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Neuroendocrine Disturbances after Brain Damage

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A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Endocrinology & Metabolism".

Deadline for manuscript submissions: closed (31 March 2015) | Viewed by 121222

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Prof. Dr. Med. Günter Stalla

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Guest Editor

President European Neuroendocrine Association, Max Planck Institute of Psychiatry, Dept. of Internal Medicine/Endocrinology and Clin. Chemistry, Kraepelinstr. 10, 80804 Munich, Germany
Interests: hypothalamo-pituitary function; pituitary disease; brain trauma; metabolic disorders

Dr. Anna Kopczak

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Max Planck Institute of Psychiatry, Kraepelinstr. 2-10, 80804 Munich, Germany
Interests: neuroendocrinology; brain injury; brain tumors; psychiatric comorbidities; hypothalamic and pituitary diseases

Special Issue Information

Dear Colleagues,

Traumatic brain injury is one of the leading causes of death and disability in young adults in industrialized countries, affecting about 185–200/100,000/year. When considering traumatic brain injury, many clinicians might think of young adults who were involved in vehicle accidents. However, traumatic brain injury is not only caused by traffic accidents, but also by blast injuries or by falls. In an ageing population, the percentage of falls in elderly patients is constantly increasing.

Neuroendocrine disturbances after traumatic brain injury have been described since 1910, but were almost forgotten for a long time. First insights suggested a high and often unrecognized prevalence rate of posttraumatic hypopituitarism. Recently, a controversial discussion regarding prevalence and clinical importance has been raised.

Hormonal disturbances of the hypothalamo-pituitary axes do not only occur after traumatic brain injury. There is increasing knowledge that, after general brain damage, such as subarachnoid hemorrhage or stroke, patients can suffer from hormonal disturbances.

With our special issue we aim to highlight the importance of posttraumatic hypopituitarism. We will present a controversial discussion on this topic and its clinical relevance and will offer an overview on neuroendocrine disturbances after brain damage.

Prof. Dr. Günter K. Stalla
Dr. Anna Kopczak
Guest Editors

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Keywords

posttraumatic hypopituitarism
neuroendocrine disturbances
hypothalamo-pituitary dysfunction
traumatic brain injury
subarachnoid hemorrhage
stroke
hormone replacement therapy
neurorehabilitation
outcome after brain damage

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Published Papers (11 papers)

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Research

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312 KiB

Open AccessArticle

Hypopituitarism in Traumatic Brain Injury—A Critical Note

by Marianne Klose and Ulla Feldt-Rasmussen

J. Clin. Med. 2015, 4(7), 1480-1497; https://doi.org/10.3390/jcm4071480 - 14 Jul 2015

Cited by 28 | Viewed by 8214

Abstract

While hypopituitarism after traumatic brain injury (TBI) was previously considered rare, it is now thought to be a major cause of treatable morbidity among TBI survivors. Consequently, recommendations for assessment of pituitary function and replacement in TBI were recently introduced. Given the high incidence of TBI with more than 100 pr. 100,000 inhabitants, TBI would be by far the most common cause of hypopituitarism if the recently reported prevalence rates hold true. The disproportion between this proposed incidence and the occasional cases of post-TBI hypopituitarism in clinical practice justifies reflection as to whether hypopituitarism has been unrecognized in TBI patients or whether diagnostic testing designed for high risk populations such as patients with obvious pituitary pathology has overestimated the true risk and thereby the disease burden of hypopituitarism in TBI. The findings on mainly isolated deficiencies in TBI patients, and particularly isolated growth hormone (GH) deficiency, raise the question of the potential impact of methodological confounding, determined by variable test-retest reproducibility, appropriateness of cut-off values, importance of BMI stratified cut-offs, assay heterogeneity, pre-test probability of hypopituitarism and lack of proper individual laboratory controls as reference population. In this review, current recommendations are discussed in light of recent available evidence. Full article

(This article belongs to the Special Issue Neuroendocrine Disturbances after Brain Damage)

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Open AccessArticle

Addisonian Crisis after Missed Diagnosis of Posttraumatic Hypopituitarism

by Christine Streetz-van der Werf, Wolfram Karges, Marcus Blaum and Ilonka Kreitschmann-Andermahr

J. Clin. Med. 2015, 4(5), 965-969; https://doi.org/10.3390/jcm4050965 - 15 May 2015

Cited by 3 | Viewed by 10684

Abstract

We report a case of a previously undiagnosed panhypopituitarism initially presenting as a full-blown Addisonian crisis with hypoglycemia, hyponatremia, hypotension and neuropsychological symptoms, more than 30 years after a severe traumatic brain injury (TBI). The patient also displayed clearly visible pathognomonic clinical signs [...] Read more.

(This article belongs to the Special Issue Neuroendocrine Disturbances after Brain Damage)

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Review

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Interrelation between Neuroendocrine Disturbances and Medical Complications Encountered during Rehabilitation after TBI

by Caroline I. E. Renner

J. Clin. Med. 2015, 4(9), 1815-1840; https://doi.org/10.3390/jcm4091815 - 22 Sep 2015

Cited by 18 | Viewed by 7430

Abstract

Traumatic brain injury is not a discrete event but an unfolding sequence of damage to the central nervous system. Not only the acute phase but also the subacute and chronic period after injury, i.e., during inpatient rehabilitation, is characterized by multiple neurotransmitter alterations, cellular dysfunction, and medical complications causing additional secondary injury. Neuroendocrine disturbances also influence neurological outcome and are easily overlooked as they often present with diffuse symptoms such as fatigue, depression, poor concentration, or a decline in overall cognitive function; these are also typical sequelae of traumatic brain injury. Furthermore, neurological complications such as hydrocephalus, epilepsy, fatigue, disorders of consciousness, paroxysmal sympathetic hyperactivity, or psychiatric-behavioural symptoms may mask and/or complicate the diagnosis of neuroendocrine disturbances, delay appropriate treatment and impede neurorehabilitation. The present review seeks to examine the interrelation between neuroendocrine disturbances with neurological complications frequently encountered after moderate to severe TBI during rehabilitation. Common neuroendocrine disturbances and medical complications and their clinical implications are discussed. Full article

(This article belongs to the Special Issue Neuroendocrine Disturbances after Brain Damage)

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323 KiB

Open AccessReview

Hypothalamic Obesity in Craniopharyngioma Patients: Disturbed Energy Homeostasis Related to Extent of Hypothalamic Damage and Its Implication for Obesity Intervention

by Christian L. Roth

J. Clin. Med. 2015, 4(9), 1774-1797; https://doi.org/10.3390/jcm4091774 - 9 Sep 2015

Cited by 60 | Viewed by 11380

Abstract

Hypothalamic obesity (HO) occurs in patients with tumors and lesions in the medial hypothalamic region. Hypothalamic dysfunction can lead to hyperinsulinemia and leptin resistance. This review is focused on HO caused by craniopharyngiomas (CP), which are the most common childhood brain tumors of nonglial origin. Despite excellent overall survival rates, CP patients have substantially reduced quality of life because of significant long-term sequelae, notably severe obesity in about 50% of patients, leading to a high rate of cardiovascular mortality. Recent studies reported that both hyperphagia and decreased energy expenditure can contribute to severe obesity in HO patients. Recognized risk factors for severe obesity include large hypothalamic tumors or lesions affecting several medial and posterior hypothalamic nuclei that impact satiety signaling pathways. Structural damage in these nuclei often lead to hyperphagia, rapid weight gain, central insulin and leptin resistance, decreased sympathetic activity, low energy expenditure, and increased energy storage in adipose tissue. To date, most efforts to treat HO have shown disappointing long-term success rates. However, treatments based on the distinct pathophysiology of disturbed energy homeostasis related to CP may offer options for successful interventions in the future. Full article

(This article belongs to the Special Issue Neuroendocrine Disturbances after Brain Damage)

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Update of Endocrine Dysfunction following Pediatric Traumatic Brain Injury

by Kent Reifschneider, Bethany A. Auble and Susan R. Rose

J. Clin. Med. 2015, 4(8), 1536-1560; https://doi.org/10.3390/jcm4081536 - 31 Jul 2015

Cited by 50 | Viewed by 10021

Abstract

Traumatic brain injuries (TBI) are common occurrences in childhood, often resulting in long term, life altering consequences. Research into endocrine sequelae following injury has gained attention; however, there are few studies in children. This paper reviews the pathophysiology and current literature documenting risk for endocrine dysfunction in children suffering from TBI. Primary injury following TBI often results in disruption of the hypothalamic-pituitary-adrenal axis and antidiuretic hormone production and release, with implications for both acute management and survival. Secondary injuries, occurring hours to weeks after TBI, result in both temporary and permanent alterations in pituitary function. At five years after moderate to severe TBI, nearly 30% of children suffer from hypopituitarism. Growth hormone deficiency and disturbances in puberty are the most common; however, any part of the hypothalamic-pituitary axis can be affected. In addition, endocrine abnormalities can improve or worsen with time, having a significant impact on children’s quality of life both acutely and chronically. Since primary and secondary injuries from TBI commonly result in transient or permanent hypopituitarism, we conclude that survivors should undergo serial screening for possible endocrine disturbances. High indices of suspicion for life threatening endocrine deficiencies should be maintained during acute care. Additionally, survivors of TBI should undergo endocrine surveillance by 6–12 months after injury, and then yearly, to ensure early detection of deficiencies in hormonal production that can substantially influence growth, puberty and quality of life. Full article

(This article belongs to the Special Issue Neuroendocrine Disturbances after Brain Damage)

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Impaired Pituitary Axes Following Traumatic Brain Injury

by Robert A. Scranton and David S. Baskin

J. Clin. Med. 2015, 4(7), 1463-1479; https://doi.org/10.3390/jcm4071463 - 13 Jul 2015

Cited by 35 | Viewed by 6630

Abstract

Pituitary dysfunction following traumatic brain injury (TBI) is significant and rarely considered by clinicians. This topic has received much more attention in the last decade. The incidence of post TBI anterior pituitary dysfunction is around 30% acutely, and declines to around 20% by one year. Growth hormone and gonadotrophic hormones are the most common deficiencies seen after traumatic brain injury, but also the most likely to spontaneously recover. The majority of deficiencies present within the first year, but extreme delayed presentation has been reported. Information on posterior pituitary dysfunction is less reliable ranging from 3%–40% incidence but prospective data suggests a rate around 5%. The mechanism, risk factors, natural history, and long-term effect of treatment are poorly defined in the literature and limited by a lack of standardization. Post TBI pituitary dysfunction is an entity to recognize with significant clinical relevance. Secondary hypoadrenalism, hypothyroidism and central diabetes insipidus should be treated acutely while deficiencies in growth and gonadotrophic hormones should be initially observed. Full article

(This article belongs to the Special Issue Neuroendocrine Disturbances after Brain Damage)

195 KiB

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Diabetes Insipidus after Traumatic Brain Injury

by Cristina Capatina, Alessandro Paluzzi, Rosalid Mitchell and Niki Karavitaki

J. Clin. Med. 2015, 4(7), 1448-1462; https://doi.org/10.3390/jcm4071448 - 13 Jul 2015

Cited by 82 | Viewed by 31235

Abstract

Traumatic brain injury (TBI) is a significant cause of morbidity and mortality in many age groups. Neuroendocrine dysfunction has been recognized as a consequence of TBI and consists of both anterior and posterior pituitary insufficiency; water and electrolyte abnormalities (diabetes insipidus (DI) and the syndrome of inappropriate antidiuretic hormone secretion (SIADH)) are amongst the most challenging sequelae. The acute head trauma can lead (directly or indirectly) to dysfunction of the hypothalamic neurons secreting antidiuretic hormone (ADH) or of the posterior pituitary gland causing post-traumatic DI (PTDI). PTDI is usually diagnosed in the first days after the trauma presenting with hypotonic polyuria. Frequently, the poor general status of most patients prevents adequate fluid intake to compensate the losses and severe dehydration and hypernatremia occur. Management consists of careful monitoring of fluid balance and hormonal replacement. PTDI is associated with high mortality, particularly when presenting very early following the injury. In many surviving patients, the PTDI is transient, lasting a few days to a few weeks and in a minority of cases, it is permanent requiring management similar to that offered to patients with non-traumatic central DI. Full article

(This article belongs to the Special Issue Neuroendocrine Disturbances after Brain Damage)

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Neuropsychology of Neuroendocrine Dysregulation after Traumatic Brain Injury

by Josef Zihl and Osborne F. X. Almeida

J. Clin. Med. 2015, 4(5), 1051-1062; https://doi.org/10.3390/jcm4051051 - 20 May 2015

Cited by 14 | Viewed by 8827

Abstract

Endocrine dysfunction is a common effect of traumatic brain injury (TBI). In addition to affecting the regulation of important body functions, the disruption of endocrine physiology can significantly impair mental functions, such as attention, memory, executive function, and mood. This mini-review focuses on alterations in mental functioning that are associated with neuroendocrine disturbances in adults who suffered TBI. It summarizes the contribution of hormones to the regulation of mental functions, the consequences of TBI on mental health and neuroendocrine homeostasis, and the effects of hormone substitution on mental dysfunction caused by TBI. The available empirical evidence suggests that comprehensive assessment of mental functions should be standard in TBI subjects presenting with hormone deficiency and that hormone replacement therapy should be accompanied by pre- and post-assessments. Full article

(This article belongs to the Special Issue Neuroendocrine Disturbances after Brain Damage)

116 KiB

Open AccessReview

Hypothalamic-Pituitary Autoimmunity and Traumatic Brain Injury

by Federica Guaraldi, Silvia Grottoli, Emanuela Arvat and Ezio Ghigo

J. Clin. Med. 2015, 4(5), 1025-1035; https://doi.org/10.3390/jcm4051025 - 19 May 2015

Cited by 27 | Viewed by 6280

Abstract

Background: Traumatic brain injury (TBI) is a leading cause of secondary hypopituitarism in children and adults, and is responsible for impaired quality of life, disabilities and compromised development. Alterations of pituitary function can occur at any time after the traumatic event, presenting in various ways and evolving during time, so they require appropriate screening for early detection and treatment. Although the exact pathophysiology is unknown, several mechanisms have been hypothesized, including hypothalamic-pituitary autoimmunity (HP-A). The aim of this study was to systematically review literature on the association between HP-A and TBI-induced hypopituitarism. Major pitfalls related to the HP-A investigation were also discussed. Methods: The PubMed database was searched with a string developed for this purpose, without temporal or language limits, for original articles assessing the association of HP-A and TBI-induced hypopituitarism. Results: Three articles from the same group met the inclusion criteria. Anti-pituitary and anti-hypothalamic antibodies were detected using indirect immunofluorescence in a significant number of patients with acute and chronic TBI. Elevated antibody titer was associated with an increased risk of persistent hypopituitarism, especially somatotroph and gonadotroph deficiency, while no correlations were found with clinical parameters. Conclusion: HPA seems to contribute to TBI-induced pituitary damage, although major methodological issues need to be overcome and larger studies are warranted to confirm these preliminary data. Full article

(This article belongs to the Special Issue Neuroendocrine Disturbances after Brain Damage)

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Neuroendocrine Disturbances after Brain Damage: An Important and Often Undiagnosed Disorder

by Fatih Tanriverdi and Fahrettin Kelestimur

J. Clin. Med. 2015, 4(5), 847-857; https://doi.org/10.3390/jcm4050847 - 28 Apr 2015

Cited by 25 | Viewed by 7240

Abstract

Traumatic brain injury (TBI) is a common and significant public health problem all over the world. Until recently, TBI has been recognized as an uncommon cause of hypopituitarism. The studies conducted during the last 15 years revealed that TBI is a serious cause of hypopituitarism. Although the underlying pathophysiology has not yet been fully clarified, new data indicate that genetic predisposition, autoimmunity and neuroinflammatory changes may play a role in the development of hypopituitarism. Combative sports, including boxing and kickboxing, both of which are characterized by chronic repetitive head trauma, have been shown as new causes of neuroendocrine abnormalities, mainly hypopituitarism, for the first time during the last 10 years. Most patients with TBI-induced pituitary dysfunction remain undiagnosed and untreated because of the non-specific and subtle clinical manifestations of hypopituitarism. Replacement of the deficient hormones, of which GH is the commonest hormone lost, may not only reverse the clinical manifestations and neurocognitive dysfunction, but may also help posttraumatic disabled patients resistant to classical treatment who have undiagnosed hypopituitarism and GH deficiency in particular. Therefore, early diagnosis, which depends on the awareness of TBI as a cause of neuroendocrine abnormalities among the medical community, is crucially important. Full article

(This article belongs to the Special Issue Neuroendocrine Disturbances after Brain Damage)

675 KiB

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Neuroendocrine Disorders in Pediatric Craniopharyngioma Patients

by Anna M. M. Daubenbüchel and Hermann L. Müller

J. Clin. Med. 2015, 4(3), 389-413; https://doi.org/10.3390/jcm4030389 - 9 Mar 2015

Cited by 55 | Viewed by 12386

Abstract

Childhood-onset craniopharyngiomas are partly cystic embryonic malformations of the sellar/parasellar region. The therapy of choice in patients with favorable tumor localization is complete resection with a specific focus on maintaining optical and hypothalamic neuroendocrine functions. In patients with unfavorable tumor localization (i.e., hypothalamic involvement), a limited hypothalamus-sparing surgical strategy followed by local irradiation is recommended. Involvement and/or surgical lesions of posterior hypothalamic areas cause major neuroendocrine sequelae. The overall survival rates are high (92%) but neuroendocrine disorders such as obesity and metabolic syndrome due to involvement and/or treatment-related hypothalamic lesions have major negative impact on survival and quality of life. Recurrences and progressions are frequent post-surgical events. Because irradiation is efficient in preventing tumor progression, appropriate timing of post-surgical irradiation is currently under investigation in a randomized multinational trial (KRANIOPHARYNGEOM 2007). Childhood-onset craniopharyngioma should be recognized as a chronic disease requiring treatment and constant monitoring of the clinical and quality of life consequences, frequently impaired due to neuroendocrine disorders, by experienced multidisciplinary teams in order to provide optimal care of surviving patients. Full article

(This article belongs to the Special Issue Neuroendocrine Disturbances after Brain Damage)

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