Brainstem auditory evoked potentials (BAEPs) were examined in 49 workers employed in a printing press, who were occupationally exposed to low concentrations of toluene for an average of 20.3 years, and in 59 subjects in a control group. In the group of exposed workers, a significant decrease was found in all wave amplitudes examined, a significant prolongation of PI wave latency, and an increased interval of interpeak latencies (P3–P5), indicating that the extramedullary and high medullary part of the auditory pathway are biologically most frequently affected by chronic exposure to low concentrations of toluene. The level of exposure to toluene in both groups was evaluated by defining the concentration of toluene in peripheral blood and the concentration of hippuric acid and ortho‐cresol in urine. © 1996 Wiley‐Liss, Inc.

An investigation of visual evoked potentials was carried out in two groups of subjects; 49 workers employed in a printing-prss where toluene has been used exclusively as an organic solvent for the last 30 years, and 59 workers not occupationally exposed to any known neurotoxic substances. The average length of work service in the printing-press was 21.4 years. The level of exposure was assessed by determination of the concentration of toluene in peripheral blood, the concentration of hippuric acid and ortho-cresol in urine in subgroups of subjects chosen at random from both groups. N75, P100 and N145 waves of the pattern reversal visual evoked potentials were analyzed. In the group of exposed subjects, significantly greater amplitudes were found in all waves, with significantly longer latency of the P100 wave.

Visual evoked potentials (VEPs) of the pattern shift reversal type were determined in a representative group of 57 prisoners of war (POWs) released in 1992 from detention camps in former Yugoslavia. The parameters were correlated with the conditions in four camps (1-4). All subjects were male, with a mean age of 34.75 years (SD +/- 8.92), average length of imprisonment 192.7 days (SD +/- 77.6), mean loss of body mass during imprisonment 19.32% (SD +/- 9.54), and the average number of reported blows to the head and neck was 25.7 (SD +/- 20.3). VEPs were determined on average 290.5 days after the last craniocerebral trauma caused by blows to the head and neck (SD +/- 152.0) i.e., on average 218.5 days after release from the camp (SD +/- 164.3). Although all the 57 POWs reported being maltreated to a certain extent, 14 reported being subjected to particularly brutal forms of torture, 5 had been held in solitary confinement and 25 had lost consciousness at least once. Solitary confinement and loss of consciousness had the most significant effect on VEPs, and the altered VEP parameters correlated significantly with the craniocerebral trauma experienced, loss of body mass and the length of time since the last craniocerebral trauma until examination, and from release until examination. However, the length of imprisonment and treatment in the camps did not have a significant effect on VEP parameters. The study confirmed that under such conditions the age of the subject is a risk factor. The results of this study also confirmed that prisoners in one camp had been subjected to the worst maltreatment.

Objectives: Our study focused on the RANKL (receptor activator of nuclear factor-κB ligand)/RANK/OPG (osteoprotegerin) axis and selected proinflammatory/immunoregulatory upstream mediators in the peripheral blood (PBL) and cerebrospinal fluid (CSF) of multiple sclerosis (MS) patients. Methods: PBL and CSF were collected from healthy controls (n = 35) and MS patients at the clinical onset of the disease (n = 33). In addition, PBL samples were obtained from relapse-remitting (RR)-MS patients (n = 30). Patients were assessed by means of the expanded disability status scale (EDSS) and routine laboratory parameters. Soluble (s)RANKL and OPG were measured in the CSF and plasma; gene expression was detected for RANKL, RANK, OPG, and selected cytokines/chemokines (interleukin [IL]-4, IL-10, IL-17, CCL2, and CXCL12) in PBL mononuclear cells. Results: The OPG level in the CSF was lower in MS patients at clinical onset than in controls. Moreover, the sRANKL/OPG ratio was higher in the CSF of MS patients at clinical onset and in the plasma of RR-MS patients than in controls. Gene expression of RANKL/RANK/OPG in PBL mononuclear cells was higher only in RR-MS patients. IL-4, CCL2, and CXCL12 were positively correlated and IL-10 was negatively correlated with RANKL/RANK expression. OPG was negatively correlated with EDSS and alkaline phosphatase level. Conclusion: Our study revealed that changes of RANKL/RANK/OPG axis are associated with MS, particularly the decreased OPG level in the CSF at disease onset. Therefore, these factors may serve as disease biomarkers and molecular targets of novel therapeutic approaches.

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