To illustrate the need to carefully consider mental health, psychosocial and motivational factors when investigating cognitive and intellectual impairment among chronic inhalant users.

Two adolescent chronic inhalant users with similar psychosocial disadvantages (eg unstable and dysfunctional families, state-based care, school absenteeism and forensic issues) and histories of comorbid drug use and mental health problems were assessed using a battery of paper and pencil and computerised neuropsychological tests.

Contrary to the expectations of her case manager, one participant performed within the normal range for her age in all domains of intellectual ability, while the other participant, in line with the expectations of her case manger, showed marked cognitive deficits and intellectual disability.

The typically complex presentation of chronic inhalant users (ie disadvantaged psychosocial backgrounds, comorbid psychopathology and poor motivation/engagement) is rarely considered when investigating associated cognitive and intellectual functioning. Future research should more carefully consider the role of such factors, given the evidence suggesting that they can considerably alter (accentuate or diminish) the association between inhalant abuse and neuropsychological impairment.

Delirium tremens (DT) is one of the most serious complications of alcohol withdrawal, affecting 5–10% of in-patients with a mortality rate up to 15%. DT, characterised by delirium and tremors, appears within 48–72 h of abstinence and persists for about 5–10 days.

We report a case of DT in a young man with delayed onset on the 15th day after the cessation of alcohol use, despite an uncomplicated detoxification with benzodiazepine treatment.

We hypothesise that the intake of country liquor in our patient, which contains higher percentages of alcohol, causes a prolonged imbalance of N-methyl-d-aspartic acid and glutamate receptor activity, leading to the picture of delayed-onset DT and that an atypical presentation at the time of admission and atypicality in early course are clinical pointers to the subsequent development of delayed-onset DT.