A prospective study of neurocognitive changes 15 years after chronic inhalant abuse Sheree Cairney 1,2 , Nicole O’ Connor 1 , Kylie M. Dingwall 1 , Paul Maruff 3,4 , Ruxanna Shafiq-Antonacci 5 , Jon Currie 5 & Bart J. Currie 1 Menzies School of Health Research, Institute of Advanced Studies, Charles Darwin University, Darwin, NT, Australia, 1 Flinders University and Northern Territory Clinical School, Darwin, NT, Australia, 2 Centre for Neuroscience, University of Melbourne, Melbourne, Vic., Australia, 3 CogState Ltd, Melbourne, Vic., Australia 4 and Department of Addiction Medicine, St Vincent’s Hospital, Melbourne, Vic., Australia 5 ABSTRACT Aims In a previous study, neurological and cognitive deficits reflecting central nervous system (CNS) disruption from chronic inhalant abuse showed substantial recovery after 2 years’ abstinence. Functional recovery was progressive, with recovery rates dependent on the degree of impairment prior to abstinence, and severity and duration of initial abuse. Persistent deficits occurred in those with previous ‘lead encephalopathy’ from leaded petrol abuse. The current study examined recovery in the same cohort 15 years after baseline. Design Prospective cohort design. Setting Two remote Aboriginal communities in Arnhem Land, Australia. Participants Using baseline group clas- sifications, 27 healthy controls, 60 ex-chronic inhalant abusers and an additional 17 with previous lead encephalopa- thy were assessed. Measurements Standard neurological, ocular-motor and cognitive functions and blood lead levels. Findings Chronic (non-encephalopathic) inhalant abusers showed elevated blood lead levels and abnormal scores on most tasks at baseline. At 2 years’ abstinence, blood lead was reduced but remained elevated and most scores had normalized. By 15 years, blood lead and all performance scores were equivalent to healthy controls for this group (P > 0.05). The encephalopathic group was more severely impaired on all scores at baseline and showed little improve- ment, if any, across all tests after both 2 and 15 years’ abstinence. Blood lead for this group declined, and was not significantly different to controls after 15 years. Conclusions Some inhalant abusers experience severe and persistent neurological deficits, suggesting irrecoverable damage attributable to lead encephalopathy. In the absence of this encephalopathy long-term abstinence from inhalants may allow recovery of normal brain function. Keywords Brain, cognitive, gasoline, inhalant abuse, neurological, petrol. Correspondence to: Sheree Cairney, Menzies School of Health Research, PO Box 41096, Casuarina, NT 0811, Australia. E-mail: Sheree.Cairney@menzies.edu.au Submitted 7 August 2012; initial review completed 4 October 2012; final version accepted 15 January 2013 INTRODUCTION Recreational inhalation of volatile hydrocarbons, known as volatile solvent abuse or inhalant abuse, occurs in a context of health and social deterioration in many disad- vantaged subpopulations. Inhalants such as spray paint, glue and petrol (i.e. gasoline) contain complex mixtures of lipophilic hydrocarbons, which are absorbed rapidly into the lipid-rich central nervous system (CNS; see [1] for review). Leaded petrol also contains tetraethyl lead. Euphoria and excitability occurs with initial intoxication, and sedation, lack of coordination (i.e. ataxia) and even coma can follow with increasing doses [2]. Leaded petrol overdose can cause lead encephalopathy, a neurological syndrome consisting of tremor, gross ataxia, eye move- ment abnormalities (i.e. nystagmus) and convulsive sei- zures [3,4]. Lead encephalopathy requires critical care and chelation treatment to remove lead from the blood over a prolonged recovery period [5]. Long-term CNS impairment with chronic inhalant abuse presents as a progressive decline of cognitive func- tions impacting memory, attention, visuospatial, execu- tive and motor functions implicating frontostriatal and cerebellar deterioration [6–9]. Neuroimaging studies of solvent abusers report brain white matter, periventricular and subcortical abnormalities and atrophy of the hippo- campus, cerebellum, cerebrum, corpus callosum and brainstem [10–20]. Neurological changes suggest that RESEARCH REPORT doi:10.1111/add.12124 © 2013 The Authors, Addiction © 2013 Society for the Study of Addiction Addiction, 108, 1107–1114