title: Cerebral impairment in chronic solvent-induced encephalopathy.
abstract: OBJECTIVE
  Worldwide, many workers experience occupational exposure to organic solvents, which may induce chronic solvent-induced encephalopathy (CSE). Disturbances within the frontostriatothalamic (FST) circuitry might explain the symptomatology of CSE. We tested the hypothesis of FST circuitry abnormalities in CSE, as well as associations with performance of psychomotor speed, attention, and solvent exposure. To detect preclinical, solvent-related effects, we also studied the FST circuitry in solvent-exposed, but asymptomatic workers.
  
  
  METHODS
  Ten CSE patients, 10 asymptomatic but solvent-exposed house painters (EC), and 11 nonexposed asymptomatic carpenters were included. Dopamine D(2) receptor (D2R) binding, central nervous system tissue metabolites, and fractional anisotropy were measured within the FST circuitry, using single-photon emission computed tomography, magnetic resonance spectroscopy, and diffusion tensor imaging. Performance of psychomotor speed and attention, and severity of solvent exposure were assessed.
  
  
  RESULTS
  Striatal D2R binding was reduced in CSE. In the solvent-exposed asymptomatic patients, striatal D2R binding and levels of N-acetylaspartate + N-acetylaspartyl-glutamate in frontal gray matter were reduced. In both exposed groups, a trend was seen for reduced choline in frontal gray matter. In CSE, the fractional anisotropy in the thalamus, caudate nucleus, and striatal D2R binding significantly predicted reduced performance of attention and psychomotor speed. In CSE, striatal D2R binding showed a negative correlation with solvent exposure.
  
  
  CONCLUSIONS
  This is the first study in CSE showing pronounced disturbances within the FST circuitry that are related to the clinical findings and to exposure severity to solvents. The comparable, but milder, abnormalities within the FST circuitry in the exposed asymptomatic workers may imply a presymptomatic phase of CSE.
authors.affiliation: Academic Psychiatric Center AMC, Amsterdam, the Netherlands. i.visser@amc.uva.nl
authors.forename: Ieke
authors.initials: I
authors.lastname: Visser
authors.forename: Cristina
authors.initials: C
authors.lastname: Lavini
authors.forename: Jan
authors.initials: J
authors.lastname: Booij
authors.forename: Liesbeth
authors.initials: L
authors.lastname: Reneman
authors.forename: Charles
authors.initials: C
authors.lastname: Majoie
authors.forename: Angela G E M
authors.initials: AG
authors.lastname: de Boer
authors.forename: Elizabeth M
authors.initials: EM
authors.lastname: Wekking
authors.forename: Elisabeth A
authors.initials: EA
authors.lastname: de Joode
authors.forename: Gert
authors.initials: G
authors.lastname: van der Laan
authors.forename: Frank J H
authors.initials: FJ
authors.lastname: van Dijk
authors.forename: Aart H
authors.initials: AH
authors.lastname: Schene
authors.forename: Gerard J
authors.initials: GJ
authors.lastname: Den Heeten
mesh_terms: D001921:Brain / Q000187:drug effects* / Q000503:physiopathology*; D001925:Brain Damage, Chronic / Q000139:chemically induced* / Q000175:diagnosis / Q000503:physiopathology*; D003072:Cognition Disorders / Q000139:chemically induced* / Q000175:diagnosis / Q000503:physiopathology*; D006801:Humans; D008297:Male; D008875:Middle Aged; D009784:Occupational Diseases / Q000139:chemically induced / Q000175:diagnosis / Q000503:physiopathology; D017448:Receptors, Dopamine D2 / Q000378:metabolism*; D012189:Retrospective Studies; D012997:Solvents / Q000506:poisoning*
chemical_list: D017448:Receptors, Dopamine D2; D012997:Solvents