scholarly journals Myocardial Injury after Stroke

2021 ◽  
Vol 11 (1) ◽  
pp. 2
Author(s):  
Michal Mihalovic ◽  
Petr Tousek
Keyword(s):  
Heart Disease ◽  
Brain Injury ◽  
Myocardial Injury ◽  
Cardiac Injury ◽  
Complex Interaction ◽  
Blood Biomarkers ◽  
Stroke Patients ◽  
Therapy Strategy ◽  
The Brain

The cardiovascular system is markedly affected by stress after stroke. There is a complex interaction between the brain and heart, and the understanding of the mutual effects has increased in recent decades. Stroke is accompanied by pathological disturbances leading to autonomic dysfunction and systemic inflammation, which leads to changes in cardiomyocyte metabolism. Cardiac injury after stroke may lead to serious complications and long-term cardiac problems. Evidence suggests that blood biomarkers and electrocardiogram analyses can be valuable for estimating the severity, prognosis, and therapy strategy in patients after stroke. It is necessary to distinguish whether these abnormalities presenting in stroke patients are caused by coexisting ischemic heart disease or are caused by brain injury directly. Distinguishing the origin can have a great impact on the treatment of patients after acute stroke. In this article, we focus on epidemiology, pathophysiological mechanisms, and the presentation of cardiac changes in patients after stroke.

scholarly journals GPR110 ligands reduce chronic optic tract gliosis and visual deficit following repetitive mild traumatic brain injury in mice

2021 ◽  
Vol 18 (1) ◽  
Author(s):  
Huazhen Chen ◽  
Karl Kevala ◽  
Elma Aflaki ◽  
Juan Marugan ◽  
Hee-Yong Kim
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Visual Evoked Potential ◽  
Evoked Potential ◽  
Optic Tract ◽  
Primary Microglia ◽  
Visual Dysfunction ◽  
The Brain

Abstract Background Repetitive mild traumatic brain injury (mTBI) can result in chronic visual dysfunction. G-protein receptor 110 (GPR110, ADGRF1) is the target receptor of N-docosahexaenoylethanolamine (synaptamide) mediating the anti-neuroinflammatory function of synaptamide. In this study, we evaluated the effect of an endogenous and a synthetic ligand of GPR110, synaptamide and (4Z,7Z,10Z,13Z,16Z,19Z)-N-(2-hydroxy-2-methylpropyl) docosa-4,7,10,13,16,19-hexaenamide (dimethylsynaptamide, A8), on the mTBI-induced long-term optic tract histopathology and visual dysfunction using Closed-Head Impact Model of Engineered Rotational Acceleration (CHIMERA), a clinically relevant model of mTBI. Methods The brain injury in wild-type (WT) and GPR110 knockout (KO) mice was induced by CHIMERA applied daily for 3 days, and GPR110 ligands were intraperitoneally injected immediately following each impact. The expression of GPR110 and proinflammatory mediator tumor necrosis factor (TNF) in the brain was measured by using real-time quantitative reverse transcription polymerase chain reaction (qRT-PCR) in an acute phase. Chronic inflammatory responses in the optic tract and visual dysfunction were assessed by immunostaining for Iba-1 and GFAP and visual evoked potential (VEP), respectively. The effect of GPR110 ligands in vitro was evaluated by the cyclic adenosine monophosphate (cAMP) production in primary microglia isolated from adult WT or KO mouse brains. Results CHIMERA injury acutely upregulated the GPR110 and TNF gene level in mouse brain. Repetitive CHIMERA (rCHIMERA) increased the GFAP and Iba-1 immunostaining of glia cells and silver staining of degenerating axons in the optic tract with significant reduction of N1 amplitude of visual evoked potential at up to 3.5 months after injury. Both GPR110 ligands dose- and GPR110-dependently increased cAMP in cultured primary microglia with A8, a ligand with improved stability, being more effective than synaptamide. Intraperitoneal injection of A8 at 1 mg/kg or synaptamide at 5 mg/kg significantly reduced the acute expression of TNF mRNA in the brain and ameliorated chronic optic tract microgliosis, astrogliosis, and axonal degeneration as well as visual deficit caused by injury in WT but not in GPR110 KO mice. Conclusion Our data demonstrate that ligand-induced activation of the GPR110/cAMP system upregulated after injury ameliorates the long-term optic tract histopathology and visual impairment caused by rCHIMERA. Based on the anti-inflammatory nature of GPR110 activation, we suggest that GPR110 ligands may have therapeutic potential for chronic visual dysfunction associated with mTBI.

Long-term Quality of Life After Decompressive Craniectomy in Severe Traumatic Brain Injury and Stroke

2021 ◽  
Author(s):  
Alex Vicino ◽  
Philippe Vuadens ◽  
Bertrand Léger ◽  
Charles Benaim
Keyword(s):  
Quality Of Life ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Acute Phase ◽  
Decompressive Craniectomy ◽  
Severe Traumatic Brain Injury ◽  
Full Time ◽  
Stroke Patients

Abstract PurposeDecompressive craniectomy (DC) can rapidly reduce intracranial pressure and save lives in the acute phase of severe traumatic brain injury (TBI) or stroke, but little is known about the long-term outcome after DC. We evaluated quality of life (QoL) a few years after DC for severe TBI/stroke.MethodsThe following data were collected for stroke/TBI patients hospitalized for neurorehabilitation after DC: 1) at discharge, motor and cognitive sub-scores of the Functional Independence Measure (motor-FIM [score 13-91] and cognitive-FIM [score 5-35]) and 2) more than 4 years after discharge, the QOLIBRI health-related QoL (HR-QoL) score (0-100; <60 representing low or impaired QoL) and the return to work (RTW: 0%, partial, 100%)ResultsWe included 88 patients (66 males, median age 38 [interquartile range 26.3-51.0], 65 with TBI/23 stroke); 46 responded to the HR-QoL questionnaire. Responders and non-responders had similar characteristics (age, sex, functional levels upon discharge). Median motor-FIM and cognitive-FIM scores were 85/91 and 27/35, with no significant difference between TBI and stroke patients. Long-term QoL was borderline low for TBI patients and within normal values for stroke patients (score 58.0[42.0-69.0] vs. 67.0[54.0-81.5], p=0.052). RTW was comparable between the groups (62% full time).ConclusionWe already knew that DC can save the lives of TBI or stroke patients in the acute phase and this study suggests that their long-term quality of life is generally quite acceptable.

Potential Role of Adult Hippocampal Neurogenesis in Traumatic Brain Injury

2021 ◽  
Vol 28 ◽  
Author(s):  
Lucas Alexandre Santos Marzano ◽  
Fabyolla Lúcia Macedo de Castro ◽  
Caroline Amaral Machado ◽  
João Luís Vieira Monteiro de Barros ◽  
Thiago Macedo e Cordeiro ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Clinical Studies ◽  
Molecular Mechanisms ◽  
Hippocampal Neurogenesis ◽  
Cognitive Outcomes ◽  
Adult Hippocampal Neurogenesis ◽  
The Brain

: Traumatic brain injury (TBI) is a serious cause of disability and death among young and adult individuals, displaying complex pathophysiology including cellular and molecular mechanisms that are not fully elucidated. Many experimental and clinical studies investigated the potential relationship between TBI and the process by which neurons are formed in the brain, known as neurogenesis. Currently, there are no available treatments for TBI’s long-term consequences being the search for novel therapeutic targets, a goal of highest scientific and clinical priority. Some studies evaluated the benefits of treatments aimed at improving neurogenesis in TBI. In this scenario, herein, we reviewed current pre-clinical studies that evaluated different approaches to improving neurogenesis after TBI while achieving better cognitive outcomes, which may consist in interesting approaches for future treatments.

Sa2015 Traumatic Brain Injury and Intestinal Dysfunction: Investigating a Putative Role of the Brain-Gut Axis in Long-Term Consequences of Injury

2015 ◽  
Vol 148 (4) ◽  
pp. S-384
Author(s):  
Elise L. Ma ◽  
Allen Smith ◽  
Neemesh Desai ◽  
Alan Faden ◽  
Terez Shea-Donohue
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Putative Role ◽  
Long Term Consequences ◽  
The Brain

scholarly journals Annexin A2 Deficiency Exacerbates Neuroinflammation and Long-Term Neurological Deficits after Traumatic Brain Injury in Mice

2019 ◽  
Vol 20 (24) ◽  
pp. 6125 ◽  
Author(s):  
Ning Liu ◽  
Yinghua Jiang ◽  
Joon Yong Chung ◽  
Yadan Li ◽  
Zhanyang Yu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Inflammatory Response ◽  
Neurovascular Unit ◽  
Annexin A2 ◽  
Tissue Loss ◽  
Neurological Deficits ◽  
Endogenous Factors ◽  
The Brain

Our laboratory and others previously showed that Annexin A2 knockout (A2KO) mice had impaired blood–brain barrier (BBB) development and elevated pro-inflammatory response in macrophages, implying that Annexin A2 (AnxA2) might be one of the key endogenous factors for maintaining homeostasis of the neurovascular unit in the brain. Traumatic brain injury (TBI) is an important cause of disability and mortality worldwide, and neurovascular inflammation plays an important role in the TBI pathophysiology. In the present study, we aimed to test the hypothesis that A2KO promotes pro-inflammatory response in the brain and worsens neurobehavioral outcomes after TBI. TBI was conducted by a controlled cortical impact (CCI) device in mice. Our experimental results showed AnxA2 expression was significantly up-regulated in response to TBI at day three post-TBI. We also found more production of pro-inflammatory cytokines in the A2KO mouse brain, while there was a significant increase of inflammatory adhesion molecules mRNA expression in isolated cerebral micro-vessels of A2KO mice compared with wild-type (WT) mice. Consistently, the A2KO mice brains had a significant increase in leukocyte brain infiltration at two days after TBI. Importantly, A2KO mice had significantly worse sensorimotor and cognitive function deficits up to 28 days after TBI and significantly larger brain tissue loss. Therefore, these results suggested that AnxA2 deficiency results in exacerbated early neurovascular pro-inflammation, which leads to a worse long-term neurologic outcome after TBI.

TGFβ1: Friend or Foe During Recovery in Encephalopathy

2018 ◽  
Vol 25 (3) ◽  
pp. 192-198 ◽  
Author(s):  
Brian H. Kim ◽  
Steven W. Levison
Keyword(s):  
Brain Injury ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Neuronal Survival ◽  
Acute Stage ◽  
Tgfβ Signaling ◽  
Immature Brain ◽  
The Brain ◽  
Survival Mechanisms

The cytokine transforming growth factor (TGF)-β1 is highly induced after encephalopathic brain injury, with data showing that it can both contribute to the pathophysiology and aid in disease resolution. In the immature brain, sustained TGFβ-signaling after injury may prolong inflammation to both exacerbate acute stage damage and perturb the normal course of development. Yet in adult encephalopathy, elevated TGFβ1 may promote a reparative state. In this review, we highlight the context-dependent actions of TGFβ-signaling in the brain during resolution of encephalopathy and focus on neuronal survival mechanisms that are affected by TGFβ1. We discuss the mechanisms that contribute to the disparate actions of TGFβ1 toward elucidating the long-term neurological and neuropsychiatric consequences that follow encephalopathic injury.

Practical Challenges in Collecting Head Impact Biomechanics Data in Real-World Scenarios via a Helmet-Based Accelerometer System

2013 ◽  
Author(s):  
Mari A. Allison ◽  
Yun Seok Kang ◽  
Matthew R. Maltese ◽  
John H. Bolte ◽  
Kristy B. Arbogast
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Mild Traumatic Brain Injury ◽  
Real World ◽  
Head Impact ◽  
Permanent Damage ◽  
Head Impact Biomechanics ◽  
Impact Biomechanics ◽  
The Brain

Recent studies have shown that mild traumatic brain injury (mTBI) can have long-term neurological consequences and may cause permanent damage to the brain [1,2]. Given estimates that millions of these injuries occur each year [3], this knowledge has created a demand for countermeasures to prevent mTBI. In order to create countermeasures, the biomechanical inputs leading to mTBI, which are still a matter of debate, must be better understood in both children and adults.

Neuropsychological Syndrome and long term effects of Exposure to Organophosphate Pesticides in Humans

2019 ◽  
Vol 10 (4) ◽  
pp. 1219-1227
Author(s):  
Dr.Maida Zameer ◽  
Dr. Sunbal Siddique ◽  
Dr.Maria Baig
Keyword(s):  
Brain Injury ◽  
Neuropsychological Assessment ◽  
Organophosphate Pesticides ◽  
Significant Morbidity ◽  
Long Term Effects ◽  
Neurological Illness ◽  
Organophosphorous Compounds ◽  
The Brain ◽  
Neuroimaging Techniques

Organophosphorous compounds, the anticholinesterases, produce significant morbidity and mortality in Pakistan. Neuropsychological assessment was traditionally carried out to assess the extent of impairment to a particular skill and to attempt to determine the area of the brain which may have been damaged following brain injury or neurological illness. With the advent of neuroimaging techniques, location of space-occupying lesions can now be more accurately determined through this method, so the focus has now moved on to the assessment of cognition and behaviour, including examining the effects of any brain injury or neuropathological process that a person may have experienced.

scholarly journals Residual Pituitary Function after Brain Injury-Induced Hypopituitarism: A Prospective 12-Month Study

2005 ◽  
Vol 90 (11) ◽  
pp. 6085-6092 ◽  
Author(s):  
Gianluca Aimaretti ◽  
Maria Rosaria Ambrosio ◽  
Carolina Di Somma ◽  
Maurizio Gasperi ◽  
Salvatore Cannavò ◽  
...  
Keyword(s):  
Brain Injury ◽  
High Risk ◽  
Gh Deficiency ◽  
Pituitary Function ◽  
Brain Injured ◽  
Injured Patients ◽  
The Brain ◽  
Over Time

Abstract Context: Traumatic brain injury (TBI) and subarachnoid hemorrhage (SAH) are conditions at high risk for the development of hypopituitarism. Objective: The objective of the study was to clarify whether pituitary deficiencies and normal pituitary function recorded at 3 months would improve or worsen at 12 months after the brain injury. Design and Patients: Pituitary function was tested at 3 and 12 months in patients who had TBI (n = 70) or SAH (n = 32). Results: In TBI, the 3-month evaluation had shown hypopituitarism (H) in 32.8%. Panhypopituitarism (PH), multiple (MH), and isolated (IH) hypopituitarism had been demonstrated in 5.7, 5.7, and 21.4%, respectively. The retesting demonstrated some degree of H in 22.7%. PH, MH, and IH were present in 5.7, 4.2, and 12.8%, respectively. PH was always confirmed at 12 months, whereas MH and IH were confirmed in 25% only. In 5.5% of TBI with no deficit at 3 months, IH was recorded at retesting. In 13.3% of TBI with IH at 3 months, MH was demonstrated at 12-month retesting. In SAH, the 3-month evaluation had shown H in 46.8%. MH and IH had been demonstrated in 6.2 and 40.6%, respectively. The retesting demonstrated H in 37.5%. MH and IH were present in 6.2 and 31.3%, respectively. Although no MH was confirmed at 12 months, two patients with IH at 3 months showed MH at retesting; 30.7% of SAH with IH at 3 months displayed normal pituitary function at retesting. In SAH, normal pituitary function was always confirmed. In TBI and SAH, the most common deficit was always severe GH deficiency. Conclusion: There is high risk for H in TBI and SAH patients. Early diagnosis of PH is always confirmed in the long term. Pituitary function in brain-injured patients may improve over time but, although rarely, may also worsen. Thus, brain-injured patients must undergo neuroendocrine follow-up over time.

scholarly journals Traumatic Injury to the Developing Brain: Emerging Relationship to Early Life Stress

2021 ◽  
Vol 12 ◽  
Author(s):  
Kaila N. Parker ◽  
Michael H. Donovan ◽  
Kylee Smith ◽  
Linda J. Noble-Haeusslein
Keyword(s):  
Brain Injury ◽  
Life Stress ◽  
Early Life ◽  
Brain Injuries ◽  
Traumatic Injury ◽  
Early Life Stress ◽  
Early Age ◽  
Functional Impairments ◽  
The Brain

Despite the high incidence of brain injuries in children, we have yet to fully understand the unique vulnerability of a young brain to an injury and key determinants of long-term recovery. Here we consider how early life stress may influence recovery after an early age brain injury. Studies of early life stress alone reveal persistent structural and functional impairments at adulthood. We consider the interacting pathologies imposed by early life stress and subsequent brain injuries during early brain development as well as at adulthood. This review outlines how early life stress primes the immune cells of the brain and periphery to elicit a heightened response to injury. While the focus of this review is on early age traumatic brain injuries, there is also a consideration of preclinical models of neonatal hypoxia and stroke, as each further speaks to the vulnerability of the brain and reinforces those characteristics that are common across each of these injuries. Lastly, we identify a common mechanistic trend; namely, early life stress worsens outcomes independent of its temporal proximity to a brain injury.

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