perivascular macrophages stuffed with coarse or linear
PAS-positive debris, and trilaminar inclusions by EM.
Extent of myelin and axonal loss in patients is highly
variable, possibly due to extent of exposure, age of onset
of toluene abuse, coexistent abuse of other substances, or
polymorphisms in the gene encoding the enzyme aldehyde
dehydrogenase. Although toluene leukoencephalopathy
is well documented in inhalant abusers, the potential
of low-level occupational or household toluene exposure
to cause brain damage is uncertain. Long term exposure
to low levels of toluene has been speculated to cause
neurobehavioral dysfunction, but the threshold of exposure
above which leukoencephalopathy occurs is debated.
Toluene abuse in pregnancy causes a constellation of teratogenic
features known as fetal solvent syndrome, whichis similar to the fetal alcohol syndrome. Advanced neuroimaging techniques such as diffusion tensor imaging,
magnetization transfer imaging, and magnetic resonance
spectroscopy promise to improve the early recognition of
leukoencephalopathy in individuals exposed to toluene
when the potential for reversibility is maximal. Animal
studies suggest that astrocytes are activated by toluene,
paralleling the reactive gliosis seen in human cases with lesser degrees of myelin damage.
Despite these animal studies, however, many questions regarding the specific effects of toluene on myelin and other cellular components of the CNS remain to be answered.