Sensitization in the neuroscience and pharmacology literatures is defined as progressive increase in the size of a response over repeated presentations of a stimulus. Types of sensitization include stimulant drug-induced time-dependent sensitization (TDS), an animal model related to substance abuse, and limbic kindling, an animal model for temporal lobe epilepsy. Neural sensitization (primarily nonconvulsive or subconvulsive) to the adverse properties of substances has been hypothesized to underlie the initiation and subsequent elicitation of heightened sensitivity to low levels of environmental chemicals. A corollary of the sensitization model is that individuals with illness from low-level chemicals are among the more sensitizable members of the population. The Working Group on Sensitization and Kindling identified two primary goals for a research approach to this problem: to perform controlled experiments to determine whether or not sensitization to low-level chemical exposures occurs in multiple chemical sensitivity (MCS) patients; and to use animal preparations for kindling and TDS as nonhomologous models for the initiation and elicitation of MCS.

Organic solvents have been implicated in a number of neuropsychiatric disturbances, though physical and neurological exams are frequently negative. An individual with acute tetrabromoethane exposure was evaluated with positron emission tomography (PET), topographical electroencephalogram (EEG), and neurobehavioral assessment. Results suggest widespread central nervous system (CNS) dysfunction consistent with a solvent-induced encephalopathy.

Cognitive and mood changes are central components of solvent encephalopathy. This study examined event-related potentials in relation to neuropsychological and psychiatric function in solvent-exposed adults. Results revealed that longer P300 latency was associated with poorer cognitive test scores, whereas reduced P300 amplitude was related to increased psychiatric symptomatology. The findings suggest that the cognitive deficits and the psychiatric disturbance following solvent exposure may have different neurophysiological bases.

No abstract