APPLICATION OF SERIAL MOTOR REACTION INDICATORS AS MARKERS OF FUNCTIONAL CONDITION DYNAMICS IN CHILDREN WITH EPILEPSY.

To monitor the functional state of the brain of children with epilepsy, we developed an original modification of the method of study ingserialmotorreactions (tapping) using touch screen devices, which all owsdistant multiple examination and to obtain aninformativeset of performance indicators and their dynamics. Clinical and anamnestic; clinical and neurological research methods were also used. Examination materials of 21 children with epilepsy (13 boys, 8 girls), aged from 6 to 18 years were analyzed. The presence of significant differences in serial motor responses between patients with recurrent seizures and children with no seizures in all age groups allows us to consider the proposed option of tapping as a reliable source of additional information about the functional state of the brain of children with epilepsy, for data processing of which can be used «Big Data¼ methods.

Cortical spreading depression induces oxidative stress in the trigeminal nociceptive system.

Indirect evidence suggests the increased production of reactive oxygen species (ROS) in migraine pathophysiology. In the current study we measured lipid peroxidation product in the rat cortex, trigeminal ganglia and meninges after the induction of cortical spreading depression (CSD), a phenomenon known to be associated with migraine aura, and tested nociceptive firing triggered by ROS in trigeminal nerves ex vivo. Application of KCl to dura mater in anesthetized rats induced several waves of CSD recorded by an extracellular electrode in the cortex. Following CSD, samples of cortex (affected regions were identified with blood oxygen level-dependent (BOLD) functional magnetic resonance imaging (fMRI)), meninges from left and right hemispheres and trigeminal ganglia were taken for biochemical analysis. We found that CSD increased the level of the lipid peroxidation product malondialdehyde (MDA) in the ipsilateral cerebral cortex and meninges, but also in both ipsi- and contralateral trigeminal ganglia. In order to test the pro-nociceptive action of ROS, we applied the mild oxidant hydrogen peroxide to isolated rat hemiskull preparations including preserved trigeminal innervations. Application of hydrogen peroxide to meninges transiently enhanced electrical spiking activity of trigeminal nerves showing a pro-nociceptive action of ROS. In the presence of hydrogen peroxide trigeminal nerves still responded to capsaicin by burst of spiking activity indicating integrity of neuronal structures. The action of hydrogen peroxide was mediated by TRPA1 receptors as it was abolished by the specific TRPA1 antagonist TCS-5861528. Using dorsal root ganglion sensory neurons as test system we found that hydrogen peroxide promoted the release of the migraine mediator calcitonin gene-related peptide (CGRP), which we previously identified as a trigger of delayed sensitization of trigeminal neurons. Our data suggest that, after CSD, oxidative stress spreads downstream within the trigeminal nociceptive system and could be involved in the coupling of CSD with the activation of trigeminovascular system in migraine pathology.