The DOI matches its Crossref record; 15 of the 15 references it cites were found in a registry or an index.
Recent Advances in Pathophysiology of Traumatic Brain Injury
Open accessAbstract
BACKGROUND: Traumatic brain injury (TBI) constitutes the primary reason for mortality and morbidity in persons worldwide below 45 years of age. 1.7 million Traumatic events occur yearly in the United States alone, considering for 50,000 deaths. In severe traumatic brain injury sufferers, a considerable achievement attained in treating short-term consequences; but till date, huge failures are occurring in researcher's capability to render severe traumatic brain injury sufferers to an elevated degree of performing. METHODS: Initial damage force results in Primary brain injury, causing tissue destruction and distortion in the early post-injury period. These secondary injuries from TBI cause changes in cell performance and dissemination of trauma via activities like free-radical generation, depolarization, and formation of edema, excitotoxicity, and disruption of blood brain barrier, calcium homeostasis, and intracranial hematoma. The expectation for developing effect in TBI sufferers is the best knowledge of these activities and enhancement of remedies that restrict secondary brain damage. RESULTS: The focal point of this study is on knowing the complex outburst of secondary impairments and studying the pathophysiology of TBI which provides alternative treatment benefits. CONCLUSION: While injured persons demonstrate dissimilar levels of harm and every case is novel with specific recovery profiles, this article strengthens the recent pathophysiological sight of TBI mainly attention on oxidative stress, excitotoxicity, cerebral oxygenation and cerebral blood flow (CBF), development of edema, and inflammatory activities. For initial research acknowledgment of these recurring factors could permit clarification of possible beneficial targets.
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“The pituitary involvement is the result of hemorrhage, infarction or shearing injury lesions, followed by hypoxic insults and an inflammatory reaction [17,18,19,20,21].”
From An Approach to Traumatic Brain Injury-Related Hypopituitarism: Overcoming the Pediatric Challenges (2023) · cites this paper as [18]
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“The mechanism through which vasospasm is caused involves persistent depolarization of vascular smooth muscles owing to decrease in potassium channel action, [110] discharge of endothelin through decreased accessibility of nitric oxide, [111] vascular smooth muscles cyclic GMP reduction, [112] potentiating prostaglandi…”
Cited by
Calina, D., Buga, A. M., Mitroi, M., Buha, A., Caruntu, C., Scheau, C., Bouyahya, A., El Omari, N., El Menyiy, N., & Docea, A. O. (2020) · Journal of Clinical Medicine · doi:10.3390/jcm9082395 · Cited by 65
An Approach to Traumatic Brain Injury-Related Hypopituitarism: Overcoming the Pediatric Challenges
Vlad, R. M., Albu, A. I., Nicolaescu, I. D., Dobritoiu, R., Carsote, M., Sandru, F., Albu, D., & Păcurar, D. (2023) · Diagnostics · doi:10.3390/diagnostics13020212 · Cited by 7
Metadata
- Authors
- Kaur, P., & Sharma, S.
- Venue
- Current Neuropharmacology
- Publisher
- Bentham Science Publishers Ltd.
- Published
- 2018-08-21
- Volume
- 16
- Issue
- 8
- Pages
- 1224-1238
- ISSN
- 1570-159X (ISSN-L)
- OpenAlex
- W2699395010
- Cited by
- 444
- References
- 15
- FWCI
- 8.95
- Type
- journal article
- Language
- en
- Open access
- green
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