scholarly journals Electrospinning-modified Pt/CeO2 nano bandage as a promising therapy to reduce secondary brain injury

2022 ◽  
Vol 13 (1) ◽  
pp. 298-304
Author(s):  
Alfiani Zukhruful Fitri Rifa’i ◽  
Rizqi Apsari Fairuz Kamila ◽  
Clara Alverina ◽  
Reny I’tishom
Keyword(s):  
Brain Injury ◽  
Brain Damage ◽  
Calcium Release ◽  
Channel Blocker ◽  
Age Groups ◽  
Secondary Brain Injury ◽  
Ros Scavenging ◽  
Secondary Brain Damage ◽  
Primary Damage ◽  
Scavenging Efficiency

Traumatic brain injury (TBI) continues to be a major contributor to morbidity, disability, and mortality in all age groups. Initial brain damage is accompanied by acute and irreversible primary damage to the parenchyma, while subsequent secondary brain damage often progresses slowly over months to years, thus providing a window for therapeutic intervention. The most frequent case which happened is excessive oxidative stress and calcium release after brain injury. Although some traditional antioxidants have been clinically approved, the efficacy is far from satisfactory due to their low ROS-scavenging efficiency, instability, toxicity, or inadequate penetration of the blood-brain barrier. Moreover, the combination of Nanozyme based-bandage with Pt/CeO2 atom catalysis with electrospinning nanofibers N-type voltage-gated calcium channel blocker (SNX-185) is predicted to be as promising as a potential novel to reduce secondary injury of TBI. Therefore, the duo could cut down morbidity and mortality rates because of TBI in the future, noninvasively.

Novel Synthetic and Natural Therapies for Traumatic Brain Injury

2021 ◽  
Vol 19 ◽  
Author(s):  
Denise Battaglini ◽  
Dorota Siwicka-Gieroba ◽  
Patricia RM Rocco ◽  
Fernanda Ferreira Cruz ◽  
Pedro Leme Silva ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Molecular Mechanisms ◽  
Antioxidant Properties ◽  
Secondary Brain Injury ◽  
Specific Recommendation ◽  
Novel Therapies ◽  
Secondary Brain Damage ◽  
Late Treatment

: Traumatic brain injury (TBI) is a major cause of disability and death worldwide. The initial mechanical insult results in tissue and vascular disruption with hemorrhages and cellular necrosis that is followed by a dynamic secondary brain damage that presumably results in additional destruction of the brain. In order to minimize deleterious consequences of the secondary brain damage-such as inflammation, bleeding or reduced oxygen supply. The old concept of the -staircase approach- has been updated in recent years by most guidelines and should be followed as it is considered the only validated approach for the treatment of TBI. Besides, a variety of novel therapies have been proposed as neuroprotectants. The molecular mechanisms of each drug involved in inhibition of secondary brain injury can result as potential target for the early and late treatment of TBI. However, no specific recommendation is available on their use in clinical setting. The administration of both synthetic and natural compounds, which act on specific pathways involved in the destructive processes after TBI, even if usually employed for the treatment of other diseases, can show potential benefits. This review represents a massive effort towards current and novel therapies for TBI that have been investigated in both pre-clinical and clinical settings. This review aims to summarize the advancement in therapeutic strategies basing on specific and distinct -target of therapies-: brain edema, ICP control, neuronal activity and plasticity, anti-inflammatory and immunomodulatory effects, cerebral autoregulation, antioxidant properties, and future perspectives with the adoption of mesenchymal stromal cells.

scholarly journals Diagnosis, monitoring and prognosis of secondary brain damage in icu patients with traumatic brain injuries

2018 ◽  
Vol 4 (2) ◽  
pp. 63
Author(s):  
Aikaterini Karipiadou ◽  
Stefanos Korfias ◽  
Evridikh Papastavrou
Keyword(s):  
Brain Injury ◽  
Brain Damage ◽  
Injury Severity ◽  
Cerebral Oxygenation ◽  
Ct Perfusion ◽  
Secondary Brain Injury ◽  
Secondary Brain Damage ◽  
Xenon Ct ◽  
Glascow Coma Scale ◽  
Systemic Level

Traumatic brain injury (TBI) is the brain injury that occurs whenever a physical force that impacts the head leads to neuropathology. The types of primary TBI are penentrating TBI or non-penetrating TBI and it can lead to intracerebral contusions, hemorrhages or extra-axial hematomas. Patients with TBI can also have skull fractures or concussions. The injury severity can be classified in many ways but the most established and common used is the Glascow Coma Scale (GCS). However, with the GCS, each of the severity criteria has limitations and might mot be an accurate predictor of TBI severity and outcome when used alone. For this reason it is often used in conjunction with other parameters (Abbreviated Injury Scale - AIS). Secondary Brain Damage is the injury that occurs to the TBI patient not at the time of the accident, but during the following minutes, hours or days. There are many mechanisms that lead to development of cerebral edema, blood-brain barrier disruption, vasospasm, increase in volume of bleeding, contusions and intracranial hypertension. These mechanisms can act either in cellular level or systemic level. The cellular mechanisms that lead to secondary brain damage include necrosis or apoptosis, mitochondrial dysfunction, excitotoxicicty, formation of free radicals, changes in cerebral glucose metabolism and inflammation. The mechanisms at systemic level include hypoxia-cerebral oxygenation, hypo or hypertension, hypo or hyper-capnia, anemia, hyponatremia and hyper or hypoglycemia. The first tool to diagnose severe TBI and secondary brain injury is neurological assessment. Neuroimaging is one of the most important ways for diagnosis. Computed Tomography (CT scan), Magnetic Resonance Imaging (MRI), cerebral angiography, transcranial Doppler, CT perfusion, Xenon CT, MRI diffusion, MRI perfusion, MRI spectrometry and Positron Emission Tomography (PET) are possible ways of imaging that not only help in the diagnosis but give important information that help in choosing the correct management. Moreover, neuromonitoring, helps in the correct management of the patient.

scholarly journals Inhaled Nitric Oxide Reduces Secondary Brain Damage after Traumatic Brain Injury in Mice

2012 ◽  
Vol 33 (2) ◽  
pp. 311-318 ◽  
Author(s):  
Nicole A Terpolilli ◽  
Seong-Woong Kim ◽  
Serge C Thal ◽  
Wolfgang M Kuebler ◽  
Nikolaus Plesnila
Keyword(s):  
Nitric Oxide ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Brain Regions ◽  
Lesion Volume ◽  
Effective Treatment Option ◽  
Secondary Brain Damage ◽  
Edema Formation ◽  
Regional Ischemia

Ischemia, especially pericontusional ischemia, is one of the leading causes of secondary brain damage after traumatic brain injury (TBI). So far efforts to improve cerebral blood flow (CBF) after TBI were not successful because of various reasons. We previously showed that nitric oxide (NO) applied by inhalation after experimental ischemic stroke is transported to the brain and induces vasodilatation in hypoxic brain regions, thus improving regional ischemia, thereby improving brain damage and neurological outcome. As regional ischemia in the traumatic penumbra is a key mechanism determining secondary posttraumatic brain damage, the aim of the current study was to evaluate the effect of NO inhalation after experimental TBI. NO inhalation significantly improved CBF and reduced intracranial pressure after TBI in male C57 Bl/6 mice. Long-term application (24 hours NO inhalation) resulted in reduced lesion volume, reduced brain edema formation and less blood–brain barrier disruption, as well as improved neurological function. No adverse effects, e.g., on cerebral auto-regulation, systemic blood pressure, or oxidative damage were observed. NO inhalation might therefore be a safe and effective treatment option for TBI patients.

Platelet-activating factor and progressive brain damage following focal brain injury

1990 ◽  
Vol 73 (2) ◽  
pp. 223-233 ◽  
Author(s):  
Kai U. Frerichs ◽  
Perttu J. Lindsberg ◽  
John M. Hallenbeck ◽  
Giora Z. Feuerstein
Keyword(s):  
Brain Injury ◽  
Brain Damage ◽  
Neuronal Death ◽  
Hippocampal Neurons ◽  
Neuronal Damage ◽  
Platelet Activating Factor ◽  
Secondary Brain Damage ◽  
Content Type ◽  
Focal Brain Injury ◽  
Fine Print

✓ The effects of a platelet-activating factor (PAF) antagonist on brain edema, cortical microcirculation, blood-brain barrier (BBB) disruption, and neuronal death following focal brain injury are reported. A neodymium:yttrium-aluminum-garnet (Nd:YAG) laser was used to induce highly reproducible focal cortical lesions in anesthetized rats. Secondary brain damage in this model was characterized by progressive cortical hypoperfusion, edema, and BBB disruption in the vicinity of the hemispheroid lesion occurring acutely after injury. The histopathological evolution was followed for up to 4 days. Neuronal damage in the cortex and the hippocampus (CA-1) was assessed quantitatively, revealing secondary and progressive loss of neuronal tissue within the first 24 hours following injury. Pretreatment with the PAF antagonist BN 50739 ameliorated the severe hypoperfusion in 12 rats (increasing local cerebral blood flow from a mean ± standard error of the mean of 40.5% ± 8.3% to 80.2% ± 7.8%, p < 0.01) and reduced edema by 70% in 10 rats (p < 0.05) acutely after injury. The PAF antagonist also reduced the progression of neuronal damage in the cortex and the CA-1 hippocampal neurons (decrease of neuronal death from 88.0% ± 3.9% to 49.8% ± 4.2% at 24 hours in the cortex and from 40.2 ± 5.0% to 13.2% ± 2.1% in the hippocampus in 30 rats; p < 0.05). This study provides evidence to support progressive brain damage following focal brain injury, associated with secondary loss of neuronal cells. In this latter process, PAF antagonists may provide significant therapeutic protection in arresting secondary brain damage following cerebral ischemia and neurological trauma.

Role of Vasopressin V1a and V2 Receptors for the Development of Secondary Brain Damage after Traumatic Brain Injury in Mice

2008 ◽  
Vol 25 (12) ◽  
pp. 1459-1465 ◽  
Author(s):  
Raimund Trabold ◽  
Sandro Krieg ◽  
Karsten Schöller ◽  
Nikolaus Plesnila
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Secondary Brain Damage

scholarly journals Influence of Organic Solvents on Secondary Brain Damage after Experimental Traumatic Brain Injury

2020 ◽  
Vol 1 (1) ◽  
pp. 148-156
Author(s):  
Johannes Walter ◽  
Julian Schwarting ◽  
Nikolaus Plesnila ◽  
Nicole A. Terpolilli
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Organic Solvents ◽  
Secondary Brain Damage ◽  
Experimental Traumatic Brain Injury

scholarly journals The Role of Bradykinin B1 and B2 Receptors for Secondary Brain Damage after Traumatic Brain Injury in Mice

2009 ◽  
Vol 30 (1) ◽  
pp. 130-139 ◽  
Author(s):  
Raimund Trabold ◽  
Christian Erös ◽  
Klaus Zweckberger ◽  
Jane Relton ◽  
Heike Beck ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Functional Outcome ◽  
Brain Edema ◽  
Brain Damage ◽  
Secondary Brain Damage ◽  
Edema Formation ◽  
Receptor Mrna ◽  
B2 Receptors

Inflammatory mechanisms are known to contribute to the pathophysiology of traumatic brain injury (TBI). Since bradykinin is one of the first mediators activated during inflammation, we investigated the role of bradykinin and its receptors in posttraumatic secondary brain damage. We subjected wild-type (WT), B1-, and B2-receptor-knockout mice to controlled cortical impact (CCI) and analyzed tissue bradykinin as well as kinin receptor mRNA and protein expression up to 48 h thereafter. Brain edema, contusion volume, and functional outcome were assessed 24 h and 7 days after CCI. Tissue bradykinin was maximally increased 2 h after trauma ( P<0.01 versus sham). Kinin B1 receptor mRNA was upregulated up to four-fold 24 h after CCI. Immunohistochemistry showed that B1 and B2 receptors were expressed in the brain and were significantly upregulated in the traumatic penumbra 1 to 24 h after CCI. B2R−/− mice had significantly less brain edema (−51% versus WT, 24 h; P<0.001), smaller contusion volumes (∼50% versus WT 24 h and 7 d after CCI; P<0.05), and better functional outcome 7 days after TBI as compared with WT mice ( P<0.05). The present results show that bradykinin and its B2 receptors play a causal role for brain edema formation and cell death after TBI.

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