scholarly journals Multiple Sites of Vasopressin Synthesis in the Injured Brain

2010 ◽  
Vol 31 (1) ◽  
pp. 47-51 ◽  
Author(s):  
Joanna Szmydynger-Chodobska ◽  
Brian J Zink ◽  
Adam Chodobski

Previous studies have indicated that the primary targets for vasopressin actions on the injured brain are the cerebrovascular endothelium and astrocytes, and that vasopressin amplifies the posttraumatic production of proinflammatory mediators. Here, the controlled cortical impact model of traumatic brain injury in rats was used to identify the sources of vasopressin in the injured brain. Injury increased vasopressin synthesis in the hypothalamus and cerebral cortex adjacent to the posttraumatic lesion. In the cortex, vasopressin was predominantly produced by activated microglia/macrophages, and, to a lesser extent, by the cerebrovascular endothelium. These data further support the pathophysiological role of vasopressin in brain injury.

2016 ◽  
Vol 07 (S 01) ◽  
pp. S076-S079 ◽  
Author(s):  
Ashok Munivenkatappa ◽  
Amit Agrawal

ABSTRACTDegree of recovery after traumatic brain injury is highly variable that lasts for many weeks to months. The evidence of brain structures involved in recovery mechanisms is limited. This review highlights evidence of the brain structure particularly thalamus in neuroplasticity mechanism. Thalamus with its complex global networking has potential role in refining the cortical and other brain structures. Thalamic nuclei activation both naturally or by neurorehabilitation in injured brain can enhance and facilitate the improvement of posttraumatic symptoms. This review provides evidence from literature that thalamus plays a key role in recovery mechanism after injury. The study also emphasize that thalamus should be specifically targeted in neurorehabilitation following brain injury.


Neurosurgery ◽  
2013 ◽  
Vol 73 (2) ◽  
pp. 305-311 ◽  
Author(s):  
Rahul Raj ◽  
Jari Siironen ◽  
Riku Kivisaari ◽  
Juha Hernesniemi ◽  
Päivi Tanskanen ◽  
...  

Abstract BACKGROUND: Markers of coagulation have shown to have important value in predicting traumatic brain injury outcome. OBJECTIVE: To externally validate and investigate the role of markers of coagulation for outcome prediction by using the International Mission for Prognosis and Analysis of Clinical Trials (IMPACT) model while adjusting for overall injury severity. METHODS: A retrospective chart analysis of traumatic brain injury patients admitted to Helsinki University Central Hospital between 2009 and 2010 was performed. Outcome was estimated by using the criteria of the IMPACT model. Admission international normalized ratio (INR) and platelet count were used as markers of coagulation. Overall injury severity was categorized with the injury severity score (ISS). Variables were added to the calculated IMPACT risk, generating new models. Model performance was assessed by analyzing and comparing the area under the curve (AUC) of the models. RESULTS: For 342 included patients, 6-month mortality was 32% and unfavorable neurological outcome was 36%. Patients with a poor outcome had lower platelets and higher INR and ISS than those with good outcome (P < .001). The IMPACT model had an AUC of 0.85 for predicting mortality and 0.81 for neurological outcome. Addition of INR but not ISS or platelets to the IMPACT predicted risk improved the predictive validity for mortality ([INCREMENT]AUC 0.02, P = .034) but not neurological outcome ([INCREMENT]AUC 0.00, P = .401). In multivariate analysis, INR remained significant for mortality but not for neurological outcome when adjusting for IMPACT risk and ISS (P = .012). CONCLUSION: The IMPACT model showed excellent performance, and INR was an independent predictor for mortality, independent of overall injury severity.


Author(s):  
Oscar D. Guillamondegui

Traumatic brain injury (TBI) is a serious epidemic in the United States. It affects patients of all ages, race, and socioeconomic status (SES). The current care of these patients typically manifests after sequelae have been identified after discharge from the hospital, long after the inciting event. The purpose of this article is to introduce the concept of identification and management of the TBI patient from the moment of injury through long-term care as a multidisciplinary approach. By promoting an awareness of the issues that develop around the acutely injured brain and linking them to long-term outcomes, the trauma team can initiate care early to alter the effect on the patient, family, and community. Hopefully, by describing the care afforded at a trauma center and by a multidisciplinary team, we can bring a better understanding to the armamentarium of methods utilized to treat the difficult population of TBI patients.


Author(s):  
Sandrine Bourgeois-Tardif ◽  
Louis De Beaumont ◽  
José Carlos Rivera ◽  
Sylvain Chemtob ◽  
Alexander G Weil

BJS Open ◽  
2021 ◽  
Vol 5 (Supplement_1) ◽  
Author(s):  
Stéphane Nguembu ◽  
Marco Meloni ◽  
Geneviève Endalle ◽  
Hugues Dokponou ◽  
Olaoluwa Ezekiel Dada ◽  
...  

Abstract Introduction Most cases of paroxysmal sympathetic hyperactivity (PSH) result from traumatic brain injury (TBI). Little is known about its pathophysiology and treatment, and several neuroprotective drugs are used including beta-blockers. The aim of our study is to collate existing evidence of the role of beta-blockers in the treatment of PSH. Method We will search MEDLINE, Web of Science, EMBASE, Cochrane, and Google Scholar. The search terms used will cover the following terms: “paroxysmal sympathetic hyperactivity”, “traumatic brain injury” and “beta-blockers.”: No language or geographical restrictions will be applied. Two independent co-authors will screen the titles and abstracts of each article following predefined inclusion and exclusion criteria. If there is a conflict the two reviewers will find a consensus and if they cannot a third co-author will decide. Using a pre-designed and pre-piloted data extraction form, data from each included citation will be collected (authors identification, study type, TBI severity, type of beta-blockers used, dosage of the drug, clinical signs of PSH, Glasgow Coma Scale, Glasgow Outcome Scale, mortality, morbidity and length of stay). Simple descriptive data analyses will be performed and the results will be presented both in a narrative and tabular form. Results The effectiveness of beta-blockers in post-TBI PHS will be evaluated through clinical signs of PHS(increased heart rate, respiratory rate, temperature, blood pressure, and sweating), Glasgow Coma Scale, and Glasgow Outcome Scale. mortality, morbidity and length of stay. Conclusion At the end of this scoping review we will design a systematic review with metaanalysis if there are a reasonable number of studies otherwise we will design a randomized controlled trial.


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