Florence Lebert

Based on the recent literature and collective experience, an international consortium developed revised guidelines for the diagnosis of behavioural variant frontotemporal dementia. The validation process retrospectively reviewed clinical records and compared the sensitivity of proposed and earlier criteria in a multi-site sample of patients with pathologically verified frontotemporal lobar degeneration. According to the revised criteria, 'possible' behavioural variant frontotemporal dementia requires three of six clinically discriminating features (disinhibition, apathy/inertia, loss of sympathy/empathy, perseverative/compulsive behaviours, hyperorality and dysexecutive neuropsychological profile). 'Probable' behavioural variant frontotemporal dementia adds functional disability and characteristic neuroimaging, while behavioural variant frontotemporal dementia 'with definite frontotemporal lobar degeneration' requires histopathological confirmation or a pathogenic mutation. Sixteen brain banks contributed cases meeting histopathological criteria for frontotemporal lobar degeneration and a clinical diagnosis of behavioural variant frontotemporal dementia, Alzheimer's disease, dementia with Lewy bodies or vascular dementia at presentation. Cases with predominant primary progressive aphasia or extra-pyramidal syndromes were excluded. In these autopsy-confirmed cases, an experienced neurologist or psychiatrist ascertained clinical features necessary for making a diagnosis according to previous and proposed criteria at presentation. Of 137 cases where features were available for both proposed and previously established criteria, 118 (86%) met 'possible' criteria, and 104 (76%) met criteria for 'probable' behavioural variant frontotemporal dementia. In contrast, 72 cases (53%) met previously established criteria for the syndrome (P < 0.001 for comparison with 'possible' and 'probable' criteria). Patients who failed to meet revised criteria were significantly older and most had atypical presentations with marked memory impairment. In conclusion, the revised criteria for behavioural variant frontotemporal dementia improve diagnostic accuracy compared with previously established criteria in a sample with known frontotemporal lobar degeneration. Greater sensitivity of the proposed criteria may reflect the optimized diagnostic features, less restrictive exclusion features and a flexible structure that accommodates different initial clinical presentations. Future studies will be needed to establish the reliability and specificity of these revised diagnostic guidelines.

To determine the spatiotemporal mapping of neurofibrillary degeneration (NFD) in normal aging and the different stages of AD.The pathophysiologic significance of AD lesions, namely amyloid plaques and neurofibrillary tangles, is still unclear, especially their interrelationship and their link with cognitive impairment.The study included 130 patients of various ages and different cognitive statuses, from nondemented control subjects (n = 60, prospective study) to patients with severe definite AD. Paired helical filaments (PHF)-tau and Abeta were used as biochemical and histologic markers of NFD and amyloid plaques, respectively.NFD with PHF-tau was systematically present in variable amounts in the hippocampal region of nondemented patients age >75 years. When NFD was found in other brain areas, it was always along a stereotyped, sequential, hierarchical pathway. The progression was categorized into 10 stages according to the brain regions affected: transentorhinal cortex (S1), entorhinal (S2), hippocampus (S3), anterior temporal cortex (S4), inferior temporal cortex (S5), medium temporal cortex (S6), polymodal association areas (prefrontal, parietal inferior, temporal superior) (S7), unimodal areas (S8), primary motor (S9a) or sensory (S9b, S9c) areas, and all neocortical areas (S10). Up to stage 6, the disease could be asymptomatic. In all cases studied here, stage 7 individuals with two polymodal association areas affected by tau pathologic states were cognitively impaired.The relationship between NFD and Alzheimer-type dementia, and the criteria for a biochemical diagnosis of AD, are documented, and an association between AD and the extent of NFD in defined brain areas is shown.

Behavioural troubles due to frontotemporal dementia (FTD) are difficult to treat. The serotonergic system is associated with frontal lobes, the degeneration of which contributes to FTD. Trazodone increases the extracellular 5-HT levels in the frontal cortex. In a randomised, double-blind, placebo-controlled cross-over study, we investigated the effect of trazodone. There was a significant decrease in the Neuropsychiatry Inventory (NPI) total score with trazodone (p = 0.028) in the 26 evaluable patients. A decrease of more than 50% in the NPI score was observed in 10 patients with trazodone. This improvement was mainly based on the improvement of 4 items of the scale (irritability, agitation, depressive symptoms and eating disorders). The Mini-Mental State Examination was not modified and trazodone was well tolerated. Results of this first placebo-controlled trial suggest that trazodone is an effective treatment for the behavioural symptoms of FTD.

To evaluate the 3-year incidence of poststroke dementia (PSD) and the influence of prestroke cognitive decline.The authors evaluated prestroke cognitive functions in 202 consecutive stroke patients > or =40 years old using the Informant Questionnaire on Cognitive Decline in the Elderly (IQCODE), with a cut-off of 104 for the diagnosis of dementia. Six months and then annually after stroke, dementia was reassessed. The diagnosis of dementia was based on the International Classification of Diseases, 10th revision criteria in survivors who underwent a visit with a neurologist, or on the IQCODE score obtained by telephone contact with the family in survivors who did not. Statistics were performed using life-table methods.Thirty-three patients were excluded because of prestroke dementia. In the 169 remaining patients, the cumulative proportion of patients with dementia was 28.5% at the end of the follow-up period, with most of PSD occurring during the first 6 months. Using multivariate analysis, independent predictors of PSD were aging, preexisting cognitive decline, severity of deficit at admission, diabetes mellitus, and silent infarcts. Leukoaraiosis was an independent predictor of PSD when prestroke cognitive decline was not taken into account. The presumed etiology of dementia was vascular dementia (VaD) in two-thirds of patients and AD in one-third.The risk of PSD is high, and increased in patients with prestroke cognitive decline, with about one-third of patients meeting the criteria for AD and two-thirds meeting the criteria for VaD. These results confirm that, in stroke patients, an underlying degenerative pathology may play a role in the development of PSD.

Frontotemporal dementia (FTD) is the second cause of degenerative dementia. Behavioral changes occur before the cognitive decline and remain the major feature. A poor perception of emotion could account for some behavioral symptoms. The aim of this study was to assess the perception of emotion in patients with FTD and to compare it with that of patients with Alzheimer disease (AD). Fifty subjects performed the tests: 20 patients with probable AD, 18 patients with FTD, and 12 matched controls. The two patient groups did not differ in age, sex, severity of dementia, duration of the disease, and language tests. Subjects had to recognize and point out the name of one of seven basic emotions (anger, disgust, happiness, fear, sadness, surprise, and contempt) on a set of 28 faces presented on slides. The three groups were equally able to distinguish a face displaying affect from one not displaying affect. Naming of emotion was worse in patients with FTD than in patients with AD (correct answers 46% vs. 62%; p = 0.0006) who did not differ significantly from controls (72%). Anger, sadness, and disgust were less recognized in FTD than in AD patients who did not differ from controls, whereas fear and contempt were poorly recognized in both groups of patients compared with controls. These findings argue for different neural substrates underlying the recognition of various basic emotions. Behavioral disorders in FTD may be partly due to an impaired interpretation of the emotional environment.

Frontotemporal lobar degeneration (FTLD) encompasses a variety of clinicopathologic entities. The antemortem prediction of the underlying pathologic lesions is reputed to be difficult. This study sought to characterize correlations between 1) the different clinical variants of primary progressive language and speech disorders and 2) the pathologic diagnosis.The latter was available for 18 patients having been prospectively monitored in the Lille Memory Clinic (France) between 1993 and 2008.The patients were diagnosed with progressive anarthria (n = 5), agrammatic progressive aphasia (n = 6), logopenic progressive aphasia (n = 1), progressive jargon aphasia (n = 2), typical semantic dementia (n = 2), and atypical semantic dementia (n = 2). All patients with progressive anarthria had a tau pathology at postmortem evaluation: progressive supranuclear palsy (n = 2), Pick disease (n = 2), and corticobasal degeneration (n = 1). All patients with agrammatic primary progressive aphasia had TDP-43-positive FTLD (FTLD-TDP). The patients with logopenic progressive aphasia and progressive jargon aphasia had Alzheimer disease. Both cases of typical semantic dementia had FTLD-TDP. The patients with atypical semantic dementia had tau pathologies: argyrophilic grain disease and corticobasal degeneration.The different anatomic distribution of the pathologic lesions could explain these results: opercular and subcortical regions in tau pathologies with progressive anarthria, the left frontotemporal cortex in TDP-43-positive frontotemporal lobar degeneration (FTLD-TDP) with agrammatic progressive aphasia, the bilateral lateral and anterior temporal cortex in FTLD-TDP or argyrophilic grain disease with semantic dementia, and the left parietotemporal cortex in Alzheimer disease with logopenic progressive aphasia or jargon aphasia. These correlations have to be confirmed in larger series.

To determine the spatiotemporal mapping of tau pathologies and insoluble pools of Abeta in aging and sporadic AD, and their contribution to the physiopathologic, clinical, and neuropathologic features.The authors studied 130 patients of various ages and different cognitive status, from nondemented controls (n = 60) to patients with severe definite AD (n = 70) who were followed prospectively. Insoluble Abeta 42 and 40 species were fully solubilized and quantified in the main neocortical areas, with a new procedure adapted to human brain tissue. Tau pathology staging was determined in 10 different brain areas, using Western blots.In AD, there is a constellation of amyloid phenotypes, extending from cases with exclusively aggregated Abeta 42 to cases with, in addition, large quantities of insoluble Abeta 40 species. Five other points were observed: 1) There was no spatial and temporal overlap in the distribution of these two insoluble Abeta species in cortical brain areas. 2) In contrast to solubilized Abeta 40 aggregates composed essentially of monomers and dimers, solubilized Abeta 42 was essentially observed as dimers and multimers. 3) Abeta 42 aggregates were observed at the early stages of tau pathology, whereas the insoluble Abeta 40 pool was found at the last stages. 4) During the progression of the disease, Abeta aggregates increase in quantity and heterogeneity, in close parallel to the extension of tau pathology. 5) There was no spatial overlap between Abeta aggregation that is widespread and heterogeneously distributed in cortical areas and tau pathology that is progressing sequentially, stereotypically, and hierarchically.These observations demonstrate that Abeta 42 aggregation, and not Abeta 40, is the marker that is close to Alzheimer etiology. It should be the main target for the early biological diagnosis of AD and modeling. Furthermore, the spatial mismatch between amyloid ss-precursor protein (APP) and tau pathologies in cortical brain areas demonstrates that neurodegeneration is not a direct consequence of extracellular Abeta neurotoxicity. Hence, there is a synergetic effect of APP dysfunction, revealed by Abeta aggregation, on the neuron-to-neuron propagation of tau pathology.

Theory of mind reasoning-the ability to understand someone else's mental states, such as beliefs, intentions and desires-is crucial in social interaction. It has been suggested that a theory of mind deficit may account for some of the abnormalities in interpersonal behaviour that characterize patients affected by behavioural variant frontotemporal dementia. However, there are conflicting reports as to whether understanding someone else's mind is a key difference between behavioural variant frontotemporal dementia and other neurodegenerative conditions such as Alzheimer's disease. Literature data on the relationship between theory of mind abilities and executive functions are also contradictory. These disparities may be due to underestimation of the fractionation within theory of mind components. A recent theoretical framework suggests that taking someone else's mental perspective requires two distinct processes: inferring someone else's belief and inhibiting one's own belief, with involvement of the temporoparietal and right frontal cortices, respectively. Therefore, we performed a neuropsychological and neuroimaging study to investigate the hypothesis whereby distinct cognitive deficits could impair theory of mind reasoning in patients with Alzheimer's disease and patients with behavioural variant frontotemporal dementia. We used a three-option false belief task to assess theory of mind components in 11 patients with behavioural variant frontotemporal dementia, 12 patients with Alzheimer's disease and 20 healthy elderly control subjects. The patients with behavioural variant frontotemporal dementia and those with Alzheimer's disease were matched for age, gender, education and global cognitive impairment. [(18)F]-fluorodeoxyglucose-positron emission tomography imaging was used to investigate neural correlates of theory of mind reasoning deficits. Performance in the three-option false belief task revealed differential impairments in the components of theory of mind reasoning; patients with Alzheimer's disease had a predominant deficit in inferring someone else's belief, whereas patients with behavioural variant frontotemporal dementia were selectively impaired in inhibiting their own mental perspective. Moreover, inhibiting one's own perspective was strongly correlated with inhibition in a Stroop task but not with other subprocesses of executive functions. This finding suggests that self-perspective inhibition may depend on cognitive processes that are not specific to the social domain. Last, the severity of the deficit in inferring someone else's beliefs correlated significantly over all subjects with hypometabolism in the left temporoparietal junction, whereas the severity of the deficit in self-perspective inhibition correlated significantly with hypometabolism in the right lateral prefrontal cortex. In conclusion, our findings provided clinical and imaging evidence to support differential deficits in two components of theory of mind reasoning (subserved by distinct brain regions) in patients with Alzheimer's disease and patients with behavioural variant frontotemporal dementia.

The aim of this study was to assess short-term and long-term explicit memory and implicit memory in frontotemporal dementia (FTD; frontal variant) and to compare FTD and Alzheimer's disease (AD) patients with similar severity of dementia. Fifteen FTD patients [mean age: 68 years; Mini-Mental State (MMS): 24], 30 probable AD patients (mean age: 72 years; MMS: 23) and 12 healthy subjects participated in the study. The three groups were comparable in terms of gender and educational level. Short-term memory was assessed with the digit span and Corsi block-tapping tests. Explicit verbal memory was assessed with the Grober and Buschke test, and implicit memory with a verbal priming task and a fragmented picture test. FTD patients demonstrated a genuine memory deficit with impaired digit span, encoding deficit and retrieval strategy difficulties, but preserved implicit verbal and visual priming. Memory patterns differed in AD and FTD: short-term memory and free recall were similarly decreased in FTD and AD but cues provided more benefit to FTD than to AD; encoding was more impaired and the forgetting rate was faster in AD than in FTD; priming was lower in AD than in FTD. AD patients with clinical and imaging frontal lobe dysfunction tended to have lower memory performance and to differ even more from FTD patients than AD patients without frontal lobe dysfunction.

Acute confusional state (ACS) is frequent in hospitalized stroke patients. We previously showed that 16% of patients admitted for a stroke have preexisting dementia. The extent to which preexisting cognitive decline is associated with a risk of ACS at the acute stage of stroke remains to be systematically examined. The aim of this study was to evaluate the prevalence of ACS in acute stroke patients, to study the influence of preexisting cognitive decline and other patient characteristics, and to evaluate the influence of ACS on outcome.We diagnosed ACS using DSM-IV criteria and the Delirium Rating Scale with a cutoff of 10 in 202 consecutive stroke patients aged 40 years or older (median age, 75 years; range, 42 to 101 years). Cognitive functioning before stroke was assessed with the Informant Questionnaire on Cognitive Decline in the Elderly.Forty-nine stroke patients (24.3%; 95% CI, 18.3% to 30.2%) had an ACS during hospitalization. Using logistic regression analysis, we found preexisting cognitive decline (P=0.006) and metabolic or infectious disorders (P=0.008) to be independent predictors of ACS. Functional, but not vital, prognosis was worse in patients with ACS at discharge and 6 months after stroke.ACS occurs in one fourth of stroke patients older than 40 years. Its occurrence requires inquiry for a preexisting cognitive decline, which usually remains unrecognized in the absence of a systematic evaluation.

This study compares semantic (category) and letter-initial verbal fluency performance in dementia of frontal lobe type, dementia of Alzheimer type, and control subjects matched for age, sex, and level of education. As well as demographic characteristics, patients were matched for severity of dementia as estimated by the mini mental scale (23.2 (SD 4.9)). All patients with dementia of frontal lobe type had a frontal hypoperfusion on single photon emission computed tomography whereas patients with dementia of Alzheimer type showed mainly posterior deficits. Patients had significantly lower verbal fluency than controls but those with dementia of frontal lobe type did not differ from those with dementia of Alzheimer type in the number of words generated, intrusions, or preservations. Category fluency was more impaired than letter fluency in both dementias. No correlation between frontal index, frontal/parietal index, and fluency was found. Verbal fluency tests are sensitive tools for detecting dementia but do not seem useful in distinguishing between patients with dementia of Alzheimer type and those with dementia of frontal lobe type in early disease.

To determine frequency, determinants, and time course of poststroke depressive symptoms (DS) and their relationship with dementia.Two hundred two consecutive stroke patients were prospectively evaluated for DS, followed up over a 3-year period. Patients with Montgomery and Asberg Depression Rating Scale (MADRS) scores of >/==" BORDER="0">7 were considered as having DS. The severity of the neurologic deficit, functional outcome, and dementia were quantified with the Orgogozo Scale, modified Rankin Scale, Informant Questionnaire on Cognitive Decline in the Elderly, and an extensive battery of neuropsychological tests.DS were present in 43% of survivors after 6 months, 36% after 12 months, 24% after 24 months, and 18% after 36 months. The severity of the neurologic deficit at admission was the only independent predictor of DS at month 6. DS at month 6 were more frequent in patients with previous depression, dementia, and right superficial lesions. Younger age and right superficial lesions were the two variables independently associated with the presence of DS at month 36. The time course of the various DS differed, sadness remaining frequent 3 years after stroke (50%), whereas slowness, psychic slowness, lack of energy, and concentration difficulties remained frequent at month 36 in patients with dementia.DS are frequent after stroke. Their time course varies and depends on the cognitive status; this variation contributes to differences among previous studies on poststroke depression.

The primary feature of dementia with Lewy bodies (DLB) is the aggregation of alpha-synuclein into characteristic lesions: Lewy bodies (LBs) and Lewy neurites. However, in most of DLB cases, LBs are associated with neurofibrillary tangles and amyloid plaques (both Alzheimer disease [AD]-related lesions). We wanted to determine if this overlap of lesions is statistical, as a result of the late onset of both diseases, or results from a specific physiopathological synergy between synucleinopathy and either tauopathy or amyloid pathology. All patients with DLB from our prospective and multidisciplinary study were analyzed. These cases were compared with cases with pure AD and patients with Parkinson disease and controls. All cases were analyzed thoroughly at the neuropathologic and biochemical levels with a biochemical staging of aggregated alpha-synuclein, tau, and Abeta species. All sporadic cases of DLB were associated with abundant deposits of Abeta x-42 that were similar in quality and quantity to those of AD. Amyloid precursor protein (APP) dysfunction is a risk factor for AD as demonstrated by pathogenic mutations and Abeta accumulation. The constant and abundant Abeta x-42 deposition in sporadic DLB suggests that synucleinopathy is also promoted by APP dysfunction. Therefore, we conclude that APP is a therapeutic target for both AD and DLB.

Collecting data on households and individuals since 1999, the Swiss Household Panel (SHP) is an ongoing, unique, large-scale, nationally representative, longitudinal study in Switzerland (N=7,383 households and N=12,119 persons interviewed in 2014). The data of the SHP provide a rich source of information to study social change in Switzerland over a significant period on a wide variety of topics. The SHP aims to provide both continuity and innovation in measurement and data collection, with the combination of retrospective and prospective longitudinal data in the most recent refreshment sample as one notable example of such an innovation. This paper provides an overview of the SHP – focusing on its origin, aims, design, content, data collection and adjustments, possibilities for cross-national comparisons, data use and accomplishments.

This study analyses the consequences of the Covid-19 crisis on stress and well-being in Switzerland. In particular, we assess whether vulnerable groups in terms of social isolation, increased workload and limited socioeconomic resources are affected more than others. Using longitudinal data from the Swiss Household Panel, including a specific Covid-19 study, we estimate change score models to predict changes in perceived stress and life satisfaction at the end of the semi-lockdown in comparison to before the crisis. We find no general change in life satisfaction and a small decrease in stress. Yet, in line with our expectations, more vulnerable groups in terms of social isolation (young adults, Covid-19 risk group members, individuals without a partner), workload (women) and socioeconomic resources (unemployed and those who experienced a deteriorating financial situation) reported a decrease in life satisfaction. Stress levels decreased most strongly among high earners, workers on short-time work and the highly educated.

Abstract Background Due to heterogeneous clinical presentation, difficult differential diagnosis with Alzheimer’s disease (AD) and psychiatric disorders, and evolving clinical criteria, the epidemiology and natural history of frontotemporal lobar degeneration (FTD) remain elusive. In order to better characterize FTD patients, we relied on the database of a regional memory clinic network with standardized diagnostic procedures and chose AD patients as a comparator. Methods Patients that were first referred to our network between January 2010 and December 2016 and whose last clinical diagnosis was degenerative or vascular dementia were included. Comparisons were conducted between FTD and AD as well as between the different FTD syndromes, divided into language variants (lvFTD), behavioral variant (bvFTD), and FTD with primarily motor symptoms (mFTD). Cognitive progression was estimated with the yearly decline in Mini Mental State Examination (MMSE). Results Among the patients that were referred to our network in the 6-year time span, 690 were ultimately diagnosed with FTD and 18,831 with AD. Patients with FTD syndromes represented 2.6% of all-cause dementias. The age-standardized incidence was 2.90 per 100,000 person-year and incidence peaked between 75 and 79 years. Compared to AD, patients with FTD syndromes had a longer referral delay and delay to diagnosis. Patients with FTD syndromes had a higher MMSE score than AD at first referral while their progression was similar. mFTD patients had the shortest survival while survival in bvFTD, lvFTD, and AD did not significantly differ. FTD patients, especially those with the behavioral variant, received more antidepressants, anxiolytics, and antipsychotics than AD patients. Conclusions FTD syndromes differ with AD in characteristics at baseline, progression rate, and treatment. Despite a broad use of the new diagnostic criteria in an organized memory clinic network, FTD syndromes are longer to diagnose and account for a low proportion of dementia cases, suggesting persistent underdiagnosis. Congruent with recent publications, the late peak of incidence warns against considering FTD as being exclusively a young-onset dementia.

At autopsy, frontotemporal dementia (FTD) account for up to 20% of degenerative dementia cases, although FTDs are underrecognized in memory clinics. FTDs are confused with Alzheimer disease (AD) or vascular dementia (VaD). These misdiagnosis may affect the results of AD pharmacological trials. The first manifestations of FTD are behavioral abnormalities. The aim of this study was to assess a behavioral scale of frontal lobe dysfunction and to determine a behavioral cutoff to diagnose early FTD and distinguish it from AD and VaD. The score of the behavioral frontotemporal lobe dysfunction assessment scale was higher in FTD than in other dementias (p < 0.0001). With a cutoff of 3 points on the scale, FTD patients were diagnosed with a specificity of 95% and sensitivity of 91%. Noncognitive symptoms known to be institutionalization factors could contribute to differences between etiologies of mild dementia.

Frontotemporal dementia (FTD) was diagnosed in 74 outpatients with a standardized assessment including neuropsychological tests, behavioural scale, structural and functional imaging. Clinical characteristics were consistent with the literature data. The cohort was followed for 2-6 years to determine the reliable variable for evaluating the progression of FTD. Every fourth patient died after a mean duration of 7 years. At first, FTD manifests itself in behavioural changes with relatively stable global cognition although language, verbal fluency and memory tests were reliable tools to follow the progression of the disease. Below 18 of Mini-Mental State Examination, mutism and apathy prevented from neuropsychological testing within the next 6 months. Behavioural disorders evolved with time but restlessness and hyperorality were long-lasting. Imaging showed the progression of a consistent pattern of anterior abnormalities with frequent leukoaraiosis.

Tauopathy is a concept to describe different genetic or metabolic dysfunctions of tau proteins that generate most of the known dementing disorders. Tauopathy is a degenerating process that also affects the entorhinal formation, and then the hippocampal formation in ageing. In Alzheimer's disease (AD), a disease due to APP dysfunction, a similar tauopathy process in observed in neocortical areas, well correlated to cognitive impairment. One important gap of knowledge is the relationship between tauopathy in the hippocampal formation, ageing, AD, and cognitive impairment. Here we show that the multidisciplinary analysis of numerous brains from non-demented and demented patients suggests the following observations: tauopathy of the hippocampal formation in humans is age-related but not an age-dependent process, also independent of AD, but amplified by APP dysfunctions. Tauopathy in the entorhinal and hippocampal formation could be another type of pathological dysfunction of tau proteins, and a therapeutic target to delay AD. Relevant animal models are desperately needed to address this issue.

&lt;i&gt;Introduction:&lt;/i&gt; Frontotemporal dementia (FTD) is a more common cause of dementia than previously recognised. Few data are available regarding the natural course of FTD in terms of survival, nursing home admission and causes of death. &lt;i&gt;Methods:&lt;/i&gt; An observational study of all consecutive patients referred to the memory centre of Lille, France, between 1995 and 1999, and examined at least twice in this centre, with a diagnosis of FTD (frontal or behavioural variant) or of Alzheimer’s disease (AD) was performed. Kaplan-Meyer analysis allowing for delayed entry was used to compare the survival functions in FTD and AD. &lt;i&gt;Results:&lt;/i&gt; 552 patients were included, of whom 49 (8.9%) were lost to follow-up at 3 years. FTD patients were younger (mean age at onset 59 years), had more often a family history of psychiatric disorders (20%), had a longer delay between first symptoms and first visit (5.9 years) and a higher Mini-Mental State Examination (MMSE) score at first visit (24.5) than patients with AD (19.9). The mean annual MMSE score decline was 0.9 point in FTD vs. 2.0 points in AD (p &lt; 0.0004). Fewer patients with FTD than with AD entered an institution (RR: 0.20, 95% CI 0.05–0.81). After adjustment for sex, age at first visit, level of education and MMSE score at first visit, survival rates in FTD and AD did not differ significantly. Patients with FTD often had a sudden death, the cause of which could not be found. The earlier the first visit after onset, the longer the survival rate, whatever the diagnosis (RR: 0.76, 95% CI 0.67–0.86, p &lt; 0.0001 per year of earlier first visit). &lt;i&gt;Conclusion:&lt;/i&gt; This large study showed that the mean duration of FTD was 2 years longer than that of AD, but the risk of death after adjustment for age and sex was similar in FTD and in AD. Sudden and unexplained causes of death were frequent and need further study. Early management increases the life span of demented patients.

<h3>Objective:</h3> Vascular dementia (VaD) and Alzheimer disease with cerebrovascular disease (AD+CVD) are the leading causes of dementia after Alzheimer disease alone (AD). Little is known about the progression of either VaD or AD+CVD. The aim of this study was to compare demographic features, cognitive decline and survival of patients with VaD, AD+CVD and AD alone attending a memory clinic. <h3>Methods:</h3> This study included 970 patients who were followed at the Lille-Bailleul memory clinic, France. Cognitive functions were measured with the Mini Mental State Examination (MMSE) and the Dementia Rating Scale (DRS). Survival rate was analysed with a left-truncated Cox model. Analyses were adjusted for age, sex, education, hypertension, diabetes and baseline MMSE and DRS. <h3>Results:</h3> Of 970 patients, 141 had VaD, 663 AD alone and 166 AD+CVD. The latter were significantly older than AD or VaD patients at onset (71 (SD 7) vs 69 (9) and 68 (9) years, p = 0.01) and at first visit (75 (6) vs 73 (8) and 72 (8) years, p = 0.0002). Baseline MMSE and DRS evaluations were highest for VaD compared with AD alone or AD+CVD patients (p&lt;0.006). Cognitive decline during follow-up was slowest for VaD, intermediate for AD+CVD and fastest for AD alone (p = 0.03). After adjustment, compared with AD patients, mortality risk was similar for those with VaD (relative mortality risk (RR) = 0.7 (0.5 to 1.1)) and tended to be lower for AD+CVD (RR = 0.7 (0.5 to 1.0)). The shorter the delay between first symptoms and first visit, the longer patients survived. <h3>Conclusion:</h3> This clinical cohort study shows that patients with VaD, AD+CVD and AD present different characteristics at baseline and during follow-up, and underlines the need to distinguish between them.

&lt;b&gt;&lt;i&gt;Background:&lt;/i&gt;&lt;/b&gt; The diagnosis of behavioral variant of frontotemporal dementia (bvFTD) relies primarily on clinical features and remains challenging. The specificity of the recently revised criteria can be disappointing, justifying development of new clinical tools. &lt;b&gt;&lt;i&gt;Objective:&lt;/i&gt;&lt;/b&gt; We produced a behavioral inventory named DAPHNE. This scale (adapted from Rascovsky's criteria) explores six domains: disinhibition, apathy, perseverations, hyperorality, personal neglect and loss of empathy. It is composed of ten items (five answer categories). The aim was (1) to assess the validity and reliability of DAPHNE and (2) to evaluate its contribution in differentiating patients. &lt;b&gt;&lt;i&gt;Methods:&lt;/i&gt;&lt;/b&gt; Two scores were computed: DAPHNE-6 (screening) from the six domains and DAPHNE-40 (diagnosis) from the ten items. Reliability and reproducibility were assessed. External validity was studied with the Frontal Behavioral Inventory (FBI) and the Frontotemporal Behavioral Scale (FBS). Finally, the diagnostic performance of DAPHNE was compared to revised criteria, FBI and FBS. &lt;b&gt;&lt;i&gt;Results:&lt;/i&gt;&lt;/b&gt; DAPHNE was administered to the caregivers of 89 patients, 36 with bvFTD, 22 with Alzheimer's disease, 15 with progressive supranuclear palsy and 16 with bipolar disorder. Reliability and reproducibility were excellent, as was external validity. DAPHNE-6 allowed bvFTD diagnosis (score ≥4) with a sensitivity of 92%, while DAPHNE-40 (score ≥15) had a specificity of 92%. &lt;b&gt;&lt;i&gt;Conclusion:&lt;/i&gt;&lt;/b&gt; We demonstrate excellent psychometric features for DAPHNE. This quick tool could help for both diagnosing and screening bvFTD.

La maladie bipolaire (MB) s’accompagne d’un déficit cognitif léger, pouvant devenir démentiel chez le sujet âgé, rappelant la notion de vésanie. L’objectif de l’étude était de caractériser cette démence. Treize patients aux antécédents de MB avant 50 ans, répondant aux critères de démence ont consulté en centre mémoire et ont été suivis au minimum deux ans. Ils étaient en euthymie, leur âge moyen était de 70,8 ans (±7,7), le début de l’état démentiel survenait en moyenne 29,2 ans (±10,1) après le début de la MB, le score moyen au minimental state examination (MMSE) était de 24,0 (±4,3). Après un suivi moyen de 6,1 ans (±2,8), le MMSE moyen était de 23,5 (±3,2). La perte moyenne annuelle au MMSE était de 0,5 (±4,4). L’imagerie morphologique ne mettait pas en évidence d’atrophie focale ou de lésions vasculaires. L’imagerie fonctionnelle montrait dans tous les cas un hypodébit frontotemporal souvent associé à un hypodébit pariétal plus modéré. Le suivi neuropsychologique notait un syndrome dyséxécutif, un trouble mnésique fronto-sous-cortical et souvent un déficit visuospatial. Un syndrome frontal comportemental modéré était observé, tandis que les hallucinations étaient rares. Même après six ans, aucun patient ne répondait aux critères de probabilité des principales démences, faisant suspecter l’hypothèse d’une démence spécifique à la MB qu’une étude prospective devrait explorer. Converging evidence suggests that people with bipolar disorder (BPD) exhibit persistent cognitive impairment independently from the emotional state. In old age BPD, the cognitive decline is more severe and can fulfill the criteria of dementia. However, the characteristics of bipolar disorder dementia are still unknown. The aim of the study was to characterise the cognitive and imaging profile of the dementia following bipolar disorder. Patients fulfilling criteria of dementia and followed-up in the memory unit for at least two years were included. Patients with substance abuse were excluded. A battery of specific (assessing verbal memory, attention, frontal executive function, construction and visuospatial impairment), and global (MMSE and Mattis dementia rating scale) neuropsychological tests, behavioural assessment using the frontotemporal behavioural scale, MRI and HMPAO–SPECT imaging were performed in all patients during euthymic state. We included 13 patients with bipolar disorder (9W/4M). The mean age was 70.8 years (±7.7). Dementia began in average 29.2 years (±10.1) after the onset of the bipolar disorder. The mean score of MMSE was 24.0 (±4.3). The mean score of the Mattis dementia rating scale was 122.5 (±8.9). After an average of 6.1 years (±2.8) of follow-up, the mean score of MMSE was 23.5 (±3.2). The annual MMSE score decrease was of 0.5 (±4.4) per year. In more than 75% of the patients, Trail-Making Test-part B, Go-nogo test, Stroop test, delayed free recall in verbal explicit long-term memory test, category fluency tasks and code test were impaired. In more than 50% of patients, free recall, delayed cued recall, clock test, visuospatial battery and temporal orientation were impaired. On the other hand, spatial orientation and recognition were within the standards. The mean of the BREF score was 10.6 (±3.2). A moderate frontal behavioural syndrome was observed, but never persistent hallucinations. Seven patients had been treated with lithium and seven with antipsychotics, but none during the neurological assessment. Moderate extrapyramidal signs were reported in 10 patients, of which the seven patients treated in the past with antipsychotics. MRI showed no focal atrophy and no vascular lesions. Functional imaging conducted in 10 patients always showed uptake decrease in the frontotemporal regions and sometimes in the parietal region too. After six years of follow-up, no patient fulfilled the probable criteria for the main dementia, Alzheimer disease, vascular dementia, frontotemporal dementia and dementia with Lewy bodies. The data of this study support a possible specific dementia postbipolar disorder and not only mild cognitive decline. This hypothesis could be tested in a prospective study. Such dementia could be a main differential diagnosis from long lasting frontotemporal dementia. The pathogenic process of this dementia could also be determined.

MAPT mutations cause autosomal dominant frontotemporal lobar degeneration. These diseases are characterized by considerable heterogeneity in their clinical, neuropathological, and biochemical presentations. We describe the full characterization of a family with autosomal dominant frontotemporal lobar degeneration caused by a novel MAPT mutation. Clinical, imaging, neuropathological, and biochemical data are presented. The proband was a woman who died at 85 years old, 25 years after the onset of a slowly progressive and isolated anarthria and opercular syndrome. The pathological examination of her brain showed marked atrophy of primary motor and premotor cortices, associated with predominant neuronal tau-positive lesions mimicking Pick bodies. At the biochemical level, the six tau isoforms aggregate to display a pathological triplet at 60, 64, and 69 kDa. Two of her sons presented at 48 and 50 years old with a right temporal variant of frontotemporal degeneration characterized by severe prosopagnosia, semantic impairment, and behavioral modifications. In these three patients, the molecular analysis of MAPT showed the c.1945C>T mutation on exon 11 resulting in the P332S substitution in tau sequence. This mutation changes the PGGG motif of the third repeat domain of the protein and therefore reduces the ability of tau to bind microtubule. From a clinical point of view, this mutation is associated with considerable intrafamilial phenotypic variation.

Amnesia is a key component of Alzheimer's disease (AD) and the most important feature of its clinical diagnosis but its specificity has recently been challenged. This study investigated the ability of amnesia to predict AD in a clinicopathological dementia series. Ninety-one patients to which free and cued verbal memory assessment was administered during early cognitive decline, were followed until autopsy. Patients' histological diagnoses were classified as pure AD, mixed AD, and non-AD pathologies. Data-driven automated classification procedures explored the correspondence between memory performance and pathological diagnoses. Classifications revealed 3 clusters of performance reflecting different levels of amnesia. Little correspondence between these clusters and the presence of AD pathology was retrieved. A third of patients with pure/mixed AD pathology were non-amnesic at presentation and ≈45% of patients without AD pathology were amnesic. Data-driven prediction of AD pathology based on memory also had a poor accuracy. Free and cued memory assessments are fair tools to diagnose an amnesic syndrome but lack accuracy to predict AD pathology.

Abstract Collecting data on households and individuals since 1999, the Swiss Household Panel (SHP) is an ongoing, unique, large-scale, nationally representative, longitudinal study in Switzerland ( N = 9828 households and N = 15,882 persons interviewed in 2020). The SHP aims to provide both continuity and innovation in measurement and data collection. Examples of innovation are the combination of retrospective and prospective longitudinal data, the combination of survey modes notably in refreshment samples and additional studies oversampling specific population groups. This article provides an overview of the SHP – focusing on the survey’s key design features, content, data collection and adjustments, possibilities for cross-national comparisons, data use and accomplishments.

Response to tacrine varies among patients with Alzheimer's disease (AD). Lewy body dementia (LBD) could be a high responder subtype of AD. The aim of the study was to compare the effects of tacrine in LBD and AD.Seventy-five consecutive outpatients with mild or moderate AD were screened. Tacrine was given at a dose of 40 mg/day during 6 weeks. During the next 6 weeks, the patients were treated with 80 mg/day and afterwards with 120 mg/day. Patients were assessed at baseline and treated with a dose of 120 mg/day tacrine for 2 weeks.Analysis was performed on 39 patients (AD, N = 20; LBD, N = 19). Eight patients were lost to follow-up, eight patients manifested with side-effects, six suffered from an intercurrent somatic disease during the study and 14 patients had poor compliance or were treated with incompatible drugs. Twenty-two patients (11 AD/11 LBD) increased their cognitive performances with tacrine. Among the 22 patients, the improvement differed between the AD and the LBD groups. In AD, conceptualization improved; in LBD, the improvements occurred in verbal initiation and digit span.This study emphasizes the importance of using appropriate tests to determine the positive effects of pharmacological treatments.

Central serotonin depletion may contribute to the anxiety, restlessness, irritability, and affective disturbance seen in a variety of psychiatric conditions, particularly dementia of the Alzheimer's type (DAT) in which brain concentrations of both 5-hydroxytryptamine (5-HT) and its 5-hydroxyindoleacetic acid (5-HIAA) metabolite are reduced.Trazodone, a serotonergic antidepressant with alpha 2-adrenergic blocking activity, was administered to 13 patients with DAT in an open 10-week pilot study at a dose of 25 mg t.i.d. Behavioral and affective disturbance was assessed pretreatment and posttreatment using semistructured interview and Jouvent's Depressed Mood and Gottfries-Brane-Steen scales.Irritability, anxiety, restlessness, and affective disturbance were all decreased (p < .05). No side effects were observed. Mean Mini Mental State scores were unaffected by treatment.The hypothesis that trazodone corrects behavioral and affective disturbance induced by serotonin depletion in DAT requires confirmation in a double-blind placebo-controlled trial.

Memory deficit is the predominant presenting symptom in dementia. To compare short-term memory (STM) deficit in early dementia of Alzheimer type (DAT) vs frontal lobe type (DFT), and determine the residual memory capacity for stimulation, the generation effect (the memory advantage of items generated rather than read) was tested on verbal and visuospatial STM in patients with DAT (n = 10), DFT (n = 9) and in age-matched normal controls (n = 12). The generation effect enhanced performance in all groups. However, the profile of STM deficit differed in the two dementias: verbal and visuospatial memory were both decreased in DAT vs verbal memory only in DFT. These results provide a further criterion for differentiating between DAT and DFT, and show that memory performance can be enhanced in early dementia using techniques such as the generation effect.

International Journal of Geriatric PsychiatryVolume 20, Issue 12 p. 1203-1204 Letter to the Editor Diogene syndrome, a clinical presentation of fronto-temporal dementia or not? Florence Lebert, Florence Lebert Centre de la Mémoire, Centre Universitaire Roger Salengro, Lille, FranceSearch for more papers by this author Florence Lebert, Florence Lebert Centre de la Mémoire, Centre Universitaire Roger Salengro, Lille, FranceSearch for more papers by this author First published: 28 November 2005 https://doi.org/10.1002/gps.1430Citations: 22AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume20, Issue12December 2005Pages 1203-1204 RelatedInformation

This article assesses the gendered impact of COVID-19 measures on changes in time that Swiss dual earner couples spent on unpaid work during the pandemic, focusing on families with children. Overcoming some of the methodological shortcomings of previous studies, high-quality representative panel data allow us to examine the change in time invested in housework and childcare before and during the pandemic, and test theoretical assumptions as to the mechanisms underlying the observed patterns. Gender inequalities are explained by the couple's work division prior to, and at the onset of, the pandemic and interpreted in the light of key theoretical approaches (economics of the family, bargaining and time availability, doing gender). Our results imply that in particular changes in the time availability of the partner are relevant for changes in time spent on housework, while in case of care work, the own time availability matters more. Moreover, we also found that the respondents' economic bargaining power within the couple matters both for housework and care work. Finally, the implemented COVID-19 measures neither led to an increase in patriarchal power structures nor did they foster an increase in equality for unpaid work among women and men. Instead, the results show that changes in time availability due to short-time, remote or overtime working schemes determined changes in time spent on unpaid care to a larger extent than gender alone.

In our memory clinic experience, memory impairment differs widely in patients with frontotemporal dementia (FTD). We searched for a correlation between explicit memory disturbance assessed with the Grober and Buschke test and medial temporal atrophy on CT scan in 22 consecutive patients with FTD. Five of the 22 patients had a medial temporal lobe (MTL) atrophy. There was no significant difference between the two groups for the demographic characteristics. Free recall, cued recall and the learning curve were significantly better in patients without MTL atrophy. The patients with MTL atrophy made more intrusions. We found a positive correlation between total recall and cued recall and the mean of medial temporal lobe measurement. These results are in agreement with the role of the hippocampal formation in the memory process. In our group, the ratio of patients with MTL atrophy is similar to the ratio of Pick’s disease in frontotemporal dementia. In histological series more severe hippocampal atrophy are reported in Pick’s disease. Therefore MTL atrophy on CT scan could be a marker of Pick’s disease in FTD.

It is unclear whether associated cerebrovascular pathology contributes to the clinical spectrum of Lewy body dementia (LBD).The present postmortem 7.0-tesla MRI study investigates the anatomical distribution of cortical microbleeds (CoMBs) in LBD brains with and without associated Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA). CoMBs predominated in the frontal section of the LBD brains and were associated to severe white matter lesions. No differences were observed when LBD brains with and without AD and CAA were compared.In LBD, there is a specific distribution of CoMBs that is different from that in other neurodegenerative diseases. The increase of frontal CoMBs is not due to the frequently associated AD and CAA features but due to the LBD itself.

The perception of job insecurity is known to be a stressful condition for employees. Less is known about employment insecurity and the ways employees and their families deal with it. This study investigates whether participation in further training is a strategy that employees adopt to reduce perceived employment insecurity. As participation in further training is often costly and time-consuming, we assume that the family context is of importance for the decision to take part in further training. To take account of possible self-selection, we apply a propensity score matching procedure on longitudinal data from the Swiss Household Panel (2004-2013). Three main findings can be emphasized: first, participation in further training is not a strategy adopted particularly by employees who perceive high employment insecurity as they are less likely to train than their secure counterparts. Second, even though further training is not a strategy that is actively adopted, employees who train subsequently report lower levels of perceived employment insecurity. Third, the family context indeed influences the likelihood to train: partnered employees are more likely to train and preschool-aged children act as a constraint on women’s but enhance men’s participation in further training. Yet, in the context of high perceived employment insecurity, children generally reduce their parents’ likelihood to train as the parents may turn to other strategies that reduce perceived employment insecurity.

Human Psychopharmacology: Clinical and ExperimentalVolume 14, Issue 4 p. 279-281 Letter to the Editor Trazodone in the treatment of behaviour in frontotemporal dementia F. Lebert, F. Lebert Hospital Roger Salengro, Centre Hospitalier Universitaire, 59037 Lille, FranceSearch for more papers by this authorF. Pasquier, F. Pasquier Hospital Roger Salengro, Centre Hospitalier Universitaire, 59037 Lille, FranceSearch for more papers by this author F. Lebert, F. Lebert Hospital Roger Salengro, Centre Hospitalier Universitaire, 59037 Lille, FranceSearch for more papers by this authorF. Pasquier, F. Pasquier Hospital Roger Salengro, Centre Hospitalier Universitaire, 59037 Lille, FranceSearch for more papers by this author First published: 23 June 1999 https://doi.org/10.1002/(SICI)1099-1077(199906)14:4<279::AID-HUP89>3.0.CO;2-1Citations: 20AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article.Citing Literature Volume14, Issue4June 1999Pages 279-281 RelatedInformation

Characterisation of sundowning syndrome, defined as 'an exacerbation of symptoms indicating increased arousal or impairment in late afternoon, evening or at night, among elderly demented individuals', is complicated by neuroleptic therapy and frequent failure to specify the nature of the associated dementia. Screening by a memory disorders unit of an institutionalized population of 30 neuroleptic-free demented patients revealed 8 sundowners, with diagnoses of probable Alzheimer's disease (n = 5), frontal lobe dementia (n = 1), Lewy body disease (n = 1), and sequelae of herpes encephalitis (n = 1). Sundowners did not differ from non-sundowners in age, Mini Mental State score, degree of temporal and spatial disorientation or perceptual delusion. Sundowning was related to restlessness (P < 0.0001), sleep disorder (P < 0.003) and a history of hypotension lipothymia (P < 0.08). These results provide further evidence for a chronobiological explanation of sundowning syndrome.

We tested the interobserver reliability of visual rating of HMPAO-SPECT imaging in 271 outpatients referred to a memory clinic, and followed over 1 year. The clinical diagnoses were Alzheimer's disease (n = 156), frontotemporal dementia (n = 47); vascular dementia (n = 21), senile dementia of Lewy body type (n = 12), anxiety/depressive disorders (n = 14) and miscellaneous memory disorders (n = 21). The interobserver agreement was good (k = 0.68). However, the heterogeneity of the patterns-independent from demographic data, age at onset and duration of the disease- and their lack of sensibility and specificity limited the contribution of SPECT for diagnostic purposes in routine practice.

Capgras' delusion (CD) may be secondary to a neurologic lesion, particularly in the right frontal or occipital regions. A 40-year-old woman with multiple sclerosis underwent SPECT during and after an episode of CD. Analysis during delusion showed an uptake defect in the right parietal cortex with an 11% index of asymmetry (normal: < or = 4%). Post-delusion SPECT showed decreased bifrontal and biparietal cortical uptake indices but a normal index of asymmetry. Functional brain imaging may provide clues to the psychopathology of CD.

Under the auspices of the French Society of Gerontology and Geriatrics, a multidisciplinary team including geriatritians, neurologists, epidemiologists, psychiatrists, pharmacologists and public health specialists developed a consensus on care for patients with severe dementia. They defined 21 recommendations for general practitioners, long-term care physicians and specialists based on knowledge available in 2005. At all stages of the disease, the objective of care is to improve as much as possible quality-of-life for the patient and his/her family, including a life project until the end of life. It is always possible to do something for these patients and their family: nutritional status, behavior disorders, and incapacities to deal with basic activities of daily life have to be taken in consideration. Resource allocation and proximity care have to be targeted. Research areas necessary to improve the care of patients with severe dementia has been selected.

Objective: Previously, a placebo-controlled cross-over trial of trazodone (300 mg/day) of 12-weeks duration showed behavioral improvement in a group of 26 patients with frontotemporal dementia. The long-term efficacy and safety of trazodone in frontotemporal dementia was unknown. Materials & methods: The placebo-controlled trial has now been followed by an open-label extension study. The 26 frontotemporal dementia patients with mild cognitive decline and severe behavioral troubles who entered the study had previously completed the double-blind study with trazodone. Patients were treated with 300 mg/day. They were followed for at least 2 years, after the end of the double-blind trial. The efficacy was evaluated by the neuropsychiatric inventory score. Results: The withdrawal rate was approximately 23% during the first year, two patients died due to unrelated causes, two patients were institutionalized and two refused the follow-up – none as a result of adverse events. The withdrawal rate was approximately ...

Among behavioral and socioemotional changes occurring before cognitive decline at the early stages of frontotemporal dementia, the patients often manifest with self-neglect and some criteria of Diogene syndrome. Despite the lack of accurate behavior regarding disgust, are they still sensitive to the emotional content of disgust-inducing words or scenes?Eleven patients with frontotemporal dementia, 11 healthy controls, and 34 young adults performed a lexical decision task, where some of the words conveyed an emotional content and a number comparison task while they were presented with emotion-inducing pictures. They were not instructed to identify the emotional content of the words and pictures.Contrary to the healthy controls paired for age, the patients provided delayed responses for disgust-inducing words in the lexical decision task and in presence of disgust-inducing pictures in the number comparison task.Although they manifest with self-neglect and inaccurate behavior regarding dirt, the patients were still sensitive to disgust, provided that this sensitivity was tested implicitly, suggesting that they above all suffer from inabilities in matching the appropriate social behavior with such emotions.

Bipolar disorder is associated with an increased risk of dementia with aging. Little is known regarding this association, limiting appropriate diagnosis and management. We aimed to describe the characteristics of bipolar patients with late cognitive impairment for whom the hypothesis of an underlying neurodegenerative disease had been raised. We performed a retrospective multicenter study, recruiting bipolar patients over 50 years old from five French tertiary memory centers who had undergone cerebrospinal fluid (CSF) biomarker assessment for Alzheimer's disease (AD). Clinical, neuropsychological, and paraclinical characteristics were analyzed and 78 patients were included. The mean age at the onset of cognitive impairment was 62.4 years (±9.2). The mean MMSE score was 22.8 (±4.5), the mean FAB was 11.7 (±3.9), and the mean FCRST was 15.8 (±7.4)/36.8 (±9.7) (free/total recall). A total of 48.6% of the patients displayed cognitive fluctuations, and 38.2% showed cognitive improvement during follow-ups; and 56.3% of the patients showed Parkinsonism, of which 12.7% had never received antipsychotics. Among patients who underwent DAT-scans, 35.3% displayed dopaminergic denervation; 10.3% of patients had CSF AD biological signature ("A+ T+" profile), while 56.4% had other abnormal CSF profiles. Thus, clinical presentation was dominated by executive dysfunction, episodic memory impairment, fluctuating cognition, and a high frequency of Parkinsonism. Specifically, high frequency of delusional episodes suggests limited tolerance of psychotropic drugs. Most patients had abnormal CSF biomarker profiles, but only a minority displayed AD's specific biomarker signature. Therefore, while our results unveil shared common neurocognitive features in bipolar patients with cognitive impairment of suspected neurodegenerative origin they suggest a participation of various underlying pathologies rather than a common degenerative mechanism in the pathophysiology of this condition.

Abstract The diagnosis of frontal lobe dementia (FLD) involves the assessment of affect. Three affective states predominate in FLD: apathy, elation and emotionalism. Nineteen FLD patients were investigated for a relationship between affective changes and premorbid personality traits. The negative results support the hypothesis that mood changes in FLD have a neurological basis and are important in early diagnosis.

Alzheimer's disease is the most frequent cause of degenerative dementia. Despite the available diagnostic criteria, improvement of diagnosic accuracy is still required. The aim of this prospective study was to assess in a large population of patients referred to a memory clinic the diagnostic value of the combination of medial temporal lobe atrophy on temporal oriented CT and decreased temporoparietal uptake on HMPAO single photon emission tomography (SPECT).The study was conducted in 125 patients aged 51-93: 64 with probable Alzheimer's disease (Mean (SD) mini mental state examination (MMSE)=18.34 (6.93)), duration of disease=6.48 (2.93) years, 13 possible Alzheimer's disease (MMSE=21.58 (5.48), duration of disease=6.08 (2.56)), 48 patients with miscellaneous memory disorders (MMSE=21.98 (6.10), duration the disease = 6.85 (3.91)).For the diagnosis of probable Alzheimer's disease, the sensitivity of this association was 0.56, the specificity 0.93, the positive predictive value 0.95, and the negative predictive value 0.45. The diagnosic accuracy was 0.68. Both medial temporal atrophy and parietotemporal decrease in uptake were present in four of 13 patients with possible Alzheimer's disease and 11 of 48 with miscellaneous memory disorders. The association was absent in 27 of 29 patients with frontotemporal dementia. In mild stages (MMSE>18; n = 32), the sensitivity of the association was 0.34, the specificity 0.93, the positive predictive value 0.85, and the negative predictive value 0.57. The diagnosic accuracy was 0.53.This association, although not sensitive, helps to select patients with high probability of Alzheimer's disease at an early stage which can be of interest for clinical and research purposes.

To get more insight into how people were affected by and fared during the first wave of the Covid-19 pandemic, the Swiss Household Panel launched an additional Covid-19 Survey among participating households. It was fielded between May and June 2020, right after the strictest regulations ended, but numerous restrictions were still in place. This paper presents the main findings of this study with respect to a wide variety of domains: the occurrence of Covid-19 infections in people’s networks, changes with respect to work, finances, time use, family life, following education from home, health and wellbeing, worries, social networks and social cohesion, and the evaluation of the political measures taken by the federal government.

Frontotemporal dementia (FTD) is poorly recognized clinically. Of the 1,517 patients examined at the Lille Outpatients Memory Clinic data bank (1991-1995), 74 fulfilled the criteria of the Lund and Manchester groups for FTD. They accounted for 5 p, 100 of all patients, 1 for 10 probable or possible Alzheimer's disease. Mean patient age was 63 years, duration of the disease was 5 years, mean Mini Mental State score was 23; 45 p. 100 belonged to the active population. Behavioral disorders occurred before the cognitive decline and remained the major feature. All patients had at least 3 of the following symptoms: self-control impairment, affective disorder, loss of interest and self-neglect. Memory impairment consisted of correct encoding and impaired retrieval processes, without major storage impairment. No patients had spatial disorientation. Language was usually reduced, EEG was normal. Two diagnoses were confirmed by autopsy: both consisted of aspecific frontal and temporal degeneration, 41 p. 100 of the patients were referred by a general practitioner, 30 p. 100 by a psychiatrist, 16 p. 100 by a neurologist, 2 p. 100 by other specialists, and 11 p. 100 following the advice of their relatives. FTD had never been suspected. Alzheimer's disease or non specified degenerative dementia was suspected in 2/3 of patients and a psychiatric disorder in 1/3. With the advent of novel pharmacological agents for the treatment of dementing disorders and for research purposes, the identification and accurate differentiation of FTD from Alzheimer's disease and psychiatric disorder is essential. Therefore, the role of multidisciplinary memory clinic is crucial to differentiate FTD from other degenerative dementias.

Sous l’égide de la Société Française de Gériatrie et Gérontologie, un groupe pluridisciplinaire de spécialistes en gériatrie, neurologie, épidémiologie, psychiatrie, neuroradiologie, pharmacologie, santé publique a entrepris une démarche de consensus sur les modalités d’évaluation, de suivi et de prise en charge globale de la démence de type Alzheimer au stade sévère. Cette réflexion, fondée sur l’état des connaissances en 2005, a permis de formuler 21 recommandations à destination des praticiens hospitaliers, médecins traitants, médecins coordonnateurs et spécialistes. Quel que soit le stade évolutif de la maladie, l’objectif de la prise en charge est d’améliorer la qualité de vie de la personne malade et de sa famille, en associant projet de soins et projet de vie et ce jusqu’en fin de vie. La prise en charge, pour être globale, doit être nécessairement pluridisciplinaire et coordonnée, en mobilisant les ressources sanitaires et médico-sociales de proximité pour optimiser leur utilisation. Le groupe a souligné également l’importance d’une recherche dynamique : recherche clinique visant à mieux connaître l’évolution des troubles, évaluation des stratégies de prise en soins. Under the auspices of the French Society of Gerontology and Geriatrics, a multidisciplinary group of experts, including geriatricians, neurologists, epidemiologists, psychiatrists, pharmacologists, and public health specialists developed consensus recommendations about care for patients with severe dementia. They defined 21 recommendations for general practitioners, long-term care physicians, and specialists, based on the knowledge currently available (2005). The aim of care at all stages is to mitigate the quality-of-life of patient, caregiver, and family insofar as possible, combining care and future planning until the end of life. Management, to take into account problems including nutritional status, behavior disorders, and ability (or inability) to perform activities of daily living, must be global, multidisciplinary, and coordinated and must optimize use of local medical and social resources. The group also stressed the importance of clinical research to improve knowledge of disease course and assess management strategies and recommended specific area for research.

Introduction: Cerebrovascular lesions are rare in frontotemporal lobar degeneration (FTLD), in contrast to other neurodegenerative diseases.Cortical microbleeds (CoMBs) are frequent in Alzheimer's disease, in particular in cases associated with cerebral amyloid angiopathy.The present study investigates the gyral topographic distribution of CoMBs in post-mortem FTLD brains with 7.0-tesla magnetic resonance imaging.Material and methods: The distribution of CoMBs in 11 post-mortem FTLD brains and in 12 control brains was compared on T2*-GRE MRI of six coronal sections of a cerebral hemisphere.The mean values of CoMBs were determined in twenty-two different gyri.The findings were correlated to those separately observed on neuropathological examination.Results: As a whole there was a trend of more CoMBs in the prefrontal section of FTLD as well as of the control brains.CoMBs were significantly increased in the superior frontal gyrus and the insular cortex (p ≤ 0.001) and also in the inferior frontal gyrus and the superior temporal gyrus (p ≤ 0.01).Conclusions: CoMBs in FTLD are only increased in the regions mainly affected by the neurodegenerative lesions.They probably do not reflect additional cerebrovascular disease.

The number of patients with young onset dementia (YOD) (first symptoms beginning before the age of 60 years) is estimated around 5,000 in France. On account of the usual severity of behavioral symptoms in these patients, the need for cognitive-behavioral specialized unit (UCC) is expected. To determine the number and characteristics of YOD patients cared for in UCC in France during the year 2013. A specific questionnaire was sent to the 84 French UCC. The questionnaire was completed by 55 UCC (65%), whose 33 received 179 YOD patients. The diagnosis was Alzheimer's disease in 50% of the cases and frontotemporal dementia in 30%. The main reasons for the hospitalization in UCC were the severity of behavioral symptoms in 86% of cases, the need to alleviate the caregiver burden in 31% and the waiting for a place in a nursing home in 23%. Mean duration of hospitalization was 40.4 ± 20.5 days. At the end of hospitalization 51% of the patients returned to their original living accomodation and 39% entered into a nursing home. The main reason of YOD patients hospitalization reject was the care team's fear in the UCC without experience. The severity of the behavioral troubles was the major issue while the necessary ethical reflection raised by the YOD patients management was a positive aspect. The teams rated how ready do they feel about taking care of YOD patients on a scale from 0 to 100, the median was 35. The welcoming of YOD patients in UCC is necessary, however the severity of the behavioral troubles and the care teams fear prompt to set up specific education and to increase of the number of staff for YOD patients management.

Behavioral disorders are major manifestations of Alzheimer's disease and other forms of dementia. They are associated with caregiver distress, increase the likelihood of institutionalization and may be associated with more rapid cognitive decline. The first step of treatment strategy is an assessment of these disorders. Treatment of behavioral signs is an etiological treatment. Acute behavioral signs are often related to an unknown somatic disease. Chronic signs are often symptoms of the neurological dementia and can be reduced, especially by serotonergic agents and anticonvulsivants. The new antipsychotics are a good alternative to classic neuroleptics known for their frequent cognitive side effects in demented patients. Anticholinesterasic drugs can positively influence noncognitive signs. The treatment of behavioral and psychological symptoms of dementia (BPSD) involves a number of specific interventions including cognitive stimulation which has shown effectiveness on both cognitive functions and quality of life. Prevention of BPSD includes safety measures such as evaluation of suicidality and violence, vigilance regarding neglect and abuse, planning for legal issues due to the patient's incapacity. Families or caregivers should be provided with counseling, education and support. The treatment of BPSD is part of a global and multimodal care which involves general practioners, nurses, social workers, physiotherapists, neuropsychologists, speech therapists, memory centers, psychogeriatric and geriatric units, and respite care units, nursing homes and long-term care facilities. The coordination of the professionals is a critical aspect of providing effective care for patients with Alzheimer's disease.

Two characteristics of senile dementia of the Lewy body type (SDLT) compared with Alzheimer's disease (AD) are relevant to treatment management: relative hypocholinergic activities and behavioural disturbances such as psychotic manifestations with neuroleptic hypersensitivity. A better tacrine responsiveness of SDLT patients has been proposed. An open trial with tacrine (120mg/day) prescribed in 22 probable AD patients (meeting NINCDS–ADRDA criteria) resulted in no memory improvement in the four patients meeting SDLT criteria. The potential of GABAergic agents, particularly carbamazepine, in the management of delirium and psychotic symptoms in SDLT is discussed.

European Journal of NeurologyVolume 6, Issue 2 p. 133-136 Neuropsychiatric afflictions of modern French Presidents: Maréchal Henri-Philippe Pétain and Paul Deschanel François Boller, François Boller NSERM U 324, Centre Paul Broca, 2 ter rue d'Alésia, 75014 Paris, FranceSearch for more papers by this authorAnnie Ganansia-Ganem, Annie Ganansia-Ganem NSERM U 324, Centre Paul Broca, 2 ter rue d'Alésia, 75014 Paris, FranceSearch for more papers by this authorFlorence Lebert, Florence Lebert Centre de la Mémoire, Déparfement de Neurologie, Hôpital Roger Salengro, Centre Hospitalier et Universitaire de Lille, 59037 Lille, FranceSearch for more papers by this authorFlorence Pasquier, Florence Pasquier Centre de la Mémoire, Déparfement de Neurologie, Hôpital Roger Salengro, Centre Hospitalier et Universitaire de Lille, 59037 Lille, FranceSearch for more papers by this author François Boller, François Boller NSERM U 324, Centre Paul Broca, 2 ter rue d'Alésia, 75014 Paris, FranceSearch for more papers by this authorAnnie Ganansia-Ganem, Annie Ganansia-Ganem NSERM U 324, Centre Paul Broca, 2 ter rue d'Alésia, 75014 Paris, FranceSearch for more papers by this authorFlorence Lebert, Florence Lebert Centre de la Mémoire, Déparfement de Neurologie, Hôpital Roger Salengro, Centre Hospitalier et Universitaire de Lille, 59037 Lille, FranceSearch for more papers by this authorFlorence Pasquier, Florence Pasquier Centre de la Mémoire, Déparfement de Neurologie, Hôpital Roger Salengro, Centre Hospitalier et Universitaire de Lille, 59037 Lille, FranceSearch for more papers by this author First published: 27 July 2007 https://doi.org/10.1111/j.1468-1331.1999.tb00005.xCitations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume6, Issue2March 1999Pages 133-136 RelatedInformation

We developed a disruptive behavior questionnaire designed for persons living close to the patient in order to assess behavior disorders in Alzheimer type dementia.The study included 111 patients with criteria for diagnosis of Alzheimer type dementia. The questionnaire was used to assess the patients 15 days after withdrawal of psychotropic drugs. A partially-structured interview was also conducted by a psychiatrist in 20 cases.There was no relationship between the different behavior disorders and the mini-mental-state score or the social and cultural situation. Answers to the questionnaire and responses given during the interview were nearly identical.There has been little effort to assess behavior disorders compared with cognitive disorders in patients with Alzheimer type dementia. Behavior assessment should be an integral part of patient evaluation since cognitive and non-cognitive disorders are independent and certain therapeutics may be effective in behavior disorders.

The very slow progression of behavioral disorders, initially isolated at the onset of frontotemporal dementia, easily results in their neglect, all the more so since the patients are anosognosic. In absence of cognitive decline, these patients, whatever carrying a neurological disease, are frequently led towards psychiatrists. Many psychiatric disorders may be evoked: depression, mania, compulsive obsessive disorder, psychopathy, alcoholic addiction, bulimia, schizophrenia, or Diogene syndrome. However, the diagnosis can often be easily corrected by a detailed clinical analysis. The knowledge of the 3 behavioral symptoms included in the diagnostic criteria can help to recognize frontotemporal dementia, even when imaging and neuropsychological data show mild abnormalities. In the last few years, various neuropsychological, biological and environmental mechanisms have been proposed to explain the behavioral disorders. These disorders are very difficult to tolerate by the caregivers because the patients appear to be asocial and show no affect. A detailed information of the changes related to the disease is important for the caregivers to accept the behavioral changes and to cope with them. However, over time, the occurrence of mutism may lead caregivers to regret the period of behavioral disorders.

Cholinesterase inhibitors (ChEIs) are effective in treating visual hallucinations (VH) in dementia with Lewy bodies (DLB). Nonetheless, approximately 35% of patients treated with rivastigmine showed no significant improvement according to the psychosis subscores of the Neuropsychiatry Inventory (NPI).1 We conducted an observational study in our memory clinic and we report the characteristics of patients who showed resistant hallucinations (RH) to ChEIs. We carried out an observational study of outpatients with DLB with hallucinations treated with ChEIs over 4 years. Probable DLB was diagnosed according to the second consensus criteria, and the severity of dementia was assessed using the Mini-Mental State Examination (MMSE) score. We excluded patients who required concomitant medications other than ChEIs that influence hallucinations or if they were treated with antipsychotics. Episodes of …

The number of patients with young onset dementia (YOD) (that is before age 65) is estimated at 32,000 in France, and 5000 with onset dementia before 60 years. These patients differ from older ones by the greater number of rares causes (29%), heterogeneity of the presentation among the usual diseases, such as non-amnestic phenotypes of Alzheimer's disease, high frequency of frontal symptoms, and possible genetic origin. These aspects must be taken into account for the diagnosis, often more difficult than in older ones because patients have a little knowledge of the YOD, excepted in the genetics forms. YOD patients can still work or drive a car, and we should choose between the respect for autonomy and the security for the patient and their carers. YOD patients can be more often included in pharmacological trials because they have lower associated disorders. Individual non-pharmacological treatment should be priviledged because they don't easily accept collective activities with other patients over 60 years of age. Excepted for the very young patients (onset before 45), the survival is longer than in late onset dementia, with sometimes severe behavioral problems related to frontal syndrome. In France, the caregiving at home has been improved since the possibility for the YOD patients to receive a financial assistance reserved for the disabled patients, but admission to a nursing home before 60 is very difficult and increases the caregiver burden and perception of unfairness. There is a discrimination between young or older demented patients related to the great difficulty to meet the needs of younger patients, due to the rigidity of the medical and social systems. The presentation of a limited offer for the YOD patients must initiate reflections on our capacities to respect the autonomy and the dignity of the Alzheimer's patients regardless of age.

Abstract Mood disorder in dementia of the Alzheimer type (DAT) is heterogeneous in presentation. A typical feature is emotionalism, defined by Allman (1991) as 'a heightened tendency to cry (or rarely laugh) such that crying occurs more frequently, more easily, more vigorously, or in circumstances that previously would have been out of character'. Given the evidence for the involvement of cerebral laterality in the control of emotion, we investigated the relationship between emotionalism and 99m Tc‐HMPAO–SPECT patterns in 14 DAT patients. Right/left frontolateral asymmetry was significantly greater in the eight emotionalism‐positive patients than in the six emotionalism‐negative patients.

Frontotemporal dementia (FTD) is the most neglected dementia by pharmacological research. Nevertheless, FTD can be now diagnosed with a good accuracy. Serotonin deficit is found in FTD and most of FTD are tauopathies. Pharmacological agents such as trazodone have showed a positive effect on behavioral symptoms, but the cognitive symptoms can not be significantly improved and parameters to follow a long-term trial in FTD remain to be identified. The recognition of the differences between FTD and Alzheimer's disease allows to determine a specific management of FTD patients and their caregivers.

RATIONALE IN ALZHEIMER'S DISEASE: Selective serotonine uptake inhibitors (SSRI) have demonstrated their effectiveness for symptomatic treatment of depression, as well as for behavioral and psychological disorders in dementia patients, particularly in Alzheimer's disease.SSRI are particularly well tolerated, particularly in comparison with tricyclic antidepressants. Nausea and vomiting may be a problem in old demented patients. Safety studies have shown that tolerance is not modified in patients with Alzheimer's disease. DRUG INTERACTIONS AND PHARMACOKINETICS: Fluoxetine and paroxetine have an inhibiting effect on metabolism of cholinesterase inhibitors which should be avoided. The compounds have a short half-life and non-active metabolites should be preferred. TRAZODONE: Studies conducted in patients with Alzheimer's disease, mixed type dementia, or fronto-temporal dementia have shown the efficacy of trazodone for diverse types of symptoms: sadness, emotional disorders, irritability, fear, psychomotor instability, delirant ideas. Efficacy of SSRI in patients with Lewy body dementia remains to be confirmed.

Circumscribed atrophy of the frontal and temporal lobes (frontotemporal lobar degeneration) accounts for about one fifth of cases of primary degenerative dementia occurring before the age of 65. It produces three prototypical clinical syndromes. The most common is frontotemporal dementia, characterized by personality change and profound alteration in social conduct and associated with bilateral atrophy of the frontal and anterior temporal lobes. Progressive non-fluent aphasia is characterized by difficulty in verbal expression, anomia and phonemic errors in the presence of relative preservation of comprehension and associated with atrophy predominantly of the left hemisphere. In semantic dementia there is fluent speech with semantic errors and severely impaired comprehension and naming, together with a visual associative agnosia, resulting from bilateral atrophy of the inferior and middle temporal gyri. The clinical syndromes occur with either of two main histological types: prominent microvacuolar change, without specific histological features (frontal lobe degeneration-type), severe astrocytic gliosis with or without ballooned cells and inclusion bodies (Pick-type). To improve clinical recognition and advance understanding of this relatively common form of cerebral degeneration, members of an international workshop on Frontotemporal Lobar Degeneration developed consensus criteria, building upon earlier published clinical diagnostic guidelines for frontotemporal dementia. The consensus criteria reported here specify core and supportive features for each of the prototypical clinical syndromes: frontotemporal dementia, progressive aphasia and semantic dementia, as well as providing broad inclusion and exclusion criteria for the generic entity of frontotemporal lobar degeneration.

Few studies have explored determinants of survival in behavioral-variant frontotemporal dementia (bvFTD). This information is important, as it can inform clinical trials and provide prognostic guidelines for patients and their families. The present study explored survival in a multi-site sample of bvFTD patients with confirmed FTLD pathology. 148 cases from the International bvFTD Criteria Consortium (FTDC) database were included. Cases met Possible bvFTD criteria at presentation and had FTLD pathology at autopsy. Kaplan Meier and Cox hazards analyses were used to determine demographic, behavioral and neurological factors affecting survival. The total sample was male predominant (61 females, 87 males) with a mean age of 57 (10.2) at initial evaluation. Median survival from disease onset was 7 years (95% CI: 6.4-7.7), and median survival was 3 years from initial evaluation (95% CI: 2.4-3.6). Kaplan Meier analyses revealed that presence of motor neuron disease (MND), extrapyramidal symptoms, motor speech deficits and disinhibition were significantly associated with reduced survival from initial evaluation, while tau-positive pathology was associated with longer overall survival. Education, family history of an FTD spectrum disorder, MMSE scores, age at onset and age at initial presentation did not significantly affect survival from initial evaluation. Excluding cases with MND (n = 26; median survival 2 years from initial evaluation), median survival increased to 8 years from disease onset (95% CI: 7.3-8.6), and 4 years from initial evaluation (95% CI: 3.4-4.6). Extrapyramidal symptoms and disinhibition remained significant predictors of decreased survival, with reduced survival in males compared to females. However, motor speech deficits and tau pathology were no longer associated with survival when excluding cases with MND. BvFTD is associated with a poor prognosis. Our findings suggest that presence of MND, extrapyramidal symptoms and disinhibition negatively impact survival in bvFTD.

La dépression du sujet âgé se distingue de celle plus précoce, par les faibles antécédents de dépression, par les fréquents facteurs de risques vasculaires, par le déclin cognitif et par des hypersignaux en imagerie cérébrale. Un sous-type de dépression est défini sous le concept de dépression vasculaire. Nous rapportons le suivi de cinq patients ayant eu une dépression vasculaire, sur une durée moyenne de 6,2 années. L'état dépressif des cinq patients était sévère, avec tentative de suicide pour trois d'entre eux. L'apathie et la résistance relative aux antidépresseurs étaient retrouvées. La prise en charge institutionnelle s'avéra efficace pour deux patients. Trois des cinq patients évoluèrent vers une démence à composante vasculaire, dont deux furent confirmées en anatomopathologie. La présence du déclin cognitif associé à l'épisode dépressif rend nécessaire de préciser dans l'avenir les limites d'avec la démence vasculaire et le trouble cognitif léger. Les originalités de traitements, de suivi et d'évolution, incitent à proposer la réalisation d'une IRM lors d'une dépression à début tardif. Late life depression differs from early life depression by no history of mood disorders, and by presence of vascular risk factors, cognitive decline and hyperintensities on MRI. A sub-type of depression is the vascular depression. We present a 6.2 years follow-up of five vascular depressed patients. The severity of depression was high with suicide attempt in three cases. Apathy and pharmacological resistance were reported. Non pharmacological management was more efficacious. Vascular dementia was the final diagnosis for three patients whose two had neuropathological diagnosis. It would be necessary to ameliorate the delimitation of the definition of vascular depression to distinguish them from mild cognitive impairment and from vascular dementia. The specificity of the treatment and the characteristics of the follow-up are arguments to realize a MRI when a patient has a late life depression.

The concept of vascular depression has recently been reassessed and more clearly delineated. The diagnostic criteria for vascular depression require a major depression associated with evidence of confluent or diffuse vascular lesions in the subcortical regions on MRI. The clinical symptoms are not specific, but they are often associated with mild cognitive decline. Ischemia is probably the main factor for vascular depression, but the relationship between ischemic lesions and clinical symptoms remains not well explained. The apolipoproteine E genotype is not a risk factor for vascular depression, but it is associated with more severe hyperintensities on MRI. A pharmacological resistance has been described in vascular depression, but, in recent studies, clinical improvement has been observed with antidepressants in more than 80% of cases. A neuropsychological follow-up is recommended, because dementia may appear with 25% of patients.

Les démences fronto-temporales (DFT) sont caractérisées cliniquement par un changement progressif des conduites sociales, du comportement et du langage en lien avec une dégénérescence des lobes frontaux et temporaux antérieurs. La présentation clinique est liée à la topographie de la dégénérescence. Au cours des vingt dernières années, des critères opérationnels plus sensibles et spécifiques ont été formalisés. L’important démembrement neuropathologique et génétique, encore inachevé, a mis en évidence les chevauchements entre DFT, sclérose latérale amyotrophique et syndromes parkinsoniens atypiques (paralysie supranucléraire progressive, dégénérescence corticobasale...). Il ouvre la voie d’une meilleure connaissance de la physiopathologie et de nouvelles cibles thérapeutiques spécifiques. Ces démences qui touchent surtout des personnes de moins de 65 ans sont mieux reconnues qu’autrefois mais encore sousdiagnostiquées et confondues initialement avec des pathologies psychiatriques, imposant une meilleure information des professionnels confrontés à ces malades. Les traitements sérotoninergiques apportent une amélioration symptomatique, mais le contrôle de l’environnement, le maintien de la communication, la prévention des troubles de déglutition et le soutien des proches est primordial. Frontotemporal dementias (FTD) are defined by a gradual change in social conduct, behavior and language, associated with frontal and anterior temporal lobe degeneration. The clinical features depend on the location of the degenerative process. In the last 20 years, increasingly specific and sensitive operational criteria have been established. Ongoing neuropathological and genetic studies have highlighted overlaps between FTD, motor neuron disease, and atypical parkinsonian syndromes (supranuclear palsy, corticobasal degeneration). They have also provided a better knowledge of the pathophysiology of FTD, and new specific therapeutic targets. These dementias, which usually occur before the age of 65 years, are now better recognized but are still underdiagnosed and often initially mistaken for psychiatric illnesses. Healthcare professionals managing these patients must therefore be better informed. Serotonergic agents provide a symptomatic improvement, but environmental adaptation, prevention of language and swallowing difficulties, and information and support for the family and caregivers remain essential.

International Journal of Geriatric PsychiatryVolume 9, Issue 7 p. 589-591 Letters To The Editor Letters to the editor John Snowdon, John Snowdon Rozelle Hospital, New South Wales, AustraliaSearch for more papers by this authorFred Lane, Fred Lane Rozelle Hospital, New South Wales, AustraliaSearch for more papers by this authorFlorence Lebert, Florence Lebert Memory Disorders Unit, Department of Neurology, University of Lille, Faculty of Medicine, Lille, FranceSearch for more papers by this authorFlorence Pasquier, Florence Pasquier Memory Disorders Unit, Department of Neurology, University of Lille, Faculty of Medicine, Lille, FranceSearch for more papers by this authorHenri Petit, Henri Petit Memory Disorders Unit, Department of Neurology, University of Lille, Faculty of Medicine, Lille, FranceSearch for more papers by this author John Snowdon, John Snowdon Rozelle Hospital, New South Wales, AustraliaSearch for more papers by this authorFred Lane, Fred Lane Rozelle Hospital, New South Wales, AustraliaSearch for more papers by this authorFlorence Lebert, Florence Lebert Memory Disorders Unit, Department of Neurology, University of Lille, Faculty of Medicine, Lille, FranceSearch for more papers by this authorFlorence Pasquier, Florence Pasquier Memory Disorders Unit, Department of Neurology, University of Lille, Faculty of Medicine, Lille, FranceSearch for more papers by this authorHenri Petit, Henri Petit Memory Disorders Unit, Department of Neurology, University of Lille, Faculty of Medicine, Lille, FranceSearch for more papers by this author First published: July 1994 https://doi.org/10.1002/gps.930090714Citations: 5AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume9, Issue7July 1994Pages 589-591 RelatedInformation

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La demence frontotemporale (DFT) est la demence la plus negligee par la recherche pharmacologique. Pourtant, la DFT peut aujourd‘hui etre correctement identifiee, le deficit serotoninergique predominant est connu et beaucoup des DFT sont integrees aux tauopathies. Parmi les molecules essayees, la trazodone a montre son efficacite sur les troubles du comportement, mais en revanche les troubles cognitifs n‘ont pas pu etre significativement ameliores et il reste a determiner les parametres d‘evaluation pour un essai a long terme. La reconnaissance des differences entre DFT et maladie d‘Alzheimer a permis d‘identifier les caracteristiques de la prise en charge des patients ayant une DFT et celle de leurs proches.

Mémoire et sens forment un ensemble qui donne corps à la subjectivité. Ils composent le registre des stratégies personnelles en organisant les formes de vie, ils permettent d’asseoir la personnalité, validant ou infirmant les choix de la personne par l’école de l’expérience, et ils structurent le lexique des émotions à travers le jeu des rites et des habitus sociaux. Sens et mémoire sont co-déterminés et co-construits au cours de la vie. Le sens étaye la mémoire, et en retour la mémoire facilite l’accès au sens perçu de l’environnement. Les conditions qui favorisent l’émergence du sens, facilitent le travail de mémoire. La dynamique des processus mis en œuvre entre sens et mémoire est ici discutée. Trois aspects seront évoqués, phénoménologique, sémiotique et neuropsychologique, ainsi que les conséquences des troubles cognitifs sur l’interdépendance sens et mémoire. Le modèle intégratif de la mémoire et ses relations avec la mise en signification de l’environnement sont présentés dans cet article.Memory and meaning form an ensemble that gives body to subjectivity. They provide the full range of personal strategies, by organizing forms of life. They establish personality, validating or countering the choices made by individuals on the basis of experience, and they structure the lexicon of emotions through the interplay of different rites and social habits. Meaning and memory are co-determined and co-built throughout life. Meaning supports memory, and in return memory facilitates the access to meaning derived from the environment. The conditions that favor meaning facilitate the work of memory. The dynamics of the processes occurring between meaning and memory are discussed here. Three aspects will be considered, phenomenological, semiotic and neuropsychological, as well as the consequences of cognitive disorders on the interdependence of meaning and memory. The integrative model of memory and its relationship with the meaning given to the environment are presented in this article.

8-Hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), a selective serotonin1A (5-HT1A) receptor agonist, was studied for its anti-immobility activity in the forced swimming test when administered into the raphe nuclei medianus and dorsalis of rats. At concentrations ranging from 0.5 to 5 μg, 8-OH-DPAT siginificantly reduced the immobility of rats when administered into the nucleus raphe dorsalis, but only 5 μg was effective when administered into the nucleus medianus. The activity of rats in an open-field under conditions identical to those used in the forced swimming test was not significantly changed by various concentrations of 8-OH-DPAT administered into the nucleus raphe dorsalis, but was significantly increased by an infusion of 5 μg 8-OH-DPAT into the nucleus raphe medianus. The effect of an infusion of 1 μg 8-OH-DPAT into the nucleus dorsalis was prevented by infusing 2.5 μg (−)-propranolol or 2.5 μg (−)-pindolol into the same area 5 min before 8-OH-DPAT or by treating the animals with sulpiride systematically (100 mg/kg i.p.) or centrally (in the nucleus accumbens; 1 μg/0.5 μl). The results suggest that 8-OH-DPAT reduces the immobility of rats by activating dopamine transmission, probably in the nucleus accumbens, as a consequence of its ability to reduce the activity of 5-HT neurons that originate in the nucleus raphe dorsalis. In view of the similarities between the effects of well-established antidepressants and 8-OH-DPAT in the forced swimming test, it is suggested that 5-HT1A receptor agonists may constitute a novel class of antidepressant agents.

Le concept de centre de la memoire repose sur la pluridisciplinarite des intervenants autour des troubles de la memoire et des demences, dont la plus frequente est la maladie d'Alzheimer. Ces centres ont pour objectifs de diagnostiquer les plaintes mnesiques et les demences, de les traiter et de les suivre, d'informer patients et familles, de former les medecins et les auxiliaires medicaux et de contribuer a la recherche. Les premiers centres, anglo-saxons, datent des annees 1980 et leur experience (majorite de maladie d'Alzheimer, diagnostics tardifs) a favorise l'ouverture d'autres centres a travers le monde. Une enquete aupres de centres francais definit le « centre ideal »: structure identifiee composee d'une consultation et d'un hopital de jour ou l'on trouve des competences neurologiques, neuropsychologiques, psychiatriques et geriatriques. Il s'integre dans un reseau de soin autour de la demence dont le pivot est le medecin generaliste et il travaille en reseau a l'echelon regional et national. Les relations entre affections cognitives et pathologies somatiques, tres frequentes chez les dements, sont encore mal connues. La demence peut retentir sur la semiologie, la conduite therapeutique et le pronostic, et meme etre liee a certaines affections par exemple cardio-vasculaires. Les affections somatiques sont generatrices de decompensations brutales de demence pouvant necessiter une hospitalisation dans l'urgence mais dans une structure adaptee. Les centres de la memoire doivent s'impliquer dans ces enjeux de soin, d'enseignement et de recherche.

Les démences, dont la cause la plus fréquente et la plus connue est la maladie d’Alzheimer (MA), sont considérées comme des pathologies de la personne âgée. Leur incidence et leur prévalence doublent tous les 5 ans dès l’âge adulte. La plupart des études épidémiologiques portent sur les personnes de plus de 65 ans, au delà duquel les courbes s’infléchissent. L’étude PAQUID a permis d’estimer le nombre de patients de plus de 75 ans atteints de MA en France à 850 000 en 2005. Les estimations pour les personnes plus jeunes provenant du groupe EURODEM (combinant plusieurs cohortes européennes) en 1991 donnaient une prévalence de démence à 0,5 % chez les femmes et 1,6 % chez les hommes entre 60 et 64 ans, et à 0,1 % chez les femmes et 0,2 % chez les hommes avant 60 ans [1], soit une estimation de 32 000 personnes de moins de 65 ans présentant une démence (toutes causes confondues) en 2004 en France [2]. L’extrapolation des données du réseau des consultations mémoire du Nord-Pas-de-Calais en 2009, comparable à une étude anglaise [3] donnent une estimation de 20 000 MA ou syndrome apparenté < 65 ans. L’institut national de veille sanitaire a recensé 8293 protocoles ALD15 (MA et affections apparentées) attribués à des personnes < 65 ans en 2009, dont 4145 < 60 ans. La MA reste la cause de démence la plus fréquente (50 %) chez les personnes jeunes (<65 ans selon la définition internationale), mais les dégénérescences lobaires fronto-temporales (DLFT), comprenant la démence fronto-temporale (DFT ou forme comportementale), l’aphasie primaire progressive, et la démence sémantique sont beaucoup plus fréquentes que chez les personnes âgées [4]. Les démences à corps de Lewy sont déroutantes en l’absence de syndrome parkinsonien, s’exprimant par une altération majeure des fonctions exécutives, visuo-spatiales, des troubles psychiatriques (dépression, hallucinations visuelles, idées délirantes, troubles du sommeil paradoxal, cauchemars…), ou des troubles végétatifs (malaises, chutes). Les démences vasculaires sous-corticales sont également trompeuses, lorsqu’elles ne s’accompagnent pas de troubles moteurs ou sensitifs ni d’épisodes vasculaires aigus [5]. Les démences sont trop tardivement identifiées chez les personnes jeunes, en moyenne 5 ans après les premiers symptômes contre 3 ans chez les patients âgés, en raison d’une méconnaissance de la population et des médecins, d’une présentation clinique y compris de la MA souvent atypique (déficit des fonctions instrumentales ou exécutives au premier plan, relative préservation de la mémoire épisodique, bonne conscience des troubles, atrophies focales progressives, sans atteinte majeure de la région hippocampique, parfois troubles moteurs associés), des diagnostics différentiels nombreux [6]. Les démences sont souvent considérées initialement comme d’origine psychiatrique (dépression, anxiété, accès maniaque, conversion…) d’autant qu’un syndrome frontal (apathie, désinhibition, agressivité, manque de tact, de jugement, de convenances sociales, troubles du comportement alimentaire…) est fréquent chez les personnes jeunes, quelle que soit la pathologie, avec des troubles de la cognition sociale rendant difficiles les relations au travail, la vie à domicile et l’acceptation dans les structures d’hébergement collectif. Les dégénérescences focales s’expriment par des troubles instrumentaux (langage, troubles neuro-visuels), égarant vers des pathologies vasculaires, ophtalmologiques ou psychiatriques. Le diagnostic étiologique des démences peut désormais être établi avec une grande fiabilité dès les stades précoces [7] grâce à l’évaluation neuropsychologique, l’imagerie structurale (IRM) et métabolique (TEP au FDG et aux traceurs de l’amyloïde, scintigraphie au DatSCAN,), les biomarqueurs du liquide céphalo-spinal (protéines Tau, phospho-Tau, b-amyloïde) et la génétique [8]. Le déclin cognitif est plus rapide, mais la survie est souvent plus longue chez les patients jeunes que les plus âgées. Une histoire familiale est plus fréquente, jusqu’à 40 % dans les DLFT dont la moitié de formes génétiques, et 10 % de forme génétique dans la MA soit 5 fois plus que chez les personnes âgées. Les découvertes génétiques récentes amènent à proposer des essais cliniques et thérapeutiques qui peuvent être très contraignants aux stades pré-symptomatiques ou prodromaux de la maladie d’Alzheimer tel que l’étude DIAN-TU [9] ou de certains sous-types de DLFT (tauopathies, mutation PGRN…). Le retentissement professionnel, familial, social, financier, juridique voire médico-légal est majeur, d’autant que le diagnostic a été tardif [10]. On déplore encore une méconnaissance de ces pathologies et de son impact, et parfois une inadéquation de la réponse médico-sociale ou professionnelle aux difficultés rencontrées. Le plan Alzheimer 2008-2012 a consacré 2 mesures aux patients jeunes : création d’un Centre National de Référence pour les Malades Alzheimer ou apparentés Jeunes (CNR-MAJ) et recensement des besoins en hébergement des malades jeunes, confiée au CNR-MAJ [11].

The investigation of job insecurity has been a growing field of research. However, little is known about the strategies employees adopt to reduce job insecurity. Former research has shown that employees who perceive high job insecurity tend to engage in voluntary turnover. Yet, we do not know whether such a strategy is successful in reducing perceived job insecurity. Based on the Swiss Household Panel (SHP), a general population survey in Switzerland, a propensity score matching procedure is applied to investigate whether voluntary turnover successfully reduces feelings of job insecurity for employees who previously perceived an above-average level of job insecurity. Assuming that individual and family conditions are important factors explaining the success of this strategy it is distinguished between men and women with high, equally shared, or low financial responsibilities and of different age and educational groups. The results show that voluntary turnover indeed reduces perceived job insecurity. Whereas the individual factors do not moderate this relationship, the level of financial responsibilities does: employees who equally share financial responsibilities with their partners are most successful in reducing perceived job insecurity through voluntary turnover. The use of a propensity score matching procedure has proven fruitful as the bias caused by differing pre-turnover characteristics can be reduced considerably.

In this paper, we study attrition in a household panel survey, where in the first wave those with a matched landline number were surveyed by telephone, while those without received a face-to-face visit. In the second wave, the face-to-face mode was dropped. We find among the first wave face-to-face households a high likelihood to attrite due to “no contact” rather than due to “cannot be tracked” or “refusal”. Socio-demographic characteristics have the expected effects. For example households with young children, with a short-term residence permit, or one-person households cannot be tracked, while those with a face-to-face visit in the first wave, or foreigners with a mother tongue that is not offered in the survey refuse more often. More first wave calls and contacts are associated with all reasons to attrite, in particular with refusal. Based on the findings, we give recommendations to tailor fieldwork to decrease attrition.

Frontotemporal lobar degeneration (FTLD) includes the behavioral variant of frontotemporal lobar degeneration (bvFTD), also called frontotemporal dementia (FTD), and two language variants, namely, semantic dementia (SD) and primary progressive agrammatic aphasia (PPA). There is a large degree of overlap between the three FTLD variants, as well as between FTLD and motor neurone disease or parkinsonism. Neuropsychiatric features, the earliest and prominent manifestations of bvFTD, are also commonly encountered in the language variants. FTLD is a pathologically heterogeneous entity, divided into several subtypes characterized by protein aggregates of different nature and distribution. The discovery of mutations on different genes made the classification of FTLD even more complex because of weak genotype-phenotype correlations, even within the same family. And a same phenotype can be caused by different mutations. Since neuropsychiatric symptoms are inaugural, bvFTD is often misdiagnosed as psychiatric conditions such as depression, bipolar disorder, obsessive-compulsive disorder, or schizophreniform psychosis, although atypical features are usually present. The main behavioral symptoms are early behavioral disinhibition; apathy or inertia; loss of sympathy or empathy; perseverative, stereotyped, or ritualistic behavior; and hyperorality and dietary changes. Psychosis is less frequent, except in some familial cases, raising the possibility of a link between FTD, schizophrenia, and bipolar disorders. There is, as yet, no specific pathophysiological treatment for FTLD. As for symptomatic treatments, few randomized placebo-controlled studies have been performed. However, serotonergic agents are recommended to treat FTD behavioral disorders.

<b><i>Background:</i></b> The diagnosis of behavioral variant of frontotemporal dementia (bvFTD) relies primarily on clinical features and remains challenging. The specificity of the recently revised criteria can be disappointing, justifying development of new clinical tools. <b><i>Objective:</i></b> We produced a behavioral inventory named DAPHNE. This scale (adapted from Rascovsky's criteria) explores six domains: disinhibition, apathy, perseverations, hyperorality, personal neglect and loss of empathy. It is composed of ten items (five answer categories). The aim was (1) to assess the validity and reliability of DAPHNE and (2) to evaluate its contribution in differentiating patients. <b><i>Methods:</i></b> Two scores were computed: DAPHNE-6 (screening) from the six domains and DAPHNE-40 (diagnosis) from the ten items. Reliability and reproducibility were assessed. External validity was studied with the Frontal Behavioral Inventory (FBI) and the Frontotemporal Behavioral Scale (FBS). Finally, the diagnostic performance of DAPHNE was compared to revised criteria, FBI and FBS. <b><i>Results:</i></b> DAPHNE was administered to the caregivers of 89 patients, 36 with bvFTD, 22 with Alzheimer's disease, 15 with progressive supranuclear palsy and 16 with bipolar disorder. Reliability and reproducibility were excellent, as was external validity. DAPHNE-6 allowed bvFTD diagnosis (score ≥4) with a sensitivity of 92%, while DAPHNE-40 (score ≥15) had a specificity of 92%. <b><i>Conclusion:</i></b> We demonstrate excellent psychometric features for DAPHNE. This quick tool could help for both diagnosing and screening bvFTD.

Classification of Frontotemporal dementia (FTLD) is currently based depending on the composition of protein aggregates and types of neuropathological lesions made of Tau proteins, TDP-43 or FUS/TLS. These proteins in the inclusions undergo modifications such as phosphorylation and truncation. We already demonstrated that biochemical analysis can be performed to increment this classification, by using different antibodies directed against modified or non-modified proteins such as Tau, TDP-43 and phospho-TDP-43. We also found that some cases presenting with TDP-43 pathology display a partial or total loss of Tau protein expression and can be referred as to “Tau less” FTLD in the classification. The goal of this study is to increment the classification by biochemical analysis and understand the mechanisms leading to this loss of Tau expression and the link to TDP-43. FTLD brains (n=18) were obtained from the Lille Neurobank, or from Rouen hospital. Neuropathology has been performed prior to biochemistry. Molecular components found in the cerebral lesions were analysed by Western-Blotting and different antibodies either directed against modified or non-modified proteins such as Tau, TDP-43 and phospho-TDP-43. Human Tau mRNA was analysed by QPCR. N1E115 cells stably expressing human Tau or not were used for overexpressing wild-type TDP-43 or mutated TDP in the nuclear export signal or in the RNA binding domain. Finally, 2D-DIGE was performed on frontal and occipital area from control and FTLD brains. We first looked at the translational level in order to explain this loss in protein expression, but no significant change in Tau mRNA could be found. The mechanisms leading to this loss may result from a dysfunction in post-transcriptional and/or -translational regulation of Tau. This will be achieved by invalidating or overexpressing TDP-43 in cellular models expressing or not Tau. Finally, 2D-DIGE analysis will help us identify proteins that could be modified during neurodegeneration. In conclusion, among FTLD-TDP, a systematic analysis of tau protein expression should be performed and associated with a sub-class of FTLD already known as “Tau less” FTLD. Finally, this study should help us to understand better the link between Tau and TDP-43.

La psychoéducation peut être définie comme une intervention didactique et psychothérapeutique systématique qui vise à informer les patients et leurs proches sur le trouble psychiatrique et à promouvoir les capacités pour y faire face. Ce n’est pas seulement une transmission d’information, mais aussi une méthode pédagogique adaptée aux troubles ayant pour but une clarification de l’identité, une appropriation du pouvoir et une modification des attitudes et des comportements. L’introduction de l’éducation dans le traitement des troubles mentaux est à l’origine du « traitement moral ». Le terme de psychoéducation naît initialement dans la littérature scientifique de la préoccupation de surmonter les difficultés d’apprentissage des enfants souffrant de problèmes de santé mentale. Cette origine est commune au terme d’éducation thérapeutique, appliqué ensuite principalement pour les problèmes de santé somatique. Le terme de psychoéducation a ensuite été utilisé dès les années 1980 pour qualifier la transmission d’un savoir sur les troubles psychiatriques à des fins thérapeutiques, d’abord aux proches, puis aux personnes souffrant de schizophrénie. Depuis la fin des années 1990, l’utilisation de la psychoéducation a ensuite été étendue à d’autres troubles psychiques comme les troubles alimentaires, les troubles bipolaires, les attaques de panique et l’agoraphobie ou le stress post-traumatique. L’efficacité thérapeutique de la psychoéducation familiale pour réduire le risque de rechute et de réadmission dans la schizophrénie constitue une révolution des thérapies familiales dans les années 1980. De manière polémique, la psychoéducation a été critiquée comme un exercice du pouvoir du médecin et de l’industrie pharmaceutique pour imposer une conception de la maladie mentale. Toutefois, dès la fin des années 1990, les patients et les proches se sont appropriés la psychoéducation comme une source de pouvoir, de savoir et de connexions sociales. En conclusion, la psychoéducation est une méthode thérapeutique qui a démontré son efficacité de manière scientifique, associée à d’autres méthodes de traitement, notamment médicamenteux ou de réhabilitation psychosociale. Dans une perspective médicale moderne, elle précède et complète en psychiatrie les notions de « consentement éclairé », de « décision partagée » ou de « littératie en santé mentale ». Les limitations sont liées aux risques de transmettre des informations obsolètes, non orientées vers le rétablissement ou inappropriées aux besoins, d’imposer un discours médical non intégré, ou de viser une rééducation plutôt qu’une appropriation du pouvoir par la personne. De plus, des programmes spécifiques indépendants du diagnostic devraient être développés pour les phases précoces des troubles psychiatriques.Psychoeducation can be defined as a systematic didactic and psychotherapeutic intervention which aims to inform patients and relatives on a psychiatric disorder and to enable their ability to cope with the illness. This is not only a transmission of information, but also a teaching method adjusted to the disorder with the objectives to clarify identity, to promote empowerment and to change attitudes and behavior. The introduction of the education in the treatment of mental disorders is at the origin of the “moral treatment”. The term of psychoeducation was born originally in the scientific literature to overcome problems in formal learning among children with mental health problems. This origin is common with the term of therapeutic education, which has been then applied mainly to somatic health problems. The term psychoeducation was then used from 1980s to describe the transmission of knowledge on psychiatric disorders for therapeutic purposes, first to relatives, then to people suffering from schizophrenia. Since the end of the 1990s, the use of psychoeducation was then extended to other psychological disorders such as eating disorders, bipolar disorder, panic attacks and agoraphobia or posttraumatic stress disorders. Therapeutic efficacy of family psychoeducation to reduce the risk of relapse and readmission in schizophrenia was a revolution in family therapy during the 1980s. In a polemical way, psychoeducation was criticized as a way to impose a conception of mental illness by medical doctors and pharmaceutical industry. However, by the end of the 1990s, psychoeducation became clearly a source of power, knowledge and social connections for patients and relatives. In conclusion, psychoeducation has an evidence-based efficacy to prevent relapse and hospitalisation when associated with other treatments, including medication or psychosocial rehabilitation. In a modern medical perspective, it precedes and supplements in psychiatry the notions of “informed consent”, “shared decision-making” or “mental health literacy”. In the limitations, psychoeducation remains not enough systemically used, some programs are not recovery compatible. Moreover, specific programs independent from diagnosis for the early phases of psychiatric disorders should be developed.

Early behavioral disinhibition, apathy, loss of empathy, perseverative behavior and dietary changes are core features of the behavioral variant of frontotemporal lobar degeneration (bvFTD). Recent reports have highlighted atypical cases characterized by a long lasting, very slowly or non progressive presentation of bvFTD but neuropathological data are usually unavailable. We report three cases with a pathologically proven diagnosis of pure vascular dementia who presented with severe behavioral core features of bvFTD. These cases were investigated in the Lille University Hospital memory clinic and neuropathology department. The first one developed from the age of 59 a long lasting bvFTD and finally died 17 years after onset. Dominant behavioral features were apathy, inertia, emotional blunting, dietary changes and self neglect. The two others, aged 52 and 60 at onset, rapidly developed severe behavioral troubles with disinhibition and compulsive behavior at foreground. They died 3 and 5 years later respectively. Although patients had various combinations of vascular risk factors their brain MRI only showed mild vascular modifications. There was neither significant frontotemporal atrophy nor hypometabolism. Pathological examination showed isolated chronic ischemic changes: severe arteriolosclerosis, perivascular spaces dilatations and microinfarcts in the frontal white matter and basal ganglia, and moderate myelin loss. These three cases illustrate that isolated subcortical microvascular pathology may underlie atypical presentation of bvFTD including the long lasting, slowly progressive variant. These observations also support the revised diagnosis criteria for bvFTD (international bvFTD criteria consortium, 2010) which require both functional decline and imaging results consistent with bvFTD to meet criteria for a probable diagnosis.

Frontotemporal dementia (FTD) is the second most common form of dementia in persons younger than 65 years after Alzheimer’s disease. The FTD spectrum is characterized by clinical, molecular and genetic heterogeneity. Core features of FTD are behavioural and language manifestations and the clinical spectrum of FTD currently includes a behavioural variant, progressive nonfluent aphasia and semantic dementia. The most common behavioural features are disinhibition, apathy, loss of empathy, hyperorality and perseveration. Neuroimaging usually demonstrates focal atrophy and hypometabolism in the anterior part of the frontal and temporal lobes. A careful history and neuropsychological examination, and judicious use of neuroimaging, can help distinguish FTD from other common forms of dementia, especially Alzheimer’s disease, vascular dementia, and dementia with Lewy bodies. Although no specific pharmacological treatments for FTD exists, symptom management with serotonin reuptake inhibitors and non pharmacological interventions have been shown to be beneficial.

OBJECTIVE: To determine whether clinical features predict tau pathology in behavioral variant frontotemporal dementia (bvFTD). BACKGROUND: Although characterized by behavior changes and frontotemporal atrophy, bvFTD is pathologically heterogeneous. With the development of tau agents for the treatment of FTD, it is increasingly important to establish underlying tau pathology during life. Therefore, we attempted to identify early clinical predictors of tau pathology in a multi-site sample of autopsy-confirmed bvFTD patients. DESIGN/METHODS: 146 cases from the International bvFTD Criteria Consortium (FTDC) database were included. Cases met Possible bvFTD criteria at presentation and had FTLD pathology at autopsy. Chi-squared analyses compared early behavioral and cognitive features in tau positive (tau+) and tau negative (non-tau) cases. RESULTS: 56 cases (38%) were classified as tau+ and 90 (62%) as non-tau. A higher proportion of non-tau cases presented with a neuropsychological profile consistent with bvFTD (i.e., executive/generation deficits with relative sparing of memory and visuospatial functions: tau+=69%, non-tau=84%, X2=4.1, p CONCLUSIONS: Our findings suggest that prediction of tau pathology in bvFTD may be difficult based on demographic, clinical or behavioral features alone. Accurate prediction of tau pathology in bvFTD may ultimately depend on more detailed cognitive/behavioral testing coupled with imaging and biofluid biomarkers. Supported by: AG17586, NS44266, P50-AG016574, P01-AG019724, P50-AG023501, CA DHS 07-65807. Disclosure: Dr. Rascovsky has nothing to disclose. Dr. Hodges has nothing to disclose. Dr. Knopman has received personal compensation for activities with Eli Lilly & Company. Dr. Knopman has received personal compensation in an editorial capacity for Neurology. Dr. Knopman has received research support from TauRx. Dr. Mendez has received personal compensation in an editorial capacity for UpToDate. Dr. Kramer has nothing to disclose. Dr. Neuhaus has nothing to disclose. Dr. Van Swieten has nothing to disclose. Dr. Seelaar has nothing to disclose. Dr. Dopper has nothing to disclose. Dr. Onyike has received research support from Forest Laboratories, Inc. Dr. Hillis has received personal compensation in an editorial capacity for Behavioural Neurology. Dr. Hillis has received research support from Allon Pharmaceutical. Dr. Josephs has nothing to disclose. Dr. Boeve has received research support from Cephalon, Inc.; Allon Therapeutics; and GE Healthcare. Dr. Kertesz has received personal compensation for activities with Pfizer and Janssen as a consultant. Dr. Kertsz has received research support from Sanofi and Janssen. Dr. Seeley has received personal compensation for activities with Korea Novartis, Summer Street Research Partners and Bristol-Myers Squibb for speaker, consulting and scientific advisory boards. Dr. Rankin has nothing to disclose. Dr. Johnson has nothing to disclose. Dr. Gorno Tempini has nothing to disclose. Dr. Rosen has nothing to disclose. Dr. Latham has nothing to disclose. Dr. Lee has nothing to disclose. Dr. Kipps has nothing to disclose. Dr. Lillo has nothing to disclose. Dr. Piguet has nothing to disclose. Dr. Rohrer has nothing to disclose. Dr. Rossor has nothing to disclose. Dr. Warren has nothing to disclose. Dr. Fox has received personal compensation in an editorial capacity for Alxforum. Dr. Fox has received license fee payments from IXICO. Dr. Fox has received research support from Elan/Janssen Alzheimer Immunotherapy, Lundbeck Research USA, Inc., and Pfizer/Wyeth Pharmaceuticals. Dr. Galasko has received personal compensation for activities with United BioSource Corporation, Pfizer, Janssen, Elan Pharmaceuticals, Lundbeck, and Balance Pharma as a consultant. Dr. Galasko has received personal compensation in an editorial capacity for Alzheimer9s Disease Research and Treatment. Dr. Galasko has received research support from Pfizer and Eli Lilly, Inc. Dr. Salmon has received personal compensation for activities with Bristol Myer Squibb as consultant. Dr. Black has recieved personal compensation for activities with Novartis Pharmaceuticals, Pfizer, GlaxoSmithKline, Roche Pharmaceuticals, and Bristol-Myers Squibb, and Elan. Dr. Black has received research support from Novartis Pharmaceuticals, Pfizer, Roche, and GlaxoSmithKline. Dr. Mesulam has nothing to disclose. Dr. Weintraub has nothing to disclose. Dr. Dickerson has received personal compensation for activities with Pfizer Inc and En Vivo as a consultant. Dr. Diehl has nothing to disclose. Dr. Pasquier has nothing to disclose. Dr. Deramecourt has nothing to disclose. Dr. Lebert has nothing to disclose. Dr. Pijnenburg has nothing to disclose. Dr. Chow has received personal compensation for activities with Bristol-Myers Squibb Company as a consultant. Dr. Manes has nothing to disclose. Dr. Grafman has nothing to disclose. Dr. Cappa has received personal compensation in an editorial capacity for Behavioral Neurology. Dr. Freedman has been listed on a provisional patent related to methods and kits for differential diagnosis of Alzheimer9s disease vs frontotemporal dementia using blood biomarkers. Dr. Freedman has received research support from Lundbeck, Canada. Dr. Miller has received personal compensation for activities with Allon Therapeuctics, Inc. and TauRx Therapeutics, Ltd. Dr. Miller has received research support from Novartis. Dr. Grossman has nothing to disclose.

■ La maladie d'Alzheimer (MA) peut toucher des personnes de moins de 60 ans, dites jeunes. ■ En France, 8000 personnes sont ainsi aujourd'hui concernees ■ Leur maintien a domicile est parfois impossible et le Plan Alzheimer 2008-2012 a choisi de consacrer une mesure a la reflexion en matiere de besoins en etablissements medico-sociaux ■ Depuis dix ans, un etablissement d'hebergement pour personnes âgees dependantes (Ehpad) du Nord de la France accueille regulierement des residents jeunes presentant une MA et rapporte, via une etude, leurs caracteristiques et leurs besoins.

Alzheimer's disease can affect people under the age of 60, considered as young patients. In France, the disease affects 8 000 such people today. Caring for them at home is sometimes impossible and the 2008-2012 Alzheimer plan comprises a measure to reflect on requirements with regard to medico-social establishments. For the last ten years, a residential home for dependent elderly people in the north of France has regularly taken in young residents with Alzheimer's disease and reports, via a study, on their characteristics and their needs.