Cognition was assessed in hepatitis C virus (HCV) patients, who did not meet the criteria for a minimal hepatic encephalopathy. Their liver function was compensated. We then disentangled potential cognitive changes associated with a sustained virologic response at 12 weeks (SVR-12), following treatment with direct antiviral agents (DAAs). We studied 23 selected HCV patients with a battery of standard neuropsychological tests, and with recordings of the P300 wave, a cerebral potential of “cognitive” significance. There was a baseline evaluation (T0) and a second one 6 months later (T1). We had 2 control groups of comparable age and sex, i.e., 15 patients suffering from non-alcoholic fatty liver disease (NAFLD) and 15 healthy subjects. At T0, we detected a significant (p < 0.05) cognitive impairment in the HCV group, which involved episodic and working memory, attention, visuospatial and verbal abilities, executive functions, and logic reasoning. The P300 latency was significantly (p < 0.05) delayed in the group. At T1, we observed some significant (p < 0.05) HCV recovery in given test domains, e.g., memory, executive functions, and reasoning. Accordingly, the P300 latency shortened significantly (p < 0.05). HCV patients exhibited subtle cognitive defects, somehow independent of their liver condition, possibly linked to direct or indirect brain involvement by the virus. These defects partly recovered following the SVR-12, as achieved through DAAs. The P300 wave was a valid neurophysiologic counterpart of these changes. DAAs can have a role in the early preservation of cognition in HCVs.

Transcranial direct current stimulation (tDCS) applied over the occipital cortex has a controversial effect on the visual cortex excitability. Paired flash visual evoked potentials (paired F-VEPs) offer a unique method to express neural inhibition within the visual system. However, no studies have explored the effects of tDCS on F-VEPs in humans. The aim of this study was to evaluate the changes of single- and paired-F-VEPs during and after tDCS in healthy humans. Twenty-six healthy volunteers participated. F-VEPs were recorded from occipital electrodes with closed eyes. Stimuli were single flashes, intermingled to flash pairs at the interstimulus interval of 125, 62.5, 50, 33.3, 16.6, and 11.1 ms (internal frequency of 8, 16, 20, 30, 60, and 90 Hz). The single F-VEP was split into a “main complex” and a “late response.” As to paired stimuli, the “test” F-VEP emerged from electronic subtraction of the single-F-VEP to the paired-F-VEP. In experiment 1, the return electrode was located on the scalp and we studied changes in F-VEPs after anodal, cathodal (1 mA, 15 min) and sham stimulation. A second experiment was performed in which F-VEPs were recorded before, during and after tDCS stimulation (anodal and cathodal) with the return electrode on the neck. F-VEPs recorded in experiment 1 did not detect any significant change after tDCS. In experiment 2 anodal polarization significantly increased the P2 latency (P = .031) and reduced the amplitude of the “late response” of the single F-VEP (P = .008). As for the paired F-VEPs, no significant changes were detected. In conclusion, low-intensity anodal tDCS has weak inhibitory aftereffects on the single F-VEP and no effects on the paired F-VEPs. Further methodological studies are needed to improve polarization efficacy.