Effect of Melatonin on Intracranial Pressure and Brain Edema Following Traumatic Brain Injury: Role of Oxidative Stresses

2013 ◽  
Vol 44 (4) ◽  
pp. 251-258 ◽  
Author(s):  
Fatemeh Dehghan ◽  
Mohammad Khaksari Hadad ◽  
Gholamreza Asadikram ◽  
Hamid Najafipour ◽  
Nader Shahrokhi
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Brain Edema ◽  
Oxidative Stresses

Effect of sex steroid hormones on brain edema, intracranial pressure, and neurologic outcomes after traumatic brain injury

2010 ◽  
Vol 88 (4) ◽  
pp. 414-421 ◽  
Author(s):  
Nader Shahrokhi ◽  
Mohammad Khaksari ◽  
Zahra Soltani ◽  
Mehdi Mahmoodi ◽  
Nouzar Nakhaee
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Steroid Hormones ◽  
Brain Edema ◽  
Sex Steroid Hormones ◽  
Female Rats ◽  
Sex Steroid ◽  
Vehicle Group ◽  
Ovx Rats

Recent studies have reported that estrogen and progesterone have a neuroprotective effect after traumatic brain injury (TBI); however, the mechanism(s) for this effect have not yet been elucidated. The aim of the present study was to investigate the role of sex steroid hormones on changes in brain edema, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) after TBI in ovariectomized (OVX) rats. In this study, 50 female rats were divided into 5 groups: control (intact), sham, and 3 TBI groups consisting of vehicle, estrogen (1 mg/kg), and progesterone (8 mg/kg). TBI was induced by the Marmarou method, and the hormones were injected i.p. 30 min after TBI. ICP was measured in the spinal cord, and CPP was calculated by subtracting the mean arterial pressure (MAP) from ICP. The results revealed that brain water content after TBI was lower (p < 0.001) in the estrogen and progesterone groups than in the vehicle group. After trauma, ICP was significantly higher in TBI rats (p < 0.001). The ICP in the estrogen and progesterone groups decreased at 4 and 24 h after TBI compared with vehicle (p < 0.001 and p < 0.05, respectively). The CPP in the estrogen and progesterone groups increased after 24 h compared with vehicle (p < 0.001). Also after TBI, the neurological score (veterinary coma scale) was significantly higher than vehicle at 1 h (p < 0.01) and 24 h (p < 0.001) in the group treated with estrogen. In conclusion, pharmacological doses of estrogen and progesterone improved ICP, CPP, and neurological scores after TBI in OVX rats, which implies that these hormones play a neuroprotective role in TBI.

scholarly journals Role of extracellular glutamate measured by cerebral microdialysis in severe traumatic brain injury

2010 ◽  
Vol 113 (3) ◽  
pp. 564-570 ◽  
Author(s):  
Roukoz Chamoun ◽  
Dima Suki ◽  
Shankar P. Gopinath ◽  
J. Clay Goodman ◽  
Claudia Robertson
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Mortality Rate ◽  
Functional Outcome ◽  
Excitatory Amino Acid ◽  
Demographic Data ◽  
Cerebral Microdialysis ◽  
Factors Affecting

Object Authors of several studies have implied a key role of glutamate, an excitatory amino acid, in the pathophysiology of traumatic brain injury (TBI). However, the place of glutamate measurement in clinical practice and its impact on the management of TBI has yet to be elucidated. The authors' objective in the present study was to evaluate glutamate levels in TBI, analyzing the factors affecting them and determining their prognostic value. Methods A prospective study of patients with severe TBI was conducted with an inclusion criterion of a Glasgow Coma Scale score ≤ 8 within 48 hours of injury. Invasive monitoring included intracranial pressure measurements, brain tissue PO2, jugular venous O2 saturation, and cerebral microdialysis. Patients received standard care including mass evacuation when indicated and treatment of elevated intracranial pressure values. Demographic data, CT findings, and outcome at 6 months of follow-up were recorded. Results One hundred sixty-five patients were included in the study. Initially high glutamate values were predictive of a poor outcome. The mortality rate was 30.3% among patients with glutamate levels > 20 μmol/L, compared with 18% among those with levels ≤ 20 μmol/L. Two general patterns were recognized: Pattern 1, glutamate levels tended to normalize over the monitoring period (120 hours); and Pattern 2, glutamate levels tended to increase with time or remain abnormally elevated. Patients showing Pattern 1 had a lower mortality rate (17.1 vs 39.6%) and a better 6-month functional outcome among survivors (41.2 vs 20.7%). Conclusions Glutamate levels measured by microdialysis appear to have an important role in TBI. Data in this study suggest that glutamate levels are correlated with the mortality rate and 6-month functional outcome.

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.

scholarly journals Polynitroxylated-Pegylated Hemoglobin Attenuates Fluid Requirements and Brain Edema in Combined Traumatic Brain Injury Plus Hemorrhagic Shock in Mice

2013 ◽  
Vol 33 (9) ◽  
pp. 1457-1464 ◽  
Author(s):  
Erik C Brockman ◽  
Hülya Bayir ◽  
Brian Blasiole ◽  
Steven L Shein ◽  
Ericka L Fink ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Hemorrhagic Shock ◽  
Brain Edema ◽  
Dry Weight ◽  
Bovine Hemoglobin ◽  
Shed Blood ◽  
Brain Water ◽  
Experimental Traumatic Brain Injury

Polynitroxylated-pegylated hemoglobin (PNPH), a bovine hemoglobin decorated with nitroxide and polyethylene glycol moieties, showed neuroprotection vs. lactated Ringer’s (LR) in experimental traumatic brain injury plus hemorrhagic shock (TBI + HS). Hypothesis: Resuscitation with PNPH will reduce intracranial pressure (ICP) and brain edema and improve cerebral perfusion pressure (CPP) vs. LR in experimental TBI + HS. C57/BL6 mice ( n = 20) underwent controlled cortical impact followed by severe HS to mean arterial pressure (MAP) of 25 to 27 mm Hg for 35 minutes. Mice ( n = 10/group) were then resuscitated with a 20 mL/kg bolus of 4% PNPH or LR followed by 10 mL/kg boluses targeting MAP > 70 mm Hg for 90 minutes. Shed blood was then reinfused. Intracranial pressure was monitored. Mice were killed and %brain water (%BW) was measured (wet/dry weight). Mice resuscitated with PNPH vs. LR required less fluid (26.0 ± 0.0 vs. 167.0 ± 10.7 mL/kg, P < 0.001) and had a higher MAP (79.4 ± 0.40 vs. 59.7 ± 0.83 mm Hg, P < 0.001). The PNPH-treated mice required only 20 mL/kg while LR-resuscitated mice required multiple boluses. The PNPH-treated mice had a lower peak ICP (14.5 ± 0.97 vs. 19.7 ± 1.12 mm Hg, P = 0.002), higher CPP during resuscitation (69.2 ± 0.46 vs. 45.5 ± 0.68 mm Hg, P < 0.001), and lower %BW vs. LR (80.3 ± 0.12 vs. 80.9 ± 0.12%, P = 0.003). After TBI + HS, resuscitation with PNPH lowers fluid requirements, improves ICP and CPP, and reduces brain edema vs. LR, supporting its development.

scholarly journals The role of ICP monitoring in meningitis

2017 ◽  
Vol 43 (5) ◽  
pp. E7 ◽  
Author(s):  
Areej Tariq ◽  
Pedro Aguilar-Salinas ◽  
Ricardo A. Hanel ◽  
Neeraj Naval ◽  
Mohamad Chmayssani
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Mortality Rate ◽  
Intracranial Hypertension ◽  
Clinical Outcomes ◽  
Icp Monitoring ◽  
Review Of The Literature ◽  
Cns Infections

Intracranial pressure (ICP) monitoring has been widely accepted in the management of traumatic brain injury. However, its use in other pathologies that affect ICP has not been advocated as strongly, especially in CNS infections. Despite the most aggressive and novel antimicrobial therapies for meningitis, the mortality rate associated with this disease is far from satisfactory. Although intracranial hypertension and subsequent death have long been known to complicate meningitis, no specific guidelines targeting ICP monitoring are available. A review of the literature was performed to understand the pathophysiology of elevated ICP in meningitis, diagnostic challenges, and clinical outcomes in the use of ICP monitoring.

Role of intracranial pressure values and patterns in predicting outcome in traumatic brain injury: a systematic review

2007 ◽  
Vol 6 (2) ◽  
pp. 104-112 ◽  
Author(s):  
Miriam M. Treggiari ◽  
Nicolas Schutz ◽  
N. David Yanez ◽  
Jacques-Andre Romand
Keyword(s):  
Systematic Review ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Predicting Outcome

The role of NLRP3 in traumatic brain injury and its regulation by pioglitazone

2020 ◽  
Vol 133 (4) ◽  
pp. 1083-1091
Author(s):  
Ho Jun Yi ◽  
Jung Eun Lee ◽  
Dong Hoon Lee ◽  
Young Il Kim ◽  
Chul Bum Cho ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Western Blot ◽  
Brain Edema ◽  
Cerebral Edema ◽  
Sham Group ◽  
Secondary Brain Injury ◽  
Treatment Groups ◽  
Perilesional Edema

OBJECTIVEPerilesional edema is a predominant mechanism underlying secondary brain injury after traumatic brain injury (TBI). Perilesional edema is characterized by inflammation, production of proinflammatory cytokines, and migration of peripheral immune cells into the brain. The nucleotide-binding domain and leucine-rich repeat (NLR) family pyrin domain–containing 3 protein (NLRP3) is a key component of secondary injury. Pioglitazone regulates NLRP3 and other inflammatory cytokines. In the present study, the role of NLRP3 and the pharmacological effects of pioglitazone were investigated in animal TBI models.METHODSBrain contusion was induced in a weight drop model involving 3 groups of mice: C57 BL/6 (sham group), NLRP3 knockout (K/O group), and pioglitazone-treated mice (treatment group). The percentage of brain water content of the 3 groups of mice was compared over a period of time. Western blot, immunohistochemistry, and immunofluorescence analyses were conducted to investigate NLRP3-related inflammasomes and the effects of pioglitazone in the TBI models.RESULTSBrain edema was the highest on day 3 after TBI in the sham group. Brain edema in both the K/O and the treatment groups was lower than in the sham group. In Western blot, the expression of inflammasomes was higher after TBI in the sham group, but the expression of interleukin-1β, caspase-1, and NLRP3 was decreased significantly following treatment with pioglitazone. The expression of GFAP (glial fibrillary acidic protein) and Iba1 was decreased in both the K/O and treatment groups. In addition, confocal microscopy revealed a decrease in microglial cell and astrocyte activation following pioglitazone therapy.CONCLUSIONSThe inflammasome NLRP3 plays a pivotal role in regulating cerebral edema and secondary inflammation. Interestingly, pioglitazone reduced cerebral edema and immune response after TBI by downregulating the effects of NLRP3. These results suggest that the clinical application of pioglitazone may be a neuroprotective strategy in TBI.

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