Abstract
Original language | English |
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Pages (from-to) | 472-476 |
Number of pages | 5 |
Journal | Journal of Neurology, Neurosurgery and Psychiatry |
Volume | 75 |
Issue number | 3 |
Publication status | Published - 2004 |
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Saccade dysfunction associated with chronic petrol sniffing and lead encephalopathy. / Cairney, Sheree; Maruff, Paul; Burns, C; CURRIE, J; Currie, Bart.
In: Journal of Neurology, Neurosurgery and Psychiatry, Vol. 75, No. 3, 2004, p. 472-476.Research output: Contribution to journal › Article › Research › peer-review
TY - JOUR
T1 - Saccade dysfunction associated with chronic petrol sniffing and lead encephalopathy
AU - Cairney, Sheree
AU - Maruff, Paul
AU - Burns, C
AU - CURRIE, J
AU - Currie, Bart
PY - 2004
Y1 - 2004
N2 - 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.
AB - 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.
KW - gasoline
KW - lead
KW - adolescent
KW - adult
KW - anamnesis
KW - article
KW - basal ganglion
KW - brain cortex
KW - brain disease
KW - brain region
KW - brain stem
KW - central nervous system
KW - cerebellum disease
KW - controlled study
KW - disease severity
KW - dysmetria
KW - evoked response
KW - gaze
KW - human
KW - latent period
KW - lead poisoning
KW - long term exposure
KW - major clinical study
KW - male
KW - nystagmus
KW - priority journal
KW - saccadic eye movement
KW - sniffing
KW - substance abuse
KW - task performance
KW - Administration, Inhalation
KW - Adolescent
KW - Adult
KW - Basal Ganglia
KW - Brain Diseases
KW - Cerebral Cortex
KW - Chronic Disease
KW - Female
KW - Humans
KW - Lead Poisoning
KW - Male
KW - Oceanic Ancestry Group
KW - Ocular Motility Disorders
KW - Petroleum
KW - Saccades
KW - Substance-Related Disorders
M3 - Article
VL - 75
SP - 472
EP - 476
JO - Journal of Neurology, Neurosurgery and Psychiatry
JF - Journal of Neurology, Neurosurgery and Psychiatry
SN - 0022-3050
IS - 3
ER -