Pinocembrin: A Natural Compound For Treatment Of Acute Intracerebral Hemorrhage And Traumatic Brain Injury

2018 ◽  
Author(s):  
Ruhai Huang ◽  
Jian Wang
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Natural Compound ◽  
Acute Intracerebral Hemorrhage

scholarly journals Translational Insights into Traumatic Brain Injury Occurring during Dabigatran or Warfarin Anticoagulation

2014 ◽  
Vol 34 (5) ◽  
pp. 870-875 ◽  
Author(s):  
Jan Hendrik Schaefer ◽  
Wendy Leung ◽  
Limin Wu ◽  
Elizabeth M Van Cott ◽  
Josephine Lok ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Oral Anticoagulants ◽  
International Normalized Ratio ◽  
Thrombin Time ◽  
Limited Data ◽  
Hemorrhage Volume ◽  
Post Hoc ◽  
Safety Advantage

To date, only limited data are available on the effects of pretreatment with novel oral anticoagulants in the event of traumatic brain injury (TBI). We determined intracerebral hemorrhage volume and functional outcome in a standardized TBI model in mice treated with warfarin or dabigatran. Additionally, we investigated whether excess concentrations of dabigatran could increase bleeding and whether this was preventable by using prothrombin complex concentrate (PCC). C57 mice were treated orally with warfarin or dabigatran; sham-treated mice served as controls. Effective anticoagulation was verified by measurement of international normalized ratio and diluted thrombin time, and TBI was induced by controlled cortical impact (CCI). Twenty-four hours after CCI, intracerebral hemorrhage volume was larger in warfarin-pretreated mice than in controls (10.1 ± 4.9 vs 4.1 ± 1.7 μL; analysis of variance post hoc P = 0.001), but no difference was found between controls and dabigatran-pretreated mice (5.3 ± 1.5 μL). PCC applied 30 minutes after CCI did not reliably reduce intracerebral hemorrhage induced by excess dabigatran concentration compared with saline (10.4 ± 11.2 vs 8.7 ± 7.1 μL). Our data suggest pathophysiological differences in TBI occurring during warfarin and dabigatran anticoagulation. The reduced hemorrhage formation under dabigatran therapy could present a safety advantage compared with warfarin. An excess dabigatran concentration, however, can increase hemorrhage.

scholarly journals Case Report: Osteomesh Cranioplasty in a 20-Year-Old Trauma Patient

2021 ◽  
pp. 1-4
Author(s):  
Erickson Torio ◽  
Jonna Maala ◽  
Erickson Torio ◽  
Roy Allan Torcuator
Keyword(s):  
Traumatic Brain Injury ◽  
Case Report ◽  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Trauma Patient ◽  
Decompressive Craniectomy ◽  
Severe Traumatic Brain Injury ◽  
Cranial Defect ◽  
Bone Filler

In this study, we present a case of a 20-year-old male who suffered from severe traumatic brain injury with intracerebral hemorrhage, thus requiring decompressive craniectomy. Five months after, the patient underwent cranioplasty with the use of Osteomesh, a scaffold bone filler in reconstructing the post-operative cranial defect.

scholarly journals TT-301 Inhibits Microglial Activation and Improves Outcome after Central Nervous System Injury in Adult Mice

2012 ◽  
Vol 116 (6) ◽  
pp. 1299-1311 ◽  
Author(s):  
Michael L. James ◽  
Haichen Wang ◽  
Viviana Cantillana ◽  
Beilei Lei ◽  
Dawn N. Kernagis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Functional Outcome ◽  
Differential Gene Expression ◽  
Morris Water Maze ◽  
Water Maze ◽  
Murine Models ◽  
Differential Gene

Background Microglial inhibition may reduce secondary tissue injury and improve functional outcome following acute brain injury. Utilizing clinically relevant murine models of traumatic brain injury and intracerebral hemorrhage, neuroinflammatory responses and functional outcome were examined in the presence of a potential microglial inhibitor, TT-301. Methods TT-301 or saline was administered following traumatic brain injury or intracerebral hemorrhage, and then for four subsequent days. The effect of TT-301 on neuroinflammatory responses and neuronal viability was assessed, as well as short-term vestibulomotor deficit (Rotorod) and long-term neurocognitive impairment (Morris water maze). Finally differential gene expression profiles of mice treated with TT-301 were compared with those of vehicle. Results Reduction in F4/80+ staining was demonstrated at 1 and 10 days, but not 28 days, after injury in mice treated with TT-301 (n = 6). These histologic findings were associated with improved neurologic function as assessed by Rotorod, which improved by 52.7% in the treated group by day 7, and Morris water maze latencies, which improved by 232.5% as a function of treatment (n = 12; P < 0.05). Similar benefit was demonstrated following intracerebral hemorrhage, in which treatment with TT-301 was associated with functional neurologic improvement of 39.6% improvement in Rotorod and a reduction in cerebral edema that was independent of hematoma volume (n = 12; P < 0.05). Differential gene expression was evaluated following treatment with TT-301, and hierarchical cluster analysis implicated involvement of the Janus kinase-Signal Transducer and Activator of Transcription pathway after administration of TT-301 (n = 3/group). Conclusions Modulation of neuroinflammatory responses through TT-301 administration improved histologic and functional parameters in murine models of acute neurologic injury.

Terson syndrome in subarachnoid hemorrhage, intracerebral hemorrhage, and traumatic brain injury

2014 ◽  
Vol 38 (1) ◽  
pp. 129-136 ◽  
Author(s):  
Patrick Czorlich ◽  
Christos Skevas ◽  
Volker Knospe ◽  
Eik Vettorazzi ◽  
Gisbert Richard ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Subarachnoid Hemorrhage ◽  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
Terson Syndrome

Intracerebral Hemorrhage

2017 ◽  
Author(s):  
Craig Anderson
Keyword(s):  
Blood Pressure ◽  
Risk Factor ◽  
Brain Injury ◽  
Intracerebral Hemorrhage ◽  
High Blood Pressure ◽  
Major Risk Factor ◽  
Rapid Control ◽  
Acute Intracerebral Hemorrhage

Acute intracerebral hemorrhage is the most serious and least treatable form of stroke. The major risk factor is high blood pressure (BP). Management is largely supportive-to reduce brain injury, prevent complications, and promote recovery. Recent evidence suggests modest benefits from rapid control of elevated BP. Surgery remains controversial.

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