Lifelong bilingualism and mechanisms of neuroprotection in Alzheimer dementia.

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

[Acute severe neuropathies in the context of SARS-CoV-2 infection]. / Neuropathies aiguës sévères induites par l'infection à SARS-CoV-2.

Various neuromuscular complications have been described in SARS-CoV-2 infection, especially Guillain-Barré syndrome (GBS) and Critical Illness neuromyopathy (CI-NM). Two representative cases are discussed below. It appears that GBS shares most of the characteristics of classical post-infectious GBS, but SARS-CoV-2 may contribute to the increased incidence of CI-NM. Other rare complications have been described, including Tapia Syndrome and Kawasaki-like multiple system inflammatory syndrome. The question of vaccination and the risk of immune-mediated neuropathies remains open, but the lack of reported cases is reassuring as these complications usually occur within 6 weeks after vaccination.

Différentes complications neuromusculaires ont été décrites suite à l'infection à SARS-CoV-2, notamment le syndrome de Guillain-Barré (SGB) et la neuromyopathie des soins intensifs (NMSI). Deux cas représentatifs sont discutés ici. Il apparaît que le SGB partage la plupart des caractéristiques du SGB postinfectieux classique, mais le SARS-CoV-2 pourrait participer à la majoration de l'incidence de la NMSI. D'autres complications rares ont été décrites, notamment le syndrome de Tapia et le syndrome inflammatoire multisystémique de type Kawasaki. La question de la vaccination et du risque de neuropathie à médiation immunitaire reste ouverte, mais l'absence de réaction rapportée est rassurante dans la mesure où ces complications surviennent habituellement dans les 6 semaines après la vaccination.

[Neurorehabilitation in the acute and post-acute phase: what did we learn from the first wave of COVID-19?] / Neurorééducation en phases aiguë et postaiguë : qu'avons-nous appris de la première vague de Covid-19 ?

The majority of patients with Coronavirus disease 2019 (COVID-19) present mild to moderate illness and recover without hospitalization. Nevertheless, 5 % of cases require hospitalization in the intensive care unit, with 15 % of them showing severe central and peripheral nervous system manifestations. These patients should be considered high risk patients and their management must include prevention of a potential accompanying cascade of negative factors. In order to optimize care, it is essential that signs of neurological damage are searched for as early as in intensive care so that appropriate neurorehabilitation can be started immediately and continued in a specific unit for patients with neurological sequelae at post-acute and outpatient phases.

La majorité des patients atteints par la maladie due au coronavirus 2019 (Covid-19) présente une évolution plutôt favorable. Cependant 5 % nécessitent une hospitalisation aux soins intensifs, dont 15 % présentent des atteintes sévères des systèmes nerveux central et périphérique. Ces patients doivent être considérés comme des personnes à haut risque de développer des séquelles graves et leur plan de traitement doit nécessairement impliquer la prévention d'une potentielle cascade de facteurs négatifs concomitants. Afin d'optimiser une telle prise en charge, il est primordial que les premiers signes d'atteintes neurologiques soient détectés dès les soins intensifs et qu'une neurorééducation puisse être débutée précocement et poursuivie dans une filière de patients neuro-lésés en phase postaiguë, puis en ambulatoire.

Terson Syndrome: Not to Be Missed in Patients with Disorders of Consciousness.

The diagnosis of clinical cognitive motor dissociation (cCMD) can be hindered by pitfalls during standardized clinical evaluation based on gold-standard neurobehavioral rating scales. We introduce here a new pitfall, by reporting two cases of Terson syndrome (TS) after subarachnoid haemorrhage (SAH) caused by the rupture of an anterior communicant artery aneurysm, hospitalized in the Acute Neurorehabilitation Unit (ANR) of CHUV. TS is reported to occur in 8-19.3% of patients suffering from SAH. It can lead to significant visual impairment and if unrecognized, may impair the patient's capacity to interact appropriately with the environment; it thus presents an important pitfall in recognizing clinical cognitive-motor dissociation (cCMD) in patients with altered states of consciousness. An early ophthalmological exam should be considered in all patients with SAH and disorders of consciousness or visual complaints.

Case Report: Behavioral Unresponsiveness in Acute COVID-19 Patients: The Utility of the Motor Behavior Tool-Revised and 18F-FDG PET/CT.

Along with the propagation of COVID-19, emerging evidence reveals significant neurological manifestations in severely infected COVID-19 patients. Among these patients admitted to the intensive care unit (ICU), behavioral unresponsiveness may occur frequently, yet, there are still only a few cases reported and with rare descriptions of their motor behavior after pathological awakening. Several hypotheses regarding central lesions in these patients are conceivable. Here, we describe two acute SARS-CoV-2- infected patients who developed neurological symptoms evoking the condition of clinical cognitive motor dissociation (CMD). This diagnosis could be confirmed first by clinical observation of a dissociation between preserved cognitive abilities and lack of initial motor interaction and second, by performing 18F- FDG PET imaging. Accurate diagnosis led to an appropriate neuro-rehabilitation regimen with long-term neuro-rehabilitation leading to an improved outcome for both patients.

Encephalopathies Associated With Severe COVID-19 Present Neurovascular Unit Alterations Without Evidence for Strong Neuroinflammation.

OBJECTIVE: Coronavirus disease (COVID-19) has been associated with a large variety of neurologic disorders. However, the mechanisms underlying these neurologic complications remain elusive. In this study, we aimed at determining whether neurologic symptoms were caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) direct infection or by either systemic or local proinflammatory mediators. METHODS: In this cross-sectional study, we checked for SARS-CoV-2 RNA by quantitative reverse transcription PCR, SARS-CoV-2-specific antibodies, and 49 cytokines/chemokines/growth factors (by Luminex) in the CSF +/- sera of a cohort of 22 COVID-19 patients with neurologic presentation and 55 neurologic control patients (inflammatory neurologic disorder [IND], noninflammatory neurologic disorder, and MS). RESULTS: We detected anti-SARS-CoV-2 immunoglobulin G in patients with severe COVID-19 with signs of intrathecal synthesis for some of them. Of the 4 categories of tested patients, the CSF of IND exhibited the highest level of cytokines, chemokines, and growth factors. By contrast, patients with COVID-19 did not present overall upregulation of inflammatory mediators in the CSF. However, patients with severe COVID-19 (intensive care unit patients) exhibited higher concentrations of CCL2, CXCL8, and vascular endothelium growth factor A (VEGF-A) in the CSF than patients with a milder form of COVID-19. In addition, we could show that intrathecal CXCL8 synthesis was linked to an elevated albumin ratio and correlated with the increase of peripheral inflammation (serum hepatocyte growth factor [HGF] and CXCL10). CONCLUSIONS: Our results do not indicate active replication of SARS-CoV-2 in the CSF or signs of massive inflammation in the CSF compartment but highlight a specific impairment of the neurovascular unit linked to intrathecal production of CXCL8.

Multisystem inflammatory syndrome with refractory cardiogenic shock due to acute myocarditis and mononeuritis multiplex after SARS-CoV-2 infection in an adult.

A 22-year-old male with a typical history of pauci-symptomatic COVID-19 3 weeks earlier, confirmed by positive serology for SARS-CoV-2 (IgG), was admitted to the intensive care unit because of severe myocarditis with refractory cardiogenic shock that required extracorporeal life support. Due to a clinical presentation suggestive of Kawasaki-like disease with coronary aneurysm and severe systemic inflammation, intravenous immunoglobulins were administered in combination with tocilizumab. The initial clinical course was favourable with these treatments. However, the patient subsequently developed a severe mononeuritis multiplex leading to bilateral foot drop, which required intensive immunosuppressive therapy (corticosteroids, cyclophosphamide and rituximab). The clinical presentation meets the criteria for multisystem inflammatory syndrome associated with SARS-CoV-2, but includes very severe organ damages. Early recognition, a multidisciplinary approach and aggressive therapeutic intervention can lead to a favourable outcome.

Poor reward sensitivity and apathy after stroke: implication of basal ganglia.

OBJECTIVE: To examine the relationship between reward sensitivity and self-reported apathy in stroke patients and to investigate the neuroanatomical correlates of both reward sensitivity and apathy. METHODS: In this prospective study, 55 chronic stroke patients were administered a questionnaire to assess apathy and a laboratory task to examine reward sensitivity by measuring motivationally driven behavior ("reinforcement-related speeding"). Fifteen participants without brain damage served as controls for the laboratory task. Negative mood, working memory, and global cognitive functioning were also measured to determine whether reward insensitivity and apathy were secondary to cognitive impairments or negative mood. Voxel-based lesion-symptom mapping was used to explore the neuroanatomical substrates of reward sensitivity and apathy. RESULTS: Participants showed reinforcement-related speeding in the highly reinforced condition of the laboratory task. However, this effect was significant for the controls only. For patients, poorer reward sensitivity was associated with greater self-reported apathy (p < 0.05) beyond negative mood and after lesion size was controlled for. Neither apathy nor reward sensitivity was related to working memory or global cognitive functioning. Voxel-based lesion-symptom mapping showed that damage to the ventral putamen and globus pallidus, dorsal thalamus, and left insula and prefrontal cortex was associated with poorer reward sensitivity. The putamen and thalamus were also involved in self-reported apathy. CONCLUSIONS: Poor reward sensitivity in stroke patients with damage to the ventral basal ganglia, dorsal thalamus, insula, or prefrontal cortex constitutes a core feature of apathy. These results provide valuable insight into the neural mechanisms and brain substrate underlying apathy.