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Saccade Dysfunction Associated with Chronic Petrol Sniffing and Lead Encephalopathy S Cairney, P Maruff, C B Burns, J Currie, B J Currie

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Saccade Dysfunction Associated with Chronic Petrol Sniffing and Lead Encephalopathy S Cairney, P Maruff, C B Burns, J Currie, B J Currie 472 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.2003.019406 on 13 February 2004. Downloaded from PAPER Saccade dysfunction associated with chronic petrol sniffing and lead encephalopathy S Cairney, P Maruff, C B Burns, J Currie, B J Currie ............................................................................................................................... J Neurol Neurosurg Psychiatry 2004;75:472–476. doi: 10.1136/jnnp.2003.019406 Background: In chronic petrol sniffers, recent exposure to high levels of leaded petrol may give rise to a lead encephalopathy characterised by tremor, chorea, ataxia, hyperreflexia, convulsive seizures, and death. Neurological abnormalities associated with lead encephalopathy involve the cortex, basal ganglia, cerebellum, and brain stem. Objective: To use saccadic eye movement tasks as an experimental tool to determine which CNS changes See end of article for are associated with chronic petrol sniffing and which with a history of lead encephalopathy, and to what authors’ affiliations ....................... extent these changes are reversible. Methods: Saccade function was assessed in chronic petrol sniffers with a history of lead encephalopathy Correspondence to: (encephalopathic sniffers), chronic petrol sniffers who had never suffered lead encephalopathy (chronic Dr Sheree Cairney, Menzies School of Health sniffers), individuals who had sniffed petrol in the past but had not done so for more than six months (ex- Research, PO Box 41096, sniffers), and individuals who had never sniffed petrol (non-sniffers). Casuarina, NT 0811, Results: Chronic sniffers showed increased latency of visually guided saccades and antisaccades and Australia; Sheree.Cairney@ increased antisaccade errors which suggested cortical and basal ganglia dysfunction. These abnormalities menzies.edu.au returned to normal in ex-sniffers. Encephalopathic sniffers showed the same abnormalities as chronic sniffers but with greater severity and additional saccadic signs including dysmetria, gaze evoked Received 24 May 2003 nystagmus, and saccade slowing which usually indicate cerebellar and brain stem dysfunction. In revised form 4 August 2003 Conclusions: Chronic petrol abuse is associated with cortical and basal ganglia abnormalities that are at Accepted 23 August 2003 least partially recoverable with abstinence. Additional long term cerebellar and brain stem abnormalities ....................... are associated with lead encephalopathy. copyright. s with other types of inhalant abuse, the acute effects Because saccades can be controlled, recorded, and quanti- of inhaling or ‘‘sniffing’’ petrol (gasoline) include fied with much greater precision than most other interactive Aeuphoria, relaxation, ataxia, diplopia, and slurred physiological variables, they have proven to be an excellent speech which reflect the neurotoxic effects of aromatic tool for detecting early and subtle changes in brain function hydrocarbons such as toluene, xylene, and benzene.12 related to neurodegenerative or neuropsychiatric disease. Intoxication from sniffing petrol containing tetraethyl lead Different classes of saccadic eye movements can be distin- may be associated with additional visual hallucinations, guished, each of which has a certain function and a distinct visual distortions, and psychosis.3 High levels of exposure to anatomical substrate and physiological organisation.10 11 To leaded petrol may also give rise to a lead encephalopathy, determine the extent of saccade abnormalities that may be which extends beyond any acute intoxication and is associated with chronic petrol sniffing or lead encephalo- http://jnnp.bmj.com/ characterised by decreased conscious state, tremor, myoclo- pathy, we assessed groups of chronic recreational petrol nus or chorea, limb and gait ataxia, hyperreflexia, motor sniffers with and without a history of hospital admission for impairment, nystagmus, and convulsive seizures. Death can lead encephalopathy on a battery of saccadic function tests. also occur4–6 (reviewed by Cairney et al1). Lead encephalo- To investigate whether any abnormal saccadic functions pathy requires emergency admission to an intensive care unit normalise with abstinence from petrol sniffing, we also with intubation and sedation. A long period of inpatient studied individuals who had been chronic petrol sniffers in treatment usually follows admission, although full recovery the past but had since abstained. 78 of cognitive, motor, and emotional function may not occur. on September 26, 2021 by guest. Protected Clinical, radiological, and necropsy studies on patients admitted to hospital with lead encephalopathy show METHODS abnormalities involving the cortex, basal ganglia, cerebellum, Participants and brain stem.4–6 8 These patients almost always have a long The study was set in two remote Aboriginal communities in history of chronic recreational petrol abuse,4–6 8 so it is Arnhem Land in northern Australia, where petrol sniffing difficult to determine whether the neurological impairments had been prevalent for many years. From these communities, and brain abnormalities are related to the chronic petrol 112 male volunteers agreed to participate in a prospective sniffing, the lead encephalopathy, or both. In recreational research trial to investigate health and social outcomes of petrol sniffers who had not suffered lead encephalopathy, we petrol abuse.912We present data on a subgroup of 96 subjects recently showed impairments in memory and attentional (age range, 13 to 35 years) for whom saccade assessments functions as well as neurological impairments that suggested were obtained at baseline. Participants were classified into abnormalities of the frontocerebellar brain regions.9 How- groups according to their history of petrol sniffing, using the ever, the cognitive and neurological tasks were unable to consensual methodology used in our earlier studies involving dissociate performance measures that suggested cortical the same participants912(see Clough et al13). impairment from those arising from cerebellar or brain stem Participants who had never sniffed petrol were classified as dysfunction. non-sniffers or controls. www.jnnp.com Saccade effects of petrol sniffing 473 J Neurol Neurosurg Psychiatry: first published as 10.1136/jnnp.2003.019406 on 13 February 2004. Downloaded from Participants who had sniffed petrol in the past for at least Saccade accuracy (gain) was calculated as the displacement six months but, at the time of the study, had not sniffed of the final eye position with respect to the target position. petrol for the last six months were classified as ex-sniffers. The percentage of hypometric saccades (,85% of target), On average, ex-sniffers had abstained from sniffing petrol for hypermetric saccades (.15% of target), and anticipatory 2.6 (SD 3.3) years. saccades (,70 ms from target onset)19 was calculated for Participants who were currently and actively sniffing petrol each participant. Duration and peak velocity for visually and had done so for a period of at least six months were guided saccades were plotted against saccade amplitude. classified as chronic sniffers. No participant from the ex- Saccade recordings were examined by visual inspection for sniffer or chronic sniffer groups had ever been admitted to the following abnormalities: post-saccadic drift reflecting hospital for lead encephalopathy from sniffing petrol. pulse–step mismatch; saccadic intrusions that are inappropri- Chronic sniffers who were currently living in the commu- ate saccades taking the eye away from the target during nity but who had been admitted to hospital previously for attempted fixation; and gaze evoked nystagmus, which lead encephalopathy from petrol sniffing were classified as shows difficulty maintaining eccentric fixation of the target encephalopathic sniffers. These individuals had required (¡10˚ and ¡15˚) characterised by an alternation between emergency hospital admission and ongoing intensive care slow drift and corrective quick movements of the eye.20 For treatment for lead encephalopathy on a median of 1.0 the antisaccade task, a central fixation point was offset previous occasions (range one to six), confirmed by records simultaneously with the onset of a peripheral target. A at the Royal Darwin Hospital (RDH). Before testing for this correct antisaccade was a deliberate eye movement to the study, the most recent admission for lead encephalopathy location in the opposite visual field of the target and among these individuals was a median of 3.5 (range 1 to 7) equidistant from the centre. Any initial reflexive eye move- years earlier, when they were admitted for a median of 25 ment towards the target was scored as an error, even if a days (5 to 118) and had a median blood lead of 4.6 mmol/l subsequent correction to the opposite side was made. The (1.69 to 7.25) on admission. Blood lead concentrations higher latency for the onset of correct antisaccades was recorded and than 0.48 mmol/l are above Australian recommended safe a percentage error calculated. limits, and concentrations above 3.85 mmol/l indicate lead poisoning.14 All of the encephalopathic sniffers, chronic sniffers, and ex-sniffers (using a retrospective rating) met Data analysis the criteria for inhalant abuse from the Diagnostic and Before analysis, the distributions of data for each perfor- Statistical Manual of Mental Disorders, fourth edition.15 These mance measure were inspected for normality and hetero- individuals had inhaled a combination
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