Traumatic brain injury is an important cause of hypopituitarism in human beings, but limited information exists in the veterinary literature regarding this condition. The primary study objective was to investigate whether hypothalamic-anterior pituitary axis dysfunction exists following traumatic brain injury in 17 client owned dogs. In this retrospective, observational, open, cohort study, information about dogs presented to four separate referral centres between April 2008 and October 2013 was reviewed. Cases were included if they had suffered from non-fatal traumatic brain injury, resulting in neurological dysfunction, and follow-up evaluation included measurement of the serum concentration of insulin-like growth factor 1 (IGF-1), endogenous adrenocorticotrophic hormone (ACTH), basal cortisol, thyroid-stimulating hormone, total thyroxine (TT4) and, if appropriate, free thyroxine. Decreased IGF-1 concentration was the most common abnormality detected (7/17, 41 per cent; median 132 ng/ml, range <15–536), followed by a decreased TT4 concentration (4/17, 23 per cent; median 19, range 4–49). Basal cortisol concentration was less than 20 nmol/l in two cases (2/17, 12 per cent; median 65, range <20–1735), with concurrently undetectable ACTH (<5 pg/ml). This study demonstrates that dogs with a history of traumatic brain injury can develop endocrine abnormalities indicative of hypothalamic-anterior pituitary dysfunction.