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Saccade dysfunction associated with chronic petrol sniffing and lead encephalopathy

Cairney, Sheree J., Maruff, P., Burns, Chris B., Currie, Jon and Currie, Bart J. (2004). Saccade dysfunction associated with chronic petrol sniffing and lead encephalopathy. Journal of Neurology, Neurosurgery and Psychiatry,75(3):472-476.

Document type: Journal Article
Citation counts: Altmetric Score Altmetric Score is 3
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Title Saccade dysfunction associated with chronic petrol sniffing and lead encephalopathy
Author Cairney, Sheree J.
Maruff, P.
Burns, Chris B.
Currie, Jon
Currie, Bart J.
Journal Name Journal of Neurology, Neurosurgery and Psychiatry
Publication Date 2004
Volume Number 75
Issue Number 3
ISSN 0022-3050   (check CDU catalogue  open catalogue search in new window)
Start Page 472
End Page 476
Total Pages 5
Place of Publication UK
Publisher BMJ Group
Field of Research 1103 - Clinical Sciences
1701 - Psychology
1702 - Cognitive Sciences
HERDC Category C1 - Journal Article (DEST)
Abstract 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 wild lead encephalopathy involve the cortex, basal ganglio, cerebellum, and brain stem.

Objective: To use saccadic eye movement tasks as an experimental tool to determine which CNS changes are associated with chronic petrol sniffing and which with a history of lead encephalopathy, and to what extent these changes are reversible.

Methods: Saccade function was assessed in chronic petrol sniffers with a history of lead encephalopathy (encephalopathic sniffers), chronic petrol sniffers who had never suffered lead encephalopathy (chronic sniffers), individuals who had sniffed petrol in the past but had not done so for more than six months (ex-sniffers), and individuals who had never sniffed petrol (non-sniffers).

Results: Chronic sniffers showed increased latency of visually guided saccades and antisaccades and increased antisaccade errors which suggested cortical and basal ganglia dysfunction. These abnormalities 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 nystagmus, and saccade slowing which usually indicate cerebellar and brain stem dysfunction.

Conclusions: Chronic petrol abuse is associated with cortical and basal ganglia abnormalities that are at least partially recoverable with abstinence. Additional long term cerebellar and brain stem abnormalities are associated with lead encephalopathy.
DOI http://dx.doi.org/10.1136/jnnp.2003.019406   (check subscription with CDU E-Gateway service for CDU Staff and Students  check subscription with CDU E-Gateway in new window)
 
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