Hypophysenveränderungen nach Schädelhirntraumen und ihre Korrelation zu Lokalisation und Überlebenszeit

Cardauns, H

doi:10.1007/bf02096434

Cited by 4 publications

(2 citation statements)

References 3 publications

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“…The first report was in 1918 associated with a basilar skull fracture [ 6 ]. Early descriptions included autopsy data associated with infarction of the anterior pituitary [ 7 , 8 , 9 , 10 ]. Understanding the true incidence is difficult given that TBI is not considered by many practitioners in the evaluation of hypopituitarism, even amongst endocrinologists [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Impaired Pituitary Axes Following Traumatic Brain Injury

Scranton

Baskin

2015

JCM

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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.

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Section: Introductionmentioning

confidence: 99%

Impaired Pituitary Axes Following Traumatic Brain Injury

Scranton

Baskin

2015

JCM

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“…Head traumatisms may involve the pituitary and cause pathological changes in its function 1,2 :for a review. In the majority of these cases, the ensuing endocrine syndrome is conspicuous and entails symptoms of a post-traumatic pituitary disease.…”

Section: Introductionmentioning

confidence: 99%

Neuroendocrine Data in Chronic Post‐traumatic Headache

et al. 1982

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Twenty chronic post-traumatic headache subjects (16 men and 4 women) were considered, together with age and sex matched normal controls. Pituitary function was challenged by means of luteinising hormone releasing hormone (100 microg, i.v.), thyrotropin (TSH) releasing hormone (200 microg, i.v.) and regular insulin (.1 U/kg, i.v.). The responses of gonadotropins, TSH, somatotropin (STH) and prolactin (PRL) were studied in the group as a whole and in clinical subgroups. No differences were found in the baseline levels of the hormones. No significant changes were observed in the responses of gonadotropins and STH. A decreased response was found for TSH and, in the female series, an enhanced response of PRL was observed. Patients complaining for a decreased libido showed a larger PRL response. The smaller response of TSH exhibits a straight inverse relationship to the clinical severity. The periodicity of PRL secretion studied in male patients with a harmonic analysis according to the Fourier's theorem showed the preservation of the physiological sleep-entrained night surge. The per cent incidence of the harmonics with a period shorter than 24 hours decreases according to the clinical severity, at variance to the finding in normal controls. The only persisting harmonic is the one with a 24 hour period. In the absence of major post-traumatic endocrine syndromes, post-traumatic headache subjects show changes of the neuroendocrine regulation of pituitary secretion. The findings are consistent with the hypothesis of an hyperactivity of serotoninergic neurotransmission.

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