Enhancement of attention processing by Kantroll in healthy humans: a pilot study.

This is the first report in humans of the effects of daily ingestion of a specific amino acid mixture, Kantroll, on cognitive event-related potentials (ERPs) associated with performance. Cognitive ERPs were generated by two computerized visual attention tasks, the Spatial Orientation Task (SOT) and Contingent Continuous Performance Task (CCPT), in normal young adult volunteers, where each subject acted as his own control for testing before and after 28-30 days of amino acid ingestion. A statistically significant amplitude enhancement of the P300 component of the ERPs was seen after Kantroll for both tasks, as well as improvement with respect to cognitive processing speeds. The enhancement of neurophysiologic function observed in this study on normal controls is consistent with the facilitation of recovery of individuals with RDS (i.e., substance use disorder, ADHD, carbohydrate bingeing) following the ingestion of the amino acid supplement, Kantroll, and warrants additional placebo-controlled, double-blind, studies to confirm and extend these results.

Evidence of temporal lobe activation by discriminative spatial orientation.

The results from this spatial orientation, or cue priming, investigation found that targets presented to the contralateral visual fields differentially activated the temporal zones. For instance, stimulation within the right visual field lead to activation of the left temporal zones, as indexed by the relative prominence of the association negativity, N2. The converse was true for left visual field stimulation. For both visual field stimulation, the N2 component also showed an occipital and parietal distribution. The P300 component, which is presumed to be modulated by medial temporal lobe structures, showed the classic centroparietal distribution. Somewhat surprisingly, differences between the primed (e.g., 'facilitated') and 'normal' conditions for the N2 component appeared restricted to the occipital zones. Here, the significant variable was the N2 peak latency. Hence, the priming cue appears to quicken the maximal development of the N2 processing component, preferentially over the occipital cortex, and this may partially explain the faster reaction times in the 'facilitated' conditions for both visual fields.

The influence of electrical variables on analgesia produced by low current transcranial electrostimulation of rats.

Pulsed low current transcranial electrostimulation (TE) has been shown to induce analgesia in rats as measured by the wet tail flick test. This study investigates the effect of varying stimulus frequency, pulse width, charge balance and polarity, as well as the influence of electrode placement and time of day at which stimulus occurred. A biphasic, charge balanced waveform with a first phase duration of 2 msec, current 10 microA and repetition rate 10 Hz was found to induce maximum tail flick latency changes. The effects of morning or nighttime stimulation were statistically indistinguishable, as were the differences between monophasic and biphasic stimulation. Analgesia was maximized when a positive first phase was delivered into the right ears of the rats, but monolateral stimulation with both electrodes on either the left or the right ear produced no measurable effect. Examination of TE responses in sham and stimulated populations reveals normal response distributions with the stimulated group skewed toward a positive effect.

Low current electrostimulation produces naloxone-reversible analgesia in rats.

A new form of transcranial electrostimulation (TE) has been shown to induce analgesia in rats, as measured by the wet tail flick test. Charge-balanced rectangular current pulses of very low amplitude were delivered bilaterally into low impedance regions of the rat pinnae. The resultant analgesia was studied as a function of systematic variations in stimulus frequency, amplitude and duration. The optimal current for inducing analgesia was found to be 10 microA, well below the startle threshold, and several orders of magnitude below effective stimulus current levels required for other treatment modalities. The optimal stimulation duration was 30 min, during which time a slow onset of analgesia was noted. Significant analgesia persisted for at least 200 min after stimulation ended, and no evidence was found of tolerance developing in the course of 5 daily stimulation sessions. Consistent with findings for other forms of electrostimulation, the analgesic effect of TE was abolished by subcutaneous injection of 3 mg/kg naloxone, suggesting that the mechanism of TE analgesia has an endogenous opioid component.