Introduction: The peri-operative use of high-dose dexamethasone to reduce cerebral oedema may result in worsening glycaemic control in people with diabetes and glucocorticoid-induced diabetes in susceptible individuals. This study aims to examine the incidence of glucocorticoid-induced diabetes in a cohort of neurosurgical patients receiving high-dose dexamethasone peri-operatively. Materials and methods: Adult non-diabetic neurosurgical patients receiving high-dose dexamethasone were prospectively studied. Exclusion criteria included pregnancy, HbA1c > 6.0%, and use of anti-diabetes therapies. The following data were collected: Family history of diabetes, body mass index, fasting glucose, insulin, C-peptide, and HbA1c (prior to surgery and 6 weeks after last dose of dexamethasone). Homeostatic model assessment values were calculated. Peri-operative glucose readings were recorded and 75 g oral glucose tolerance tests performed at the end of 6 weeks. Paired student t tests and multiple linear regressions were used. Results: Data from 21 participants (11 women) were available. The mean total dose of dexamethasone was 96 ± 34 mg, and treatment duration was 17 ± 7 days. A total of 105 random blood glucose levels were documented peri-operatively (mean 7.0 ± 1.0 mmol/L). Six weeks following cessation of dexamethasone course, none of the participants developed diabetes, defined either by fasting glucose or by 75 g OGTT. There was a statistically significant increase in the mean HOMA-β from 81.5 to 102.1% (p = 0.01) and a significant decrease in the mean fasting glucose from 5.7 to 4.8 mmol/L (p = 0.001). Conclusions: The use of high-dose dexamethasone in this cohort of neurosurgical patients did not result in glucocorticoid-induced diabetes. Hyperglycaemia was transient and had resolved by 6 weeks.