Neuroendocrine dysfunction in patients recovering from subarachnoid hemorrhage.
ABSTRACT Subarachnoid hemorrhage (SAH) is a recently identified risk factor for hypopituitarism, particularly growth hormone (GH) and corticotrophins deficiencies. The aim of our study was to identify possible predictor(s) for neuroendocrine dysfunction in SAH survivors.
Pituitary function was evaluated in 93 patients (30 males, 63 females), aged 48.0+/-1.1 years (mean+/-SE), and with a Glasgow Outcome Scale score of 4.6+/-0.6 (mean+/-SE) more than one year following SAH. In the acute phase, SAH was complicated by vasospasm (VS) in 18 and by hydrocephalus (HDC) in 9 patients. Baseline serum values of insulin growth factor 1 (IGF-I), cortisol, thyroxine (T4), thyroid stimulating hormone (TSH), follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone (in males), estradiol (in females) and prolactin were determined.
According to the results of baseline hormonal evaluation, 47 patients (50.5%) had no hormonal abnormalities. Seven patients (7.5%) had multiple pituitary hormone deficiencies: Four patients (4.3%) had two (GH and cortisol), one patient had three (gonadal, adrenal and GH) and two patients had deficiency of all pituitary axes. Thirty-nine patients (42%) had one abnormal axis (13 adrenal, 2 thyroid, 4 gonadal and 20 GH). None of the subjects was treated with desmopressin or exhibited symptomatic polyuria. The VS and HDC during the acute phase of SAH were related to abnormal pituitary status (VS with low IGF-I levels and HDC with low cortisol levels).
Through a screening procedure, neuroendocrine dysfunction was identified in a substantial number of asymptomatic patients with previous SAH. Cerebral VS and HDC at the time of SAH emerged as risk factors possibly predicting development of pituitary dysfunction. Low basal levels of IGF 1 and cortisol may help in selecting patients requiring further evaluation of pituitary function.
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ABSTRACT: Background Fatigue, slowness, apathy and decrease in level of activity are common long-term complaints after a subarachnoid haemorrhage (SAH). They resemble the symptoms frequently found in patients with endocrine dysfunction. Pituitary dysfunction may be the result of SAH or its complications. We therefore hypothesized that it may explain some of the long-term complaints after SAH.We reviewed the literature to clarify the occurrence, pattern and severity of endocrine abnormalities and we attempted to identify risk factors for hypopituitarism after SAH. We also assessed the effect of hypopituitarism on long-term functional recovery after SAH.Methods In a MEDLINE search for studies published between 1995 and 2014, we used the term subarachnoid haemorrhage in combination with pituitary, hypopituitarism, growth hormone, gonadotropin, testosterone, cortisol function, thyroid function and diabetes insipidus. We selected all case-series and cohort studies reporting endocrine function at least 3 months after SAH and studied their reported prevalence, pathogenesis, risk factors, clinical course and outcome.ResultsWe identified 16 studies describing pituitary function in the long term after SAH. The reported prevalence of endocrine dysfunction varied from 0 to 55% and the affected pituitary axes differed between studies. Due to methodological issues no inferences on risk factors, course and outcome could be made.Conclusions Neuroendocrine dysfunction may be an important and modifiable determinant of poor functional outcome after SAH. There is an urgent need for well-designed prospective studies to more precisely assess its incidence, clinical course and effect on mood, behaviour and quality of life.BMC Neurology 10/2014; 14(1):205. DOI:10.1186/s12883-014-0205-0 · 2.49 Impact Factor
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ABSTRACT: Objective: Sodium dysregulation in the course after aneurysmal subarachnoid hemorrhage (aSAH) has been identified as one contributor to adverse clinical outcome. However, the correlation of acute dysnatremia and early brain injury (EBI) remains unclear. We investigated the early course and prognostic relevance of changes in serum sodium concentrations and its relation to EBI after aSAH. Methods: Retrospectively, the serum sodium concentration (SSC) of 264 patients with aSAH was analyzed. The first SSC was obtained within 8 h after initial ictus and then repeatedly analyzed every 8 h over the first five days. Incidence of hypernatremia (defined as SSC > 145 mmol/l) was correlated with initial neurological condition according to World Federation of Neurological Surgeons grade (WFNS), incidence of delayed cerebral ischemia (DCI) and clinical outcome at 12 month according to modified Rankin Scale (mRS). Results: Within 56h. 82 patients (31.1%) developed hypernatremia which correlated significantly with initial neurological condition (p <0.001). Initial SSC within 8 h after SAH did not correlate with patient outcome at 12 month (r= -0.026, p = 0.694), however SSC obtained 56 h after ictus did significantly (r= 0.365, p < 0.001; OR 4.14 95% Cl (1.84-9.31)). A correlation with the incidence of DCI was not found (r=0.079, p=0.217). Conclusion: The occurrence of hypernatremia within 56 h after aSAH was shown to be an independent predictor for poor neurological outcome. Early serum sodium levels after aSAH can be considered as surrogate markers to predict outcome after aSAH irrespective to the occurrence of DCI. However, prospective studies are necessary to validate this concept.Clinical Neurology and Neurosurgery 06/2014; 123C:164-168. DOI:10.1016/j.clineuro.2014.05.022 · 1.25 Impact Factor
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ABSTRACT: A number of neuroendocrine changes have been described after stroke, which may serve adaptive or deleterious functions. The neuroendocrine changes include activation of the hypothalamo-pituitary-adrenal axis, sympathetic nervous system and alterations of several hormonal levels. Alterations of the HPA axis, increased catecholamines, natriuretic peptides and, decreased melatonin and IGF-1 levels are associated with poor post-stroke outcome, although there is no definitive proof of causality. Therefore, it remains to be established whether alteration of neuroendocrine responses could be used as a potential therapeutic target to improve stroke outcome. This article gives an overview of the major neuroendocrine pathways altered by stroke and highlights their potential for clinical use and further neurotherapeutic development by summarizing the evidence for their association with stroke outcome including functional outcome, post-stroke infection, delirium, depression and stroke-related myocardial injury.Expert Review of Neurotherapeutics 01/2014; DOI:10.1586/14737175.2014.877841 · 2.83 Impact Factor