Traumatic Infarction of the Anterior Lobe of the Pituitary Gland

Daniel, P. M.; Prichard, Marjorie M. L.; Treip, C. S.

doi:10.1016/s0140-6736(59)91583-1

Cited by 160 publications

(96 citation statements)

References 10 publications

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“…Pittman et al (1971) supposed their patient as hypothalamic hypothyroidism, who had hypothyroidism and undetectable serum TSH levels, with a normal response to TRH. Daniel et al(1959) proposed that if the section level of pituitary stalk by trauma was above the site of entry of the hypophyseal arteries into the, stalk, there was no pituitary necrosis. They also found that the section at a lower level of pituitary stalk caused, necrosis of the central portion of the anterior lobe, while a small area adjacent to the posterior lobe, supplied by short hypophyseal portal vessels, usually survived.…”

Section: Discussionmentioning

confidence: 99%

A Case of Posttraumatic Hypopituitarism

et al. 1972

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SynopsisA case of posttraumatic hypopituitarism was studied. A 46-years-old man suffered from adrenal crisis after he showed symptoms of hypopituitarism which was caused by the head injury of 26 years ago. Hyponatremia was prominent at the time of admission. Clinical and laboratory studies revealed hypothyroidism, hypofunction of adrenal gland and hypogonadism. Blood pituitary hormones-ACTH, GH, TSH and LH were determined by radioimmunoassay. Plasma ACTH levels were not detectable (below 10 pg/ml) even after metyrapone administration. Base-line serum GH level was low and did not respond to the administration of insulin or L-arginine. Although the response was subnormal, serum TSH levels were increased in response to synthetic thyrotropin releasing hormone (TRH). Serum LH levels were low. Mechanism about the hyponatremia at the time of adrenal crisis in this case was discussed.

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Section: Discussionmentioning

confidence: 99%

A Case of Posttraumatic Hypopituitarism

et al. 1972

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“…This suggests that secondary insults such as increased intracranial pressure, ischaemic and/or hypoxic damage may account for the pituitary lesions (14). It is thought that severed portal vessels can regenerate and grow down into viable anterior pituitary tissue with demonstration of mitotic figures in the surviving cells in early histopathological studies (15). This revascularisation may lead to the restoration of anterior pituitary function.…”

Section: Traumatic Brain Injurymentioning

confidence: 99%

MANAGEMENT OF ENDOCRINE DISEASE: Neuroendocrine surveillance and management of neurosurgical patients

Garrahy

Sherlock

Thompson

2017

European Journal of Endocrinology

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Advances in the management of traumatic brain injury, subarachnoid haemorrhage and intracranial tumours have led to improved survival rates and an increased focus on quality of life of survivors. Endocrine sequelae of the acute brain insult and subsequent neurosurgery, peri-operative fluid administration and/or cranial irradiation are now well described. Unrecognised acute hypopituitarism, particularly ACTH/cortisol deficiency and diabetes insipidus, can be life threatening. Although hypopituitarism may be transient, up to 30% of survivors of TBI have chronic hypopituitarism, which can diminish quality of life and hamper rehabilitation. Patients who survive SAH may also develop hypopituitarism, though it is less common than after TBI. The growth hormone axis is most frequently affected. There is also accumulating evidence that survivors of intracranial malignancy, who have required cranial irradiation, may develop hypopituitarism. The time course of the development of hormone deficits is varied, and predictors of pituitary dysfunction are unreliable. Furthermore, diagnosis of GH and ACTH deficiency require dynamic testing that can be resource intensive. Thus the surveillance and management of neuroendocrine dysfunction in neurosurgical patients poses significant logistic challenges to endocrine services. However, diagnosis and management of pituitary dysfunction can be rewarding. Appropriate hormone replacement can improve quality of life, prevent complications such as muscle atrophy, infection and osteoporosis and improve engagement with physiotherapy and rehabilitation.

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“…Necrosis processes seem to be due to the vulnerability of the long hypophysial portal vessels when they pass through the diaphragma sellae, where they are particularly vulnerable to mechanical compression from both brain and pituitary swelling and direct stalk injury. 21,42 Direct injury of the pituitary gland, pituitary stalk, 31,47 and/or hypothalamus can be caused by the following mechanisms: rotational and shearing injuries of the brainstem and hypothalamic-pituitary axis, and fractures through the skull base and sella turcica. 11,21 This direct injury also can be reinforced by subsequent hemorrhage into the sella turcica or into the pituitary gland.…”

Section: The Most Common Theoriesmentioning

confidence: 99%

Sports-related chronic repetitive head trauma as a cause of pituitary dysfunction

Dubourg

Messerer

2011

FOC

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Traumatic brain injury (TBI) is recognized as a cause of hypopituitarism even after mild TBI. Although over the past decade, a growing body of research has detailed neuroendocrine changes induced by TBI, the mechanisms and risk factors responsible for this pituitary dysfunction are still unclear. Around the world, sports—especially combative sports—are very popular. However, sports are not generally considered as a cause of TBI in most epidemiological studies, and the link between sports-related head trauma and hypopituitarism has not been investigated until recently. Thus, there is a paucity of data regarding this important concern. Because of the large number of young sports participants with near-normal life expectancy, the implications of undiagnosed or untreated postconcussion pituitary dysfunction can be dramatic. Understanding the pathophysiological mechanisms and risk factors of hypopituitarism caused by sports injuries is thus an important issue that concerns both medical staff and sponsors of sports. The aim of this paper was to summarize the best evidence for understanding the pathophysiological mechanisms and to discuss the current data and recommendations on sports-related head trauma as a cause of hypopituitarism.

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Traumatic Infarction of the Anterior Lobe of the Pituitary Gland

Cited by 160 publications

References 10 publications

A Case of Posttraumatic Hypopituitarism

A Case of Posttraumatic Hypopituitarism

MANAGEMENT OF ENDOCRINE DISEASE: Neuroendocrine surveillance and management of neurosurgical patients

Sports-related chronic repetitive head trauma as a cause of pituitary dysfunction

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