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Article ; Online: Evaluating a Pupillometry App Considering Sedation's Impact: A Step Unexplored.

Zanier, Elisa R / Citerio, Giuseppe

2023 Volume 41, Issue 1-2, Page(s) 294–295

MeSH term(s)	Mobile Applications ; Pupil
Language	English
Publishing date	2023-10-30
Publishing country	United States
Document type	Letter ; Comment
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2023.0431
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Article ; Online: Correction: Accuracy of Manual Intracranial Pressure Recording Compared to a Computerized High-Resolution System: A CENTER-TBI Analysis.

Zoerle, Tommaso / Birg, Tatiana / Carbonara, Marco / Smielewski, Peter / Placek, Michal M / Zanier, Elisa R / Åkerlund, Cecilia A I / Ortolano, Fabrizio / Stocchetti, Nino

Neurocritical care

2023 Volume 38, Issue 3, Page(s) 833–834

Language	English
Publishing date	2023-04-14
Publishing country	United States
Document type	Published Erratum
ZDB-ID	2381896-7
ISSN	1556-0961 ; 1541-6933
ISSN (online)	1556-0961
ISSN	1541-6933
DOI	10.1007/s12028-023-01722-4
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Article ; Online: Angiotensin-(1-7) as a Potential Therapeutic Strategy for Delayed Cerebral Ischemia in Subarachnoid Hemorrhage.

Annoni, Filippo / Moro, Federico / Caruso, Enrico / Zoerle, Tommaso / Taccone, Fabio Silvio / Zanier, Elisa R

Frontiers in immunology

2022 Volume 13, Page(s) 841692

Abstract: Aneurysmal subarachnoid hemorrhage (SAH) is a substantial cause of mortality and morbidity worldwide. Moreover, survivors after the initial bleeding are often subject to secondary brain injuries and delayed cerebral ischemia, further increasing the risk ... ...

Abstract	Aneurysmal subarachnoid hemorrhage (SAH) is a substantial cause of mortality and morbidity worldwide. Moreover, survivors after the initial bleeding are often subject to secondary brain injuries and delayed cerebral ischemia, further increasing the risk of a poor outcome. In recent years, the renin-angiotensin system (RAS) has been proposed as a target pathway for therapeutic interventions after brain injury. The RAS is a complex system of biochemical reactions critical for several systemic functions, namely, inflammation, vascular tone, endothelial activation, water balance, fibrosis, and apoptosis. The RAS system is classically divided into a pro-inflammatory axis, mediated by angiotensin (Ang)-II and its specific receptor AT
MeSH term(s)	Angiotensin I/metabolism ; Angiotensin II/metabolism ; Brain Ischemia ; Humans ; Peptide Fragments/metabolism ; Subarachnoid Hemorrhage/complications
Chemical Substances	Peptide Fragments ; Angiotensin II (11128-99-7) ; Angiotensin I (9041-90-1) ; angiotensin I (1-7) (IJ3FUK8MOF)
Language	English
Publishing date	2022-03-09
Publishing country	Switzerland
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.841692
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Article ; Online: Brain Protection after Anoxic Brain Injury: Is Lactate Supplementation Helpful?

Annoni, Filippo / Peluso, Lorenzo / Gouvêa Bogossian, Elisa / Creteur, Jacques / Zanier, Elisa R / Taccone, Fabio Silvio

Cells

2021 Volume 10, Issue 7

Abstract: While sudden loss of perfusion is responsible for ischemia, failure to supply the required amount of oxygen to the tissues is defined as hypoxia. Among several pathological conditions that can impair brain perfusion and oxygenation, cardiocirculatory ... ...

Abstract	While sudden loss of perfusion is responsible for ischemia, failure to supply the required amount of oxygen to the tissues is defined as hypoxia. Among several pathological conditions that can impair brain perfusion and oxygenation, cardiocirculatory arrest is characterized by a complete loss of perfusion to the brain, determining a whole brain ischemic-anoxic injury. Differently from other threatening situations of reduced cerebral perfusion, i.e., caused by increased intracranial pressure or circulatory shock, resuscitated patients after a cardiac arrest experience a sudden restoration of cerebral blood flow and are exposed to a massive reperfusion injury, which could significantly alter cellular metabolism. Current evidence suggests that cell populations in the central nervous system might use alternative metabolic pathways to glucose and that neurons may rely on a lactate-centered metabolism. Indeed, lactate does not require adenosine triphosphate (ATP) to be oxidated and it could therefore serve as an alternative substrate in condition of depleted energy reserves, i.e., reperfusion injury, even in presence of adequate tissue oxygen delivery. Lactate enriched solutions were studied in recent years in healthy subjects, acute heart failure, and severe traumatic brain injured patients, showing possible benefits that extend beyond the role as alternative energetic substrates. In this manuscript, we addressed some key aspects of the cellular metabolic derangements occurring after cerebral ischemia-reperfusion injury and examined the possible rationale for the administration of lactate enriched solutions in resuscitated patients after cardiac arrest.
MeSH term(s)	Acidosis/etiology ; Acidosis/pathology ; Acidosis/prevention & control ; Animals ; Brain Injuries, Traumatic/etiology ; Brain Injuries, Traumatic/pathology ; Brain Injuries, Traumatic/prevention & control ; Cell Death/drug effects ; Cerebrovascular Circulation/drug effects ; Energy Metabolism/drug effects ; Heart Arrest/complications ; Heart Arrest/pathology ; Heart Arrest/therapy ; Humans ; Hypertonic Solutions ; Hypoxia-Ischemia, Brain/etiology ; Hypoxia-Ischemia, Brain/pathology ; Hypoxia-Ischemia, Brain/prevention & control ; Lactic Acid/therapeutic use ; Neurons/drug effects ; Neurons/metabolism ; Neurons/pathology ; Neuroprotective Agents/therapeutic use ; Oxidative Stress/drug effects ; Reperfusion Injury/etiology ; Reperfusion Injury/pathology ; Reperfusion Injury/prevention & control ; Resuscitation/methods
Chemical Substances	Hypertonic Solutions ; Neuroprotective Agents ; Lactic Acid (33X04XA5AT)
Language	English
Publishing date	2021-07-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells10071714
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Article ; Online: Neuro-Inflammation Modulation and Post-Traumatic Brain Injury Lesions: From Bench to Bed-Side.

Jacquens, Alice / Needham, Edward J / Zanier, Elisa R / Degos, Vincent / Gressens, Pierre / Menon, David

International journal of molecular sciences

2022 Volume 23, Issue 19

Abstract: Head trauma is the most common cause of disability in young adults. Known as a silent epidemic, it can cause a mosaic of symptoms, whether neurological (sensory-motor deficits), psychiatric (depressive and anxiety symptoms), or somatic (vertigo, tinnitus, ...

Abstract	Head trauma is the most common cause of disability in young adults. Known as a silent epidemic, it can cause a mosaic of symptoms, whether neurological (sensory-motor deficits), psychiatric (depressive and anxiety symptoms), or somatic (vertigo, tinnitus, phosphenes). Furthermore, cranial trauma (CT) in children presents several particularities in terms of epidemiology, mechanism, and physiopathology-notably linked to the attack of an immature organ. As in adults, head trauma in children can have lifelong repercussions and can cause social and family isolation, difficulties at school, and, later, socio-professional adversity. Improving management of the pre-hospital and rehabilitation course of these patients reduces secondary morbidity and mortality, but often not without long-term disability. One hypothesized contributor to this process is chronic neuroinflammation, which could accompany primary lesions and facilitate their development into tertiary lesions. Neuroinflammation is a complex process involving different actors such as glial cells (astrocytes, microglia, oligodendrocytes), the permeability of the blood-brain barrier, excitotoxicity, production of oxygen derivatives, cytokine release, tissue damage, and neuronal death. Several studies have investigated the effect of various treatments on the neuroinflammatory response in traumatic brain injury in vitro and in animal and human models. The aim of this review is to examine the various anti-inflammatory therapies that have been implemented.
MeSH term(s)	Animals ; Brain/pathology ; Brain Injuries, Traumatic/complications ; Brain Injuries, Traumatic/pathology ; Child ; Cytokines/pharmacology ; Disease Models, Animal ; Humans ; Inflammation/complications ; Microglia ; Oxygen/pharmacology
Chemical Substances	Cytokines ; Oxygen (S88TT14065)
Language	English
Publishing date	2022-09-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms231911193
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Article ; Online: Mesenchymal stromal cell secretome for traumatic brain injury: Focus on immunomodulatory action.

Pischiutta, Francesca / Caruso, Enrico / Cavaleiro, Helena / Salgado, Antonio J / Loane, David J / Zanier, Elisa R

Experimental neurology

2022 Volume 357, Page(s) 114199

Abstract: The severity and long-term consequences of brain damage in traumatic brain injured (TBI) patients urgently calls for better neuroprotective/neuroreparative strategies for this devastating disorder. Mesenchymal stromal cells (MSCs) hold great promise and ... ...

Abstract	The severity and long-term consequences of brain damage in traumatic brain injured (TBI) patients urgently calls for better neuroprotective/neuroreparative strategies for this devastating disorder. Mesenchymal stromal cells (MSCs) hold great promise and have been shown to confer neuroprotection in experimental TBI, mainly through paracrine mechanisms via secreted bioactive factors (i.e. secretome), which indicates significant potential for a cell-free neuroprotective approach. The secretome is composed of cytokines, chemokines, growth factors, proteins, lipids, nucleic acids, metabolites, and extracellular vesicles; it may offer advantages over MSCs in terms of delivery, safety, and variability of therapeutic response for brain injury. Immunomodulation by molecular factors secreted by MSCs is considered to be a key mechanism involved in their multi-potential therapeutic effects. Regulated neuroinflammation is required for healthy remodeling of central nervous system during development and adulthood. Moreover, immune cells and their secreted factors can also contribute to tissue repair and neurological recovery following acute brain injury. However, a chronic and maladaptive neuroinflammatory response can exacerbate TBI and contribute to progressive neurodegeneration and long-term neurological impairments. Here, we review the evidence for MSC-derived secretome as a therapy for TBI. Our framework incorporates a detailed analysis of in vitro and in vivo studies investigating the effects of the secretome on clinically relevant neurological and histopathological outcomes. We also describe the activation of immune cells after TBI and the immunomodulatory properties exerted by mediators released in the secretome. We then describe how ageing modifies central and systemic immune responses to TBI and discuss challenges and opportunities of developing secretome based neuroprotective therapies for elderly TBI populations. Finally, strategies aimed at modulating the secretome in order to boost its efficacy for TBI will also be discussed.
MeSH term(s)	Adult ; Aged ; Brain Injuries/pathology ; Brain Injuries, Traumatic/pathology ; Humans ; Immunity ; Immunomodulation ; Mesenchymal Stem Cells/metabolism ; Secretome
Language	English
Publishing date	2022-08-08
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	207148-4
ISSN	1090-2430 ; 0014-4886
ISSN (online)	1090-2430
ISSN	0014-4886
DOI	10.1016/j.expneurol.2022.114199
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Article ; Online: ECoG spiking activity and signal dimension are early predictive measures of epileptogenesis in a translational mouse model of traumatic brain injury.

Di Sapia, Rossella / Rizzi, Massimo / Moro, Federico / Lisi, Ilaria / Caccamo, Alessia / Ravizza, Teresa / Vezzani, Annamaria / Zanier, Elisa R

Neurobiology of disease

2023 Volume 185, Page(s) 106251

Abstract: The latency between traumatic brain injury (TBI) and the onset of epilepsy (PTE) represents an opportunity for counteracting epileptogenesis. Antiepileptogenesis trials are hampered by the lack of sensitive biomarkers that allow to enrich patient's ... ...

Abstract	The latency between traumatic brain injury (TBI) and the onset of epilepsy (PTE) represents an opportunity for counteracting epileptogenesis. Antiepileptogenesis trials are hampered by the lack of sensitive biomarkers that allow to enrich patient's population at-risk for PTE. We aimed to assess whether specific ECoG signals predict PTE in a clinically relevant mouse model with ∼60% epilepsy incidence. TBI was provoked in adult CD1 male mice by controlled cortical impact on the left parieto-temporal cortex, then mice were implanted with two perilesional cortical screw electrodes and two similar electrodes in the hemisphere contralateral to the lesion site. Acute seizures and spikes/sharp waves were ECoG-recorded during 1 week post-TBI. These early ECoG events were analyzed according to PTE incidence as assessed by measuring spontaneous recurrent seizures (SRS) at 5 months post-TBI. We found that incidence, number and duration of acute seizures during 3 days post-TBI were similar in PTE mice and mice not developing epilepsy (No SRS mice). Control mice with cortical electrodes (naïve, n = 5) or with electrodes and craniotomy (sham, n = 5) exhibited acute seizures but did not develop epilepsy. The daily number of spikes/sharp waves at the perilesional electrodes was increased similarly in PTE (n = 15) and No SRS (n = 8) mice vs controls (p < 0.05, n = 10) from day 2 post-injury. Differently, the daily number of spikes/sharp waves at both contralateral electrodes showed a progressive increase in PTE mice vs No SRS and control mice. In particular, spikes number was higher in PTE vs No SRS mice (p < 0.05) at 6 and 7 days post-TBI, and this measure predicted epilepsy development with high accuracy (AUC = 0.77, p = 0.03; CI 0.5830-0.9670). The cut-off value was validated in an independent cohort of TBI mice (n = 12). The daily spike number at the contralateral electrodes showed a circadian distribution in PTE mice which was not observed in No SRS mice. Analysis of non-linear dynamics at each electrode site showed changes in dimensionality during 4 days post-TBI. This measure yielded the best discrimination between PTE and No SRS mice (p < 0.01) at the cortical electrodes contralateral to injury. Data show that epileptiform activity contralateral to the lesion site has the the highest predictive value for PTE in this model reinforcing the hypothesis that the hemisphere contralateral to the lesion core may drive epileptogenic networks after TBI.
MeSH term(s)	Male ; Mice ; Animals ; Epilepsy, Post-Traumatic/complications ; Brain Injuries, Traumatic/complications ; Seizures/complications ; Epilepsy/etiology ; Electrocorticography
Language	English
Publishing date	2023-08-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	1211786-9
ISSN	1095-953X ; 0969-9961
ISSN (online)	1095-953X
ISSN	0969-9961
DOI	10.1016/j.nbd.2023.106251
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Article ; Online: Accuracy of Manual Intracranial Pressure Recording Compared to a Computerized High-Resolution System: A CENTER-TBI Analysis.

Zoerle, Tommaso / Birg, Tatiana / Carbonara, Marco / Smielewski, Peter / Placek, Michal M / Zanier, Elisa R / Åkerlund, Cecilia A I / Ortolano, Fabrizio / Stocchetti, Nino

Neurocritical care

2023 Volume 38, Issue 3, Page(s) 781–790

Abstract: Background: Monitoring intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is crucial in the management of the patient with severe traumatic brain injury (TBI). In several institutions ICP and CPP are summarized hourly and entered manually ...

Abstract	Background: Monitoring intracranial pressure (ICP) and cerebral perfusion pressure (CPP) is crucial in the management of the patient with severe traumatic brain injury (TBI). In several institutions ICP and CPP are summarized hourly and entered manually on bedside charts; these data have been used in large observational and interventional trials. However, ICP and CPP may change rapidly and frequently, so data recorded in medical charts might underestimate actual ICP and CPP shifts. The aim of this study was to evaluate the accuracy of manual data annotation for proper capturing of ICP and CPP. For this aim, we (1) compared end-hour ICP and CPP values manually recorded (MR) with values recorded continuously by computerized high-resolution (HR) systems and (2) analyzed whether MR ICP and MR CPP are reliable indicators of the burden of intracranial hypertension and low CPP. Methods: One hundred patients were included. First, we compared the MR data with the values stored in the computerized system during the first 7 days after admission. For this point-to-point analysis, we calculated the difference between end-hour MR and HR ICP and CPP. Then we analyzed the burden of high ICP (> 20 mm Hg) and low CPP (< 60 mm Hg) measured by the computerized system, in which continuous data were stored, compared with the pressure-time dose based on end-hour measurements. Results: The mean difference between MR and HR end-hour values was 0.02 mm Hg for ICP (SD 3.86 mm Hg) and 1.54 mm Hg for CPP (SD 8.81 mm Hg). ICP > 20 mm Hg and CPP < 60 mm Hg were not detected by MR in 1.6% and 5.8% of synchronized measurements, respectively. Analysis of the pathological ICP and CPP throughout the recording, however, indicated that calculations based on manual recording seriously underestimated the ICP and CPP burden (in 42% and 28% of patients, respectively). Conclusions: Manual entries fairly represent end-hour HR ICP and CPP. However, compared with a computerized system, they may prove inadequate, with a serious risk of underestimation of the ICP and CPP burden.
MeSH term(s)	Humans ; Brain Injuries ; Brain Injuries, Traumatic/diagnosis ; Cerebrovascular Circulation ; Hospitalization ; Intracranial Hypertension/diagnosis ; Intracranial Pressure
Language	English
Publishing date	2023-03-15
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2381896-7
ISSN	1556-0961 ; 1541-6933
ISSN (online)	1556-0961
ISSN	1541-6933
DOI	10.1007/s12028-023-01697-2
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Article ; Online: Acute Blood Levels of Neurofilament Light Indicate One-Year White Matter Pathology and Functional Impairment in Repetitive Mild Traumatic Brain Injured Mice.

Moro, Federico / Lisi, Ilaria / Tolomeo, Daniele / Vegliante, Gloria / Pascente, Rosaria / Mazzone, Edoardo / Hussain, Riaz / Micotti, Edoardo / Dallmeier, Julian / Pischiutta, Francesca / Bianchi, Elisa / Chiesa, Roberto / Wang, Kevin K / Zanier, Elisa R

Journal of neurotrauma

2023 Volume 40, Issue 11-12, Page(s) 1144–1163

Abstract: Mild traumatic brain injury (mTBI) mostly causes transient symptoms, but repeated (r)mTBI can lead ...

Abstract	Mild traumatic brain injury (mTBI) mostly causes transient symptoms, but repeated (r)mTBI can lead to neurodegenerative processes. Diagnostic tools to evaluate the presence of ongoing occult neuropathology are lacking. In a mouse model of rmTBI, we investigated MRI and plasma biomarkers of brain damage before chronic functional impairment arose. Anesthetized adult male and female C57BL/6J mice were subjected to rmTBI or a sham procedure. Sensorimotor deficits were evaluated up to 12 months post-injury in SNAP and Neuroscore tests. Cognitive function was assessed in the novel object recognition test at six and 12 months. Diffusion tensor imaging (DTI) and structural magnetic resonance imaging (MRI) were performed at six and 12 months to examine white matter and structural damage. Plasma levels of neurofilament light (NfL) were assessed longitudinally up to 12 months. Brain histopathology was performed at 12 months. Independent groups of mice were used to examine the effects of 2-, 7- and 14-days inter-injury intervals on acute plasma NfL levels and on hyperactivity. Twelve months after an acute transient impairment, sensorimotor functions declined again in rmTBI mice (
MeSH term(s)	Rats ; Mice ; Animals ; Male ; Female ; White Matter/pathology ; Diffusion Tensor Imaging ; Intermediate Filaments ; Rats, Sprague-Dawley ; Mice, Inbred C57BL ; Brain/pathology ; Brain Concussion/complications ; Brain Concussion/diagnostic imaging ; Brain Concussion/pathology ; Brain Injuries, Traumatic/complications
Language	English
Publishing date	2023-03-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	645092-1
ISSN	1557-9042 ; 0897-7151
ISSN (online)	1557-9042
ISSN	0897-7151
DOI	10.1089/neu.2022.0252
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Article: A novel organotypic cortical slice culture model for traumatic brain injury: molecular changes induced by injury and mesenchymal stromal cell secretome treatment.

Pischiutta, Francesca / Cavaleiro, Helena / Caruso, Enrico / Tribuzio, Francesca / Di Marzo, Noemi / Moro, Federico / Kobeissy, Firas / Wang, Kevin K / Salgado, António J / Zanier, Elisa R

Frontiers in cellular neuroscience

2023 Volume 17, Page(s) 1217987

Abstract: Traumatic brain injury (TBI) is a major worldwide neurological disorder with no neuroprotective treatment available. Three-dimensional (3D) ...

Abstract	Traumatic brain injury (TBI) is a major worldwide neurological disorder with no neuroprotective treatment available. Three-dimensional (3D)
Language	English
Publishing date	2023-07-18
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2023.1217987
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