De novo Artistic Behaviour following Brain Injury

2007 ◽  
pp. 75-88 ◽  
Author(s):  
Thomas A. Pollak ◽  
Catherine M. Mulvenna ◽  
Mark F. Lythgoe
Keyword(s):  
Brain Injury ◽  
De Novo

Development of a de novo arteriovenous malformation after severe traumatic brain injury

2014 ◽  
Vol 14 (4) ◽  
pp. 418-420 ◽  
Author(s):  
Brandon A. Miller ◽  
David I. Bass ◽  
Joshua J. Chern
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebral Cortex ◽  
Brain Injury ◽  
Arteriovenous Malformation ◽  
Severe Traumatic Brain Injury ◽  
Arteriovenous Malformations ◽  
De Novo ◽  
First Report ◽  
Congenital Lesions

Arteriovenous malformations (AVMs) are typically considered congenital lesions, although there is growing evidence for de novo formation of these lesions as well. The authors present the case of an AVM in the same cerebral cortex that had been affected by a severe traumatic brain injury (TBI) more than 6 years earlier. To the best of the authors' knowledge, this is the first report attributing the formation of an AVM directly to TBI.

scholarly journals Acute transient cognitive dysfunction and acute brain injury induced by systemic inflammation occur by dissociable IL-1-dependent mechanisms

2017 ◽  
Author(s):  
Donal T. Skelly ◽  
Éadaoin W. Griffin ◽  
Carol L. Murray ◽  
Sarah Harney ◽  
Conor O’Boyle ◽  
...  
Keyword(s):  
Working Memory ◽  
Brain Injury ◽  
Cognitive Dysfunction ◽  
Systemic Inflammation ◽  
De Novo ◽  
Hippocampal Slices ◽  
Memory Deficits ◽  
Acute Brain Injury ◽  
Contextual Fear Conditioning

AbstractSystemic inflammation can impair cognition with relevance to dementia, delirium and post-operative cognitive dysfunction. Acute episodes of delirium also contribute significantly to rates of long-term cognitive decline, implying that de novo pathology occurs during these acute episodes. Whether systemic inflammation-induced acute dysfunction and acute brain injury occur by overlapping or discrete mechanisms has not been investigated. Here we show that systemic inflammation, induced by bacterial LPS, produces both working memory deficits and acute brain injury in the degenerating brain and that these occur by dissociable IL-1-dependent processes. In normal C57BL/6 mice, LPS (100μg/kg) did not affect working memory but robustly impaired contextual fear conditioning (CFC). However prior hippocampal synaptic loss left mice selectively vulnerable to LPS-induced working memory deficits. Systemically administered IL-1 receptor antagonist (IL-1RA) was protective against, and systemic IL-1β replicated, these working memory deficits. Although LPS-induced deficits still occured in IL-1RI-/- mice, systemic TNF-α was sufficient to induce similar deficits, indicating redundancy among these cytokines. Dexamethasone abolished systemic cytokine synthesis and was protective against working memory deficits despite failing to block brain IL-1β synthesis. Direct application of IL-1β to ex vivo hippocampal slices induced non-synaptic depolarisation and irrevesible loss of membrane potential in CA1 neurons from diseased animals and systemic LPS increased apoptosis in the degenerating brain, in an IL-1RI-/- dependent-fashion. The data suggest that LPS induces working memory dysfunction via circulating IL-1β but dysfunction leading to neuronal death is mediated by hippocampal IL-1β. The data suggest that acute systemic inflammation produces both reversible cognitive deficits, resembling delirium, and acute brain injury that may lead to long-term cognitive impairment but that these events are mechanistically dissociable. This would have significant implications for management of cognitive dysfunction and decline during acute illness.

Drug Repurposing in Neurological Disorders: Implications for Neurotherapy in Traumatic Brain Injury

2020 ◽  
pp. 107385842096107
Author(s):  
Zaynab Shakkour ◽  
Karl John Habashy ◽  
Moussa Berro ◽  
Samira Takkoush ◽  
Samar Abdelhady ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Drug Administration ◽  
Neurological Disorders ◽  
De Novo ◽  
Food And Drug Administration ◽  
Drug Repurposing ◽  
Adverse Outcomes ◽  
Minimal Risk ◽  
Wide Range

Traumatic brain injury (TBI) remains a significant leading cause of death and disability among adults and children globally. To date, there are no Food and Drug Administration–approved drugs that can substantially attenuate the sequelae of TBI. The innumerable challenges faced by the conventional de novo discovery of new pharmacological agents led to the emergence of alternative paradigm, which is drug repurposing. Repurposing of existing drugs with well-characterized mechanisms of action and human safety profiles is believed to be a promising strategy for novel drug use. Compared to the conventional discovery pathways, drug repurposing is less costly, relatively rapid, and poses minimal risk of the adverse outcomes to study on participants. In recent years, drug repurposing has covered a wide range of neurodegenerative diseases and neurological disorders including brain injury. This review highlights the advances in drug repurposing and presents some of the promising candidate drugs for potential TBI treatment along with their possible mechanisms of neuroprotection. Edaravone, glyburide, ceftriaxone, levetiracetam, and progesterone have been selected due to their potential role as putative TBI neurotherapeutic agents. These drugs are Food and Drug Administration–approved for purposes other than brain injuries; however, preclinical and clinical studies have shown their efficacy in ameliorating the various detrimental outcomes of TBI.

scholarly journals Typical Spike-and-Wave Activity in Hypoxic-Ischemic Brain Injury and its Implications for classifying Nonconvulsive Status Epilepticus

2012 ◽  
Vol 5 ◽  
pp. CCRep.S9861 ◽  
Author(s):  
Edward C. Mader ◽  
Nicole R. Villemarette-Pittman ◽  
Sergei V. Kashirny ◽  
Lenay Santana-Gould ◽  
Piotr W. Olejniczak
Keyword(s):  
Status Epilepticus ◽  
Brain Injury ◽  
De Novo ◽  
Wave Activity ◽  
Nonconvulsive Status Epilepticus ◽  
Ischemic Brain Injury ◽  
Brain Disorder ◽  
Ischemic Brain ◽  
History Of ◽  
Hypoxic Ischemic Brain Injury

Introduction Typical spike-and-wave activity (TSWA) in the electroencephalogram (EEG) indicates idiopathic generalized epilepsy (IGE). IGE-related nonconvulsive status epilepticus (NCSE) is typically an absence status epilepticus (ASE). ASE and TSWA respond dramatically to benzodiazepines. Patients with no history of seizure/epilepsy may develop ASE “de novo” in the context of an acute brain disorder. However, we are aware of only one previous case of de novo ASE with TSWA in hypoxic-ischemic brain injury. Case Presentation A 65-year-old man, with congestive heart failure and history of substance abuse, survived cardiorespiratory arrest after 18 minutes of cardiopulmonary resuscitation. Post-resuscitation, the patient was in coma with intact brainstem function. Toxicology was positive for cocaine and marijuana. Eyelid myoclonus suggested NCSE, which was initially treated with lorazepam and fosphenytoin. EEG monitoring showed sustained TSWA confirming NCSE and demonstrating de novo ASE (the patient and his family never had seizure/epilepsy). The TSWA was resistant to lorazepam, levetiracetam, and low-dose midazolam; it was eliminated only with midazolam at a dose that resulted in burst-suppression (≥1.2 mg/kg/hour). Conclusion This is an unusual case of TSWA and hypoxic-ischemic brain injury in a patient with no history of seizure/epilepsy. The TSWA was relatively resistant to benzodiazepines suggesting that cerebral hypoxia-ischemia spared the thalamocortical apparatus generating TSWA but impaired the cortical/thalamic inhibitory circuits where benzodiazepines act to suppress TSWA. Albeit rare, ‘posthypoxic’ TSWA offers us some valuable insights for classifying and managing nonconvulsive status epilepticus.

scholarly journals Hipopituitarismo postraumático: reporte de un caso

2017 ◽  
Vol 2 (4) ◽  
pp. 55-59
Author(s):  
Carlos Alfonso Builes Barrera ◽  
Juliana Sierra Zuluaga
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Adrenal Insufficiency ◽  
De Novo ◽  
Past Medical History ◽  
Severe Hyponatremia ◽  
Central Hypothyroidism ◽  
Initial Manifestation ◽  
Moderate Traumatic Brain Injury

Se presenta el caso de un paciente con diagnóstico de novo de hipopituitarismo, cuya manifestación inicial fue con hiponatremia grave, secundaria a una insuficiencia suprarrenal central. Adicionalmente se documentó hipotiroidismo e hipogonadismo centrales. El paciente tuvo una lesión cerebral traumática cuatro décadas atrás y se encontraron en la resonancia nuclear de hipófisis hallazgos de hipoplasia hipofisaria y aracnoidocele selar, apoyando el diagnóstico de hipopituitarismo anterior. El caso resalta la presentación de hipopituitarismo diagnosticado décadas después de una lesión cerebral traumática. Se propone un enfoque para el diagnóstico, tratamiento y seguimiento de estos pacientes en nuestro medio.Abstract We present the case of a patient with previously undiagnosed hypopituitarism, it presents whose initial manifestation was a severe hyponatremia secondary to a central adrenal insufficiency, and besides this deficit he had central hypothyroidism and hypogonadism. In his past medical history he had a moderate traumatic brain injury almost 40 years before. The case highlights the presentation of hypopituitarism decades after a traumatic brain injury. An approach to the diagnosis, treatment and follow-up of these patients in our environment is proposed.

scholarly journals PD-L1-expressing astrocytes act as a gate-keeper for neuroinflammation in the central nervous system of mice with traumatic brain injury

2021 ◽  
Author(s):  
Xiang Gao ◽  
Wei Li ◽  
Fahim Syed ◽  
Fang Yuan ◽  
Ping Li ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
De Novo ◽  
Gene Knockout ◽  
Reactive Astrocytes ◽  
Immune Checkpoints ◽  
Enhanced Production ◽  
The Brain

Background: Tissue damage and cellular destruction are the major events in traumatic brain injury (TBI), which trigger sterile neuroimmune and neuroinflammatory responses in the brain. While appropriate acute and transient neuroimmune and neuroinflammatory responses facilitate the repair and adaptation of injured brain tissues, prolonged and excessive neuroimmune and neuroinflammatory responses exacerbate brain damage. The mechanisms that control the intensity and duration of neuroimmune and neuroinflammatory responses in TBI largely remain elusive. Methods: We used the controlled cortical impact (CCI) model of TBI to study the role of immune checkpoints (ICPs), key regulators of immune homeostasis, in the regulation of neuroimmune and neuroinflammatory responses in the brain in vivo. Results: We found that de novo expression of PD-L1, a potent inhibitory ICP, was robustly and transiently induced in reactive astrocytes, but not in microglial cells, neurons, or oligodendrocyte progenitor cells (OPCs). These PD-L1+ reactive astrocytes were highly enriched to form a dense zone around the TBI lesion. Blockade of PD-L1 signaling enlarged brain tissue cavity size, increased infiltration of inflammatory Ly-6CHigh monocytes/macrophages (M/Mɸ) but not tissue-repairing Ly-6CLow/F4/80+ M/Mɸ, and worsened TBI outcomes in mice. PD-L1 gene knockout enhanced production of CCL2 that interacted with its cognate receptor CCR2 on Ly-6CHigh M/Mϕ to chemotactically recruit these cells into inflammatory sites. Mechanically, PD-L1 signaling in astrocytes likely exhibits dual inhibitory activities for the prevention of excessive neuroimmune and neuroinflammatory responses to TBI through (1) the PD-1/PD-L1 axis to suppress the activity of brain-infiltrating PD-1+ immune cells such as PD-1+ T cells, and (2) PD-L1 reverse signaling to regulate the timing and intensity of astrocyte reactions to TBI. Conclusions: PD-L1+ astrocytes act as a gatekeeper to the brain to control TBI-related neuroimmune and neuroinflammatory responses, thereby opening a novel avenue to study the role of ICP-neuroimmune axes in the pathophysiology of TBI and other neurological disorders.

scholarly journals Neuroprotective Effects of Resveratrol in Ischemic Brain Injury

NeuroSci ◽  
2021 ◽  
Vol 2 (3) ◽  
pp. 305-319
Author(s):  
Noelia D. Machado ◽  
Gorka Villena Armas ◽  
Mariana A. Fernández ◽  
Santiago Grijalvo ◽  
David Díaz Díaz
Keyword(s):  
Brain Injury ◽  
Cerebral Ischemia ◽  
De Novo ◽  
Neuroprotective Effect ◽  
Ischemic Brain Injury ◽  
In Vivo Models ◽  
Ischemic Brain ◽  
Number Of Patients

Cerebral ischemia represents the third cause of death and the first cause of disability in adults. This process results from decreasing cerebral blood flow levels as a result of the occlusion of a major cerebral artery. This restriction in blood supply generates low levels of oxygen and glucose, which leads to a decrease in the energy metabolism of the cell, producing inflammation, and finally, neurological deterioration. Currently, blood restoration of flow is the only effective approach as a therapy in terms of ischemic stroke. However, a significant number of patients still have a poor prognosis, probably owing to the increase in the generation of reactive oxygen species (ROS) during the reperfusion of damaged tissue. Oxidative stress and inflammation can be avoided by modulating mitochondrial function and have been identified as potential targets for the treatment of cerebral ischemia. In recent years, the beneficial actions of flavonoids and polyphenols against cerebrovascular diseases have been extensively investigated. The use of resveratrol (RSV) has been shown to markedly decrease brain damage caused by ischemia in numerous studies. According to in vitro and in vivo experiments, there is growing evidence that RSV is involved in several pathways, including cAMP/AMPK/SIRT1 regulation, JAK/ERK/STAT signaling pathway modulation, TLR4 signal transduction regulation, gut/brain axis modulation, GLUT3 up-regulation inhibition, neuronal autophagy activation, and de novo SUR1 expression inhibition. In this review, we summarize the recent outcomes based on the neuroprotective effect of RSV itself and RSV-loaded nanoparticles in vitro and in vivo models focusing on such mechanisms of action as well as describing the potential therapeutic strategies in which RSV plays an active role in cases of ischemic brain injury.

Cognitive control constrains memory attributions

2019 ◽  
Vol 42 ◽  
Author(s):  
Colleen M. Kelley ◽  
Larry L. Jacoby
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Cognitive Control

Abstract Cognitive control constrains retrieval processing and so restricts what comes to mind as input to the attribution system. We review evidence that older adults, patients with Alzheimer's disease, and people with traumatic brain injury exert less cognitive control during retrieval, and so are susceptible to memory misattributions in the form of dramatic levels of false remembering.

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