Annual incidence of severe traumatic brain injuries (TBI) varies from 180 to 300 out of 100.000. Mortality or severe sequelae risk is increased 8 fold after a TBI. Studies in adults showed an ante-hypophyseal deficit in 28 to 68 % of patients with a TBI. The most common deficit is Growth Hormone Deficit (GHD); followed by gonadotropic and corticotropic (AdrenoCorticoTropic Hormone (ACTH)) insufficiencies. Thyrotropic deficits (Thyroid-Stimulating Hormone (TSH)) are less frequent. From a pathophysiological point of view, the lesional mechanism responsible for hypopituitarisms would be a damage of hypophyseal vessels or hypothalamic-pituitary vessels. The frequency of pituitary deficits and the potential beneficial effects of replacement therapy on quality of life, tiredness, loss of energy and productivity, justify the systematic detection of the deficits in patients with moderate to severe TBI.

Study hypotheses :

At the present time, the lack of data in children does not give us the opportunity to affirm that one part of the symptoms showed by children with post-TBI neuropsychological sequelae, are linked to pituitary deficiency and that they can be improved with a replacement therapy.

Firstly, it is essential to better understand the natural history of post-TBI pituitary deficiencies, studying the connexion between observed deficiencies in acute and late phase of sequelae.

Inclusion Criteria:

• children from 2 months to 16 years
• in the intensive care unit
• TBI : moderate (Glasgow Coma Scale (GCS) between 9 and 12) to severe (GCS <9), whatever the mechanism involved
• informed consent form signed by parents

Exclusion Criteria:

• obesity (Body Mass Index (BMI) > 97th percentile for the age)
• patient already under replacement therapy.
• patient taking AntiEpileptic Drugs (AEDs)
• patient with long-term systemic corticotherapy
• history of neurological disease or learning difficulties
• no covered by a national health insurance