AMY, tau-PET is presented before amyloid-PET. Two neurologists independently assessed all reports with a balanced randomized design, and expressed etiological diagnosis and diagnostic confidence (50–100%) three times: (i) at baseline based on the routine diagnostic workup, (ii) after the first exam (amyloid-PET for the AMY-TAU pathway, and tau-PET for the TAU-AMY pathway), and (iii) after the remaining exam. The main outcomes were changes in diagnosis (from AD to non-AD or vice versa) and in diagnostic confidence. Results Amyloid-PET and tau-PET, when presented as the first exam, resulted in a change of etiological diagnosis in 28% (p = 0.006) and 28% (p p p p > 0.05). We observed a stronger impact of a negative amyloid-PET versus a negative tau-PET (p = 0.014). When added as the second exam, amyloid-PET and tau-PET resulted in a further change in etiological diagnosis in 6% (p = 0.077) and 9% (p = 0.149) of cases, and diagnostic confidence increased by 4% (p p p > 0.05). Conclusion Amyloid-PET and tau-PET significantly impacted diagnosis and diagnostic confidence in a similar way, although a negative amyloid-PET has a stronger impact on diagnosis than a negative tau-PET. Adding either of the two as second exam further improved diagnostic confidence. Trial number PB 2016-01346.

Background and Purpose Coronavirus disease 2019 (COVID-19) caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with several complications of the central nervous system (CNS), including acute encephalopathy. Methods In this pilot study, we report a series of 39 patients (66.5 ± 9.2 years; 10.3% female) with acute encephalopathy, who underwent a standard brain magnetic resonance imaging (MRI) at 1.5 T during the acute symptomatic phase. In addition to diffusion-weighted imaging, MR angiography and susceptibility-weighted images, high-resolution vascular black blood sequences (in 34 cases) were used to investigate the vasculature of the brain. Results In 29 out of 34 patients with COVID-19 encephalopathy (85%) with high-resolution vessel wall imaging, we found a circular enhancement and thickening of the basilar and vertebral arteries, without any correlation with ischemia or microbleeds (reported in 21% and 59%, respectively). Conclusion We report a high prevalence of vascular changes suggestive of endotheliitis as reported in other organs. This could suggest an inflammatory mechanism underlying this encephalopathy.