Endocrine dysfunction following traumatic brain injury: mechanisms, pathophysiology and clinical correlations

Neurointensive care (NIC) has contributed to great improvements in clinical outcomes for patients with severe traumatic brain injury (TBI) by preventing, detecting, and treating secondary insults and thereby reducing secondary brain injury. Traditional NIC management has mainly focused on generally applicable escalated treatment protocols to avoid high intracranial pressure (ICP) and to keep the cerebral perfusion pressure (CPP) at sufficiently high levels. However, TBI is a very heterogeneous disease regarding the type of injury, age, comorbidity, secondary injury mechanisms, etc. In recent years, the introduction of multimodality monitoring, including, e.g., pressure autoregulation, brain tissue oxygenation, and cerebral energy metabolism, in addition to ICP and CPP, has increased the understanding of the complex pathophysiology and the physiological effects of treatments in this condition. In this article, we will present some potential future approaches for more individualized patient management and fine-tuning of NIC, taking advantage of multimodal monitoring to further improve outcome after severe TBI.

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The Use of a Cellular Strain Injury Criterion and Diffusion Tensor Imaging in a Computational Model of Traumatic Brain Injury

ASME 2010 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2010-19562 ◽

2010 ◽

Author(s):

Rika M. Wright ◽

K. T. Ramesh

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Mechanical Loading ◽

Computational Models ◽

Diffusion Tensor ◽

Diffuse Axonal Injury ◽

Element Model ◽

Cellular Level ◽

Cellular Injury ◽

Injury Mechanisms

With the increase in the number of soldiers sustaining traumatic brain injury from military incidents and the recent attention on sports related traumatic brain injury, there has been a focused effort to develop preventative and treatment methods for traumatic brain injury (TBI). Traumatic brain injury is caused by mechanical loading to the head, such as from impacts, sudden accelerations, or blast loading, and the pathology can range from focal damage in the brain to widespread diffuse injury [1]. In this study, we investigate the injury mechanisms of diffuse axonal injury (DAI), which accounts for the second largest percentage of deaths due to brain trauma [2]. DAI is caused by sudden inertial loads to the head, and it is characterized by damage to neural axons. Despite the extensive research on DAI, the coupling between the mechanical loading to the head and the damage at the cellular level is still poorly understood. Unlike previous computational models that use macroscopic stress and strain measures to determine injury, a cellular injury criterion is used in this work as numerous studies have shown that cellular strain can be related to the functional damage of neurons. The effectiveness of using this cellular injury criterion to predict damage in a finite element model of DAI is investigated.

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The Management of Endocrine Dysfunction in Traumatic Brain Injury

Manual of Traumatic Brain Injury ◽

10.1891/9781617052699.0048 ◽

2016 ◽

Author(s):

Lucy-Ann Behan ◽

Amar Agha

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Endocrine Dysfunction

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Blast Traumatic Brain Injury Mechanisms

Neurotrauma ◽

10.1093/med/9780190279431.003.0010 ◽

2018 ◽

pp. 111-122

Author(s):

Elizabeth McNeil ◽

Zachary Bailey ◽

Allison Guettler ◽

Pamela VandeVord

Keyword(s):

Traumatic Brain Injury ◽

Finite Element ◽

Brain Injury ◽

Head Injury ◽

Mechanism Of Injury ◽

Primary Blast ◽

Blast Traumatic Brain Injury ◽

Injury Mechanisms ◽

Biomechanical Investigation

Blast traumatic brain injury (bTBI) is a leading cause of head injury in soldiers returning from the battlefield. Primary blast brain injury remains controversial with little evidence to support a primary mechanism of injury. The four main theories described herein include blast wave transmission through skull orifices, direct cranial transmission, thoracic surge, and skull flexure dynamics. It is possible that these mechanisms do not occur exclusively from each other, but rather that several of them lead to primary blast brain injury. Biomechanical investigation with in-vivo, cadaver, and finite element models would greatly increase our understanding of bTBI mechanisms.

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Temporal Lobe Epilepsy, Stroke, and Traumatic Brain Injury: Mechanisms of Hyperpolarized, Depolarized, and Flow-Through Ion Channels Utilized as Tri-Coordinate Biomarkers of Electrophysiologic Dysfunction

OBM Neurobiology ◽

10.21926/obm.neurobiol.1802009 ◽

2018 ◽

Vol 2 (2) ◽

pp. 1-1 ◽

Cited By ~ 6

Author(s):

Gina Sizemore ◽

◽

Brandon Lucke-Wold ◽

Charles Rosen ◽

James W. Simpkins ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Ion Channels ◽

Temporal Lobe Epilepsy ◽

Temporal Lobe ◽

Injury Mechanisms ◽

Flow Through

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Dysfunction of hypothalamic-hypophysial axis after traumatic brain injury in adults

Journal of Neurosurgery ◽

10.3171/2009.10.jns09930 ◽

2010 ◽

Vol 113 (3) ◽

pp. 581-584 ◽

Cited By ~ 56

Author(s):

David Krahulik ◽

Jirina Zapletalova ◽

Zdenek Frysak ◽

Miroslav Vaverka

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Glasgow Coma Scale ◽

Scale Score ◽

Glasgow Coma Scale Score ◽

Clinical Symptoms ◽

Empty Sella ◽

Pituitary Hormone ◽

Endocrine Dysfunction ◽

Coma Scale

Object Traumatic brain injury (TBI) is a major cause of serious morbidity and mortality. The incidence is 100–500/100,000 inhabitants/year. Chronic pituitary dysfunction is increasingly recognized after TBI. To define the incidence of endocrine dysfunction and risk factors, the authors describe a prospectively assessed group of patients in whom they documented hormonal functions, early diagnosis, and treatment of neuroendocrine dysfunction after TBI. Methods Patients aged 18–65 years were prospectively observed from the time of injury to 1 year postinjury; the Glasgow Coma Scale score ranged from 3 to 14. Patients underwent evaluation of hormonal function at the time of injury and at 3, 6, and 12 months postinjury. Magnetic resonance imaging was also conducted at 1 year postinjury. Results During the study period, 89 patients were observed. The mean age of the patients was 36 years, there were 23 women, and the median Glasgow Coma Scale score was 7. Nineteen patients (21%) had primary hormonal dysfunction. Major deficits included growth hormone dysfunction, hypogonadism, and diabetes insipidus. Patients in whom the deficiency was major had a worse Glasgow Outcome Scale score, and MR imaging demonstrated empty sella syndrome more often than in patients without a deficit. Conclusions To the authors' knowledge, this is the third largest study of its kind worldwide. The incidence of chronic hypopituitarism after TBI was higher than the authors expected. After TBI, patients are usually observed on the neurological and rehabilitative wards, and endocrine dysfunction can be overlooked. This dysfunction can be life threatening and other clinical symptoms can worsen the neurological deficit, extend the duration of physiotherapy, and lead to mental illness. The authors recommend routine pituitary hormone testing after moderate or severe TBI within 6 months and 1 year of injury.

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