EEG photic driving in workers exposed to mercury vapors

OBJECTIVE: To assess the potential of EEG photic driving (PD) as an indicator of an early neurotoxic effect of long-term, low-level exposure to mercury vapors. SUBJECTS AND METHODS: Twenty-four chloralkali workers exposed to mercury vapors; twenty-four age- and gender-matched control subjects. Level of exposure was determined by urinary mercury excreted both spontaneously and after administration of a chelating agent, sodium 2,3-dimercapto-1-propane sulfonate. A computerized method for quantitative evaluation of PD was developed. Five parameters describing PD were compared. RESULTS: The number of stimulation frequencies eliciting PD was higher in the exposed group, with a median of 17 frequencies, as compared to 10 frequencies in the control group (P < 0.001). The maximum value of PD was higher in the exposed group, with a median of 24.6 z-units as compared to 9.4 in the control group (P < 0.001). The median of the stimulation frequency with maximum PD was shifted from 15 Hz in the control group to 20 Hz in the exposed group (P < 0.01). The median of the sum of PD and the median of the index of PD were significantly higher in the exposed than in the control group (P < 0.001). The increased PD was particularly prominent at high stimulation frequencies in the beta range. There was no significant association between the measures of PD and the measures of exposure. CONCLUSIONS: In comparison with a control group, significantly increased photic driving was observed in a group of workers exposed to mercury vapors. The issue of whether or nor the intergroup differences in PD are mercury related, could not be determined on the basis of our results. Should the enhanced PD be caused by mercury, then this electrophysiological phenomenon might be regarded as a marker of the CNS hyperexcitability due to an early neurotoxic effect of mercury, the clinical expression of which is erethism.     

Trigeminal somatosensory evoked potentials in workers handling trichloroethylene

Trigeminal somatosensory evoked potentials (TSEP) were studied in 33 workers manipulating trichlorethylene for 3 to 22 years and in 33 control subjects. A significant excessive latency delay of N13, P17 and N45 waves in workers was found. Evoked potential abnormalities found in 15 exposed subjects (45%) were as following: excessive latency delay in 9 cases (27%), decrease of amplitude in 2 cases (6%) and asymmetrical responses in 4 cases (12%). Among 5 workers (15%) presenting clinical abnormalities of trigeminal nerve impairment, only one had normal evoked potential. TSEP were altered in 11 workers (33%) who had no clinical impairment. We suggest that TSEP should be confirm trigeminal impairment in chronic cases of workers exposed to carbon tetrachloride and to predict infraclinic lesions.     

Visual evoked potentials in children prenatally exposed to methylmercury

Prenatal exposure to methylmercury can cause both neurobehavioral deficits and neurophysiological changes. However, evidence of neurotoxic effects within the visual nervous system is inconsistent, possibly due to incomplete statistical adjustment for beneficial nutritional factors. We evaluated the effect of prenatal methylmercury exposure on visual evoked potential (VEP) latencies in Faroese children with elevated prenatal methylmercury exposure. A cohort of 182 singleton term births was assembled in the Faroe Islands during 1994–1995. At age 7 years, VEP tracings were obtained from 139 cohort subjects after exclusion of subjects with abnormal vision conditions. We used multiple regression analysis to evaluate the association of mercury concentrations in cord blood and maternal hair at parturition with VEP latencies after adjustment for potential confounders that included the cord-serum phospholipid concentration of n-3 polyunsaturated fatty acids (PUFAs) and the duration of breastfeeding. Unadjusted correlations between mercury exposure and VEP latencies were equivocal. Multiple regression models showed that increased mercury concentrations, especially in maternal hair, were associated with delayed latencies for VEP peak N145. After covariate adjustment, a delay of 2.22 ms (p = 0.02) was seen for each doubling of the mercury concentration in maternal hair. In agreement with neuropsychological findings, the present study suggests that prenatal methylmercury exposure may have an adverse effect on VEP findings despite the absence of clinical toxicity to the visual system. However, this association was apparent only after adjustment for n-3 PUFA status.     

Visual evoked potentials and the time of motor reaction to visual stimuli in chronic metallic mercury poisoning

In a group of 10 patients with diagnosed occupational chronic poisoning with metallic mercury a correlation was sought between the parameters of the visual evoked potentials and the results of the psychological test evaluating the rapidity of motor response to the visual stimuli. The analysis suggest a cerebral dysfunction of the visual neurons and reduced rate of visual information transformation to the motor effector at the level of the cortical association centre.     

Visual and somatosensory evoked cortical potentials in multiple sclerosis.

The diagnostic value of the pattern reversal evoked cortical potential (VEP) and the somatosensory evoked cortical potential (SEP) has been compared in 50 patients with established or suspected multiple sclerosis. A prolonged latency of VEP was found in 96% of definite cases of multiple sclerosis, 58% of probable cases, and 20% of possible cases. A prolonged latency of SEP by stimulation of median or peroneal nerves or both was found in 86% of definite cases of multiple sclerosis, 83% of probable cases, and 50% of possibe cases. When combining the results of all three tests the diagnostic yield increased to 100%, 92%, and 50%, respectively.     

Neural conduction in workers after long-term exposure to mercury vapors]

36 workers exposed to mercury vapour intoxication were examined to estimate the abnormalities in peripheral nervous system. 18 workers showed on physical examination features of polyneuropathy and in this group 15 workers had on emg examination sensory polyneuropathy. Statistical analysis was performed to show correlations between polyneuropathy on emg and age, time of exposure to mercury vapour and urinary mercury level. No such correlations were demonstrated.     

Changes in somatosensory evoked potentials in pharmacogenic myoclonia]

Transient increases of the early cortical somatosensory evoked potentials (SSEP) were observed in 9 patients who received antidepressant and/or neuroleptic treatment. All patients developed myoclonus, and 2 had grand mal seizures. Three cases--one 20-, one 17- and one 15-year-old patient--are presented in detail. Similar observations have been reported in elderly patients. Possible underlying mechanisms and the potential value of the SSEP in identifying and monitoring patients at risk of developing psychotropic drug-induced side-effects are briefly discussed.     

Visual and somatosensory evoked potentials in vitamin E deficiency with cystic fibrosis

Patients with cystic fibrosis (CF) and pancreatic malabsorption frequently have vitamin E deficiency. Affected patients may develop spinocerebellar degeneration with dysarthria, ataxia, proximal weakness, proprioceptive loss and areflexia. Of a highly selected group of 10 patients with vitamin E levels below 5 micrograms/ml (normal 5-20 micrograms/ml), 7 had abnormal neurological examinations, predominantly affecting vibration and joint position perception with some severely affected patients manifesting diminished visual acuity, tremor, ataxia and diffuse weakness. Evoked potential studies showed marked abnormalities in 3 patients, demonstrating deficits in the optic pathways and in the cervical cord dorsal column pathways. Evoked potential studies may supplement careful neurological examination in patients with CF before and after supplementation with vitamin E to evaluate their progression and response to treatment.     

Long-latency somatosensory evoked potentials

Theoretically, long-latency somatosensory evoked potentials (SEPs) provide information on the function of somatosensory associative cortical structures. Their potential role in clinical studies and research has been hampered by the lack of standardized methodology in the use of these SEPs. Other factors, such as drugs, simultaneous stimuli, and state of consciousness, also have far-reaching influences on the various parameters of long-latency SEPs. The knowledge of the origin of most SEP components is at best fragmentary; studies on clinical-electrophysiological correlations seem to be hopeful in this respect. As yet, clinical applications of long-latency SEPs are limited; for future research, studies of disturbances of SEPs are most promising, mainly with regard to diseases of the gray matter, the influence of drugs on the cerebral function, and psychopathology.     

Visual evoked potentials in normal and sulfite oxidase deficient rats exposed to ingested sulfite

Sulfite oxidase (SOX) is an essential enzyme in the pathway of the oxidative degradation of sulfur amino acids, and protects cells from sulfite (SO(3)(2-)) toxicity. Rats do not mimic responses seen in human, because of their relatively high SOX activity levels. Therefore, the present study used SOX deficient rats since they are a more appropriate model for studying sulfite toxicity. The aim of the study was to investigate the effect of sulfite exposure on visual evoked potentials (VEPs) and thiobarbituric acid reactive substances (TBARS) in normal and sulfite oxidase deficient rats. Rats were assigned to six groups (n=10 rats/group) as follows; control (C), sulfite (S), sulfite+vitamin E (SE), deficient (D), deficient+sulfite (DS) and deficient+sulfite+vitamin E (DSE). Sulfite oxidase deficiency was established by feeding rats a low molybdenum diet and adding to their drinking water 200 ppm tungsten (W). Sulfite (25img/kg) was administered to the animals via their drinking water. At the end of the experimental period, flash visual evoked potentials were recorded, and TBARS, hepatic sulfite oxidase levels and plasma S-sulphonate concentrations were determined. Sulfite treatment caused a significant delay in P1, N1P2, and P3 components of VEPs in the S and DS groups compared with the C group. These prolonged mean latencies of VEP components were reversed by vitamin E treatment in SE and DSE groups. In addition, the mean latencies of P1 and P3 components were increased in SOX deficient groups compared with the C group. Lipid peroxidation was increased in the brain in S, D, DS and DSE groups compared with the control group. There were also significant increases in the retina TBARS levels of S and DS groups. Vitamin E caused a significant decrease in brain and retina TBARS levels of SE and DSE groups with respect to their corresponding controls. However, there were no important changes in amplitudes of other groups. In conclusion, our results showed that sulfite treatment caused an increase in the lipid peroxidation process that was accompanied by changes in VEPs. Furthermore, sulfite exposure resulted in greater lipid peroxidation and more electrophysiological alterations in the SOX deficient rats than in the control rats. Additionally, the reduction of all VEP latencies in the DSE group with respect to the DS group clearly indicated that vitamin E has the potential to prevent sulfite induced-VEP changes arising from dysfunction of the SOX enzyme.     

Magnetic stimulation motor evoked potential in multiple sclerosis. Comparison with visual evoked potentials, brain stem auditory evoked potentials and somatosensory evoked potentials]

This study consists of 45 patients with clinically definite MS, laboratory supported definite MS and clinically probable MS. We compared MEP results with other multimodal evoked potentials (VEP, BAEP and SEP). The abnormal rate of MEP was 87.6%, which was the highest. Abnormal MEP showed prolonged central motor conduction time (CMCT), consistent with pathological change of the demyelination. There was a evident correlation between the abnormal MEP and VEP, which is consistent with the most common MS (Devic Syndrome) in our country.     

Three-dimensional human somatosensory evoked potentials

Median nerve somatosensory evoked potentials were recorded from 30 normal adults using conventional scalp derivations and an orthogonal bipolar surface electrode montage. This allowed the determination of the spatial orientation of the hypothetical centrally located equivalent dipole derived from the evoked response recorded in 3-dimensional voltage space. The 3-dimensional voltage trajectory describing changes in equivalent dipole orientation and magnitude revealed 4 major apices between 5 and 25 msec, 3 of which corresponded to the traditional P14, N20 and P25 peaks. A fourth apex at 17 msec was not as evident in the conventional recordings and signaled a transition from a vertical P14-N18 generator process to a horizontal N20 generator process. The normal within- and between-subject variability of trajectory apices, segments and planes are described, along with the theoretical and practical implications of this recording technique.     

Early somatosensory evoked potentials.

The early somatosensory evoked potential secondary to median nerve stimulation in the human had an onset latency of 9--12 msec when recorded from scalp electrodes at vertex-to-mastoid, vertex-to-inion or at the base of the skull. Similar latencies were observed from responses recorded over the cervical dorsal columns during neurologic surgery. A latency difference of 1.5 msec was observed between the early response and the responses recorded from the junction of medial lemniscus and nucleus ventralis posterior lateralis of the thalamus during human stereotaxic surgery. Cervical cord transections and transection at the midpontine levels of the monkey showed that the evoked potential was due to generators between these levels. Depth recording of the monkey indicate that the early evoked potential originates in the region of dorsal column nuclei, while the later components are secondary to generators in cerebral cortex.     

Segmentally specific somatosensory evoked potentials

The recording of segmentally specific somatosensory evoked potentials (SEPs) is time-consuming and the findings have generally been clinically unhelpful. This article critically evaluates the role of these SEPs in patients with disorders of the spinal cord or nerve roots.     

Pain-Related somatosensory evoked potentials.

The authors reviewed basic and clinical reports of pain-related somatosensory evoked potentials (SSEP) after high-intensity electrical stimulation [pain SSEP(E)] and painful laser stimulation [pain SSEP(L)]. The conduction velocity of peripheral nerves for both pain SSEP(E) and pain SSEP(L) is approximately 10 to 15 m/second, in a range of Adelta fibers. The generator sources are considered to be the secondary somatosensory cortex and insula, and the limbic system, including the cingulate cortex, amygdala, or hippocampus of the bilateral hemispheres. The latencies and amplitudes are clearly affected by vigilance, attention-distraction, and various kinds of stimulation applied simultaneously with pain. Abnormalities of pain SSEP(L) reflect an impairment of pain-temperature sensation, probably relating to dysfunction of A5 fibers of the peripheral nerve and spinothalamic tract. In contrast, conventional SSEP after nonpainful electrical stimulation reflects an impairment of tactile, vibratory, and deep sensation, probably relating to dysfunction of Aalpha or Abeta fibers of the peripheral nerve and dorsal column. Therefore, combining the study of pain SSEP(L) and conventional SSEP is useful to detect physiologic abnormalities, and sometimes subclinical abnormalities, of patients with peripheral and central nervous system lesions.     

Cerebral evoked potentials and somatosensory perception

In normal subjects, somatosensory evoked potentials (SEPs) were produced by increases or decreases of the load on the biceps muscle during voluntary contraction. The stimuli lasted only 20 msec and caused less than 2 degrees of elbow flexion or extension. When the stimulus was applied during voluntary movement of the elbow, the SEP was attenuated, and the subject was less able to discriminate between loading and unloading pulses. In each of eight subjects, there was a positive correlation between the percentage of correct responses and the size of the SEP. The measurement of both SEPs and perceptual accuracy under various test conditions provides a refined technique for studying the relations between electrical events and sensory processes.     

Effects of age and body height on somatosensory evoked potentials]

The influence of age and height on somatosensory evoked potentials (SEP) following median and tibial nerve stimulation was studied. Age correlated with increase of latencies and decrease of amplitudes; exceptionally the amplitude of cortical N20 component increased with age. The central conduction time P31-P40 (tibial nerve stimulation) was longer in elderly subjects, whereas the time N13-N20 (median nerve stimulation) was independent of age. Height showed a positive correlation with latencies and peripheral conduction times; central conduction times (N13-N20 and P31-P40) were independent on height. The correlations of SEP parameters with age and height were expressed quantitatively by regression equations. The presented equations should be treated as a valuable complement to normative data in interpretation of SEP testing results.