Diabetes Insipidus Following Closed Head Injury

Porter, Roger J.; Miller, Ronald

doi:10.1136/jnnp.11.4.258

Cited by 52 publications

(9 citation statements)

References 10 publications

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“…In this context, Kornblum 10 found 62 cases of histological pituitary damage in 100 patients who died of head trauma. Porter and Miller 13 have emphasized a traumatic elongation of the stalk, while Crompton 2 has considered ischemic and haemorrhagic lesions in the hypothalamus, infundibulum, and pituitary stalk as the cause of the underlying pathology. These lesions may cause denervation of the posterior lobe, with Wallerian degeneration progressing upward, resulting in a disappearance of the normal hyperintense signal on T1-weighted sequences, as shown in our case.…”

Section: Discussionmentioning

confidence: 98%

Bilateral abducens nerve palsy associated with diabetes insipidus following crushing head injury: A case report

Yamakawa¹,

Enomoto²,

Tanigawara³

et al. 2005

Injury Extra

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Section: Discussionmentioning

confidence: 98%

Bilateral abducens nerve palsy associated with diabetes insipidus following crushing head injury: A case report

Yamakawa¹,

Enomoto²,

Tanigawara³

et al. 2005

Injury Extra

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“…Pathological studies have reported either haemorrhagic or ischaemic lesions in the hypothalamus (Crompton 1971), or, more commonly, severance of pituitary stalk, or extensive infarction of the anterior pituitary due to a localized ischaemic insult of the pituitary stalk (Daniel et al 1959). Impair¬ ment of the posterior pituitary function after head trauma occurs with much greater frequency than anterior pituitary deficiency (Porter & Miller 1948); in the latter however, adrenal and thyroid deficiency may mask a diabetes insipidus. In those cases, studies performed several months following the head trauma, and after a replacement therapy, revealed either a partial impairment of ADH func¬ tion (Kanade et al 1978) or a normal hypothalamoposterior pituitary axis (Paxson & Brown 1976).…”

Section: Discussionmentioning

confidence: 99%

Panhypopituitarism secondary to head trauma: evidence for a hypothalamic origin of the deficit

Jambart¹,

Turpin²,

Gennes³

1980

Acta Endocrinologica

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A complete endocrinological exploration was performed in a 23 year old male patient who presented clinical signs of an acquired panhypopituitarism which appeared two months after a severe head trauma, in order to determine whether the deficit lay in the hypothalamus or in the pituitary. TSH had normal basal levels, but presented a delayed rise after TRH administration. PRL rose normally after TRH administration, but presented a blunted response to both metoclopramide and insulin tolerance test. Cortisol rose significatively after lysine vasopresssin, but failed to rise during insulin hypoglycaemia. These results are consistent with a hypothalamic defect. Extensive endocrinological data are often lacking in the few similar cases reported in the literature. Prl and TSH were usually found to have normal basal levels while other pituitary hormones were profoundly lowered. This was interpretated as a pituitary defect with some intact areas of the anterior lobe. However, this may also suggest a hypothalamic defect which could have been assessed by more discriminative tests.Hypothalamo-pituitary deficits following head trauma have rarely been reported and endocrine exploration was generally inadequate in those cases (). This re¬ port concerns a well documented case of posttraumatic panhypopituitarism in which a hypo¬ thalamic, rather than pituitary, origin has been established. Case reportA 23 year old white male patient was referred to our hospital with typical clinical signs of panhypopituitarism that had appeared five years earlier, following a car accident. He suffered severe head trauma with three hours loss of consciousness, vertebral fractures, left conjunctival haemorrhage and multiple skin injuries.Past medical history was unremarkable; no neonatal anoxia, slight overweight during childhood, normal growth with a height of 169 cm attained at 18 years. The onset of puberty was at 14 years. Sexual hair was normal¬ ly distributed but scanty. Erections and ejaculations were present. History of meningoencephalitis or of head or neck external irradiation was lacking.Two months after the head trauma, secondary sex characteristics regressed completely with abolition of sexual activity. Meanwhile, the patient complained of pallor, physical and mental asthenia, but did not show cold intolerance and was not constipated. He had a ten kilograms weight-gain in the year following the accident, his weight on admission was 95 kg. On physical examination, the blood pressure was 120-80 mmHg and the pulse rate was 60/min. Pubic and axillary hair were absent but the testes measured 2.5 x 2 cm and were of normal consistency. The penis was normal-sized. No galactorrhoea nor gynaecomastia were found, but adipomastia with abdominotruncular obesity were noted. The skin was slightly infiltrated. Features suggesting increased intracranial pressure were absent (no headache, papilloedema, nor polyuria-polydypsia). The patient was tuberculine-positive. There was no arachnodactylia nor retinitis pigmentosa. The bone age was determined to be 17...

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“…Since the 1940's, the medical literature has documented TBI as a cause of endocrine disruption (Escamilla & Lisser, 1942;Porter & Miller, 1946;Altman & Puzanski, 1961;Bevenga, Campeni, Ruggieri, & Trimarchi, 2000). TBI has been linked to neuroendocrine insufficiencies mediated by pituitary, such as: thyroid and adrenal functioning (Tsargarakis, Tzanela, & Dimopoulou, 2005), diabetes insipidus (Griffin, Hartley & Crow, 1976), growth hormone deficiencies (Lorenzo et al, 2006;Lopez et al, 1992), and hyperprolactinemia (Bondanelli et al, 2004).…”

Section: Incidence and Prevalence Of Endocrine Disruptionmentioning

confidence: 99%

Traumatic brain injury and neuro-endocrine disruption: Medical and psychosocial rehabilitation

Webb

Little

Loupee-Wilson

2014

NRE

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INTRODUCTION: Traumatic Brain Injury (TBI) initiates a cascade of neuromodulatory damage that blurs the distinctions between physical and psychological medicine. Monitoring endocrine function through labs is not part of the medical care algorithm for treatment of TBI, but the clinical symptoms are easily misidentified as they include: depression, fatigue, poor concentration, irritability and a decline in overall cognitive functioning. The reciprocal flow of change between neuroendocrine health and psychosocial health is well established within the field of neuroscience, social psychology, endocrinology and behavioral neurology, but has not translated into patient care. OBJECTIVES: This paper outlines common neuroendocrine disruptions secondary to TBI and their clinical implications for treating mental health professionals. CONCLUSION: Wider adoption of the consensus guidelines on the detection and monitoring of endocrine abnormalities post-TBI may diminish the severity of functional impairment and improve quality of life.

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Diabetes Insipidus Following Closed Head Injury

Cited by 52 publications

References 10 publications

Bilateral abducens nerve palsy associated with diabetes insipidus following crushing head injury: A case report

Bilateral abducens nerve palsy associated with diabetes insipidus following crushing head injury: A case report

Panhypopituitarism secondary to head trauma: evidence for a hypothalamic origin of the deficit

Traumatic brain injury and neuro-endocrine disruption: Medical and psychosocial rehabilitation

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