Localization of sensorimotor cortex in neurosurgery by recording of somatosensory evoked potentials

The current method of localizing somatosensory and motor cortex during neurosurgical removal of abnormal tissue is Penfield's method of cortical stimulation. While useful, this method has drawbacks, in particular the need to operate under local anesthesia. Another method of localization, described here, involves intra-operative recording of short-latency somatosensory evoked potentials to stimulation of the contralateral median nerve, from electrodes placed directly on central cortex. Proper localization involves identification of potentials which invert in polarity across the central sulcus, identification of other potentials which are largest in the medial portion of the hand area of somatosensory cortex and do not polarity invert, and determination of the region of maximal potential amplitude. This method of localization works equally well whether the patient is under local or general anesthesia, but it occasionally fails in patients with tumors abutting or invading the hand area of sensorimotor cortex.     

Hemodynamics evoked by microelectrical direct stimulation in rat somatosensory cortex

The aim of this study was to estimate the timing (latency) of the increase in red blood cell (RBC) velocity and RBC concentration, and the magnitude of response in local cerebral blood flow (LCBF) for neuronal activation. We measured LCBF change during activation of the somatosensory cortex by direct microelectrical stimulation. Electrical stimuli of 5, 10 and 50 Hz of 1 ms pulse with 10-15 microA, were given for 5 s. LCBF, RBC velocity and RBC concentration were monitored by laser-Doppler flowmetry (LDF) in alpha-chloralose anesthetized rats (n = 7). LCBF, RBC velocity and RBC concentration increased nearly proportionally to stimulus frequency, i.e. neuronal activity. LCBF rose approximately 0.5 s after the onset of stimulation, and there was no significant time lag of the latencies among LCBF, RBC velocity and RBC concentration at the same stimulus frequency. We interpret these results to mean that the onset of LCBF increase on cortical activation is reflected by a rapid change in arteriole (resistance vessel) dilation and capillary volume. The data also elucidate the linear relationship between LCBF increase and cortical activity.     

Presurgical functional localization of primary somatosensory cortex by dipole tracing method of scalp-skull-brain head model applied to somatosensory evoked potential

The aim of the present study was to explore the utility of dipole tracing (DT) of a scalp-skull-brain (SSB) head model in preoperative functional localization of the human brain. Nine patients who underwent surgery of mass lesions around the central sulcus (CS) were employed. By using SSB/DT, dipole source location of early cortical components of the somatosensory evoked potential (SEP) was estimated before surgery. Motor cortex, CS and primary somatosensory cortex were determined by cortical SEP during surgery. After surgery precise functional mapping was reproduced in MRI, and the accuracy of DT was evaluated by measuring the distance between estimated dipole source and the posterior bank of the CS. We defined this distance as localization error of DT. In 4 cases without structural change around the sensorimotor cortex, localization error ranged from 1 to 4 mm with an average of 2 mm. In 5 cases with structural alteration of sensorimotor cortex, localization error ranged from 6 to 10 mm with an average of 8 mm. The difference in localization error between the two groups was statistically significant, and may have been caused by changes of conductance near sensorimotor cortex in the latter group. Functional localization by DT was accurate and useful. But localization error could not be ignored in cases with structural alteration in the sensorimotor cortex.     

Ipsilateral median somatosensory evoked potentials recorded from human somatosensory cortex

Somatosensory evoked potentials (SEP) to ipsilateral and contralateral median nerve stimulations were recorded from subdural electrode grids over the perirolandic areas in 41 patients with medically refractory focal epilepsies who underwent evaluation for epilepsy surgery. All patients showed clearly defined, high-amplitude contralateral median SEPs. In addition, four patients showed ipsilateral SEPs. Compared with the contralateral SEPs, ipsilateral SEPs were very localized, had a different spatial distribution, were of considerably lower amplitude, had a longer latency (1.2–17.8 ms), did not show an initial negativity, and were markedly attenuated during sleep. Stimulation of the subdural electrodes overlying the sensory hand area was associated with contralateral hand paresthesias, but no ipsilateral hand paresthesias occurred. It was concluded that subdurally recorded cortical SEPs to ipsilateral stimulation of the median nerve (M) reflect unconscious sensory input from the hand possibly serving fast bimanual hand control. The anatomical pathway of these ipsilateral short-latency MSEPs is not yet known. Transcallosal transmission seems unlikely because of the short delay between the ipsilateral and contralateral responses in selected cases. The infrequent occurrence of ipsilateral subdurally recorded SEPs and their low amplitude and limited distribution suggest that they contribute very little to the short-latency ipsilateral median SEPs recorded on the scalp.     

Frontal distribution of early cortical somatosensory evoked potentials to median nerve stimulation

The topography of early frontal SEPs (P20 and N26) to left median nerve stimulation was studied in 30 normal subjects and 3 patients with the left frontal bone defect. The amplitudes of P20 and N26 were maximum at the frontal electrode (F4) contralateral to the stimulation and markedly decreased at frontal electrodes ipsilateral to the site of stimulation. There was, however, no latency difference of P20 and N26 between ipsilateral and contralateral frontal electrodes. These results suggest that the origin of the ipsilateral and contralateral P20 and N26 is the same. The wide distribution of P20 and N26 over both frontal areas could be explained by assuming a smearing effect from generators actually located in the rolandic fissure and motor cortex.     

Scalp topography and distribution of cortical somatosensory evoked potentials to median nerve stimulation

Topographies and distributions of cortical SEPs to median nerve stimulation were studied in 8 normal adults and 5 neurological patients. SEPs recorded from C4, P4, Pz, T6-A1A2 derivations to left median nerve stimulation were composed of 2 early negative (N16, N20) and 2 positive components (P12, P23), whereas those recorded from frontal electrodes (Fz, Fp1, Fp2) disclosed 2 early negativities (N16, N24) and 2 early positivities (P12, P20). N20 and P20, and P23 and N24, reversed across the rolandic fissure with no significant difference in their peak latencies. P23 was of slightly shorter latency at C4 than at more posterior electrodes (P4, T6, Pz).In 3 patients with complete hemiplegia but normal sensation, all the early SEP components were normal in scalp distribution and peak latencies except for a decrease of N24 amplitude. In 2 patients with complete hemiplegia and sensory loss no early cortical SEPs were seen. These findings suggest that N20 and P20 are generated as a single horizontal dipole in the central fissure, whereas P23 and N24 are a reflection of multiple generators in pre- and postrolandic regions.     

Effect of stimulus intensity on subcortical and cortical somatosensory evoked potentials by posterior tibial nerve stimulation

The effect of stimulus intensity on subcortical and cortical somatosensory evoked potentials (SEPs) to posterior tibial nerve (PTN) stimulation were studied in 16 normal controls. Stimulus intensity was evaluated as a function of sensory threshold (S). Motor threshold (M) varied between 1 S and 2 S.The amplitude of N18 (afferent volley immediately before it enters the spinal canal) increased approximately linearly up to at least 4.5 S. N20 (dorsal cord potential) also demonstrated a linear increase up to at least 4 S but the rate of increase was significantly smaller. All central components (subcortical brain-stem components P27 and N30, and cortical components N1 and P2) showed an even smaller rate of increase which was non-linear and reached a plateau at 3 S.The relatively higher rate of increase of N18 as compared with N20 was most probably due to the recording of sensory impulses plus antidromic impulses in motor fibers. The smaller rate of increase and early saturation of all the central components compared with N20 suggests that all the afferent fibers generating N20 only the low threshold fibers participate in the generation of more central components.Stimulus intensities of 3 S are recommended for clinical studies of the central SEPs to PTN stimulation.     

Somatotopy of human hand somatosensory cortex revealed by dipole source analysis of early somatosensory evoked potentials and 3D-NMR tomography

Somatosensory evoked potentials (SEPs) to median nerve and finger stimulation were analyzed by means of spatio-temporal dipole modelling combined with 3D-NMR tomography in 8 normal subjects. The early SEPs were modelled by 3 equivalent dipoles located in the region of the brain-stem (B) and in the region of the contralateral somatosensory cortex (T and R). Dipole B explained peaks P14 and N18 at the scalp. Dipole T was tangentially oriented and explained the N20-P20, dipole R was radially oriented and modelled the P22. The tangential dipole sources T were located within a distance of 6 mm on the average and all were less than 9 mm from the posterior bank of the central sulcus. In 6 subjects the tangential sources related to finger stimulation arranged along the central sulcus according to the known somatotopy. The radial sources did not show a consistent somatotopic alignment across subjects. We conclude that the combination of dipole source analysis and 3D-NMR tomography is a useful tool for functional localization within the human hand somatosensory cortex.     

Depression of evoked potentials in rat thalamic ventro-basal complex and somatosensory cortex after reticular stimulation

Experiments on unanesthetized rats immobilized with D-tubocurarine showed that electrical stimulation (100/sec) of the central gray matter and the mesencephalic and medullary reticular formation considerably depressed potentials in the somatic thalamic relay nucleus and somatosensory cortex evoked by stimulation of the forelimb or medial lemniscus. The mean threshold values of the current used for electrical stimulation of these structures did not differ significantly and were 70 (20–100), 100 (20–120), and 120 (50–200) µA, respectively. On comparison of the amplitude-temporal characteristics of inhibition of evoked potentials during electrical stimulation of the above-mentioned structures by a current of twice the threshold strength, no significant differences were found. Immediately after the end of electrical stimulation the amplitude of the cortical evolved potential and the post-synaptic components of the thalamic evoked potential was 50–60% (P<0.01) below the control values. The duration of this depression varied from 0.5 to 1 sec. An increase in the intensity of electrical stimulation of brain-stem structures to between three and five times the threshold led to depression of the presynaptic component of the thalamic evoked potential also. Depression of the evoked potential as described above was found with various ratios between the intensities of conditioning and testing stimuli.M. V. Lomonosov Moscow State University. Translated from Neirofiziologiya, Vol. 8, No. 5, pp. 467–475, September–October, 1976.     

Neurometric evaluation of the cortical somatosensory evoked potential in acute incomplete spinal cord injuries

The clinical application of evoked potentials has at times been criticized for its failure to provide an objective quantifiable assessment of the processing of sensory information and a reflection of nervous system integrity at least comparable in accuracy to other methods of assessment. The challenge is to quantify the SEP in a manner that accurately reflects the function of the somatosensory system.Therefore, neurometrics, an approach which emphasizes the transformation of the neurophysiological data to a common metric of relative probability by reference to normative standards and the classification of critical features of data by multivariate statistics, was employed.The 3-part study involved the evaluation of the diagnostic, prognostic and localization functions of the cortical tibial SEP in patients with incomplete spinal cord injuries. Two neurometric indices which correlated well with concurrent and future neurological status were developed. The distributions of influence of dorsal columns and spino-thalamic tracts on the SEP were established.     

Development of cortical somatosensory evoked potentials in rats.

The development of the contra- and ipsilateral cortical potential evoked by electrical sciatic nerve stimulation was studied in 77 male albino rats aged 5 to 45 days. A contralateral response was already recorded, as double negativity, in the youngest animals, while an ipsilateral evoked potential was not reliably present until the 10th day. At this time, however, both responses started with an inconstant positive wave and their shape was practically the same. During subsequent development the responses differed only in respect to their dominant component: in the contralateral response, the N1 wave had the highest amplitude for most of the time, while in the ipsilateral response the delayed N2 wave was the largest component. The latent periods of contralateral responses were somewhat shorter than those of ipsilateral evoked potentials. During development we noticed a phase of abrupt shortening of the latent period, which took place before the 15th day in the contralateral response and before the 20th day in the ipsilateral response. We also found a difference in the fatigability of the responses, which was greater in immature rats than in adult animals; in the ipsilateral evoked potential it approached adult values more slowly. The development of the ipsilateral response is thus delayed compared with the development of the contralateral response.     

Characterization of visual percepts evoked by noninvasive stimulation of the human posterior parietal cortex

Phosphenes are commonly evoked by transcranial magnetic stimulation (TMS) to study the functional organization, connectivity, and excitability of the human visual brain. For years, phosphenes have been documented only from stimulating early visual areas (V1-V3) and a handful of specialized visual regions (V4, V5/MT+) in occipital cortex. Recently, phosphenes were reported after applying TMS to a region of posterior parietal cortex involved in the top-down modulation of visuo-spatial processing. In the present study, we systematically characterized parietal phosphenes to determine if they are generated directly by local mechanisms or emerge through indirect activation of other visual areas. Using technology developed in-house to record the subjective features of phosphenes, we found no systematic differences in the size, shape, location, or frame-of-reference of parietal phosphenes when compared to their occipital counterparts. In a second experiment, discrete deactivation by 1 Hz repetitive TMS yielded a double dissociation: phosphene thresholds increased at the deactivated site without producing a corresponding change at the non-deactivated location. Overall, the commonalities of parietal and occipital phosphenes, and our ability to independently modulate their excitability thresholds, lead us to conclude that they share a common neural basis that is separate from either of the stimulated regions.     

Reorganizing the intrinsic functional architecture of the human primary motor cortex during rest with non-invasive cortical stimulation

The primary motor cortex (M1) is the main effector structure implicated in the generation of voluntary movements and is directly involved in motor learning. The intrinsic horizontal neuronal connections of M1 exhibit short-term and long-term plasticity, which is a strong substrate for learning-related map reorganization. Transcranial direct current stimulation (tDCS) applied for few minutes over M1 has been shown to induce relatively long-lasting plastic alterations and to modulate motor performance. Here we test the hypothesis that the relatively long-lasting synaptic modification induced by tDCS over M1 results in the alteration of associations among populations of M1 neurons which may be reflected in changes of its functional architecture. fMRI resting-state datasets were acquired immediately before and after 10 minutes of tDCS during rest, with the anode/cathode placed over the left M1. For each functional dataset, grey-matter voxels belonging to Brodmann area 4 (BA4) were labelled and afterwards BA4 voxel-based synchronization matrices were calculated and thresholded to construct undirected graphs. Nodal network parameters which characterize the architecture of functional networks (connectivity degree, clustering coefficient and characteristic path-length) were computed, transformed to volume maps and compared before and after stimulation. At the dorsolateral-BA4 region cathodal tDCS boosted local connectedness, while anodal-tDCS enhanced long distance functional communication within M1. Additionally, the more efficient the functional architecture of M1 was at baseline, the more efficient the tDCS-induced functional modulations were. In summary, we show here that it is possible to non-invasively reorganize the intrinsic functional architecture of M1, and to image such alterations.