Paolo Calabresi (Italy)

Università Cattolica del Sacro Cuore Neurosciences

Author Of 5 Presentations

Free Communication

DELIRIUM IN ACUTE STROKE: A SINGLE CENTRE, PROSPECTIVE, CROSS-SECTIONAL, COHORT STUDY

Session Type
Free Communication
Date
03.10.2021, Sunday
Session Time
09:30 - 11:00
Room
Free Communication A
Lecture Time
09:50 - 10:00
Presenter
  • Eleonora Rollo (Italy)

Abstract

Background and Aims:

Delirium is an acute fluctuating disorder of attention and awareness. The endpoints of our study were: 1) incidence of delirium in acute stroke; 2) risk factors for delirium; 3) impact of delirium on the outcome of stroke.

Methods:

Patients were consecutively enrolled in a stroke unit from April to October 2020. Inclusion criteria were: age ≥18 years, acute stroke and NIHSS≥1. Exclusion criteria were: negative neuroimaging, stroke mimics, and need for ICU treatment. All patients were evaluated by means of Richmond Agitation-Sedation Scale (RASS) and Confusion Assessment Method-Intensive Care Unit (CAM-ICU) scores at baseline, within 72 hours or when patients developed symptoms suggesting delirium. The outcome was assessed by means of modified Rankin Scale at 90 days.

Results:

The overall incidence of delirium was 36/120 (30%). Delirium was associated with aphasia (OR 9.77; CI 1.2-79.6), chronic obstructive pulmonary disease (COPD) (OR 16.67; CI 1.1-263.0), deep Fazekas score (OR 5.05; CI 1.7-14.8), and physical restraint (OR 45.02; CI 1.4-1411.5). At 3 months follow-up evaluation, patients with delirium had more disability (DLR+: mRS=4; DLR–: mRS=1; Beta=1.43; CI 0.61-2.24; p=0.001) and shorter survival (DLR+: 84±20 days; DLR–: 87±13 days; p=0.048).

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Conclusions:

Nearly one-third of patients (30%) had delirium in the acute phase of stroke. This finding supports the notion that delirium is a common complication of stroke. Delirium was associated with speech disorder, leukoencephalopathy, COPD and early use of physical restraint. Delirium was associated with increased risk of disability and shorter survival after stroke.

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THEORY OF MIND: A CLUE TO FUNCTIONAL MOVEMENT DISORDERS DIAGNOSIS

Session Type
Free Communication
Date
03.10.2021, Sunday
Session Time
11:30 - 13:00
Room
Free Communication C
Lecture Time
12:20 - 12:30
Presenter
  • Sonia Di Tella (Italy)

Abstract

Background and Aims:

Functional movement disorders (FMD) are a group of manifestations that are incongruent with known neurological diseases, interpreted as conversion disorders. Abnormal activation has been documented in regions crucial for the elaboration of social cognition aspects, such as Theory of Mind (ToM). ToM defines the ability to attribute mental states to ourselves and others that allows us to understand others’ motivation in generating actions during social interaction. We hypothesized that ToM disorders which result in reduced ability to make inferences about others’ mental states, might underlie FMD.

Methods:

Eighteen subjects with FMD and 28 matched healthy controls (HC) were given First- and Second-Order False Beliefs, the Faux-Pas Recognition Test and the Reading the Mind in the Eyes test (RMET). Subjects were also administered the DES-II questionnaire for measuring dissociative symptoms. The severity of FMD was rated with the Simplified-FMD Rating Scale (S-FMDRS).

Results:

HC scored better than the FMD group on Second-Order False Beliefs, RMET and Faux Pas Recognition Test. The mean score of the FMD group on the DES-II Scale was 20.00 (range 1.79-72.14), which indicates borderline personality disorders. No correlation emerged between S-FMDRS and any measure of ToM ability or the DES-II scale.

Conclusions:

ToM disorder might underlie FMD as expression of the inability to read the intention of the other individuals in motor behaviour. Reduced scores on the DES-II scale suggest that FMD might also originate from the inability to read one’s own mental state. FMD could represent an experimental model for understanding the relationship between 'organic' and functional manifestations.

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COGNITIVE DECLINE RISK STRATIFICATION IN PEOPLE WITH LATE-ONSET EPILEPSY OF UNKNOWN ETIOLOGY: AN ELECTROENCEPHALOGRAPHIC CONNECTIVITY AND GRAPH THEORY PILOT STUDY

Session Type
Free Communication
Date
04.10.2021, Monday
Session Time
09:30 - 11:00
Room
Free Communication A
Lecture Time
09:50 - 10:00
Presenter
  • Cinzia Costa (Italy)

Abstract

Background and Aims:

Although people with late onset epilepsy of unknown etiology (LOEU) are at higher risk of cognitive decline compared to the general population, we still lack affordable tools to predict and stratify their risk of dementia. Electroencephalography (EEG) network small-world (SW) analysis has been proven cost-effective, feasible and reliable in predicting cognitive decline in mild cognitive impairment (MCI). This pilot-study investigates the potential application of EEG network SW properties in predicting cognitive decline among patients with LOEU.

Methods:

People diagnosed with LOEU and normal cognitive examination at the time of epilepsy diagnosis were included. Cerebrospinal fluid biomarkers, brain imaging and neuropsychological assessment were performed at the time of epilepsy diagnosis. Baseline EEG was analyzed for SW properties. Patients were followed-up over time with neuropsychological tests.

Results:

Over 5.1 years of follow-up, among 24 patients diagnosed with LOEU, thirteen developed MCI, and four dementia. Patients with LOEU developing MCI had lower values of SW coefficients in the in the delta (p=.03) band and higher SW values in the alpha frequency bands (p=.02) compared to patients having normal cognition at last follow-up. A similar gradient was confirmed for patients developing dementia compared to those with normal cognitive function as well as to those developing MCI.

Conclusions:

EEG network SW properties might be able to identify people with LOEU at risk of cognitive decline. Given EEG is frequently performed in LOEU. Baseline EEG analysis through SW is worth investigating as an affordable, widely available tool to stratify people for their risk of cognitive decline.

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INTERLEUKIN-17 AXIS IN THE MODULATION OF CORTICAL AND SUBCORTICAL SYNAPTIC PLASTICITY ACROSS DISEASE STAGES IN EXPERIMENTAL MULTIPLE SCLEROSIS

Session Type
Free Communication
Date
05.10.2021, Tuesday
Session Time
09:30 - 11:00
Room
Free Communication C
Lecture Time
09:30 - 09:40
Presenter
  • Andrea Mancini (Italy)

Abstract

Background and Aims:

Interleukin-17A (IL-17) is known to be deeply involved in the immunopathogenesis of multiple sclerosis (MS), but recent reports suggest that it may also participate in synaptic modulation. The aim of our study was to explore the role exerted by IL-17 axis in the regulation of hippocampal and striatal synaptic plasticity in physiological conditions and across different stages of experimental MS.

Methods:

Electrophysiological recordings were performed in the hippocampus (CA1 area) and in the striatum of control mice, mice affected by experimental autoimmune encephalomyelitis (EAE) and mice lacking IL-17 or IL-17 receptor (IL-17R). IL-17 levels were assessed through ELISA assays and IL-17 and IL-17R expression patterns through immunohistochemical analysis.

Results:

Functional IL-17 axis is required for physiological hippocampal and striatal synaptic plasticity, since the absence of IL-17R and the exposure to high IL-17 levels were associated with altered LTP induction. Hippocampal long-term potentiation (LTP) was disrupted during pre-acute and acute EAE phases, in parallel with increased IL-17 hippocampal expression levels. The recovery phase of EAE was characterized by a restoration of hippocampal LTP and by a reduction of IL-17 production. Hippocampal-dependent cognitive tasks are preserved when EAE is induced in mice lacking IL-17. Immunohistochemical analysis suggested that microglial-produced IL-17 may directly act on IL-17Rs expressed by hippocampal neurons. The inhibition of IL-17R axis (p38MAPK) or the in vitro exposure to anti-IL-17 antibodies limited the IL-17-dependent disruption of hippocampal LTP.

Conclusions:

Targeting IL-17 axis may help counteract the loss of brain plastic properties contributing to disease progression and cognitive impairment during MS.

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MOTOR AND NEUROPHYSIOLOGICAL FEATURES OF SLEEP IN HUNTINGTON DISEASE: A SINGLE-CENTER, PROSPECTIVE, CROSS-SECTIONAL, COHORT STUDY

Session Type
Free Communication
Date
07.10.2021, Thursday
Session Time
09:30 - 10:50
Room
Free Communication B
Lecture Time
09:30 - 09:40
Presenter
  • Danilo Genovese (Italy)

Abstract

Background and Aims:

Sleep changes are reported since early stages of HD and sleep disturbances represent a prominent feature of the advanced disease. The aims our study were: to evaluate sleep-related motor activity, EEG functional connectivity in the sensory-motor network, and autonomic modulation in HD patients.

Methods:

Thirty HD patients, 16 women and 14 men (mean age 57.3±12.2) and 30 matched healthy controls (mean age 56.5±11.8 y) were enrolled. Subjective evaluation of sleep quality and daytime sleepiness was performed. All patients underwent full-night attended video-polysomnography. HRV analysis was conducted on EKG traces obtained during polysomnographic recording. EEG connectivity analysis was performed in a subset of patients by means of exact Low-Resolution Electric Tomography.

Results:

hd  figura generale (1).pngHD patients, compared to controls, showed shorter sleep duration, reduced sleep efficiency, and increased arousals and awakenings. Periodic limb movements during wake and sleep were observed in all patients, but no episode of RBD was observed. During wake and NREM sleep HD patients had higher heart rate than controls, but not during REM sleep. HD patients showed increased lagged phase synchronization among sensory-motor areas (Brodmann areas 1,2,3,4,6,8) during wake and sleep.

Conclusions:

HD patients showed a severe sleep disruption with an overall increase of motor activity, often triggered by periodic limb movements. HRV analysis confirmed the involvement of autonomic nervous system in HD, with a peculiar modulation in sleep. The findings of EEG connectivity may reflect an abnormal function of motor areas or, alternatively, the effort to counterbalance the pathological motor output.

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Moderator of 1 Session

Free Communication
Session Time
09:30 - 11:00
Room
Free Communication B
Chair(s)
  • Paolo Calabresi (Italy)