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

Abstract

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...

Lateral impact in closed head injury: A substantially increased risk for diffuse axonal injury—A preliminary study

“…There is a clear relationship between DAI and cognitive, neuropsychological and behavioural deficits such as impaired processing speed and alterations with impaired day-to-day function (Tate et al, 1991;Felmingham et al, 2004). Somatic deficits such as isolated decreases of pituitary hormones (Klingbeil and Cline, 1985) or even panhypopituitarism (Jambart et al, 1980) and other intracerebral biochemical pathway disorders have been reported (van Woerkom et al, 1977;Rossi, 1998).…”