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In healthy volunteers (HVs), we recently observed that the rules of the time-dependent paired-associative plasticity found in the sensorimotor system are valid also for the visual system. With the latter method, here, we have tested whether dysfunctioning associative plasticity might characterize the visual system in patients with episodic migraine without aura (MO), where abnormalities in both inhibitory and excitatory paired-associative sensorimotor plasticity have been observed between attacks (1). In 11 MO between attacks and in 14 HVs, we performed a visual paired associative stimulation (vPAS) protocol by coupling 90 black-and-white checkerboard reversals with low-frequency TMS pulses over the occipital cortex at 2 interstimulus intervals in separate sessions by subtracting or adding 25 ms to the visual evoked potential (VEP) P100 latency. We recorded VEPs (600 sweeps) before, after, and 10-min later each vPAS session. VEPs were partitioned in 6 blocks of 100 sweeps. We analysed VEP N1-P1 first block amplitude and delayed habituation. While vPAS-25 significantly enhanced and vPAS + 25 reduced VEP amplitude habituation in HVs, they both did not significantly change VEP amplitude habituation in MO between attacks. We provide evidence for lack of excitability depressing and enhancing short-term associative plasticity mechanisms within the visual system in interictal migraine.

Associative stimulation of peripheral afferents paired with low-frequency transcranial magnetic stimulation (LF-TMS) over the motor area (PAS) at an interstimulus interval (ISI) slightly shorter or longer than the time needed for the afferent inputs to reach the cerebral cortex, can decrease or increase the excitability of the motor system. None has proven whether the same time-dependent plasticity rules may also be valid for the visual system. In 12 healthy subjects, we performed a visual PAS (vPAS) protocol by coupling 90 black-and-white checkerboard reversals with LF-TMS pulses over the occipital cortex at 4 ISIs in separate sessions chosen by subtracting or adding 25/50 ms to the visual evoked potential (VEP) P1 latency. We recorded VEPs (600 sweeps) before, after, and 10-min later each vPAS session. VEPs were partitioned in 6 blocks of 100 sweeps. We analyzed VEP N1-P1 first amplitude and delayed habituation. VEP amplitude of the first block was reduced immediately after PAS+25, while it remained unchanged after the other vPAS protocols. Delayed VEP habituation significantly increased after PAS−25, and decreased after PAS+25. Associative bidirectional synaptic plasticity is not confined to the corticomotor system, but can also be a feature of the visual system.

Previous studies suggested that both robotic rehabilitation and non-invasive brain stimulation could produce improvement in chronic stroke patients. It is still unknown whether their combination can produce synergistic effects. We designed a proof-of-principle, double-blinded, semi-randomized, sham-controlled trial to assess the safety and efficacy of this combination. Twenty severe upper limb-impaired chronic stroke patients were randomized to robot-assisted therapy associated with real or sham cTBS, delivered for 10 working days. Eight real and nine sham patients completed the study. Change in Fugl-Meyer was chosen as primary outcome, while changes in several quantitative indicators of motor performance extracted by the robot as secondary outcomes. The treatment was well-tolerated and there were no adverse events. All patients achieved a small, but significant, Fugl-Meyer improvement. The difference between the real and the sham cTBS groups was not significant. Among several secondary end points, only the Success Rate improved more in the real than in the sham cTBS group. This study shows that a short intensive robot-assisted rehabilitation produces a slight improvement in severe upper-limb impaired, even years after the stroke. The association with homeostatic metaplasticity-promoting non-invasive brain stimulation does not augment the clinical gain in patients with severe stroke.

It has been proved that Transcranial DCS (tDCS) can modulate cortical excitability, enhancing or decreasing, respectively by anodal or cathodal polarity. The short-term and lasting alterations induced by tDCS are strictly related to the charge density, duration of stimulation and the depth of neuron below the skull. Epilepsy represents a pathophysiological model of unbalanced relation between cortical excitation and inhibition. In this line, tDCS can be exploited to counterbalance the neuronal hyper-excitation through electric neural modulation. This paper aims at providing the efficacy of cathodal tDCS in reducing seizures’ frequency in drug-resistant focal epilepsy. The study was single blind and sham-controlled and compared seizure rate in the 7 days before and after tDCS and after sham in a cross-over design. 9 patients affected by focal resistant epilepsy were enrolled. After tDCS 3 out 9 patients have not any change in seizure rate. 6 patients reduced their seizure frequency >50%. No significant modification were recorded after sham. This study represents the proof that cathodal tDCS may be efficient in reducing seizures’frequency in focal resistant epilepsy.

It has been proved that Transcranial DCS (tDCS) can modulate cortical excitability, enhancing or decreasing, respectively by anodal or cathodal polarity. The short-term and lasting alterations induced by tDCS are strictly related to the charge density, duration of stimulation and the depth of neuron below the skull. Epilepsy represents a pathophysiological model of unbalanced relation between cortical excitation and inhibition. In this line, tDCS can be exploited to counterbalance the neuronal hyper-excitation through electric neural modulation. This paper aims at providing the efficacy of cathodal tDCS in reducing seizures’ frequency in drug-resistant focal epilepsy. The study was single blind and sham-controlled and compared seizure rate in the 7 days before and after tDCS and after sham in a cross-over design. 9 patients affected by focal resistant epilepsy were enrolled. After tDCS 3 out 9 patients have not any change in seizure rate. 6 patients reduced their seizure frequency >50%. No significant modification were recorded after sham. This study represents the proof that cathodal tDCS may be efficient in reducing seizures’frequency in focal resistant epilepsy.

Objective Delta waves are the most prominent electroencephalographic (EEG) feature of non-rapid eye movement sleep with cortical origin. Several human studies suggested they are sensor of synaptic weight and possible effectors of sleep-dependent synaptic plasticity. During wakefulness delta waves are almost absent in physiological conditions, but they come out when a subcortical brain lesion occurs. For these reasons delta waves during wakefulness are considered as a lesional sign but no definitive data about its functional significance were provided. Our aim was to verify whether delta waves can be a sign of plastic cortical modifications. Materials and methods 11 young healthy subjects (28 ± 3) were enrolled in the study. Intermittent theta burst stimulation (iTBS) was administered on left primary motor cortex to induce enduring cortical motor plasticity. High density scalp EEG (32 channels) was recorded all along the experiment. PSD for standard frequency bands (delta 1–3.5 Hz, theta 4–7.5 Hz, alpha 8–12 Hz, beta 13–22 Hz) was calculated in each longitudinal bipolar derivation. 5-min resting opened-eyes EEG was analyzed pre-iTBS (T0) and immediately after iTBS (T1), after 15 (T2) and 30 (T3) min. MEP amplitude and visual analogic scales about sleepiness, alertness, and the Stanford Sleepiness Scale were analyzed at the same time-points to explore motor plasticity induction and alertness status. Results iTBS induced a 9%-increase of MEP amplitude which remained stable until 30 min after stimulation (T1vsT0 p = 0.005; T2vsT1 p = 0.560; T3vsT2 p = 0.158). A selective increase (+87.5%) in delta band PSD was evident at T1 vs T0, remaining stable all along the experiment (T1vsT0 p = 0.019, T2vsT1 p = 0.724, T3vsT2 p = 1). Significant changes were bilaterally present only in fronto-central derivations ( p Discussion Our experiment firstly demonstrated a large and enduring increase in EEG delta activity in cortical areas undergoing plasticity induction during wakefulness. Present results may open new scenarios in interpreting scalp EEG slow waves after brain lesions not only as sign of lesion but also as sign of neuronal plastic rearrangement not with a negative value.

Aim of this study is to investigate, for the first time by means of an EEG-TMS co-registration study, whether and how direct bidirectional connection between brain and hand prosthesis impacts on sensorimotor cortical topography. Within an experimental protocol for robotic hand control, a 26 years-old, left-hand amputated male was selected to have implanted four intrafascicular electrodes (tf-LIFEs-4) in the median and ulnar nerves of the stump for 4 weeks. Before tf-LIFE-4s implant (T0) and after the training period, once electrodes have been removed (T1), experimental subject’s cortico-cortical excitability, connectivity and plasticity were directly tested via neuronavigated EEG–TMS. The statistical analysis demonstrated a significant modulation of EEG activity between 30 and 100 ms post-stimulus for the stimulation of the right hemisphere. When looking at the individual latencies in that time range, significant differences between T0 and T1 condition at 30 ms, ms and 60 ms latencies were present. Finally, also a clear local decrement in N46 amplitude over C4 was evident. No differences between conditions were observed for the stimulation of the left hemisphere. The results of this study confirm the hypothesis that bidirectional neural interface could redirect cortical areas -deprived of their original input/output functions- toward restorative neuroplasticity.