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Peripheral errors in writing, that is errors produced download the spelling, have been occasionally described in primary progressive aphasia (PPA), but the possibility that these errors might be a marker of parkinsonism associated to some subtypes of PPA has not been explored. We investigated whether errors of peripheral nature characterize the writing disorder in PPA when associated with parkinsonian signs (PSs). Subgroups of PPA without PSs and with PSs were studied. The proportion of the central and peripheral errors in writing words and pseudowords was calculated in each group. In writing words, central errors significantly exceeded peripheral errors in subgroups without PSs. The higher the number of peripheral errors, the higher the probability of presenting PSs. No relation emerged between any error and the Unified Parkinson's Disease Rating Scale, but both types of errors correlated with measures of cognitive ability. Peripheral errors emerge when PSs are associated with PPA and may be linked to a decay of the cognitive control on movement, possibly involving the right hemisphere. Peripheral errors have clinical relevance in PPA, to the extent that they may assume the significance of a marker of specific subtypes and can help to outline the specific clinical picture of individual patients.

We explored the association between cognitive reserve (CR) and Parkinson' s disease (PD) related cognitive deterioration.Forty PD patients and 12 matchedhealthy controls (HC) were enrolled. The PD group was balanced for the presence/absence of cognitive impairment All participants underwent MOCA. CR was measured by the Brief Intelligence Test, and a new comprehensive tool, named Cognitive Reserve Test (CoRe-T), including sections on leisure activities and creativity.Participants with higher CR obtained a better MOCA score irrespective of the group they belonged to. At the same time, irrespective of the CR level, the performance of the HC group was always better in comparison to the PD group. Within the PD group, a higher frequency of leisure activities was associated to be cognitively unimpaired, independently by the severity of motor symptoms and age .CR could help to cope with PD-related cognitive decline. Its multidimensional nature could have important applications in prevention and rehabilitation interventions.

Based on the available literature, women living with HIV (WLWH) seem to show greater cognitive and emotional disadvantages than men living with HIV (MLWH). Our aim was to compare the cognitive performance of MLWH and WLWH in an Italian cohort of People Living With HIV (PLWH) and to analyse factors potentially contributing to sex differences in cognitive function. We ran a retrospective, cross-sectional analysis of a monocentric dataset of PLWH who were administered a standardized neuropsychological test battery (SNB) during routine clinical care. We enrolled 161 Italian PLWH who are on combined antiretroviral therapy (cART): 114 (70.8%) MLWH and 47 (29.2%) WLWH. Global cognitive performance (composite z score) (GCP) was significantly higher in MLWH than WLWH [mean 0.19 (SD 0.85) vs − 0.13 (SD 0.96); p = 0.039]. Moreover, WLWH obtained significantly higher scores on the Zung Depression Scale than MLWH [mean 41.8 (SD 10.9) vs 36.7 (SD 9.2); p = 0.003]. However, there was no statistically significant direct effect between male sex and better GCP (p = 0.692) in the context of a mediation model. On the contrary, the associations between male sex and better GCP were mediated by higher level of education (a*b = + 0.15, Bootstrap CI95 = 0.05 and 0.27) and a lower Zung depression score (a*b = + 0.10, Bootstrap CI95 = 0.02 and 0.21). In conclusion, the global cognitive performance of WLWH is lower than that of MLWH. However, other demographic and clinical factors besides sex might help explain differences in their neurocognitive functions and make it possible for us to monitor them and identify those patients most in need.

Objective: We explored the relationship between a visual scanning strategy and a facial emotion recognition deficit in Parkinson's disease (PD). Method: Thirty nondemented PD patients (balanced for symptom side at onset) and 20 age, education and gender-matched healthy controls (HC) were enrolled. The PD group underwent a comprehensive neuropsychological battery also exploring the executive functions. In both groups, eye movements were recorded while subjects categorized facial emotion from Ekman's 60-faces test. We were particularly interested in the location of fixations on facial pictures (top vs. bottom) and in emotional valence (positive vs. negative). We also compared performance of the two groups on a verbal emotion attribution task. Results: Compared to HC, PD patients performed worse on visual recognition of negative emotions such as anger, fear, and sadness (where the upper part of the face is more informative than the lower part); the two groups did not differ on the verbal emotion attribution task. HC modified their visual scanning strategy (both number and overall time duration of fixations) according to the valence of the emotion; by contrast, PD showed the same pattern regardless of the valence. In the PD group, accuracy in the visual recognition of negative emotions and fixation pattern correlated with performance on tasks exploring executive functions; however, no associations were observed with severity of motor state. Conclusions: Our results suggest that visual scanning strategy contributes significantly to the facial emotion recognition deficit of PD patients, especially at a "high level" related to cognitive control of eye movements.

The care engagement of people living with HIV (PLWH) measured with the patient health engagement (PHE) model and its association with HIV-related internalized stigma are not well established. Indeed, currently there are no data yet about the engagement of PLWH measured with the PHE model. This study aimed to evaluate the effects of HIV-related internalized stigma on care engagement and mental health and to fill the lack of data on PHE model applied to PLWH. We found that the internalized stigma score was significantly higher for PLWH (n=82) in worse care engagement phase and both higher internalized stigma scores and worse engagement were associated to major depression symptoms.In conclusion, our findings describe for the first time the engagement in care of PLWH measured with PHE and highlight the importance of PLWH support to find strategies to cope stigma-related stress and optimize their care engagement.

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Objectives: Cognitive screening is not widely used in acute stroke patients, and usually is based on tests developed for dementia. Our aim was to explore the feasibility of a new tool designed for stroke survivors, as the Oxford Cognitive Screen (OCS). Materials: 3–10 days after stroke, patients underwent the OCS, providing a five domain-specific cognitive profile: attention and executive function, language, memory, number processing and praxis. Pre-morbid functional and cognitive status was evaluated by caregiver interview. The National Institute of Health and Stroke Scale (NIHSS) estimated the stroke severity. Method: This cross-sectional study consecutively enrolled stroke patients (both ischemic and hemorrhagic). Exclusion criteria: Pre-morbid cognitive decay, difficulties with the Italian language, visual impairment or other preexisting conditions affecting cognitive status. OCS was considered non-applicable when patients failed the preliminary subtest. Ischemic brain lesions were classified according to the Bamford criteria: Total Anterior Circulation Stroke (TACS), Partial Anterior Circulation Stroke (PACS), Posterior Circulation Syndrome (POCS), Lacunar Syndrome (LACS). Results: Between October and December 2019, 45 out of 62 patients admitted to the Stroke Unit of Poliambulanza Foundation of Brescia were enrolled. Eight patients were non-eligible, 2 died, and 7 did not fit the time window inclusion criteria. Characteristics of the sample were: 43 (95.6%) Italian born, 33 (73.3%) male, 37 (82.2%) with ischemic stroke, mean age (years) 68.00 (DS 15.45), mean initial NIHSS score 7.02 (DS 7.67). Overall, 25 (55.6%) patients had a left sided brain lesion, 13/37 (35%) were affected by TACS, 19 (42.2%) were discharged at home without any cognitive follow-up indications, and 9 (20%) were transferred to neurologic rehabilitation. OCS was applicable in 37/45 (82.2%) patients. Twenty-eight (75.7%) patients showed at least one impaired cognitive domain. At multivariate

Aims: The prognosis and the clinical manifestations of HIV infection have changed with the introduction of the potent combination antiretroviral therapy (cART); however, up to 50% of patients meet research criteria for "HIV-associated neurocognitive disorders" (HAND) according with current nosology. The majority of patients affected by HAND, especially in cohorts with suppressed plasma viremia, showed an Asymptomatic Neurocognitive Impairment (ANI), without any functional impairment. After more than 10 years from the introduction of the current so-called "Frascati criteria", this mini-review aimed to address the emerging limitations in current diagnosis procedures. Methods: We discussed the most relevant literature on HAND prevalence, etiology, and diagnosis. Results: We addressed three main emerging issues: (1) the unclear clinical relevance of ANI entity; (2) the evidences that Frascati criteria could produce a significant overestimation of HAND; (3) the need to better identify patients with a higher risk to develop HAND requiring routine neuropsychological examinations. Conclusions: Frascati criteria should be updated to better respond to the present characteristics of HIV + cohorts and to help clinicians in their cognitive and global management.

Both cognitive diseases and alexithymia may be associated with HIV. Moreover, alexithymia has been linked to cardiovascular (CV) diseases. Our aim was to explore the prevalence of alexithymia and its associations with neurocognitive disorders (HAND) and CV risk factors in a well-controlled HIV-positive population. We consecutively enrolled 140 HIV-positive individuals on antiretroviral therapy and 35 healthy subjects matched for age, education and gender. In all participants alexithymia was explored by the 20-item Toronto Alexithymia Scale. For HIV-positive subjects also data about CV risk factors were collected, and a comprehensive neuropsychological examination was administered; HAND was defined according to Frascati criteria. Patients and controls did not differ in the proportion of alexithymic status (10% vs. 11%; p=0.761). Among HIV-positive patients, alexithymic participants presented a higher prevalence of diabetes (21% vs. 3%, p=0.035) and hypertension (36% vs. 13%, p= 0.037) compared to non-alexithymic. About 30% (n=41) of HIV-positive patients met criteria for asymptomatic HAND. Alexithymia was not independently associated with a higher risk of HAND (p=0.189). Analyzing each cognitive domain, alexithymia showed an independent association with an abnormal performance (OR 1.08; p=0.037) only in psychomotor speed. In conclusion, in the context of a well-controlled HIV infection, we found a low prevalence of alexithymia comparable to healthy controls. Alexithymia was linked to higher risk of CV disease in the HIV-positive population, but with a rate similar to that previously estimated in the HIV-negative alexithymic. Finally, alexithymia was clearly associated to cognitive impairment only in the psychomotor speed domain, suggesting a common fronto-striatal system dysregulation.

Purpose: Our aim was to better explore the association between liver fibrosis (LF) and neurocognitive impairment (NCI) in people living with HIV (PLWH). Methods: We performed a cross-sectional cohort study by consecutively enrolling PLWH at two clinical centers. All subjects underwent a comprehensive neuropsychological battery; NCI was defined as having a pathological performance (1.5 SD below the normative mean) on at least two cognitive domains. LF was explored using FIB4 index; in a subgroup of PLWH, LF was also assessed by transient elastography. Results: A total of 386 subjects were enrolled, of whom 17 (4.4%) had FIB4 > 3.25. In the subgroup of PLWH (N = 127) performing also liver transient elastography, 14 (11%) had liver stiffness > 14 kPa. Overall, 47 subjects (12%) were diagnosed with NCI. At multivariate regression analyses, participants with FIB4 > 1.45 showed a higher risk of NCI in comparison with those with lower values (aOR 3.04, p = 0.044), after adjusting for education (aOR 0.71, p < 0.001), past AIDS-defining events (aOR 2.91, p = 0.014), CD4 cell count, past injecting drug use (IDU), HIV-RNA < 50 copies/mL, and HCV co-infection. Also a liver stiffness > 14 kPa showed an independent association with a higher risk of NCI (aOR 10.13, p = 0.041). Analyzing any single cognitive domain, a higher risk of abnormal psychomotor speed was associated with a liver stiffness > 14 kPa (aOR 223.17, p = 0.019) after adjusting for education (aOR 0.57, p = 0.018), HIV-RNA < 50 copies/mL (aOR 0.01, p = 0.007), age, past IDU, and HCV co-infection. Conclusions: In PLWH, increased LF, estimated through non-invasive methods, was associated to a higher risk of NCI independently from HCV status.

We explored the association between cognitive reserve (CR) and Parkinson' s disease (PD) related cognitive deterioration. Forty PD patients and 12 matchedhealthy controls (HC) were enrolled. The PD group was balanced for the presence/absence of cognitive impairment All participants underwent MOCA. CR was measured by the Brief Intelligence Test, and a new comprehensive tool, named Cognitive Reserve Test (CoRe-T), including sections on leisure activities and creativity. Participants with higher CR obtained a better MOCA score irrespective of the group they belonged to. At the same time, irrespective of the CR level, the performance of the HC group was always better in comparison to the PD group. Within the PD group, a higher frequency of leisure activities was associated to be cognitively unimpaired, independently by the severity of motor symptoms and age. CR could help to cope with PD-related cognitive decline. Its multidimensional nature could have important applications in prevention and rehabilitation interventions.

The aim of this study was to explore the psychological impact of the initial stage of the 2019 coronavirus (CO-VID-19) pandemic on people living with HIV (PLWH), a population at increased risk of psychological distress. PLWH participated in an online survey exploring demographic and clinical data, physical symptoms, con-tact history, knowledge and concerns, precautionary measures and additional information about COVID-19 during the first phase of the pandemic in Italy. The Impact of Event Scale-Revised (IES-R) (identifying the COVID-19 pandemic as a specific traumatic life event) and the Depression, Anxiety and Stress Scale (DASS-21) also formed part of the survey. Out of 98 participants, 45% revealed from mild to severe psychological impact from COVID-19 according to IES-R. A lower percentage, instead, complained of significant levels of depression (14%), anxiety (11%) or stress (6%) according to DASS-21. Higher education, being unemployed, number of perceived COVID-19 physical symptoms, concerns about risk of contracting COVID-19 and the pandemic situation in Italy, and needing additional information to prevent COVID-19 infection were positively associated to a higher risk of negative psychological impact. More-over, among the participants, female gender, age, fewer years from HIV diagnosis and not being aware of their own viremia were associated to a higher risk of negative psychological outcomes. Almost half of our PLWH sample experienced significant levels of distress related to the COVID-19 pandemic. Women, elderly patients and those with recent HIV diagnosis appear to be the more psychologically fragile subgroups. Our findings could help identify patients most in need of psychological interventions to improve the wellbeing of PLWH.

Objectives: Vascular and degenerative damage are so different brain pathologies that the impact on cognition cannot be expected to be the same. The present study aims to identify possible markers able to distinguish vascular and neurodegenerative aphasias. Materials: 18 logopenic variant/mixed primary progressive aphasias (lv-mPPA) and 11 fluent post-stroke aphasics (psA) of comparable severity, and 12 matched healthy controls (HC) were enrolled. All participants underwent a comprehensive neuropsychological battery, and the examination of macro and microlinguistic aspects of language. Methods: A Principal Component Analysis (PCA) was performed (after z-transformation of the scores) to identify factors explaining the overall performance on patient groups only; factor scores were entered into a cluster analysis by fixing 2-groups solution in order to verify if lv-mPPA and psA were assigned to different clusters. Results: The PCA extracted two factors, “global cognition/lexical semantic factor” and “morphosyntactic factor”, accounting for 42.9% of variability, and two factors loading macrolinguistic variables (accounting for 22.7% of variability). A two-step cluster analysis, exclusively based on behavioural data, allowed to some extent the re-emergence of the two etiologies: a first cluster composed of 18 subjects (78% lv-mPPA and 22% PSA), a second cluster composed of 11 subjects (64% PSA and 36%lvPPA patients). Subjects of the first cluster were more impaired both in global cognition/lexical semantic and morphosyntactic factors. Macrolinguistic factors did not differentiate instead, the two clusters. Lv-mPPA that fell in the first cluster showed widespread cortical thinning in both the cerebral hemispheres (with left prevalence) including the temporal poles; atrophy was confined in the left hemisphere, and the temporal pole was relatively spared in lv-mPPA of the second cluster. The ischemic area was distributed in the posterior regions of the left middle cerebral a

Objectives: To investigate the long-term safety and efficacy of a treatment switch to dual ART with atazanavir/ritonavir + lamivudine versus continuing a standard regimen with atazanavir/ritonavir + 2NRTI in virologically suppressed patients. Methods: ATLAS-M is a 96 week open-label, randomized, non-inferiority (margin -12%) trial enrolling HIV-infected adults on atazanavir/ritonavir + 2NRTI, with stable HIV-RNA <50 copies/mL and CD4 counts >200 cells/mm3. At baseline, patients were randomized 1:1 to switch to atazanavir/ritonavir + lamivudine or to continue the previous regimen. Here, we report the 96 week efficacy and safety data. The study was registered with ClinicalTrials.gov, number NCT01599364. Results: Overall, 266 subjects were enrolled (133 in each arm). At 96 weeks, in the ITT population, patients free of treatment failure totalled 103 (77.4%) with atazanavir/ritonavir + lamivudine and 87 (65.4%) with triple therapy (difference +12.0%, 95% CI +1.2/+22.8, P = 0.030), demonstrating the superiority of dual therapy. Two (1.5%) and 9 (6.8%) virological failures occurred in the dual-therapy arm and the triple-therapy arm, respectively, without development of resistance to any study drug. Clinical adverse events occurred at similar rates in both arms. A higher frequency of grade 3-4 hyperbilirubinemia (66.9% versus 50.4%, P = 0.006) and hypertriglyceridaemia (6.8% versus 1.5%, P = 0.031) occurred with dual therapy, although this never led to treatment discontinuation. A significant improvement in renal function and lumbar spine bone mineral density occurred in the dual-therapy arm. The evolution of CD4, HIV-DNA levels and neurocognitive performance was similar in both arms. Conclusions: In this randomized study, a treatment switch to atazanavir/ritonavir + lamivudine was superior over the continuation of atazanavir/ritonavir + 2NRTI in virologically suppressed patients, with a sustained benefit in terms of improved renal function and bone mineral density.

Parkinson’s disease (PD) typically occurs in elderly people and some degree of cognitive impairment is usually present. Cognitive reserve (CR) theory was proposed to explain the discrepancy between the degree of brain pathologies and clinical manifestations. We administered a comprehensive neuropsychological battery to 35 non-demented participants affected by PD. All participants underwent also the Cognitive Reserve Index questionnaire and the Brief Intelligence Test as proxies for CR. Relationships between CR and cognitive performance were investigated by linear regression analyses, adjusting for significant confounding factors. At linear regression analyses, higher CR scores were independently associated with a better performance on Word Fluency (p ≤ 0.04) and Digit Span (backward) (p ≤ 0.02); no associations were observed between CR and other cognitive tests. Our data provide empirical support to the relation between CR and cognitive impairment in PD. In particular, this study suggests that CR may have greater effects on the cognitive areas mostly affected in PD as executive functions.

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Objective:To investigate whether the characteristics of language disorders of degenerative and vascular aphasias depend on the underlying neuropathology.Methods:Logopenic variant/mixed primary progressive aphasics (lvmPPA; n=18) and poststroke fluent aphasics (PSA; n=11) underwent a neuropsychological examination and an assessment of the macro-and microlinguistic aspects of language. A principal component analysis and a cluster analysis applying a two-group solution were performed on the scores obtained from the neuropsychological and language examination.Results:Global cognition, lexical-semantic, and morphosyntactic components, and two components loading macrolinguistic variables, were extracted by the principal component analysis. A first cluster of 18 participants (14 lvmPPA and 4 PSA) and a second cluster of 11 participants (4 lvmPPA and 7 PSA) were identified. Participants in the first cluster were significantly more impaired than those in the second cluster in global cognition, lexical-semantic, and morphosyntactic components. Macrolinguistic components did not differentiate the two clusters. lvmPPA in the first cluster showed bilateral cortical thinning (greater on the left), whereas lvmPPA in the second cluster showed atrophy only in the left. Participants with PSA in both clusters showed vascular lesions encompassing the posterior left perisylvian regions. Underestimation of the severity of the leukoencephalopathy and damage of the interhemispheric connectivity might be responsible for the inclusion of PSA individuals in the first cluster, despite a unilateral lesion.Conclusions:Lesion localization is the main factor that determines the characteristics of aphasic deficits. Etiology indirectly acts through a different sensitivity of the brain regions to various pathologies.

Background: Neuropsychiatric symptoms (NPs) have been reported with dolutegravir use. We hypothesized that increasing dolutegravir trough concentrations (Ctrough) and/or polymorphism in the SLC22A2 gene, encoding the organic cation transporter-2 (OCT2), which is involved in monoamine clearance in the CNS and is inhibited by dolutegravir, might be associated with NPs. Methods: A cross-sectional cohort of HIV-positive patients treated with a dolutegravir-containing regimen underwent determination of allelic discrimination for SLC22A2 808 C → A polymorphism and dolutegravir Ctrough. The Symptom Checklist-90-R [investigating 10 psychiatric dimensions and reporting a general severity index (GSI)], a self-reported questionnaire and the Mini-International Neuropsychiatric Interview were offered to investigate current NPs. The effects of dolutegravir Ctrough and the SLC22A2 gene variant on NPs were explored by multivariable logistic regression. Results: A cohort of 203 patients was analysed: 71.4% were male, with median age 51 years and 11 years of ART exposure. Median time on dolutegravir was 18 months. Dolutegravir was associated with different antiretroviral combinations (mainly lamivudine, 38.9%, and abacavir/lamivudine, 35.5%). SLC22A2 CA genotype was independently associated with an abnormal GSI [adjusted OR (aOR) 2.43; P = 0.072], anxiety (aOR 2.61; P = 0.044), hostility (aOR 3.76; P = 0.012) and with moderate to severe headache (aOR 5.55; P = 0.037), and dolutegravir Ctrough was associated with hostility (fourth versus first quartile aOR 6.70; P = 0.007) and psychoticism (fourth versus first quartile aOR 19.01; P = 0.008). Other NPs were not associated with SLC22A2 polymorphism or dolutegravir Ctrough. Conclusions: A variant of the OCT2-encoding gene, in addition to or in synergy with higher dolutegravir Ctrough, is associated with a set of NPs observed during dolutegravir therapy.

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HIV+ population is getting older because of progress in treatments. Yet, there are concerns that Older HIV+ individuals (OHIV+) may be more vulnerable for developing a "cortical" dementia such as Alzheimer Disease (AD). Our aim was to explore the hypothesis that the cognitive deficit extends to ''cortical'' functions in OHIV+ by comparing serial position effects (SPE) in different groups of participants affected by "cortical" or "subcortical" damage. We enrolled a total of 122 subjects: 22 OHIV+ (≥60 years of age), 31 Younger HIV+ (YHIV+) (<60 years of age), 18 participants with AD, 23 subjects with Parkinson Disease (PD), and 28 healthy subjects. All subjects performed verbal learning tasks (VLT) to explore SPE. Factorial analysis of covariance showed a significant effect of "group" (p < 0.001) and "task" (Primacy vs Recency) (p < 0.001), but no significant group*task (p = 0.257) interaction. Compared with healthy subjects (p = 0.003), AD had the most severe reduction of Primacy, confirming a primary "encoding deficit," while PD confirmed a "frontal pattern." OHIV+ showed a memory profile similar to that of PD with a worsening of the cognitive performance in comparison with YHIV+. In conclusion, we did not confirm the "cortical" hypothesis in OHIV+, at least in terms of learning and memory functions.

The aim of our study was to better understand the dynamics between cardiovascular risk factors and immunological parameters in the evolution of cognitive performance in HIV+ patients.

AtLaS was a single-arm pilot study that demonstrated promising efficacy and safety of treatment simplification to a dual regimen with atazanavir/ritonavir + lamivudine in virologically suppressed HIV-positive patients. Here, we report data from the 144 week follow-up.

The aim of the study was to explore how viral resistance and antiretroviral central nervous system (CNS) penetration could impact on cognitive performance of HIV-infected patients.

According to recent evidence about boosted protease inhibitors (PIs/r)-simplified regimens, the combination of 3TC and DRV/r 800/100 mg could represent a feasible option for optimizing antiretroviral therapy (ART) in treatment-experienced HIV+ patients.

The aim of our study was to investigate the potential relationship between liver fibrosis (LF) and cognitive performance in HIV+ patients.

Raltegravir intensification is associated with an increase in 2-LTR episomal HIV DNA= circles, indicating a persistent low-level replication, in some individuals in ART with suppressed HIV RNA. We aimed at monitoring residual plasma HIV RNA and cellular HIV DNA in virologically suppressed patients switching to a raltegravir-based regimen.

The aim of our study was to better understand the dynamics between cardiovascular risk factors and immunological parameters in the evolution of cognitive performance in HIV+ patients.

We investigated whether primary progressive aphasias (PPA) reflect non-random degradation of linguistic dimensions that might be supported by different neural subsystems and to what extent this degradation contributes to the emergence of clinical entities: semantic (S), logopenic (L) and nonfluent (NF) aphasia; apraxia of speech was also considered if associated with language disorders (AOS/aph). Forty-two aphasic patients are reported. Two main definable patterns of linguistic deficits tended to emerge that corresponded with identifiable patterns of brain atrophy, and probably diseases: the S variant, which principally expresses the impact of a "deep" cognitive (semantic) disorder on language, and AOS/aph in which "peripheral" executive components play a significant role. By contrast, NF aphasia emerged as a heterogeneous variant due to disorganization of various dimensions within the linguistic domain, that assumes different patterns depending on the differential distribution of atrophy in the perisylvian regions.

"BACKGROUND: "Posterior shift" of the neuropathological changes of Alzheimer's disease (AD) produces a syndrome (posterior cortical atrophy) (PCA) dominated by high-level visual deficits. OBJECTIVE: To explore in patients with AD-type pathology whether a data-driven analysis (cluster analysis) based on neuropsychological findings resulted in the emergence of different subgroups of patients; in particular to find out whether it was possible to identify patients with visuospatial deficits consistent with the hypothesis that PCA is a "dorsal stream" syndrome or, rather, whether there were subgroups of patients with different types of impairment within the high-level visual domain. METHODS: 23 PCA and 16 DAT patients were studied. By a principal component analysis performed on a wide range of neuropsychological tasks, 15 variables were obtained that loaded onto five main factors (memory, language, perceptual, visuospatial, and calculation) which entered a hierarchical cluster analysis. RESULTS: Four clusters of cognitive impairment emerged: visuospatial/perceptual, memory, perceptual/calculation, and language. Only in the first cluster a visuospatial deficit clearly emerged. conclusions: AD pathology produces not only variants dominated by memory (DAT) and, to a lesser extent, visuospatial deficit (PCA), but also other distinct syndromic subtypes with disorders in visual perception and language which reflect a different vulnerability of specific functional networks.

Objectives: Ipofluency, phonological errors and mild agrammatism are the microlinguistic markers of the logopenic variant-Primary Progressive Aphasia (lvPPA); it is less clear if patients may also experience pragmatic difficulties in the construction of coherent narratives. The present study aimed to describe narrative discourse impairment in patients with lvPPA. Materials: 18 lvPPA patients (mean age 74,56 ± 7,91; 11 males, 7 females) and 18 matched healthy controls (HCs) were enrolled. Speech samples were recorded and transcribed. Method: Connected speech was analyzed according to Marini et al.’s criteria (2011) focusing on microlinguistic (speech rate; well-formed sentence ratio; principal/subordinate clause ratio; closed/open class word ratio; % phonemic and % semantic paraphasias; % fragments) and macrolinguistic (mean length of utterance (MLU); % cohesive errors; % local and global coherence errors, informativeness) measures. A preliminary two-step cluster analysis was conducted to confirm the clustering of HCs and lvPPA patients on the whole performance. A Principal Component Analysis (PCA) was then performed to identify factors explaining measures of micro and macrolinguistic deficits on patients only; factor scores were entered into a cluster analysis to evaluate the presence of different subgroups. Differences between subgroups were tested by one-way ANOVAs. Results: lvPPA patients were significantly different from HCs in both micro and macrolinguistic measures. The PCA performed on patients only (Bartlett’s χ2 = 111.83, p < .0001) showed a first factor accounting for production of % semantic paraphasias, well-formed sentence ratio, MLU, closed/open class words ratio; a second factor accounting for production of % cohesive errors, principal/subordinate clause ratio, informativeness and a third factor for the production of % global coherence errors. The two-step cluster analysis on factorial scores showed a 3-cluster solution. A first cluster (2 cases) had

Our aim was to explore the interplay between human immunodeficiency virus (HIV) and hepatitis C virus (HCV) infections in the expression of cognitive disorders.

The objective of our study was to compare two different central nervous system penetration-effectiveness (CPE) scores for the prediction of cognitive dysfunction in HIV-infected patients.

Background: Facial emotion recognition depends on cortical and subcortical networks. HIV infection of the central nervous system can damage these networks, leading to impaired facial emotion recognition. Methods: We performed a cross-sectional single cohort study consecutively enrolling HIV + subjects during routine outpatient visits. Age, gender and education-matched HIV-negative healthy individuals were also selected. Subjects were submitted to a Facial Emotion Recognition Test, which assesses the ability to recognize six basic emotions (disgust, anger, fear, happiness, surprise, sadness). The score for each emotion and a global score (obtained by summing scores for each emotion) were analyzed. General cognitive status of patients was also assessed. Results: A total of 49 HIV + and 20 HIV−subjects were enrolled. On the Facial Emotion Recognition Test, ANOVA revealed a significantly lower performance of HIV + subjects than healthy controls in recognizing fear. Moreover, fear facial emotion recognition was directly correlated with Immediate Recall of Rey Words. The lower the patients’ neurocognitive performance the less accurate they were in recognizing happiness. AIDS-defining events were negatively related to the correct recognition of happiness. Conclusions: Fear recognition deficit in HIV + patients might be related to the impaired function of neural networks in the frontostriatal system. AIDS events, including non-neurological ones, may have a negative effect on this system. Inclusion of an emotion recognition test in the neuropsychological test battery could help clinicians during the long term management of HIV-infected patients, to better understand the cognitive mechanisms involved in the reduction of emotion recognition ability and the impact of this impairment on daily life

OBJECTIVES: To explore 48 week safety and efficacy of treatment simplification to atazanavir/ritonavir + lamivudine in HIV-infected patients with virological suppression on a stable atazanavir/ritonavir-based standard triple regimen. METHODS: This was a single-arm pilot study, enrolling 40 patients on atazanavir/ritonavir + two nucleos(t)ide reverse transcriptase inhibitors (NRTIs), without previous treatment failure, with HIV-RNA <50 copies/mL for >3 months and CD4 >200 cells/mm(3). At baseline, patients were switched to 300/100 mg of atazanavir/ritonavir + 300 mg of lamivudine once daily. Laboratory parameters, atazanavir plasma levels, self-reported adherence, quality of life, neurocognitive performance, bone composition and body fat distribution were monitored. Virological failure was defined as HIV-RNA >50 copies/mL on two consecutive determinations or a single level >1000 copies/mL. RESULTS: After 48 weeks, 4/40 (10%) regimen discontinuations occurred: 1 death (brain haemorrhage), 1 study withdrawal (inadequate atazanavir plasma levels), 1 re-induction with two NRTIs due to pregnancy and 1 virological failure without development of resistance. Seven moderate to severe adverse events were recorded (including four renal colics, possibly treatment-related) in six patients. At week 48, increases in total (mean change +17 mg/dL, P = 0.001), high-density lipoprotein (+6 mg/dL, P < 0.001) and low-density lipoprotein (+8 mg/dL, P = 0.052) cholesterol were observed. The glomerular filtration rate improved (+7 mL/min/1.73 m(2), P < 0.001), as did scores exploring self-reported physical and mental health (+11, P = 0.009 and +13, P < 0.001 on a 0-100 scale), neuropsychological performance (-1 pathological task, P = 0.002) and total bone mineral density (+0.03 g/cm(2), P = 0.026). There were no significant changes in CD4 cell count, bilirubin, atazanavir plasma levels, adherence and body fat distribution over time. CONCLUSIONS: Simplification to ata

The aim of the study was to investigate the relationship between metabolic comorbidities, cardiovascular risk factors or common carotid intima-media thickness (cIMT) and cognitive performance in HIV-infected patients.

To explore the combined effects of aging and human immunodeficiency virus (HIV) infection on cognitive decay.

An impairment for verbs has been described in patients with Parkinson's disease (PD), suggesting that a disruption of frontal-subcortical circuits may result in dysfunction of the neural systems involved in action-verb processing. A previous study suggested that deep brain stimulation (DBS) of the subthalamic nucleus (STN) during verb generation may affect the ability to select from many competing lexical alternatives. In this study, 12 PD patients who had undergone bilateral STN DBS and completed an 8-year follow-up and 14 matched normal controls were administered action and object naming tasks and verb and noun reading tasks. Their responses were recorded using a microphone, resulting in a signal that marked the onset of the verbal response and allowed to measure response times (RTs). Accuracy was scored manually. RESULTS: Overall performance in naming (independently of stimulation): In naming task controls were faster and more accurate than PD patients. In both groups, performance (accuracy and RTs) was worse on action naming than object naming. PD patients were significantly slower than controls in naming actions. Effect of stimulation: Compared with the OFF stimulation condition, in ON stimulation condition PD patients showed improved performance on object and action naming tasks (increased accuracy, faster RTs), with a decreased number of semantic errors. Some evidence also emerged that action naming in the ON stimulation condition improved more than object naming. On noun and verb reading tasks, although accuracy was at ceiling in both groups and no significant difference was observed in RTs for nouns and verbs, PD patients were slower than controls. CONCLUSIONS: Our findings suggest that STN DBS may improve lexical search in PD patients. We hypothesize that STN stimulation may facilitate the motor components involved in naming and reading tasks (increased speed of speech onset), resulting in shorter RTs in both naming and reading and, to some extent, in incr

Despite the availability of potent antiretroviral regimens (combination antiretroviral therapy [cART]), HIV-associated neurocognitive disorders (HAND) are increasingly recognized. Our aim was to investigate the prevalence and treatment-related correlates of HAND, exploring the potential neurotoxicity of antiretrovirals on cognitive functions.

Objective: In an attempt to interpret neglect as a disconnection syndrome, it is currently proposed that the disorder results from disorganization of large-scale networks involved in attentional spatial processes rather than of individual brain areas. We hypothesize that as degenerative brain diseases are “system pathologies,” degeneration could be restricted to some of the neural subsystems implicated in the functional organization of spatial attention and different neglect syndromes could emerge depending on the patterns of the subsystems involved. Method: We studied five neglect patients: one with corticobasal degeneration (CBD), three with Posterior Cortical Atrophy (PCA) and one with frontotemporal dementia (FTD). Results: The patient with CBD and left parietoccipital atrophy showed right allocentric neglect; the three patients with PCA mostly distributed in the right posterior regions showed left egocentric extrapersonal neglect; the patient with FTD, who displayed more severe frontotemporal atrophy on the right, had left motor-executive neglect for both personal and extrapersonal space. All patients also presented a deep breakdown of spatial working memory. Conclusion: Our data would confirm that left neglect is more frequent than right neglect also in degenerative pathology and that damage to different neural substrates can produce different types of neglect. Our findings are also consistent with the hypothesis that both lateralized and nonlateralized attention disorders contribute to generate the syndrome. We suggest that evidence from degenerative diseases may contribute to construction of models of spatial attention.

We studied five patients with semantic memory disorders, four with semantic dementia and one with herpes simplex virus encephalitis, to investigate the involvement of semantic conceptual knowledge in object use. Comparisons between patients who had semantic deficits of different severity, as well as the follow-up, showed that the ability to use objects was largely preserved when the deficit was mild but progressively decayed as the deficit became more severe. Naming was generally more impaired than object use. Production tasks (pantomime execution and actual object use) and comprehension tasks (pantomime recognition and action recognition) as well as functional knowledge about objects were impaired when the semantic deficit was severe. Semantic and unrelated errors were produced during object use, but actions were always fluent and patients performed normally on a novel tools task in which the semantic demand was minimal. Patients with severe semantic deficits scored borderline on ideational apraxia tasks. Our data indicate that functional semantic knowledge is crucial for using objects in a conventional way and suggest that non-semantic factors, mainly non-declarative components of memory, might compensate to some extent for semantic disorders and guarantee some residual ability to use very common objects independently of semantic knowledge.