154 results match your criteria: "Post Head Injury Endocrine Complications"
Brain Res
March 2011
Department of Neurosurgery, Tianjin Medical University General Hospital, Tianjin 300052, PR China.
Emerging evidence demonstrates that severe illness could induce critical illness-related corticosteroid insufficiency (CIRCI) and cause poor prognosis. The purpose of this study was to test the hypothesis that methylprednisolone (MP), a synthetic glucocorticoid, promotes post-traumatic apoptosis in both the hypothalamus and pituitary, resulting in acute CIRCI and increased mortality in the acute phase of traumatic brain injury (TBI). We tested this hypothesis by measuring acute CIRCI in rats subjected to fluid percussion injury (FPI) and treated with MP (5-30mg/kg).
View Article and Find Full Text PDFHormones (Athens)
March 2011
Clinical Experimental Department of Medicine and Pharmacology, Section of Endocrinology, Policlinico Universitario G. Martino, University of Messina, Messina, Italy.
Objective: Hypopituitarism is a recognized complication of Traumatic Brain Injury (TBI). Resolution of established anterior pituitary hormones deficiency is rare.
Case Report: A woman was initially presented at the age of 22 years with amenorrhoea.
Interv Neuroradiol
September 2010
Department of Neurosurgery, Fudan University, Shanghai, China.
A 26-year-old man presented with symptoms of progressive bilateral exophthalmos and swelling of the eyelids after a severe head injury. Angiography confirmed a direct carotid-superior hypophyseal arterial (SHA) cavernous fistula with petrosal sinus and intracavernous sinus drainage. Successful transarterial coil embolization of the fistula was performed with resolution of the patient's symptoms.
View Article and Find Full Text PDFBrain Inj
February 2011
PM&R, San Jose, CA, USA.
Objective: Define associations between post-traumatic brain injury (TBI) fatigue and abnormalities in neuroendocrine axes, sleep, mood, cognition and physical functioning.
Design: Survey.
Setting: Large community hospital-based rehabilitation centre.
Ned Tijdschr Geneeskd
June 2010
De Gelderse Roos, afd. Ouderen, Arnhem, The Netherlands.
A manic episode in old age presents a diagnostic challenge to the clinician due to the different symptomatology often difficult to distinguish from delirium, dementia, agitated depression and psychosis. To complicate matters further, a first episode of mania in later life is very often based on underlying physical and cerebral pathology ('secondary mania'). Many causes of 'secondary mania', including neurological, systemic or endocrine diseases, infections, intoxications, apnoea, post-thoracic surgery and vitamin B12 deficiency have been described to date, but there have been no reports on subdural haematomas in this context.
View Article and Find Full Text PDFOral Maxillofac Surg Clin North Am
May 2010
Section of Oral and Maxillofacial Surgery, 23-009 UCLA School of Dentistry, University of California, 10833 Le Conte Avenue, Los Angeles, CA 90095-1668, USA.
After facial trauma, a distinct subset of patients goes on to develop mental health problems including recalcitrant psychopathology. Early identification of maladaptive stress reactions provides opportunities for initiating preemptive mental health interventions and hinges on the surgeon's ability to differentiate between transient distress and precursors of recalcitrant psychiatric sequelae. The comprehensive care of injured patients will benefit greatly from objective adjuncts and decision-making tools to complement the clinical evaluation.
View Article and Find Full Text PDFArq Bras Endocrinol Metabol
November 2009
Hospital Universitário, Universidade Federal de Santa Catarina, Florianópolis, SC, Brasil.
Objective: The purpose of this study is to evaluate pituitary function impairment in order to verify the prevalence of sex hormone deficiency and to analyze the profile of TBI population.
Methods: Thirty patients were studied, 22 were male and 8 were female. All patients had their gonadal function assessed and they were evaluated at a median of 4 years post-trauma.
Arq Bras Endocrinol Metabol
November 2009
Hospital Universitário, Universidade Federal de Santa Catarina, Florianópolis, SC, Brasil.
Traumatic brain injury (TBI) is the most common cause of death and disability in young adults. Post-TBI neuroendocrine disorders have been increasingly acknowledged in recent years due to their potential contribution to morbidity and, probably, to mortality after trauma. Marked alterations of the hypothalamic-pituitary axis during the post-TBI acute and chronic phases have been reported.
View Article and Find Full Text PDFBMJ Case Rep
September 2010
Department of Rehabilitation Medicine, Rookwood Hospital, Cardiff, UK.
The following case illustrates a 10-year delay in the diagnosis of hypopituitarism after severe traumatic brain injury in a 22-year-old man crushed by a forklift truck. His symptoms of mood changes, headaches and sleep pattern disturbances were attributed to post traumatic brain injury syndrome resulting in a delay in diagnosing the underlying pathology. Following recurrent episodes of symptomatic hyponatraemia, hypopituitarism was diagnosed.
View Article and Find Full Text PDFSurgery
December 2009
Division of Endocrine Surgery, Department of Surgery, Università Cattolica del Sacro Cuore, Rome, Italy.
Background: Voice and swallowing symptoms are frequently reported early after thyroidectomy even in the absence of laryngeal nerves injury. We evaluated the short-term and long-term outcomes of these functional alterations.
Methods: Consenting patients undergoing total thyroidectomy (TT) were enrolled.
Brain Inj
December 2009
Department of Physical Medicine and Rehabilitation, China Medical University Hospital, Taichung, Taiwan, PR China.
Aim: The patients in the permanent diabetes insipidus (DI) group are more likely to have more severe TBI, which is defined by a post-resuscitational and pre-sedational Glasgow Coma Scale (GCS) score of 8/15 or less. This study presents a case of permanent, central DI following mild traumatic brain injury with post-resuscitation GCS 13/15.
Case Report: A 17-year-old boy suffered from mild brain injury and experienced permanent DI without any anatomical changes on image in the early stage of traumatic brain injury.
Nearly 64% of people with mild traumatic brain injury (MTBI) experience prolonged symptoms and functional impairments lasting months or years postinjury. Explanations for delayed recovery have varied and lacked a guiding framework, hindering intervention science. Using theory substruction and adapting McLean and associates' biopsychosocial model for chronic pain after trauma, we suggest that perceived psychological stress and associated neurobiological responses may predict risk for functional impairment.
View Article and Find Full Text PDFJ Neurotrauma
August 2009
Department of Emergency Medicine, Emory University School of Medicine, Atlanta, GA 30322, USA.
Unlabelled: In humans, traumatic brain injury (TBI) causes pathological changes in the hypothalamus (HT) and the pituitary. One consequence of TBI is hypopituitarism, with deficiency of single or multiple hormones of the anterior pituitary (AP), including growth hormone (GH). At present no animal model of TBI with ensuing hypopituitarism has been demonstrated.
View Article and Find Full Text PDFJ Clin Neurosci
June 2009
Department of Neurosurgery, Johannes Gutenberg University Mainz, Mainz, Germany.
Between January 2004 and June 2007 we conducted a retrospective analysis to assess post-operative complications related to endoscopic pituitary surgery in a series of 150 patients. Patients were treated with an endoscopic endonasal transsphenoidal approach to the sellar region for removal of pathological sellar and suprasellar lesions. We analysed the complications in groups according to the anatomical structures of the approach and the functional systems of the pituitary gland (anterior and posterior endocrine systems), and compared them to a large historical series using the traditional microsurgical transsphenoidal approach.
View Article and Find Full Text PDFJ Neurol Neurosurg Psychiatry
July 2008
Academic Department of Endocrinology, Beaumont Hospital and RCSI Medical School, Dublin, Ireland.
Traumatic brain injury (TBI) is the most common cause of death and disability in young adults living in industrialised countries, in which 180-250 persons per 100 000 per year die or are hospitalised as a result. Neuroendocrine derangements after TBI have received increasing recognition in recent years because of their potential contribution to morbidity, and possibly mortality, after trauma. Marked changes of the hypothalamo-pituitary axis have been documented in the acute phase of TBI, with as many as 80% of patients showing evidence of gonadotropin deficiency, 18% of growth hormone deficiency, 16% of corticotrophin deficiency and 40% of patients demonstrating vasopressin abnormalities leading to diabetes insipidus or the syndrome of inappropriate anti-diuresis.
View Article and Find Full Text PDFPituitary
September 2008
Department of Medical Endocrinology, PE2131, Copenhagen University Hospital, Rigshospitalet, Blegdamsvej 9, 2100, Copenhagen, Denmark.
Several studies have reported a close association between traumatic brain injury (TBI) and pituitary dysfunction, and expert panels have recently proposed recommendations for hormone assessment and replacement for pituitary insufficiency after TBI. Given the high incidence of TBI, identification of reliable predictors is of utmost importance in order to secure a cost-effective screening strategy. It has not yet been possible to identify early hormone alterations as a useful tool for the prediction of long-term post-traumatic hypopituitarism, whereas indicators of increased trauma severity have been reported as predictive in an increasing number of studies.
View Article and Find Full Text PDFCurr Opin Crit Care
April 2008
Department of Neurosurgery, University of Texas Medical School, Houston, Texas 77030, USA.
Purpose Of Review: Hypoadrenalism occurs in approximately 25% of patients soon after traumatic brain injury. Neurosurgeons or critical care physicians should be prepared to diagnose and treat this and other related hormonal deficiencies.
Recent Findings: The severity of traumatic brain injury, location of basilar skull fractures and edema or hemorrhage within the hypothalamic-pituitary axis appear correlated with secondary adrenal failure.
Horm Res
March 2008
Department of Paediatrics, University of Cambridge, Cambridge, UK.
Background: Anterior pituitary hormone dysfunction may be an important feature of long-term morbidity in survivors of traumatic brain injury (TBI). The hypothalamic-pituitary structures are vulnerable to damage following head injury. Therefore, pituitary dysfunction, which may be detected months or years after injury, is now well recognised as a long-term consequence of TBI in adults.
View Article and Find Full Text PDFIntensive Care Med
March 2008
University Division of Anaesthesia, Cambridge University Foundation Hospitals NHS Trust, Hills Road, Box 93, CB2 2QQ Cambridge, Cambridgeshire, UK.
Objective: The objective was to study the anatomical changes in the pituitary gland following acute moderate or severe traumatic brain injury (TBI).
Design: Retrospective, observational, case-control study.
Setting: Neurosciences Critical Care Unit of a university hospital.
Clin Endocrinol (Oxf)
October 2007
Department of Medical Endocrinology, the University Hospital of Copenhagen, Denmark.
Objective: To assess the prevalence of hypopituitarism following traumatic brain injury (TBI), describe the time-course and assess the association with trauma-related parameters and early post-traumatic hormone alterations.
Design: A 12-month prospective study.
Patients: Forty-six consecutive patients with TBI (mild: N = 22; moderate: N = 9; severe: N = 15).
Clin Endocrinol (Oxf)
February 2008
Neurological Clinic Bad Aibling, Kolbermoorer Strasse, Bad Aibling, Germany.
Background: Several studies have reported a high prevalence of hypopituitarism after traumatic brain injury (TBI). Risk stratification is a prerequisite for cost-effective hormonal screening of these patients. However, it is still unclear which risk factors predispose patients to develop anterior hypopituitarism after TBI.
View Article and Find Full Text PDFBrain Inj
June 2007
Department of Laboratory Medicine, University of Toronto, Toronto, Ontario, Canada.
Purpose: Approximately 25% of patients with traumatic brain injury (TBI) may develop partial or complete hypopituitarism. The causative mechanisms involved in its development are not clear. To the authors' knowledge, there have been no recent morphologic studies of the pituitary following TBI.
View Article and Find Full Text PDFBrain Inj
June 2007
Rehabilitation Research Center, San Jose, CA 95128, USA.
Objective: Evaluate the association between neuroendocrine findings and fatigue after traumatic brain injury (TBI) Research design: Prospective, observational.
Methods And Procedures: Sixty-four individuals at least 1 year post-TBI underwent neuroendocrine testing including thyroid, adrenal, gonadal axes and growth hormone (GH) after glucagon stimulation with assessment of fatigue using the Global Fatigue Index (GFI) and the Fatigue Severity Scale (FSS).
Main Outcomes And Results: GFI and FSS scores were significantly higher within this sample compared to published control data.
Pituitary
January 2008
Department of Paediatrics, University of Cambridge, Addenbrooke's Hospital, Level 8/Box 116, Cambridge CB2 2QQ, UK.
In survivors of traumatic brain injury (TBI), impairment in anterior pituitary hormone function may be an important cause of long-term morbidity. Histopathological evidence from post-mortem studies suggests that the hypothalamic-pituitary structures are vulnerable to damage following head injury. Pituitary dysfunction, present months or years after injury, is now well recognised in adults, however, little evidence is known about this potential complication in children and adolescents.
View Article and Find Full Text PDFHead Neck
December 2007
Department of Otolaryngology-Head and Neck Surgery, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
Background: The aim of this study was to review our experience with reoperative thyroid bed surgery (RTBS) for recurrent/persistent papillary thyroid cancer (PTC), and present an algorithm for safe and effective RTBS.
Methods: This is a retrospective study. Records of 33 consecutive patients who underwent RTBS for recurrent/persistent PTC in a previously operated thyroid bed, and were operated upon by the senior author (R.