Neuromagnetic Activation of Primaryand Secondary Somatosensory Cortex Following Tactile-on and Tactile-off Stimulation

Objective Magnetoencephalography (MEG) recordings were performed to investigate the cortical activation following tactile-on and tactile-off stimulation. Methods We used a 306-ch whole-head MEG system and a tactile stimulator driven by a piezoelectric actuator. Tactile stimuli were applied to the tip of right index finger. The interstimulus interval was set at 2000 ms, which included a constant stimulus of 1000 ms duration. Results Prominent somatosensory evoked magnetic fields were recorded from the contralateral hemisphere at 57.5 ms and 133.0 ms after the onset of tactile-on stimulation and at 58.2 ms and 138.5 ms after the onset of tactile-off stimulation. All corresponding equivalent current dipoles (ECDs) were located in the primary somatosensory cortex (SI). Moreover, long-latency responses (168.7 ms after tactile-on stimulation, 169.8 ms after tactile-off stimulation) were detected from the ipsilateral hemisphere. The ECDs of these signals were identified in the secondary somatosensory cortex (SII). Conclusions The somatosensory evoked magnetic fields waveforms elicited by the two tactile stimuli (tactile-on and tactile-off stimuli) with a mechanical stimulator were strikingly similar. These mechanical stimuli elicited both contralateral SI and ipsilateral SII activities. Significance Tactile stimulation with a mechanical stimulator provides new possibilities for experimental designs in studies of the human mechanoreceptor system

Dynamic imaging of somatosensory cortical activity in the rat visualized by flavoprotein autofluorescence

We used autofluorescence of mitochondrial flavoproteins to image cortical neural activity in the rat. Green autofluorescence in blue light was examined in slices obtained from rat cerebral cortex. About half of the basal autofluorescence was modulated by the presence or absence of O2 or glucose in the medium. Repetitive electrical stimulation at 20 Hz for 1 s produced a localized fluorescence increase in the slices. The amplitude of the increase was 27 ± 2 % (mean ± s.d., n = 35). Tetrodotoxin or diphenyleneiodonium, an inhibitor of flavoproteins, blocked the autofluorescence responses. The autofluorescence responses were not observed in slices perfused with calcium-, glucose- or O2-free medium. In the primary somatosensory cortex of rats anaesthetized with urethane (1.5 g kg−1, i.p.), an activity-dependent increase in autofluorescence of 20 ± 4 % (n = 6) was observed after electrical cortical stimulation at 100 Hz for 1 s, and an increase of 2.6 ± 0.5 % (n = 33) after vibratory skin stimulation at 50 Hz for 1 s applied to the plantar hindpaw. These responses were large enough to allow visualization of the neural activity without having to average a number of trials. The distribution of the fluorescence responses after electrical or vibratory skin stimulation was comparable to that of the cortical field potentials in the same rats. The fluorescence responses were followed by an increase in arterial blood flow. The former were resistant to an inhibitor of nitric oxide synthase, while the latter was inhibited. Thus, activity-dependent changes in the autofluorescence of flavoproteins are useful for functional brain imaging in vivo

Epileptic network of hypothalamic hamartoma: An EEG-fMRI study.

To investigate the brain networks involved in epileptogenesis/encephalopathy associated with hypothalamic hamartoma (HH) by EEG with functional MRI (EEG-fMRI), and evaluate its efficacy in locating the HH interface in comparison with subtraction ictal SPECT coregistered to MRI (SISCOM). Eight HH patients underwent EEG-fMRI. All had gelastic seizures (GS) and 7 developed other seizure types. Using a general linear model, spike-related activation/deactivation was analyzed individually by applying a hemodynamic response function before, at, and after spike onset (time-shift model = −8–+4 s). Group analysis was also performed. The sensitivity of EEG-fMRI in identifying the HH interface was compared with SISCOM in HH patients having unilateral hypothalamic attachment. EEG-fMRI revealed activation and/or deactivation in subcortical structures and neocortices in all patients. 6/8 patients showed activation in or around the hypothalamus with the HH interface with time-shift model before spike onset. Group analysis showed common activation in the ipsilateral hypothalamus, brainstem tegmentum, and contralateral cerebellum. Deactivation occurred in the default mode network (DMN) and bilateral hippocampi. Among 5 patients with unilateral hypothalamic attachment, activation in or around the ipsilateral hypothalamus was seen in 3 using EEG-fMRI, whereas hyperperfusion was seen in 1 by SISCOM. Group analysis of this preliminary study may suggest that the commonly activated subcortical network is related to generation of GS and that frequent spikes lead to deactivation of the DMN and hippocampi, and eventually to a form of epileptic encephalopathy. Inter-individual variance in neocortex activation explains various seizure types among patients. EEG-fMRI enhances sensitivity in detecting the HH interface compared with SISCOM