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1
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Wang XJ. Research progress of postoperative delirium in neurosurgery. World J Psychiatry 2025; 15:104708. [DOI: 10.5498/wjp.v15.i4.104708] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/29/2024] [Revised: 01/25/2025] [Accepted: 03/07/2025] [Indexed: 03/25/2025] Open
Abstract
Delirium is a transient and acute syndrome of encephalopathy, characterized by disturbances in consciousness, orientation, cognition, perception, and emotional regulation, often accompanied by hallucinations, illusions, psychomotor agitation, and restlessness. Postoperative delirium (POD), a common complication particularly in elderly patients, significantly impacts recovery by prolonging mechanical ventilation, neurosurgical intensive care unit stays, and overall hospitalization durations, while severely diminishing patients’ quality of life after discharge. Despite its prevalence, POD remains underrecognized in clinical practice, with significant gaps in its diagnosis and management. This review explores the definition, diagnostic criteria, underlying pathogenesis, and associated risk factors of POD in neurosurgical patients, aiming to offer valuable insights for improving clinical diagnosis and therapeutic strategies.
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Affiliation(s)
- Xue-Jian Wang
- Department of Neurosurgery, Affiliated Hospital 2 of Nantong University, Nantong 226000, Jiangsu Province, China
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2
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Aljboor GS, Tulemat A, Al-Saedi AR, Radoi MP, Toader C, Papacocea TM. Acute and chronic hypopituitarism following traumatic brain injury: a systematic review and meta-analysis. Neurosurg Rev 2024; 47:841. [PMID: 39527353 PMCID: PMC11554839 DOI: 10.1007/s10143-024-03088-3] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/11/2024] [Revised: 10/17/2024] [Accepted: 11/03/2024] [Indexed: 11/16/2024]
Abstract
Traumatic brain injury (TBI) is associated with various endocrine abnormalities, including pituitary axis dysfunction. Understanding the prevalence and temporal patterns of these dysfunctions is crucial for effective clinical management. This study aimed to systematically review the literature and conduct a meta-analysis to determine the prevalence of pituitary axis dysfunction following TBI, assess temporal patterns across different post-injury durations, and identify potential contributing factors. A comprehensive search was conducted across multiple electronic databases between 1st of January 2000 until 31st March 2024. Studies reporting the prevalence of pituitary axis dysfunction post-TBI were included. Pooled estimates with 95% confidence intervals (CIs) were calculated using random-effects models in the R statistical software. Subgroup analyses were performed based on duration post-TBI (< 3 months, 3-6 months, 6-12 months, > 12 months) to explore temporal variations. Heterogeneity was assessed using the I^2 statistic. A total of 52 studies were included in the meta-analysis, encompassing 7367 participants. The pooled estimate for the prevalence of any pituitary axis dysfunction post-TBI was 33% (95% CI [28%; 37%]). Subgroup analysis by duration revealed varying prevalence rates: < 3 months (40%, 95% CI [27%; 53%]), 3-6 months (31%, 95% CI [15%; 47%]), 6-12 months (26%, 95% CI [19%; 33%]), and > 12 months (32%, 95% CI [26%; 38%]). Prevalence of multiple axes affection was 7% (95% CI [6%; 9%]), with varying rates across durations. Specific axes affection varied: Growth Hormone (GH) deficiency was 18% (95% CI [14%; 21%]), adrenocorticotropic hormone (ACTH) deficiency was 10% (95% CI [8%; 13%]), pituitary-gonadal axis hormones deficiency was 16% (95% CI [12%; 19%]), and thyroid-stimulating hormone (TSH) deficiency was 6% (95% CI [5%; 7%]). This meta-analysis highlights a significant prevalence of pituitary axis dysfunction following TBI, with temporal variations observed across different post-injury durations. The findings underscore the importance of tailored clinical management strategies based on the duration and type of dysfunction. Further research addressing potential contributing factors is warranted to enhance understanding and management of these conditions.
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Affiliation(s)
- Ghaith S Aljboor
- Department of Neurosurgery. 020021, University of Medicine and Pharmacy "Carol Davila", Bucharest, Romania.
- Neurosurgical Department, . Pantelimon Emergency Hospital, Bucharest, Romania.
| | - Aoun Tulemat
- Department of Neurosurgery. 020021, University of Medicine and Pharmacy "Carol Davila", Bucharest, Romania
| | - Ali Ridha Al-Saedi
- Department of Neurosurgery. 020021, University of Medicine and Pharmacy "Carol Davila", Bucharest, Romania
| | - Mugurel Petrinel Radoi
- Department of Neurosurgery. 020021, University of Medicine and Pharmacy "Carol Davila", Bucharest, Romania
- Department of Neurosurgery, National Institute of Neurology and Neurovascular Diseases, 020021, Bucharest, Romania
| | - Corneliu Toader
- Department of Neurosurgery. 020021, University of Medicine and Pharmacy "Carol Davila", Bucharest, Romania
- Department of Neurosurgery, National Institute of Neurology and Neurovascular Diseases, 020021, Bucharest, Romania
| | - Toma Marius Papacocea
- Department of Neurosurgery. 020021, University of Medicine and Pharmacy "Carol Davila", Bucharest, Romania
- Neurosurgical Department, . Pantelimon Emergency Hospital, Bucharest, Romania
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Marina D, Feldt-Rasmussen U, Klose M. Long-term pituitary function and functional and patient-reported outcomes in severe acquired brain injury. Eur J Endocrinol 2024; 190:382-390. [PMID: 38679947 DOI: 10.1093/ejendo/lvae047] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/30/2023] [Revised: 03/05/2024] [Accepted: 03/11/2024] [Indexed: 05/01/2024]
Abstract
OBJECTIVE Assessment of posttraumatic hypothalamic-pituitary dysfunctions is expected to be the most relevant assessment to offer patients with severe intracranial affection. In this study, we aim to investigate the prevalence of hypopituitarism in patients with severe acquired traumatic brain injury (TBI) compared with nontraumatic brain injury (NTBI) and to relate pituitary insufficiency to functional and patient-reported outcomes. DESIGN This is a prospective study. METHODS We included patients admitted for inpatient neurorehabilitation after severe TBI (N = 42) and NTBI (N = 18). The patients underwent a pituitary function assessment at a mean of 2.4 years after the injury. Functional outcome was assessed by using Functional Independence Measure and Glasgow Outcome Scale-Extended (both 1 year after discharge from neurorehabilitation) and patient-reported outcome was assessed by using Multiple Fatigue Inventory-20 and EQ-5D-3L. RESULTS Hypopituitarism was reported in 10/42 (24%) patients with TBI and 7/18 (39%) patients with NTBI (P = .23). Insufficiencies affected 1 axis in 14/17 (82%) patients (13 hypogonadotropic hypogonadism and 1 growth hormone [GH] deficiency) and 2 axes in 3/17 (18%) patients (1 hypogonadotropic hypogonadism and GH deficiency, and 2 hypogonadotropic hypogonadism and arginin vasopressin deficiency). None had central hypoadrenalism or central hypothyroidism. In patients with both TBI and NTBI, pituitary status was unrelated to functioning and ability scores at 1 year and to patient-reported outcome scores at a mean of 2.4 years after the injury. CONCLUSION Patients with severe acquired brain injury may develop long-term hypothalamus-pituitary insufficiency, with an equal occurrence in patients with TBI and NTBI. In both types of patients, mainly isolated deficiencies, most commonly affecting the gonadal axis, were seen. Insufficiencies were unrelated to functional outcomes and patient-reported outcomes, probably reflecting the complexity and heterogeneous manifestations in both patient groups.
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Affiliation(s)
- Djordje Marina
- Department of Medical Endocrinology and Metabolism PE2131, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark
| | - Ulla Feldt-Rasmussen
- Department of Medical Endocrinology and Metabolism PE2131, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark
- Faculty of Health and Clinical Sciences, Institute of Clinical Medicine, Copenhagen University, Copenhagen, Denmark
| | - Marianne Klose
- Department of Medical Endocrinology and Metabolism PE2131, Rigshospitalet, Copenhagen University Hospital, Copenhagen, Denmark
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Fernández Rodriguez E, Villar Taibo R, Bernabeu I. Hypopituitarism after traumatic brain injury in adults: Clinical guidelines of the neuroendocrinology area of the Spanish Society of Endocrinology and Nutrition (SEEN). ENDOCRINOL DIAB NUTR 2023; 70:584-591. [PMID: 37977921 DOI: 10.1016/j.endien.2023.11.002] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/12/2023] [Accepted: 07/20/2023] [Indexed: 11/19/2023]
Abstract
Traumatic brain injury (TBI) is associated with hypopituitarism with a variable incidence, depending on the time and methods used to diagnosis, and on factors related to the trauma, such as its severity, its anatomical location and the drugs used in the acute phase. The pituitary gland can be damaged directly by the impact or secondary to factors such as ischemia, inflammation, excitotoxicity or immunity. In acute phases ACTH deficiency is the most relevant, since failure to detect and treat it can compromise the patient's life. Clinical manifestations are typical of each hormone deficient axes, although the combination hypopituitarism-trauma has been associated with cognitive deterioration, worse metabolic profile and greater impairment of quality of life. One of the clinical challenges is to determine which patients benefit from a systematic hormonal evaluation, and therefore from hormone replacement, and what is the appropriate time to do so and the most suitable diagnostic methods.
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Affiliation(s)
- Eva Fernández Rodriguez
- Servicio de Endocrinología y Nutrición, Complejo Hospitalario Universitario de Ourense, Ourense, Spain
| | - Rocío Villar Taibo
- Servicio de Endocrinología y Nutrición, Complejo Hospitalario Universitario de Santiago de Compostela, Santiago de Compostela, A Coruña, Spain
| | - Ignacio Bernabeu
- Servicio de Endocrinología y Nutrición, Complejo Hospitalario Universitario de Santiago de Compostela, Santiago de Compostela, A Coruña, Spain.
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Wexler TL, Reifschneider K, Backeljauw P, Cárdenas JF, Hoffman AR, Miller BS, Yuen KCJ. Growth Hormone Deficiency following Traumatic Brain Injury in Pediatric and Adolescent Patients: Presentation, Treatment, and Challenges of Transitioning from Pediatric to Adult Services. J Neurotrauma 2023. [PMID: 36825511 DOI: 10.1089/neu.2022.0384] [Citation(s) in RCA: 6] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 02/25/2023] Open
Abstract
Traumatic brain injury (TBI) is increasingly recognized, with an incidence of approximately 110 per 100,000 in pediatric populations and 618 per 100,000 in adolescent and adult populations. TBI often leads to cognitive, behavioral, and physical consequences, including endocrinopathies. Deficiencies in anterior pituitary hormones (e.g., adrenocorticotropic hormone, thyroid-stimulating hormone, gonadotropins, and growth hormone [GH]) can negatively impact health outcomes and quality of life post-TBI. This review focuses on GH deficiency (GHD), the most common post-TBI pituitary hormone deficiency. GHD is associated with abnormal body composition, lipid metabolism, bone mineral density, executive brain functions, behavior, and height outcomes in pediatric, adolescent, and transition-age patients. Despite its relatively frequent occurrence, post-TBI GHD has not been well studied in these patients; hence, diagnostic and treatment recommendations are limited. Here, we examine the occurrence and diagnosis of TBI, retrospectively analyze post-TBI hypopituitarism and GHD prevalence rates in pediatric and adolescent patients, and discuss appropriate GHD testing strategies and GH dosage recommendations for these patients. We place particular emphasis on the ways in which testing and dosage recommendations may change during the transition phase. We conclude with a review of the challenges faced by transition-age patients and how these may be addressed to improve access to adequate healthcare. Little information is currently available to help guide patients with TBI and GHD through the transition phase and there is a risk of interrupted care; therefore, a strength of this review is its emphasis on this critical period in a patient's healthcare journey.
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Affiliation(s)
- Tamara L Wexler
- Department of Rehabilitation Medicine, NYU Langone Health, New York, New York, USA
- Division of Endocrinology, Diabetes, and Metabolism, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, USA
| | - Kent Reifschneider
- Children's Hospital of The King's Daughters, Eastern Virginia Medical Center, Norfolk, Virginia, USA
| | - Philippe Backeljauw
- Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA
| | - Javier F Cárdenas
- Barrow Concussion and Brain Injury Center, Barrow Neurological Institute, University of Arizona College of Medicine and Creighton School of Medicine, Phoenix, Arizona, USA
| | - Andrew R Hoffman
- Department of Medicine, Division of Endocrinology, Metabolism and Gerontology, Stanford University School of Medicine, Stanford, California, USA
| | - Bradley S Miller
- Department of Pediatrics, Division of Pediatric Endocrinology, University of Minnesota Medical School, M Health Fairview Masonic Children's Hospital, Minneapolis, Minnesota, USA
| | - Kevin C J Yuen
- Barrow Pituitary Center, Barrow Neurological Institute, University of Arizona College of Medicine and Creighton School of Medicine, Phoenix, Arizona, USA
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6
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Bakalkin G. The left-right side-specific endocrine signaling in the effects of brain lesions: questioning of the neurological dogma. Cell Mol Life Sci 2022; 79:545. [PMID: 36219330 PMCID: PMC9553812 DOI: 10.1007/s00018-022-04576-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/26/2022] [Revised: 09/26/2022] [Accepted: 09/27/2022] [Indexed: 11/25/2022]
Abstract
Each cerebral hemisphere is functionally connected to the contralateral side of the body through the decussating neural tracts. The crossed neural pathways set a basis for contralateral effects of brain injury such hemiparesis and hemiplegia as it has been already noted by Hippocrates. Recent studies demonstrated that, in addition to neural mechanisms, the contralateral effects of brain lesions are mediated through the humoral pathway by neurohormones that produce either the left or right side-specific effects. The side-specific humoral signaling defines whether the left or right limbs are affected after a unilateral brain injury. The hormonal signals are released by the pituitary gland and may operate through their receptors that are lateralized in the spinal cord and involved in the side-specific control of symmetric neurocircuits innervating the left and right limbs. Identification of features and a proportion of neurological deficits transmitted by neurohormonal signals vs. those mediated by neural pathways is essential for better understanding of mechanisms of brain trauma and stroke and development of new therapies. In a biological context, the left-right side-specific neuroendocrine signaling may be fundamental for the control of the left- and right-sided processes in bilaterally symmetric animals.
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Affiliation(s)
- Georgy Bakalkin
- Department of Pharmaceutical Biosciences, Uppsala University, Box 591, SE-751 24, Uppsala, Sweden.
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Akira M, Yuichi T, Tomotaka U, Takaaki K, Kenichi M, Chimi M. The Outcome of Neurorehabilitation Efficacy and Management of Traumatic Brain Injury. Front Hum Neurosci 2022; 16:870190. [PMID: 35814948 PMCID: PMC9256961 DOI: 10.3389/fnhum.2022.870190] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/06/2022] [Accepted: 05/31/2022] [Indexed: 11/13/2022] Open
Abstract
For public health professionals, traumatic brain injury (TBI) and its possible protracted repercussions are a significant source of worry. In opposed to patient neurorehabilitation with developed brain abnormalities of different etiologies, neurorehabilitation of affected persons has several distinct features. The clinical repercussions of the various types of TBI injuries will be discussed in detail in this paper. During severe TBI, the medical course frequently follows a familiar first sequence of coma, accompanied by disordered awareness, followed by agitation and forgetfulness, followed by return of function. Clinicians must be aware of common medical issues that might occur throughout the various stages of neurorehabilitation, for example, posttraumatic hydrocephalus, paroxysmal sympathetic hyperactivity and posttraumatic neuroendocrine disorders, at each step of the process. Furthermore, we address problems about the scheduling of various rehabilitation programs as well as the availability of current data for comprehensive rehabilitative neuropsychology techniques.
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Affiliation(s)
- Miyamoto Akira
- Faculty of Rehabilitation Sciences, Nishikyushu University, Kanzaki, Japan
| | - Takata Yuichi
- Faculty of Human Science, Hokkaido Bunkyo University, Eniwa, Japan
| | - Ueda Tomotaka
- Faculty of Rehabilitation Sciences, Nishikyushu University, Kanzaki, Japan
| | - Kubo Takaaki
- Division of Physical Therapy, Department of Rehabilitation, Faculty of Health Science, Kumamoto Health Science University, Kumamoto, Japan
| | - Mori Kenichi
- Omote Orthopedic Osteoporosis Clinic, Toyonaka, Japan
| | - Miyamoto Chimi
- Department of Occupational Therapy, Faculty of Health Science, Aino University, Ibaraki, Japan
- *Correspondence: Miyamoto Chimi,
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8
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Abstract
The epidemiology of male hypogonadism has been understudied. Of the known causes of endogenous androgen deficiency, only Klinefelter syndrome is common with a likely population prevalence of greater than 5:10,000 men (possibly as high as 10-25:10,000). Mild traumatic injury might also be a common cause of androgen deficiency (prevalence 5-10:10,000 men), but large, long-term studies must be completed to confirm this prevalence estimation that might be too high. The classic causes of male androgen deficiency-hyperprolactinemia, pituitary macroadenoma, endogenous Cushing syndrome, and iron overload syndrome-are rare (prevalence < 10,000 men).
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Affiliation(s)
- Arthi Thirumalai
- Department of Medicine, University of Washington School of Medicine, Box 356420, 1959 Northeast Pacific Avenue, Seattle, WA 98195, USA
| | - Bradley D Anawalt
- Department of Medicine, University of Washington School of Medicine, Box 356420, 1959 Northeast Pacific Avenue, Seattle, WA 98195, USA.
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Wang TY, Xia FY, Gong JW, Xu XK, Lv MC, Chatoo M, Shamsi BH, Zhang MC, Liu QR, Liu TX, Zhang DD, Lu XJ, Zhao Y, Du JZ, Chen XQ. CRHR1 mediates the transcriptional expression of pituitary hormones and their receptors under hypoxia. Front Endocrinol (Lausanne) 2022; 13:893238. [PMID: 36147561 PMCID: PMC9487150 DOI: 10.3389/fendo.2022.893238] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/10/2022] [Accepted: 08/03/2022] [Indexed: 11/13/2022] Open
Abstract
Hypothalamus-pituitary-adrenal (HPA) axis plays critical roles in stress responses under challenging conditions such as hypoxia, via regulating gene expression and integrating activities of hypothalamus-pituitary-targets cells. However, the transcriptional regulatory mechanisms and signaling pathways of hypoxic stress in the pituitary remain to be defined. Here, we report that hypoxia induced dynamic changes in the transcription factors, hormones, and their receptors in the adult rat pituitary. Hypoxia-inducible factors (HIFs), oxidative phosphorylation, and cAMP signaling pathways were all differentially enriched in genes induced by hypoxic stress. In the pituitary gene network, hypoxia activated c-Fos and HIFs with specific pituitary transcription factors (Prop1), targeting the promoters of hormones and their receptors. HIF and its related signaling pathways can be a promising biomarker during acute or constant hypoxia. Hypoxia stimulated the transcription of marker genes for microglia, chemokines, and cytokine receptors of the inflammatory response. Corticotropin-releasing hormone receptor 1 (CRHR1) mediated the transcription of Pomc, Sstr2, and Hif2a, and regulated the function of HPA axis. Together with HIF, c-Fos initiated and modulated dynamic changes in the transcription of hormones and their receptors. The receptors were also implicated in the regulation of functions of target cells in the pituitary network under hypoxic stress. CRHR1 played an integrative role in the hypothalamus-pituitary-target axes. This study provides new evidence for CRHR1 involved changes of hormones, receptors, signaling molecules and pathways in the pituitary induced by hypoxia.
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Affiliation(s)
- Tong Ying Wang
- Department of Neurobiology, Department of Neurology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
- National Health Commission and Chinese Academy of Medical Sciences Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China
- Department of Research and Development, Jiuyuan Gene Engineering, Hangzhou, China
| | - Fang Yuan Xia
- Department of Neurobiology, Department of Neurology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
- National Health Commission and Chinese Academy of Medical Sciences Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China
| | - Jing Wen Gong
- Department of Pathology, and Department of Medical Oncology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
| | - Xiao Kang Xu
- Department of Neurobiology, Department of Neurology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
- National Health Commission and Chinese Academy of Medical Sciences Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China
| | - Min Chao Lv
- Department of Orthopedics, The Quzhou Affiliated Hospital of Wenzhou Medical University, Quzhou People's Hospital, Quzhou, China
| | - Mahanand Chatoo
- Department of Neurobiology, Department of Neurology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
- National Health Commission and Chinese Academy of Medical Sciences Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China
| | - Bilal Haider Shamsi
- Department of Neurobiology, Department of Neurology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
- National Health Commission and Chinese Academy of Medical Sciences Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China
| | - Meng Chen Zhang
- Department of Neurobiology, Department of Neurology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
- National Health Commission and Chinese Academy of Medical Sciences Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China
| | - Qian Ru Liu
- Department of Neurobiology, Department of Neurology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
- National Health Commission and Chinese Academy of Medical Sciences Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China
| | - Tian Xing Liu
- Department of Cell and System Biology, University of Toronto, St. George, NB, Canada
| | - Dan Dan Zhang
- Department of Pathology, and Department of Medical Oncology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
| | - Xin Jiang Lu
- Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China
| | - Yang Zhao
- Department of Physiology, Zhejiang University School of Medicine, Hangzhou, China
| | - Ji Zeng Du
- National Health Commission and Chinese Academy of Medical Sciences Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China
| | - Xue Qun Chen
- Department of Neurobiology, Department of Neurology of the Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
- National Health Commission and Chinese Academy of Medical Sciences Key Laboratory of Medical Neurobiology, Ministry of Education Frontier Science Center for Brain Research and Brain Machine Integration, School of Brain Science and Brain Medicine, Zhejiang University, Hangzhou, China
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First Case of Chronic Post-Traumatic Anterior Pituitary Dysfunction in a Professional Rugby Player: A Case Report. ANNALES D'ENDOCRINOLOGIE 2022; 83:142-146. [DOI: 10.1016/j.ando.2021.12.005] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Received: 12/05/2021] [Revised: 12/16/2021] [Accepted: 12/24/2021] [Indexed: 11/24/2022]
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Zhang Y, Huang Z, Xia H, Xiong J, Ma X, Liu C. The benefits of exercise for outcome improvement following traumatic brain injury: Evidence, pitfalls and future perspectives. Exp Neurol 2021; 349:113958. [PMID: 34951984 DOI: 10.1016/j.expneurol.2021.113958] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/15/2021] [Revised: 12/04/2021] [Accepted: 12/15/2021] [Indexed: 12/15/2022]
Abstract
Traumatic brain injury (TBI), also known as a silent epidemic, is currently a substantial public health problem worldwide. Given the increased energy demands following brain injury, relevant guidelines tend to recommend absolute physical and cognitive rest for patients post-TBI. Nevertheless, recent evidence suggests that strict rest does not provide additional benefits to patients' recovery. By contrast, as a cost-effective non-pharmacological therapy, exercise has shown promise for enhancing functional outcomes after injury. This article summarizes the most recent evidence supporting the beneficial effects of exercise on TBI outcomes, focusing on the efficacy of exercise for cognitive recovery after injury and its potential mechanisms. Available evidence demonstrates the potential of exercise in improving cognitive impairment, mood disorders, and post-concussion syndrome following TBI. However, the clinical application for exercise rehabilitation in TBI remains challenging, particularly due to the inadequacy of the existing clinical evaluation system. Also, a better understanding of the underlying mechanisms whereby exercise promotes its most beneficial effects post-TBI will aid in the development of new clinical strategies to best benefit of these patients.
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Affiliation(s)
- Yulan Zhang
- Cognitive & Sports Neuroscience Laboratory, National Demonstration Center for Experimental Sports Science Education, College of Physical Education and Sports Science, South China Normal University, Guangzhou, Guangdong 510006, China; Laboratory of Laser Sports Medicine, College of Physical Education and Sports Science, South China Normal University, Guangzhou, Guangdong 510006, China
| | - Zhihai Huang
- Cognitive & Sports Neuroscience Laboratory, National Demonstration Center for Experimental Sports Science Education, College of Physical Education and Sports Science, South China Normal University, Guangzhou, Guangdong 510006, China
| | - Honglin Xia
- Laboratory of Regenerative Medicine in Sports Science, College of Physical Education and Sports Science, South China Normal University, Guangzhou, Guangdong 510006, China
| | - Jing Xiong
- Cognitive & Sports Neuroscience Laboratory, National Demonstration Center for Experimental Sports Science Education, College of Physical Education and Sports Science, South China Normal University, Guangzhou, Guangdong 510006, China; Laboratory of Laser Sports Medicine, College of Physical Education and Sports Science, South China Normal University, Guangzhou, Guangdong 510006, China
| | - Xu Ma
- Cognitive & Sports Neuroscience Laboratory, National Demonstration Center for Experimental Sports Science Education, College of Physical Education and Sports Science, South China Normal University, Guangzhou, Guangdong 510006, China; Laboratory of Laser Sports Medicine, College of Physical Education and Sports Science, South China Normal University, Guangzhou, Guangdong 510006, China
| | - Chengyi Liu
- Laboratory of Laser Sports Medicine, College of Physical Education and Sports Science, South China Normal University, Guangzhou, Guangdong 510006, China.
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Kumaria A, Robertson IJA, Tolias CM. Autoimmunity following traumatic brain injury: hypopituitarism and beyond. Br J Neurosurg 2021; 35:796. [DOI: 10.1080/02688697.2019.1645300] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/26/2022]
Affiliation(s)
- Ashwin Kumaria
- Department of Neurosurgery, Queen’s Medical Centre, Nottingham, UK
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Lukoyanov N, Watanabe H, Carvalho LS, Kononenko O, Sarkisyan D, Zhang M, Andersen MS, Lukoyanova EA, Galatenko V, Tonevitsky A, Bazov I, Iakovleva T, Schouenborg J, Bakalkin G. Left-right side-specific endocrine signaling complements neural pathways to mediate acute asymmetric effects of brain injury. eLife 2021; 10:e65247. [PMID: 34372969 PMCID: PMC8354641 DOI: 10.7554/elife.65247] [Citation(s) in RCA: 10] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/27/2020] [Accepted: 07/07/2021] [Indexed: 12/14/2022] Open
Abstract
Brain injuries can interrupt descending neural pathways that convey motor commands from the cortex to spinal motoneurons. Here, we demonstrate that a unilateral injury of the hindlimb sensorimotor cortex of rats with completely transected thoracic spinal cord produces hindlimb postural asymmetry with contralateral flexion and asymmetric hindlimb withdrawal reflexes within 3 hr, as well as asymmetry in gene expression patterns in the lumbar spinal cord. The injury-induced postural effects were abolished by hypophysectomy and were mimicked by transfusion of serum from animals with brain injury. Administration of the pituitary neurohormones β-endorphin or Arg-vasopressin-induced side-specific hindlimb responses in naive animals, while antagonists of the opioid and vasopressin receptors blocked hindlimb postural asymmetry in rats with brain injury. Thus, in addition to the well-established involvement of motor pathways descending from the brain to spinal circuits, the side-specific humoral signaling may also add to postural and reflex asymmetries seen after brain injury.
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Affiliation(s)
- Nikolay Lukoyanov
- Departamento de Biomedicina da Faculdade de Medicina da Universidade do Porto, Instituto de Investigação e Inovação em Saúde, Instituto de Biologia Molecular e CelularPortoPortugal
| | - Hiroyuki Watanabe
- Department of Pharmaceutical Biosciences, Uppsala UniversityUppsalaSweden
| | - Liliana S Carvalho
- Departamento de Biomedicina da Faculdade de Medicina da Universidade do Porto, Instituto de Investigação e Inovação em Saúde, Instituto de Biologia Molecular e CelularPortoPortugal
| | - Olga Kononenko
- Department of Pharmaceutical Biosciences, Uppsala UniversityUppsalaSweden
| | - Daniil Sarkisyan
- Department of Pharmaceutical Biosciences, Uppsala UniversityUppsalaSweden
| | - Mengliang Zhang
- Neuronano Research Center, Department of Experimental Medical Science, Lund UniversityLundSweden
- Department of Molecular Medicine, University of Southern DenmarkOdenseDenmark
| | | | - Elena A Lukoyanova
- Departamento de Biomedicina da Faculdade de Medicina da Universidade do Porto, Instituto de Investigação e Inovação em Saúde, Instituto de Biologia Molecular e CelularPortoPortugal
| | - Vladimir Galatenko
- Faculty of Mechanics and Mathematics, Lomonosov Moscow State UniversityMoscowRussian Federation
| | - Alex Tonevitsky
- Faculty of Biology and Biotechnology, National Research University Higher School of EconomicsMoscowRussian Federation
- Shemyakin–Ovchinnikov Institute of Bioorganic Chemistry RASMoscowRussian Federation
| | - Igor Bazov
- Department of Pharmaceutical Biosciences, Uppsala UniversityUppsalaSweden
| | - Tatiana Iakovleva
- Department of Pharmaceutical Biosciences, Uppsala UniversityUppsalaSweden
| | - Jens Schouenborg
- Neuronano Research Center, Department of Experimental Medical Science, Lund UniversityLundSweden
| | - Georgy Bakalkin
- Department of Pharmaceutical Biosciences, Uppsala UniversityUppsalaSweden
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14
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Feldt-Rasmussen U, Effraimidis G, Klose M. The hypothalamus-pituitary-thyroid (HPT)-axis and its role in physiology and pathophysiology of other hypothalamus-pituitary functions. Mol Cell Endocrinol 2021; 525:111173. [PMID: 33549603 DOI: 10.1016/j.mce.2021.111173] [Citation(s) in RCA: 42] [Impact Index Per Article: 10.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 12/09/2020] [Revised: 01/14/2021] [Accepted: 01/18/2021] [Indexed: 12/16/2022]
Abstract
The hypothalamus-pituitary-thyroid axis is one of several hormone regulatory systems from the hypothalamus to the pituitary and ultimately to the peripheral target organs. The hypothalamus and the pituitary gland are in close anatomical proximity at the base of the brain and extended through the pituitary stalk to the sella turcica. The pituitary stalk allows passage of stimulatory and inhibitory hormones and other signal molecules. The target organs are placed in the periphery and function through stimulation/inhibition by the circulating pituitary hormones. The several hypothalamus-pituitary-target organ axis systems interact in very sophisticated and complicated ways and for many of them the interactive and integrated mechanisms are still not quite clear. The diagnosis of central hypothyroidism is complicated by itself but challenged further by concomitant affection of other hypothalamus-pituitary-hormone axes, the dysfunction of which influences the diagnosis of central hypothyroidism. Treatment of both the central hypothyroidism and the other hypothalamus-pituitary axes also influence the function of the others by complex mechanisms involving both central and peripheral mechanisms. Clinicians managing patients with neuroendocrine disorders should become aware of the strong integrative influence from each hypothalamus-pituitary-hormone axis on the physiology and pathophysiology of central hypothyroidism. As an aid in this direction the present review summarizes and highlights the importance of the hypothalamus-pituitary-thyroid axis, pitfalls in diagnosing central hypothyroidism, diagnosing/testing central hypothyroidism in relation to panhypopituitarism, pointing at interactions of the thyroid function with other pituitary hormones, as well as local hypothalamic neurotransmitters and gut-brain hormones. Furthermore, the treatment effect of each axis on the regulation of the others is described. Finally, these complicating aspects require stringent diagnostic testing, particularly in clinical settings with lower or at least altered à priori likelihood of hypopituitarism than in former obvious clinical patient presentations.
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Affiliation(s)
- Ulla Feldt-Rasmussen
- Department of Medical Endocrinology and Metabolism, Rigshospitalet, Copenhagen University Hospital, Denmark; Institute of Clinical Medicine, Faculty of Health and Medical Sciences, Copenhagen University, Denmark.
| | - Grigoris Effraimidis
- Department of Medical Endocrinology and Metabolism, Rigshospitalet, Copenhagen University Hospital, Denmark
| | - Marianne Klose
- Department of Medical Endocrinology and Metabolism, Rigshospitalet, Copenhagen University Hospital, Denmark
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15
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Garmes HM, Boguszewski CL, Miranda PAC, Martins MRA, da Silva SRC, Abucham JZ, de Castro Musolino NR, Vilar L, Portari LHC, Gadelha MR, Kasuki L, Naves LA, Czepielewski MA, de Almeida TS, Duarte FHG, Glezer A, Bronstein MD. Management of hypopituitarism: a perspective from the Brazilian Society of Endocrinology and Metabolism. ARCHIVES OF ENDOCRINOLOGY AND METABOLISM 2021; 65:212-230. [PMID: 33905631 PMCID: PMC10065316 DOI: 10.20945/2359-3997000000335] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 11/23/2022]
Abstract
Hypopituitarism is a disorder characterized by insufficient secretion of one or more pituitary hormones. New etiologies of hypopituitarism have been recently described, including head trauma, cerebral hemorrhage, and drug-induced hypophysitis. The investigation of patients with these new disorders, in addition to advances in diagnosis and treatment of hypopituitarism, has increased the prevalence of this condition. Pituitary hormone deficiencies can induce significant clinical changes with consequent increased morbidity and mortality rates, while hormone replacement based on current guidelines protects these patients. In this review, we will first discuss the different etiologies of hypopituitarism and then address one by one the clinical aspects, diagnostic evaluation, and therapeutic options for deficiencies of TSH, ACTH, gonadotropin, and GH. Finally, we will detail the hormonal interactions that occur during replacement of pituitary hormones.
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Affiliation(s)
- Heraldo Mendes Garmes
- Unidade de Neuroendocrinologia, Divisão de Endocrinologia e Metabologia, Departamento de Clínica Médica, Faculdade de Ciências Médicas, Universidade Estadual de Campinas (Unicamp), Campinas, SP, Brasil,
| | - César Luiz Boguszewski
- Serviço de Endocrinologia e Metabologia, Departamento de Clínica Médica, Universidade Federal do Paraná (SEMPR), Curitiba, PR, Brasil,
| | | | | | - Silvia Regina Correa da Silva
- Unidade de Neuroendocrinologia, Divisão de Endocrinologia e Metabolismo, Escola Paulista de Medicina, Universidade Federal de São Paulo (EPM-Unifesp), São Paulo, SP, Brasil
| | - Julio Zaki Abucham
- Unidade de Neuroendocrinologia, Divisão de Endocrinologia e Metabolismo, Escola Paulista de Medicina, Universidade Federal de São Paulo (EPM-Unifesp), São Paulo, SP, Brasil
| | - Nina Rosa de Castro Musolino
- Unidade de Neuroendocrinologia, Divisão de Neurocirurgia Funcional, Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, DP, Brasil
| | - Lucio Vilar
- Serviço de Endocrinologia, Hospital das Clínicas da Universidade Federal de Pernambuco, Recife, PE, Brasil
| | - Luiz Henrique Corrêa Portari
- Unidade de Neuroendocrinologia, Divisão de Endocrinologia e Metabolismo, Escola Paulista de Medicina, Universidade Federal de São Paulo (EPM-Unifesp), São Paulo, SP, Brasil
| | - Mônica Roberto Gadelha
- Unidade de Neuroendocrinologia, Instituto Estadual do Cérebro Paulo Niemeyer, Centro de Pesquisa de Neuroendocrinologia, Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brasil
| | - Leandro Kasuki
- Unidade de Neuroendocrinologia, Instituto Estadual do Cérebro Paulo Niemeyer, Centro de Pesquisa de Neuroendocrinologia, Hospital Universitário Clementino Fraga Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ, Brasil
| | - Luciana Ansaneli Naves
- Serviço de Endocrinologia, Faculdade de Medicina da Universidade de Brasília, Brasília, DF, Brasil
| | - Mauro Antônio Czepielewski
- Serviço de Endocrinologia, Hospital de Clínicas de Porto Alegre; Faculdade de Medicina, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brasil
| | - Tobias Skrebsky de Almeida
- Serviço de Endocrinologia, Hospital de Clínicas de Porto Alegre; Faculdade de Medicina, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brasil
| | | | - Andrea Glezer
- Unidade de Neuroendocrinologia, Laboratório de Endocrinologia Celular e Molecular LIM-25, Divisão de Endocrinologia e Metabolismo, Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brasil
| | - Marcello Delano Bronstein
- Unidade de Neuroendocrinologia, Laboratório de Endocrinologia Celular e Molecular LIM-25, Divisão de Endocrinologia e Metabolismo, Hospital das Clínicas, Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP, Brasil
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16
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Campos-Pires R, Onggradito H, Ujvari E, Karimi S, Valeo F, Aldhoun J, Edge CJ, Franks NP, Dickinson R. Xenon treatment after severe traumatic brain injury improves locomotor outcome, reduces acute neuronal loss and enhances early beneficial neuroinflammation: a randomized, blinded, controlled animal study. Crit Care 2020; 24:667. [PMID: 33246487 PMCID: PMC7691958 DOI: 10.1186/s13054-020-03373-9] [Citation(s) in RCA: 19] [Impact Index Per Article: 3.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/13/2020] [Accepted: 11/04/2020] [Indexed: 02/01/2023] Open
Abstract
BACKGROUND Traumatic brain injury (TBI) is a major cause of morbidity and mortality, but there are no clinically proven treatments that specifically target neuronal loss and secondary injury development following TBI. In this study, we evaluate the effect of xenon treatment on functional outcome, lesion volume, neuronal loss and neuroinflammation after severe TBI in rats. METHODS Young adult male Sprague Dawley rats were subjected to controlled cortical impact (CCI) brain trauma or sham surgery followed by treatment with either 50% xenon:25% oxygen balance nitrogen, or control gas 75% nitrogen:25% oxygen. Locomotor function was assessed using Catwalk-XT automated gait analysis at baseline and 24 h after injury. Histological outcomes were assessed following perfusion fixation at 15 min or 24 h after injury or sham procedure. RESULTS Xenon treatment reduced lesion volume, reduced early locomotor deficits, and attenuated neuronal loss in clinically relevant cortical and subcortical areas. Xenon treatment resulted in significant increases in Iba1-positive microglia and GFAP-positive reactive astrocytes that was associated with neuronal preservation. CONCLUSIONS Our findings demonstrate that xenon improves functional outcome and reduces neuronal loss after brain trauma in rats. Neuronal preservation was associated with a xenon-induced enhancement of microglial cell numbers and astrocyte activation, consistent with a role for early beneficial neuroinflammation in xenon's neuroprotective effect. These findings suggest that xenon may be a first-line clinical treatment for brain trauma.
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Affiliation(s)
- Rita Campos-Pires
- Anaesthetics, Pain Medicine and Intensive Care Section, Department of Surgery and Cancer, Imperial College London, Sir Ernst Chain Building, South Kensington, London, SW7 2AZ, UK
- Royal British Legion Centre for Blast Injury Studies, Department of Bioengineering, Imperial College London, Bessemer Building, South Kensington, London, SW7 2AZ, UK
- Charing Cross Hospital Intensive Care Unit, Critical Care Directorate, Imperial College Healthcare NHS Trust, London, UK
| | - Haldis Onggradito
- Anaesthetics, Pain Medicine and Intensive Care Section, Department of Surgery and Cancer, Imperial College London, Sir Ernst Chain Building, South Kensington, London, SW7 2AZ, UK
| | - Eszter Ujvari
- Anaesthetics, Pain Medicine and Intensive Care Section, Department of Surgery and Cancer, Imperial College London, Sir Ernst Chain Building, South Kensington, London, SW7 2AZ, UK
| | - Shughoofa Karimi
- Anaesthetics, Pain Medicine and Intensive Care Section, Department of Surgery and Cancer, Imperial College London, Sir Ernst Chain Building, South Kensington, London, SW7 2AZ, UK
| | - Flavia Valeo
- Anaesthetics, Pain Medicine and Intensive Care Section, Department of Surgery and Cancer, Imperial College London, Sir Ernst Chain Building, South Kensington, London, SW7 2AZ, UK
| | - Jitka Aldhoun
- Anaesthetics, Pain Medicine and Intensive Care Section, Department of Surgery and Cancer, Imperial College London, Sir Ernst Chain Building, South Kensington, London, SW7 2AZ, UK
| | - Christopher J Edge
- Department of Life Sciences, Imperial College London, Sir Ernst Chain Building, South Kensington, London, SW7 2AZ, UK
- Department of Anaesthetics, Royal Berkshire Hospital NHS Foundation Trust, London Road, Reading, RG1 5AN, UK
| | - Nicholas P Franks
- Department of Life Sciences, Imperial College London, Sir Ernst Chain Building, South Kensington, London, SW7 2AZ, UK
| | - Robert Dickinson
- Anaesthetics, Pain Medicine and Intensive Care Section, Department of Surgery and Cancer, Imperial College London, Sir Ernst Chain Building, South Kensington, London, SW7 2AZ, UK.
- Royal British Legion Centre for Blast Injury Studies, Department of Bioengineering, Imperial College London, Bessemer Building, South Kensington, London, SW7 2AZ, UK.
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17
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Ntali G, Tsagarakis S. Pituitary dysfunction after traumatic brain injury: prevalence and screening strategies. Expert Rev Endocrinol Metab 2020; 15:341-354. [PMID: 32967470 DOI: 10.1080/17446651.2020.1810561] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/14/2020] [Accepted: 08/12/2020] [Indexed: 12/11/2022]
Abstract
INTRODUCTION Pituitary gland is vulnerable to traumatic brain injury (TBI). As a result a series of neuroendocrine changes appear after head injury; in many occasions they reverse with time, while occasionally new late onset changes may develop. AREAS COVERED In this review, we focus on the prevalence of anterior and posterior pituitary hormonal changes in the acute and chronic post-TBI period in both children and adults. Moreover, we present evidence supporting the need for evaluating pituitary function along with the current suggestions for the most appropriate screening strategies. We attempted to identify all published literature and we conducted an online search of PubMed, from January 1970 to June 2020. EXPERT OPINION Adrenal insufficiency and water metabolism disorders are medical emergencies and should be promptly recognized. Awareness for long-term hormonal derangements is necessary, as they may lead to a series of chronic health issues and compromise quality of life. There is a need for well-designed prospective long-term studies that will estimate pituitary function during the acute and chronic phase after head injury.
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Affiliation(s)
- Georgia Ntali
- Department of Endocrinology, Diabetes and Metabolism, Evangelismos Hospital , Athens, Greece
| | - Stylianos Tsagarakis
- Department of Endocrinology, Diabetes and Metabolism, Evangelismos Hospital , Athens, Greece
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18
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Yang Q, Zhou Y, Sun Y, Luo Y, Shen Y, Shao A. Will Sirtuins Be Promising Therapeutic Targets for TBI and Associated Neurodegenerative Diseases? Front Neurosci 2020; 14:791. [PMID: 32848564 PMCID: PMC7411228 DOI: 10.3389/fnins.2020.00791] [Citation(s) in RCA: 16] [Impact Index Per Article: 3.2] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/21/2020] [Accepted: 07/06/2020] [Indexed: 12/17/2022] Open
Abstract
Traumatic brain injury (TBI), a leading cause of morbidity worldwide, induces mechanical, persistent structural, and metabolic abnormalities in neurons and other brain-resident cells. The key pathological features of TBI include neuroinflammation, oxidative stress, excitotoxicity, and mitochondrial dysfunction. These pathological processes persist for a period of time after TBIs. Sirtuins are evolutionarily conserved nicotinamide-adenine dinucleotide (NAD+)-dependent deacetylases and mono-ADP-ribosyl transferases. The mammalian sirtuin family has seven members, referred to as Sirtuin (SIRT) 1-7. Accumulating evidence suggests that SIRT1 and SIRT3 play a neuroprotective role in TBI. Although the evidence is scant, considering the involvement of SIRT2, 4-7 in other brain injury models, they may also intervene in similar pathophysiology in TBI. Neurodegenerative diseases are generally accepted sequelae of TBI. It was found that TBI and neurodegenerative diseases have many similarities and overlaps in pathological features. Besides, sirtuins play some unique roles in some neurodegenerative diseases. Therefore, we propose that sirtuins might be a promising therapeutic target for both TBI and associated neurodegenerative diseases. In this paper, we review the neuroprotective effects of sirtuins on TBI as well as related neurodegeneration and discuss the therapeutic potential of sirtuin modulators.
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Affiliation(s)
- Qianjie Yang
- Department of Ophthalmology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
| | - Yunxiang Zhou
- Department of Surgical Oncology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
| | - Yuting Sun
- Department of Surgical Oncology, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
| | - Yi Luo
- The Second Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
| | - Ye Shen
- Department of Ophthalmology, The First Affiliated Hospital, Zhejiang University School of Medicine, Hangzhou, China
| | - Anwen Shao
- Department of Neurosurgery, The Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China
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19
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Hacioglu A, Kelestimur F, Tanriverdi F. Long-term neuroendocrine consequences of traumatic brain injury and strategies for management. Expert Rev Endocrinol Metab 2020; 15:123-139. [PMID: 32133881 DOI: 10.1080/17446651.2020.1733411] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/15/2019] [Accepted: 02/19/2020] [Indexed: 12/15/2022]
Abstract
Introduction: Traumatic brain injuries (TBI) are reported to cause neuroendocrine impairment with a prevalence of 15% with confirmatory testing. Pituitary dysfunction (PD) may have detrimental effects on vital parameters as well as on body composition, cardiovascular functions, cognition, and quality of life. Therefore, much effort has been made to identify predictive factors for post-TBI PD and various screening strategies have been offered.Areas covered: We searched PubMed and reviewed the recent data on clinical perspectives and long-term outcomes as well as predictive factors and screening modalities of post-TBI PD. Inconsistencies in the literature are overviewed and new areas of research are discussed.Expert opinion: Studies investigating biomarkers that will accurately predict TBI patients with a high risk of PD are generally pilot studies with a small number of participants. Anti-pituitary and anti-hypothalamic antibodies, neural proteins, micro-RNAs are promising in this field. As severity of TBI has been the most commonly associated risk factor for post-TBI PD, we suggest prospective screening based on severity of head trauma until new evidence emerges. There is also a need for more studies investigating the clinical effects of hormone replacement in TBI patients with PD.
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Affiliation(s)
- Aysa Hacioglu
- Department of Endocrinology and Metabolism, Erciyes University Medical School, Kayseri, Turkey
| | - Fahrettin Kelestimur
- Department of Endocrinology and Metabolism, Yeditepe University Medical Faculty, Istanbul, Turkey
| | - Fatih Tanriverdi
- Department of Endocrinology and Metabolism, Memorial Kayseri Hospital, Kayseri, Turkey
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20
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Krishna G, Beitchman JA, Bromberg CE, Currier Thomas T. Approaches to Monitor Circuit Disruption after Traumatic Brain Injury: Frontiers in Preclinical Research. Int J Mol Sci 2020; 21:ijms21020588. [PMID: 31963314 PMCID: PMC7014469 DOI: 10.3390/ijms21020588] [Citation(s) in RCA: 14] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/16/2019] [Revised: 01/03/2020] [Accepted: 01/13/2020] [Indexed: 12/19/2022] Open
Abstract
Mild traumatic brain injury (TBI) often results in pathophysiological damage that can manifest as both acute and chronic neurological deficits. In an attempt to repair and reconnect disrupted circuits to compensate for loss of afferent and efferent connections, maladaptive circuitry is created and contributes to neurological deficits, including post-concussive symptoms. The TBI-induced pathology physically and metabolically changes the structure and function of neurons associated with behaviorally relevant circuit function. Complex neurological processing is governed, in part, by circuitry mediated by primary and modulatory neurotransmitter systems, where signaling is disrupted acutely and chronically after injury, and therefore serves as a primary target for treatment. Monitoring of neurotransmitter signaling in experimental models with technology empowered with improved temporal and spatial resolution is capable of recording in vivo extracellular neurotransmitter signaling in behaviorally relevant circuits. Here, we review preclinical evidence in TBI literature that implicates the role of neurotransmitter changes mediating circuit function that contributes to neurological deficits in the post-acute and chronic phases and methods developed for in vivo neurochemical monitoring. Coupling TBI models demonstrating chronic behavioral deficits with in vivo technologies capable of real-time monitoring of neurotransmitters provides an innovative approach to directly quantify and characterize neurotransmitter signaling as a universal consequence of TBI and the direct influence of pharmacological approaches on both behavior and signaling.
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Affiliation(s)
- Gokul Krishna
- Barrow Neurological Institute at Phoenix Children’s Hospital, Phoenix, AZ 85016, USA; (G.K.); (J.A.B.); (C.E.B.)
- Department of Child Health, University of Arizona College of Medicine-Phoenix, Phoenix, AZ 85004, USA
| | - Joshua A. Beitchman
- Barrow Neurological Institute at Phoenix Children’s Hospital, Phoenix, AZ 85016, USA; (G.K.); (J.A.B.); (C.E.B.)
- Department of Child Health, University of Arizona College of Medicine-Phoenix, Phoenix, AZ 85004, USA
- College of Graduate Studies, Midwestern University, Glendale, AZ 85308, USA
| | - Caitlin E. Bromberg
- Barrow Neurological Institute at Phoenix Children’s Hospital, Phoenix, AZ 85016, USA; (G.K.); (J.A.B.); (C.E.B.)
- Department of Child Health, University of Arizona College of Medicine-Phoenix, Phoenix, AZ 85004, USA
| | - Theresa Currier Thomas
- Barrow Neurological Institute at Phoenix Children’s Hospital, Phoenix, AZ 85016, USA; (G.K.); (J.A.B.); (C.E.B.)
- Department of Child Health, University of Arizona College of Medicine-Phoenix, Phoenix, AZ 85004, USA
- Phoenix VA Healthcare System, Phoenix, AZ 85012, USA
- Correspondence: ; Tel.: +1-602-827-2348
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21
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Toro-Urrego N, Turner LF, Avila-Rodriguez MF. New Insights into Oxidative Damage and Iron Associated Impairment in Traumatic Brain Injury. Curr Pharm Des 2020; 25:4737-4746. [DOI: 10.2174/1381612825666191111153802] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/22/2019] [Accepted: 10/28/2019] [Indexed: 12/14/2022]
Abstract
:
Traumatic Brain Injury is considered one of the most prevalent causes of death around the world; more
than seventy millions of individuals sustain the condition per year. The consequences of traumatic brain injury on
brain tissue are complex and multifactorial, hence, the current palliative treatments are limited to improve patients’
quality of life. The subsequent hemorrhage caused by trauma and the ongoing oxidative process generated
by biochemical disturbances in the in the brain tissue may increase iron levels and reactive oxygen species. The
relationship between oxidative damage and the traumatic brain injury is well known, for that reason, diminishing
factors that potentiate the production of reactive oxygen species have a promissory therapeutic use. Iron chelators
are molecules capable of scavenging the oxidative damage from the brain tissue and are currently in use for ironoverload-
derived diseases.
:
Here, we show an updated overview of the underlying mechanisms of the oxidative damage after traumatic brain
injury. Later, we introduced the potential use of iron chelators as neuroprotective compounds for traumatic brain
injury, highlighting the action mechanisms of iron chelators and their current clinical applications.
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Affiliation(s)
- Nicolas Toro-Urrego
- Laboratorio de Citoarquitectura y Plasticidad Neuronal, Instituto de Investigaciones Cardiológicas, Universidad de Buenos Aires, Consejo Nacional de Investigaciones Científicas y Técnicas, Buenos Aires, Argentina
| | - Liliana F. Turner
- Grupo Modelos Experimentales para las Ciencias Zoohumanas - Departamento de Biología Facultad de Ciencias, Universidad del Tolima- Ibagué, Tolima, Colombia
| | - Marco F. Avila-Rodriguez
- Grupo Modelos Experimentales para las Ciencias Zoohumanas - Departamento de Ciencias Clínicas- Facultad de Ciencias de la Salud, Universidad del Tolima- Ibagué, Tolima, Colombia
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22
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Royes LFF, Gomez-Pinilla F. Making sense of gut feelings in the traumatic brain injury pathogenesis. Neurosci Biobehav Rev 2019; 102:345-361. [PMID: 31102601 DOI: 10.1016/j.neubiorev.2019.05.012] [Citation(s) in RCA: 18] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/15/2019] [Revised: 05/13/2019] [Accepted: 05/14/2019] [Indexed: 02/06/2023]
Abstract
Traumatic brain injury (TBI) is a devastating condition which often initiates a sequel of neurological disorders that can last throughout lifespan. From metabolic perspective, TBI also compromises systemic physiology including the function of body organs with subsequent malfunctions in metabolism. The emerging panorama is that the effects of TBI on the periphery strike back on the brain and exacerbate the overall TBI pathogenesis. An increasing number of clinical reports are alarming to show that metabolic dysfunction is associated with incidence of long-term neurological and psychiatric disorders. The autonomic nervous system, associated hypothalamic-pituitary axis, and the immune system are at the center of the interface between brain and body and are central to the regulation of overall homeostasis and disease. We review the strong association between mechanisms that regulate cell metabolism and inflammation which has important clinical implications for the communication between body and brain. We also discuss the integrative actions of lifestyle interventions such as diet and exercise on promoting brain and body health and cognition after TBI.
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Affiliation(s)
- Luiz Fernando Freire Royes
- Exercise Biochemistry Laboratory, Center of Physical Education and Sports, Federal University of Santa Maria - UFSM, Santa Maria, RS, Brazil
| | - Fernando Gomez-Pinilla
- Departments of Neurosurgery, and Integrative and Biology and Physiology, UCLA Brain Injury Research Center, University of California, Los Angeles, USA.
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23
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Rogol A. Long-term endocrine consequences of traumatic brain injury in children. Eur J Endocrinol 2019; 180:C5-C8. [PMID: 30893646 DOI: 10.1530/eje-19-0186] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.3] [Reference Citation Analysis] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/12/2019] [Accepted: 03/20/2019] [Indexed: 11/08/2022]
Affiliation(s)
- Alan Rogol
- Department of Pediatrics, University of Virginia, Charlottesville, Virginia, USA
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24
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Neurorehabilitation of Traumatic Brain Injury (TBI): A Clinical Review. Med Sci (Basel) 2019; 7:medsci7030047. [PMID: 30889900 PMCID: PMC6473767 DOI: 10.3390/medsci7030047] [Citation(s) in RCA: 35] [Impact Index Per Article: 5.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/20/2018] [Revised: 03/02/2019] [Accepted: 03/08/2019] [Indexed: 12/19/2022] Open
Abstract
Traumatic brain injury (TBI) and its potential long-term consequences are of major concern for public health. Neurorehabilitation of affected individuals has some specific characteristics in contrast to neurorehabilitation of patients with acquired brain lesions of other aetiology. This review will deal with the clinical consequences of the distinct lesions of TBI. In severe TBI, clinical course often follows a typical initial sequence of coma; followed by disturbed consciousness; later, post-traumatic agitation and amnesia; and finally, recovery of function occurs. In the different phases of neurorehabilitation, physicians should be aware of typical medical complications such as paroxysmal sympathetic hyperactivity, posttraumatic hydrocephalus, and posttraumatic neuroendocrine dysfunctions. Furthermore, we address questions on timing and on existing evidence for different rehabilitation programmes and for holistic neuropsychological rehabilitation approaches.
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Fama' F, Vita R, Sindoni A, Vinci SL, Giorgianni G, Grasso L, Gioffre'-Florio M, Benvenga S. High frequency of empty sella, with gender differences, in the early neuroradiology evaluation of patients with traumatic brain injury. A prospective study. JOURNAL OF CLINICAL AND TRANSLATIONAL ENDOCRINOLOGY 2018; 15:54-61. [PMID: 30622899 PMCID: PMC6317284 DOI: 10.1016/j.jcte.2018.12.008] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 11/12/2018] [Revised: 12/11/2018] [Accepted: 12/29/2018] [Indexed: 01/04/2023]
Abstract
One-hundred four persons aged ≥ 18 years (62 males and 42 females) who were admitted for traumatic brain injury (TBI) underwent brain computed tomography (CT) scan and assay of serum cortisol, insulin-like growth factor 1 (IGF-1), thyrotropin (TSH) and free thyroxine (FT4). The main purpose was to assess any gender difference and the rate of empty sella (ES). Women were more likely to have empty sella (19/42 [45.2%] vs 19/62 [30.6%], P = 0.15, OR = 1.9), which was more frequently total ES or TES (16/19 [84.2%] vs 3/19 [15.8%], P = 0.0025, OR = 11.6). Neuroradiology was normal in the remaining 65 patients. Patients with TES were approximately 20–30 years older than both patients with partial ES (PES) and normal sella, but only the comparison with normal sella was significant (P = 0.001 all patients, P = 0.005 males). Presumed deficiency of IGF-1, cortisol or TSH occurred in 33 persons (31.7%; 20 Males [32.2%], 13 Females [30.9%]), 14 (13.5%; 10 M [16.2%], 4F [9.5%]) or 8 (7.7%; 1 M [1.7%], 7F [16.7%]), with only TSH deficiency having significant intergender difference (P = 0.007). The highest or lowest rates of IGF-1 deficiency occurred in men with PES (41.7%) or men with TES (14.3%), of cortisol deficiency in men with PES (33.3%) or women with PES (zero), and TSH deficiency in women with TES (18.7%) or both men and women with PES (zero) and men with normal sella (zero). Within ES, males with no deficiency were older compared to males with at least one hormone deficiency (75.7 ± 17.4 vs 55.6 ± 18.9, P = 0.022); in turn, the former males were also older compared with normal sella males having no hormone deficiency (54.1 ± 25.2, P = 0.023). In conclusion, ES is detectable in almost 40% of persons who undergo CT within 24 h from TBI. A number of intergender differences concerning ES and the hormones evaluated are apparent.
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Affiliation(s)
- Fausto Fama'
- Department of Human Pathology in Adulthood and Childhood "G. Barresi", University of Messina, Italy
| | - Roberto Vita
- Department of Clinical and Experimental Medicine, University of Messina, Italy
| | - Alessandro Sindoni
- Department of Public Health and Infectious Diseases, Sapienza University of Rome, Italy
| | - Sergio Lucio Vinci
- Department of Biomedical and Dental Sciences, Morphological and Functional Images, University of Messina, Italy
| | - Grazia Giorgianni
- Department of Biomedical and Dental Sciences, Morphological and Functional Images, University of Messina, Italy
| | - Loredana Grasso
- Department of Biomedical and Dental Sciences, Morphological and Functional Images, University of Messina, Italy
| | - Maria Gioffre'-Florio
- Department of Human Pathology in Adulthood and Childhood "G. Barresi", University of Messina, Italy
| | - Salvatore Benvenga
- Department of Clinical and Experimental Medicine, University of Messina, Italy.,Master Program on Childhood, Adolescent and Women's Endocrine Health, University of Messina, Italy.,Interdepartmental Program on Molecular & Clinical Endocrinology, and Women's Endocrine Health, University Hospital of Messina, 98125 Messina, Italy
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Benvenga S, Klose M, Vita R, Feldt-Rasmussen U. Less known aspects of central hypothyroidism: Part 1 - Acquired etiologies. J Clin Transl Endocrinol 2018; 14:25-33. [PMID: 30416972 PMCID: PMC6205405 DOI: 10.1016/j.jcte.2018.09.003] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/06/2018] [Revised: 09/24/2018] [Accepted: 09/25/2018] [Indexed: 12/24/2022] Open
Abstract
Central hypothyroidism (CH) is a rare cause of hypothyroidism. CH is frequently overlooked, as its clinical picture is subtle and includes non-specific symptoms; furthermore, if measurement of TSH alone is used to screen for thyroid function, TSH concentrations can be normal or even above the upper normal reference limit. Indeed, certain patients are at risk of developing CH, such as those with a pituitary adenoma or hypophysitis, those who have been treated for a childhood malignancy, have suffered a head trauma, sub-arachnoid hemorrhage or meningitis, and those who are on drugs capable to reduce TSH secretion.
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Key Words
- ADH, antidiuretic hormone
- AT/RT, atypical teratoid/rhabdoid tumor
- CH, central hypothyroidism
- CNS, central nervous system
- CPI, conformal primary-site irradiation
- CRI, cranial irradiation
- Central hypothyroidism
- Congenital hypothyroidism
- DDMS, Dyke-Davidoff-Masson syndrome
- FSH, follicle-stimulating hormone
- FT3, free triiodothyronine
- FT4, free thyroxine
- GCT, germ cell tumor
- GH, growth hormone
- Hypopituitarism
- IGF-1, insulin growth factor-1
- LH, luteinizing hormone
- MB, medulloblastoma
- PD-1, programmed cell death-1 receptor
- PNET, primitive neuroectodermal tumor
- PRL, prolactin
- SAH, subarachnoid hemorrhage
- TBI, traumatic brain injury
- TRH, TSH-releasing hormone
- TSH, thyrotropin
- Thyrotropin deficiency
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Affiliation(s)
- Salvatore Benvenga
- Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy
- Master Program on Childhood, Adolescent and Women’s Endocrine Health, University of Messina, Messina, Italy
- Interdepartmental Program of Molecular & Clinical Endocrinology, and Women’s Endocrine Health, University Hospital Policlinico G. Martino, Messina, Italy
| | - Marianne Klose
- Department of Medical Endocrinology and Metabolism, Rigshospitalet, National University Hospital, Copenhagen University, Copenhagen, Denmark
| | - Roberto Vita
- Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy
| | - Ulla Feldt-Rasmussen
- Department of Medical Endocrinology and Metabolism, Rigshospitalet, National University Hospital, Copenhagen University, Copenhagen, Denmark
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Feldt-Rasmussen U, Klose M, Benvenga S. Interactions between hypothalamic pituitary thyroid axis and other pituitary dysfunctions. Endocrine 2018; 62:519-527. [PMID: 30191443 DOI: 10.1007/s12020-018-1738-6] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/10/2018] [Accepted: 08/23/2018] [Indexed: 12/16/2022]
Abstract
Central hypothyroidism is defined as low circulating free thyroxine (free T4) with inappropriately low circulating thyrotropin (TSH), in context of a hypothalamic pituitary pathology. Rare cases of idiopathic central hypothyroidism caused by a functional defect may occur, and the condition is often overlooked due to difficulty in achieving the correct diagnosis, sparse symptomatology of the condition and a high risk of misinterpretion of the biochemical changes in central hypothyroidism. Central hypothyroidism is mainly seen in patients with hypothalamic-pituitary pathology due to one of many possible aetiologies, where other hormone deficiencies often co-exist, and both the presence of other deficiencies and their replacement have a strong influence on the measurement of the thyroid-related hormones and thereby interpretation of the thyroid function variables in relation to the clinical impact of thyroid hormone substitution therapy. Conversely, lack of thyroid hormone has a similar strong influence on the interpretation of other pituitary hormone axes, as well as their replacement. Undertreating patients with central hypothyroidism may have serious metabolic consequences with a potentially increased risk of cardiovascular morbidity. The present review thus aims at describing central hypothyroidism, by an overview of interactions of hypothyroidism with other pituitary hormones, diagnosing/testing for central hypothyroidism, and focusing on consequences of undertreatment. Finally, it is mentioned how to deal with new diagnostic settings with lower a priori likelihood of hypopituitarism, particularly in view of the importance of stringent diagnostic testing in order to avoid overdiagnosing central hypothyroidism.
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Affiliation(s)
- Ulla Feldt-Rasmussen
- Department of Medical Endocrinology and Metabolism, Rigshospitalet, National University Hospital, Copenhagen University, Copenhagen, Denmark.
| | - Marianne Klose
- Department of Medical Endocrinology and Metabolism, Rigshospitalet, National University Hospital, Copenhagen University, Copenhagen, Denmark
| | - Salvatore Benvenga
- Department of Clinical and Experimental Medicine, University of Messina, Messina, Italy
- Master Program on Childhood, Adolescent and Women's Endocrine Health, University of Messina, Messina, Italy
- Interdepartmental Program of Molecular and Clinical Endocrinology, and Women's Endocrine Health, University hospital Policlinico G. Martino, Messina, Italy
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Lithgow K, Debert CT, Kline GA. Limited Adherence to Growth Hormone Replacement in Patients with Traumatic Brain Injury. JOURNAL OF REHABILITATION MEDICINE - CLINICAL COMMUNICATIONS 2018; 3:1000008. [PMID: 33884124 PMCID: PMC8011678 DOI: 10.2340/20030711-1000008] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Subscribe] [Scholar Register] [Accepted: 09/25/2018] [Indexed: 11/16/2022]
Abstract
Background Growth hormone deficiency is a recognized consequence of traumatic brain injury. The aim of this study was to determine adherence to human growth hormone therapy among patients with traumatic brain injury compared with patients with hypothalamic or pituitary disease. Methods A retrospective chart review of patients with traumatic brain injury referred for growth hormone stimulation testing since December 2013. Within the same electronic medical record, patients who were started on human growth hormone for aetiologies other than traumatic brain injury were reviewed. Adherence to therapy at 1-year followup was compared. Results Of the patients with traumatic brain injury, 12/23 (52%) returned for follow-up at 1 year to continue human growth hormone treatment, whereas 11/23 (48%) did not return at 1 year. Amongst the patients with non-traumatic brain injury: 25/29 (86%) continued human growth hormone treatment, vs 4/29 (14%) who did not return. A higher proportion of patients with non-traumatic brain injury continued human growth hormone treatment; x2 (1, n = 52)p = 7.238, p = 0.007. Conclusion There may be differences in the patient-perceived benefits of human growth hormone between these patient populations. However, it is important to consider the potential influences of cognitive and psychosocial dysfunction that can occur in patients with brain injuries.
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Affiliation(s)
- Kirstie Lithgow
- Division of Endocrinology, Department of Medicine, Cumming School of Medicine, University of Calgary, Calgary, Canada
| | - Chantel T Debert
- Division of Physical Medicine and Rehabilitation, Department of Clinical Neurosciences Cumming School of Medicine, University of Calgary, Calgary, Canada
| | - Gregory A Kline
- Division of Endocrinology, Department of Medicine, Cumming School of Medicine, University of Calgary, Calgary, Canada
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Molaie AM, Maguire J. Neuroendocrine Abnormalities Following Traumatic Brain Injury: An Important Contributor to Neuropsychiatric Sequelae. Front Endocrinol (Lausanne) 2018; 9:176. [PMID: 29922224 PMCID: PMC5996920 DOI: 10.3389/fendo.2018.00176] [Citation(s) in RCA: 43] [Impact Index Per Article: 6.1] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/05/2018] [Accepted: 04/03/2018] [Indexed: 12/19/2022] Open
Abstract
Neuropsychiatric symptoms following traumatic brain injury (TBI) are common and contribute negatively to TBI outcomes by reducing overall quality of life. The development of neurobehavioral sequelae, such as concentration deficits, depression, anxiety, fatigue, and loss of emotional well-being has historically been attributed to an ambiguous "post-concussive syndrome," considered secondary to frank structural injury and axonal damage. However, recent research suggests that neuroendocrine dysfunction, specifically hypopituitarism, plays an important role in the etiology of these symptoms. This post-head trauma hypopituitarism (PHTH) has been shown in the past two decades to be a clinically prevalent phenomenon, and given the parallels between neuropsychiatric symptoms associated with non-TBI-induced hypopituitarism and those following TBI, it is now acknowledged that PHTH is likely a substantial contributor to these impairments. The current paper seeks to provide an overview of hypothesized pathophysiological mechanisms underlying neuroendocrine abnormalities after TBI, and to emphasize the significance of this phenomenon in the development of the neurobehavioral problems frequently seen after head trauma.
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Affiliation(s)
- Amir M. Molaie
- Tufts University School of Medicine, Boston, MA, United States
| | - Jamie Maguire
- Department of Neuroscience, Sackler School of Graduate Biomedical Sciences, Boston, MA, United States
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