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Alessia Riglietti,1,* Francesco Fanfulla,2,* Massimo Pagani,3 Daniela Lucini,3,4 Mara Malacarne,3,4 Mauro Manconi,5– 7 Guido Ferretti,8,9 Fabio Esposito,10,11 Carlo W Cereda,12 Marco Pons1 1Department of Pulmonology, Regional Hospital of Lugano (EOC), Lugano, 6900, Switzerland; 2Respiratory Function and Sleep Unit – Istituti Clinici Scientifici Maugeri IRCCS, Pavia, Italy; 3Exercise Medicine Unit, Istituto Auxologico Italiano, MIlan, 20133, Italy; 4University of Milan, BIOMETRA Department, Milan, Italy; 5Sleep and Epilepsy Center, Neurocenter of the Southern Switzerland, Regional Hospital (EOC) of Lugano, Lugano, Switzerland; 6Faculty of Biomedical Sciences, Università della Svizzera Italiana, Lugano, Switzerland; 7Department of Neurology, University Hospital, Inselspital, Bern, Switzerland; 8Department APSI, University of Geneva, Geneva, Switzerland; 9Department of Molecular and Translational Medicine, University of Brescia, Brescia, Italy; 10Department of Biomedical Sciences for Health, Università degli Studi di Milano, Milan, Italy; 11IRCCS Istituto Ortopedico Galeazzi, Milan, Italy; 12Stroke Center EOC, Department of Neurology, Neurocenter of Southern Switzerland Regional Hospital (EOC) of Lugano, Lugano, Switzerland*These authors contributed equally to this workCorrespondence: Mauro ManconiRegional Hospital of Lugano, Via Tesserete, 46, Lugano, 6903, SwitzerlandTel +41-91-8116825Email mauro.manconi@eoc.chIntroduction: Sleep-related breathing disorders are highly prevalent in patients with ischemic stroke. Among sleep-disordered breathing disorders, obstructive sleep apnea is the most represented one, but central sleep apnea, isolated or in the context of a periodic breathing/Cheyne–Stokes respiration, is frequently reported in these patients. Altered baroreflex responses have been reported in the acute phases of a cerebral event.Methods: We conducted, in a group of patients with ischemic stroke (n=60), a prospective 3-month follow-up physiological study to describe the breathing pattern during sleep and baroreflex sensitivity in the acute phase and in the recovery phase.Results: In the acute phase, within 10 days from the onset of symptoms, 22.4% of patients had a normal breathing pattern, 40.3% had an obstructive pattern, 16.4% had a central pattern, and 29.9% showed a mixed pattern. Smaller variations in the Apnea–Hypopnea Index were found in normal breathing and obstructive groups (ΔAHI 2.1± 4.1 and − 2.8± 11.6, respectively) in comparison with central and mixed patterns (ΔAHI − 6.9± 15.1 and − 12.5± 13.1, respectively; ANOVA p=0.01). The obstructive pattern became the most frequent pattern, in 38.3% of patients at baseline and 61.7% of patients at follow-up. Modification of baroreflex sensitivity over time was influenced by the site of the lesion and by the sleep disorder pattern in the acute phase (MANOVA p=0.005).Conclusion: We suggest that a down-regulation of autonomic activity, possibly related to reduced vagal modulation, may help the recovery after stroke, or a transitory disconnection from the cortical node that participates in the regulation of sympathetic outflow.Keywords: sleep-disordered breathing, baroreflex, chemoreflex, brain lesion

Göran Högberg1,2, Davide Nardo3, Tore Hällström4,5, Marco Pagani6,71Department of Women's and Children's Health, Child and Adolescent Psychiatric Unit, Astrid Lindgren Children's Hospital, Karolinska Institutet, Stockholm, Sweden; 2BUP Huddinge Child and Adolescent Psychiatry, Stockholm, Sweden; 3Neuroimaging Laboratory, Santa Lucia Foundation, Rome, Italy; 4Department of Clinical Neuroscience, Section for Psychiatry/Huddinge, Karolinska Institutet, Stockholm, Sweden; 5Department of Neuroscience, Section of Psychiatry and Neurochemistry, Unit for Neuropsychiatric Epidemiology, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden; 6Department of Nuclear Medicine, Karolinska Hospital, Stockholm, Sweden; 7Institute of Cognitive Sciences and Technologies, CNR, Rome, ItalyAbstract: This paper reviews the affective neuroscience dealing with the effects of traumatic events. We give an overview of the normal fear reactions, the pathological fear reaction, and the character of emotional episodic memories. We find that both emotions and emotional memories are a tripartite unit of sensory information, autonomic reaction, and motor impulse (the PRM complex). We propose that emotions and movements are part and parcel of the same complex. This is our main finding from the review of affective neuroscience, and from here we focus on psychotherapy with post-trauma reactions. The finding of the process of memory reconsolidation opens up a new treatment approach: affective psychotherapy focused on reconsolidation. The meaning of reconsolidation is that an emotional memory, when retrieved and being active, will rest in a labile form, amenable to change, for a brief period of time, until it reconsolidates in the memory. This leads us to the conclusion that emotions, affects, must be evoked during the treatment session and that positive emotion must come first, because safety must be part of the new memories. In the proposed protocol of affective psychotherapy based on reconsolidation the emotional episodic memory is relived in a safe and positive setting, focused in turn on the sensory experience, the autonomic reaction, and the motor impulse. Then it is followed by a fantasy of a different positive version of the same event. All in all treatment should provide a series of new memories without fear related to the original event. With the focus on the motor program, and the actions, there is a natural link to art therapy and to the mode of play, which can rehearse and fantasize new positive actions.Keywords: post-traumatic, PTSD, affective neuroscience, memory reconsolidation, psychotherapy, play

Increasing evidence suggests that early neurodevelopmental defects in Huntington's disease (HD) patients could contribute to the later adult neurodegenerative phenotype. Here, by using HD-derived induced pluripotent stem cell lines, we report that early telencephalic induction and late neural identity are affected in cortical and striatal populations. We show that a large CAG expansion causes complete failure of the neuro-ectodermal acquisition, while cells carrying shorter CAGs repeats show gross abnormalities in neural rosette formation as well as disrupted cytoarchitecture in cortical organoids. Gene-expression analysis showed that control organoid overlapped with mature human fetal cortical areas, while HD organoids correlated with the immature ventricular zone/subventricular zone. We also report that defects in neuroectoderm and rosette formation could be rescued by molecular and pharmacological approaches leading to a recovery of striatal identity. These results show that mutant huntingtin precludes normal neuronal fate acquisition and highlights a possible connection between mutant huntingtin and abnormal neural development in HD.