Cerebral evoked potentials after rectal stimulation

We obtained reproducible cortical evoked potentials (EPs) in response to electrical stimulation of the rectum with 1 Hz frequency. We found 2 distinctly different EPs in response to rectal stimulation. In 5 females, the EP had an early onset latency (mean 26 msec) with multiple positive and negative peaks. In 10 females, the EP had a later onset latency (mean 52 msec) and a trifid configuration, having a very prominent negative peak. The early onset EPs after rectal stimulation appeared very similar to the wave form of the cortical EPs recorded after pudendal nerve stimulation. Finding similar interpeak latencies in the early onset EP after rectal stimulation and the EP after pudendal nerve stimulation suggests that either the same pathway was used or that rectal stimulation also stimulated the pudendal nerve. It appears that we stimulated visceral afferents when we recorded late onset EPs, because the large EP amplitude declined rapidly with faster stimulation rates and also with greater number of averaging, and the sensation threshold was very unstable, all different to somatosensory EPs.     

Dynamics of changes in somatosensory input to the motor cortex following lesion of somatosensory cortical areas in dogs

The pattern of change produced in somatosensory evoked potential (EP) in the forelimb projection area within the motor cortex (MI) following lesion of the projection area of the same limb in the somatosensory cortex (SI) or in parietal cortex area 5 was investigated during chronic experiments on waking dogs. Amplitude of the initial positive — negative wave of EP declined to 28–63% of preoperational level in all cases. No significant recovery of EP was noted for three weeks. Thus, a correlation between change in EP and spontaneous recuperation of the precision motor response occurring within two weeks after lesion of the SI did not exist. Nor was EP reinstated in the MI after ablation of area 5, despite complete but gradual reinstatement of EP (after an initial decline to 53%) in the nearby SI region. This protracted depression of EP seems to have been associated with breakdown of somatotopic sensory input from the SI or from area 5 to the MI, since EP in the motor cortex of the intact hemisphere and the hindlimb projection area within the MI on the lesioned side either remained unchanged or recovered within a week or two.Institute of Higher Nervous Activity and Neurophysiology, Academy of Sciences of the USSR, Moscow. Translated from Neirofiziologiya, Vol. 22, No. 1, pp. 61–68, January–February, 1990.     

Evoked potentials in the rat neostriatum during local cooling of the cortex in the zone of primary response to the applied stimulus

The effect of local cooling of the surface of the somatosensory cortex was studied while recording primary response (PR) in the center of a cooled area and evoked potentials (EP) in the striatum to the forepaw stimulation. The cooling which served to arise the amplitude of the PR, served also to arise the amplitude of the EP in the striatum. EP to the stimulus, the sensory representation of which in the cortex was cooled, were facilitated only. Facilitation of the striatal EP was more intense than facilitation of the cortical PR in the cooled area. The level of facilitation of the EP was the same in the region of the striatum which receives corticofugal fibers from the cooled area of the cortex and in other regions of the striatum, receiving the corticofugal fibers from other parts of the cortex. The data show a possibility for the interactions in the striatum of the corticofugal signals from different cortical areas with each other and with the ascending afferent signals.     

Effect of sleep stage on somatosensory evoked potentials by median nerve stimulation

The effects of sleep stage on early cortical somatosensory evoked potentials (SEPs) and short-latency components elicited by median nerve stimulation were studied in 12 normal volunteers. The latency of P13 in the awake stage was not significantly different from that in any sleep stage. The latencies of N16, N20 and P20 were significantly prolonged while the amplitude of N20 was decreased during the non-rapid eye movement (NREM) sleep stage. P22, P23 and N24 components showed double peaks (P23a, P23b, N24a, N24b) during the NREM sleep stage in 6 subjects, while N24 showed a single peak and only P22 and P23 showed double peaks in 5 other subjects. The latencies and morphologies of SEPs during rapid eye movement sleep stage were almost the same as those during the awake stage. These findings suggest that NREM sleep affects the latency, amplitude and morphology of N16 and early cortical components.     

Selective gating of lower limb cortical somatosensory evoked potentials (SEPs) during passive and active foot movements

We evaluated subcortical and cortical somatosensory evoked potentials (SEPs) in response to posterior tibial nerve stimulation in 4 experimental conditions of foot movement and compared them with the baseline condition of full relaxation. The experimental conditions were: (a) active flexion-extension of the stimulated foot; (b) active flexion-extension of the non-stimulated foot; (c) passive flexion-extension of the stimulated foot in complete relaxation; (d) tonic active flexion of the stimulated foot. We analyzed latencies and amplitudes of the subcortical P30 potential, of the contralateral pre-rolandic N37 and P50 responses and of the P37, N50 and P60 potentials recorded over the vertex. Latencies did not vary in any of the paradigms. The amplitude of subcortical P30 potential did not change during any of the paradigms. Among the cortical waves, P37, N50 and P60 amplitudes were significantly attenuated in all conditions except active movement of the non-stimulated foot (b). This attenuation was less during passive (c) than during active movements of the stimulated foot (a and d). The contralateral pre-rolandic waves N37 and P50 showed no significant decrease during any of the paradigms. These results suggest that gating occurs rostrally to the cervico-medullary junction, probably at cortical level. The different behavior of N37, P50 and P37, N50 cortical responses during movement of the stimulated foot provides evidence suggestive of a highly localized gating process occurring at cortical level. These potentials could reflect activation of separate, functionally distinct generators.     

Pain-related somatosensory evoked potentials following CO2 laser stimulation of foot in man

Since our previous study of pain somatosensory evoked potentials (SEPs) following CO₂ laser stimulation of the hand dorsum could not clarify whether the early cortical component NI was generated from the primary somatosensory cortex (SI) or the secondary somatosensory cortex (SII) or both, the scalp topography of SEPs following CO₂ laser stimulation of the foot dorsum was studied in 10 normal subjects and was compared with that of the hand pain SEPs and the conventional SEPs following electrical stimulation of the posterior tibial nerve recorded in 8 and 6 of the 10 subjects, respectively. Three components (N1, N2 and P2) were recorded for both foot and hand pain SEPs. N1 of the foot pain SEPs was maximal at the midline electrodes (Cz or CPz) in all data where that potential was recognized, but the potential field distribution was variable among subjects and even between two sides within the same subject. N1 of the hand pain SEPs was maximal at the contralateral central or midtemporal electrode. The scalp distribution of N2 and P2, however, was not different between the foot and hand pain SEPs. The mean peak latency of N1 following stimulation of foot and hand was found to be 191 msec and 150 msec, respectively, but there was no significant difference in the interpeak latency of Nl-N2 between foot and hand stimulation. It is therefore concluded that NI of the foot pain SEPs is generated mainly from the foot area of SI. The variable scalp distribution of the N7 component of the foot pain SEPs is likely due to an anatomical variability among subjects and even between sides.     

脚内核在电针镇痛及兴奋尾壳核镇痛中的作用

用行为学和电生理学的方法 ,探讨脚内核在电针镇痛及兴奋尾壳核镇痛中的作用。脚内核微量注射红藻氨酸 7d后 ,电针对辐射热引起的大鼠缩腿潜伏期无明显影响 ,电针或兴奋尾壳核对丘脑束旁核神经元的伤害性反应亦无明显影响。与正常对照组电针或兴奋尾壳核产生的抑制作用相比有显著性差异 (P <0 .0 5 ) ;与脚内核微量注射生理盐水 7d后 ,电针可提高大鼠缩腿潜伏期 ,及电针或兴奋尾壳核对束旁核神经元伤害性反应的抑制作用相比 ,有显著性差异 (P <0 0 5 )。上述结果提示 ,脚内核在电针及兴奋尾壳核镇痛中发挥重要作用     

Meeting report

Neuronal responses in somatosensory cortical areas 3b and 1- 2 (S1) were recorded during an attention task involving cue directed selection of one of three simultaneous stimuli: dual sinewave shaped vibrotactile stimuli applied to mirror sites on both hands or a similarly timed auditory tone. The cued stimulus occurred with one of two equally probable patterns: a constant amplitude vibration or the latter with a superimposed brief sinewave amplitude pulse midway during stimulation. Uncued stimuli always contained amplitude pulses. Two monkeys signaled the absence or presence of an amplitude pulse by appropriately moving a foot pedal up or down. Cues initiated trials by marking the location where the monkey had to discriminate the stimulus pattern. Cue location and stimulus pattern varied randomly per trial. Approximately 50% of cells (44/77 in 3b and 39/77 in 1- 2) had significantly different firing rates to stimulation cued to the contralateral hand relative to spatially cuing the ipsilateral hand or cross-modally the auditory stimulus. Relatively suppressed firing rates during times prior to the epoch containing amplitude pulses improved signal-to-noise ratios for responses to amplitude pulses. Instances of significant enhanced activity during and after intervals with amplitude pulses were rare and relative to suppressed activity when cues directed attention to the ipsilateral hand or auditory stimulus. The present findings suggest that attention influences even the earliest stage somatosensory cortical processing. Findings were more modest in S1 than those previously seen in S2 (Burton et al. , Somatosens Mot Res 14 : 237-267, 1997), which supports the concept of multistage attention processes for touch.     

Tactile-spatial and cross-modal attention effects in the primary somatosensory cortical areas 3b and 1-2 of rhesus monkeys

Neuronal responses in somatosensory cortical areas 3b and 1-2 (S1) were recorded during an attention task involving cue directed selection of one of three simultaneous stimuli: dual sinewave shaped vibrotactile stimuli applied to mirror sites on both hands or a similarly timed auditory tone. The cued stimulus occurred with one of two equally probable patterns: a constant amplitude vibration or the latter with a superimposed brief sinewave amplitude pulse midway during stimulation. Uncued stimuli always contained amplitude pulses. Two monkeys signaled the absence or presence of an amplitude pulse by appropriately moving a foot pedal up or down. Cues initiated trials by marking the location where the monkey had to discriminate the stimulus pattern. Cue location and stimulus pattern varied randomly per trial. Approximately 50% of cells (44/77 in 3b and 39/77 in 1-2) had significantly different firing rates to stimulation cued to the contralateral hand relative to spatially cuing the ipsilateral hand or cross-modally the auditory stimulus. Relatively suppressed firing rates during times prior to the epoch containing amplitude pulses improved signal-to-noise ratios for responses to amplitude pulses. Instances of significant enhanced activity during and after intervals with amplitude pulses were rare and relative to suppressed activity when cues directed attention to the ipsilateral hand or auditory stimulus. The present findings suggest that attention influences even the earliest stage somatosensory cortical processing. Findings were more modest in S1 than those previously seen in S2 (Burton et al., Somatosens Mot Res 14: 237-267, 1997), which supports the concept of multistage attention processes for touch.     

Dissociation induced by voluntary movement between two different components of the centro-parietal P40 SEP to tibial nerve stimulation

Whether the two earliest cortical somatosensory evoked potentials (SEPs) to tibial nerve stimulation (N37 and P40) are generated by the same dipolar source or, instead, originate from different neuronal populations is still a debated problem. We recorded the early scalp SEPs to tibial nerve stimulation in 10 healthy subjects at rest and during voluntary movement of the stimulated foot. We found that the P40, which reached its highest amplitude on the vertex at rest, changed its topography during movement, since its amplitude was reduced much more in the central than in the parietal traces. These findings suggest that two different components contribute to the centro-parietal positivity at rest: (1) the P37 response, which is parietally distributed and is not modified by movement, and (2) the `real' P40 SEP, which is focused on the vertex and is reduced in amplitude during voluntary movement. Since, also, the N37 response did not vary its amplitude under interference condition, it is possible that the N37 and P37 potentials are generated by the same dipolar source. Other later components, namely P50 and N50, were significantly reduced in amplitude during foot movement. Lastly, the subcortical P30 far-field remained unchanged and this suggests that the phenomenon of amplitude reduction during movement (i.e. gating) occurs above the cervico-medullary junction.     

Correlation of subjective assessments with somatosensory evoked potentials to electrical stimulation of the finger in man

The relationship between 5 positive components of somatosensory evoked potentials (EPs) and subjective response to electrical stimuli, which were recorded in the same human subjects, was assessed in the present study. Five levels of tactile stimuli and 6 levels of noxious stimuli were applied to the tip of the right index finger. The relationship between the magnitude of subjective response and stimulus intensity was well expressed by a power function. Of 5 major positive components in an EP, P30 and P50 were localized at contralateral primary somatic projection area, while P90, P190 and P270 were at the vertex area. The amplitude of the 5 components systematically increased as increasing stimulus intensity, and also increased with the magnitude of subjective response. A significant correlation between the amplitude of P30 or P50 and stimulus intensity was found when the effect of subjective response was partially out. By contrast, the amplitudes of P190 and P270 were associated with subjective response when the effect of stimulus intensity was partially out. These results suggest that the earlier EP components reflect sensory signal processing, while the latter ones concern the subjective evaluating system.     

正常小儿胫神经诱发短潜伏时头皮体感区电位及脑瘫对该电位的影响

本研究观察了20例正常小儿和49例脑瘫小儿的下肢胫后神经刺激性短潜伏时头皮体感诱发电位(PTN-SSEP)。正常小儿在刺激后出现6个反应波(P18、N23、P31、N42、P54和N68),大脑左右两体感头皮的SSEP波形相似;时相基本相等,t检验表明两侧间无差异;电压除波P31外其余波也无显著差异。脑瘫小儿PTN-SSEP异常率达91.84％,有4种类型:正常型占8.16％、混合异常型57.14％、反应低下型6.12％及电压不对称型28.57％。经统计患儿左右头皮的SSEP、潜伏时和电压均有显著差异(P<0.05),其中P31和N42电压差值>50％。与正常小儿比较,患儿双侧反应降低,多数波潜伏时延长。患侧电压损失率>50％(P<0.001),波P18、N23和P31的潜伏时差异显著。结果提示.(1)正常小儿体感通路反应稳定,左右侧活动基本对称;(2)脑瘫小儿体感通路左右侧活动不对称,患侧传导机能下降,体感皮层反应减退。     

The effects of stimulus rates upon median,ulnar and radial nerve somatosensory evoked potentials

We examined the effect of stimulus rates on the somatosensory evoked potential (SEP) amplitude following stimulation of the median nerve (MN) and the ulnar nerve (UN) at the elbow or wrist, and the radial nerve (RN) at the wrist in 12 normal subjects. We measured the amplitude of frontal (P14-N18-P22-N30) and parietal peaks (P14-N20-P26-N34) at a stimulus rate of 1.1, 3.5 and 5.7 Hz. The amplitude attenuation was found at frontal P22 and N30 and to a lesser degree at parietal N20 and P26 peaks with an increasing stimulus rate from 1.1 to 5.7 Hz. The amplitude attenuation was greatest at the elbow when compared to the wrist stimulation for both MN and UN. The attenuation was least for wrist stimulation for the RN. The UN block by local anesthesia just distal to the stimulus electrode at the elbow abolished the amplitude attenuation caused by the fast stimulus rate. The observed amplitude attenuation with the faster stimulus rate is probably due, in part, to interference from the “secondary” afferent inputs. The secondary afferent inputs arise from peripheral receptor stimulation (muscle, joint and/or cutaneous) as a subsequent effect of efferent volleys initiated from the point of stimulation. The greater number of peripheral receptors being activated as more proximal sites of stimulation in a mixed nerve would result in greater attenuation of the SEP recorded from scalp electrodes. We postulate that the attenuation of frontal peaks by the fast stimulus rate is due to the frontal projection of interfering “secondary” afferent inputs.     

Topography of somatosensory evoked potentials to median nerve stimulation in patients with cerebral lesions

Scalp distributions and topographies of early cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were studied in 22 patients with 5 different types of cerebral lesion due to cerebrovascular disease or tumor (thalamic, postcentral subcortical, precentral subcortical, diffuse subcortical and parieto-occipital lesions) in order to investigate the origins of frontal (P20, N24) and central-parietal SEPs (N20, P22, P23).In 2 patients with thalamic syndrome, N16 was delayed in latency and N20/P20 were not recorded. No early SEP except for N16 was recorded in 2 patients with pure hemisensory loss due to postcentral subcortical lesion. In all 11 patients with pure hemiparesis or hemiplegia due to precentral subcortical lesion N20/P20 and P22, P23/N24 components were of normal peak latencies. The amplitude of N24 was significantly decreased in all 3 patients with complete hemiplegia. These findings support the hypothesis that N20/P20 are generated as a horizontal dipole in the central sulcus (3b), whereas P23/N24 are a reflection of multiple generators in pre- and post-rolandic fissures. P22 was very localized in the central area contralateral to the stimulation.Topographical studies of early cortical SEPs are useful for detecting each component in abnormal SEPs     

Sustained negative BOLD response in human fMRI finger tapping task

In this work, we investigated the sustained negative blood oxygen level-dependent (BOLD) response (sNBR) using functional magnetic resonance imaging during a finger tapping task. We observed that the sNBR for this task was more extensive than has previously been reported. The cortical regions involved in sNBR are divided into the following three groups: frontal, somatosensory and occipital. By investigating the spatial structure, area, amplitude, and dynamics of the sNBR in comparison with those of its positive BOLD response (PBR) counterpart, we made the following observations. First, among the three groups, the somatosensory group contained the greatest number of activated voxels and the fewest deactivated voxels. In addition, the amplitude of the sNBR in this group was the smallest among the three groups. Second, the onset and peak time of the sNBR are both larger than those of the PBR, whereas the falling edge time of the sNBR is less than that of the PBR. Third, the long distance between most sNBR foci and their corresponding PBR foci makes it unlikely that they share the same blood supply artery. Fourth, the couplings between the sNBR and its PBR counterpart are distinct among different regions and thus should be investigated separately. These findings imply that the origin of most sNBR foci in the finger-tapping task is much more likely to be neuronal activity suppression rather than "blood steal."     

Lithium effects on the somatosensory cortical evoked response in the rat and cat

The early positive cortical evoked potential to somatosensory stimuli is regularly increased in amplitude in patients receiving lithium carbonate treatment. This may reflect a unique neurochemical effect of lithium since similar changes have not been observed in humans following other drugs. To investigate this finding, cortical evoked potentials to peripheral somatosensory stimulation were obtained in rats and cats with implanted epidural electrodes. In rats, increasing doses of oral lithium chloride, up to 5 meq/kg/d which approached the LD 50, produced no reliable change in the early positive evoked response amplitude. In cats, an increased amplitude of the early positive-negative cortical potential was observed in every instance and the serum lithium levels were within the range used clinically in humans. The increased cortical evoked response amplitude in cats did not directly correlate with serum lithium levels but was delayed 1 to 5 days after serum lithium levels reached their peak. The findings in cats are similar to the human studies. The negative results observed in rats may reflect important species differences regarding lithium.     

Characteristics of evoked potentials and single neuron responses in the cat sensorimotor cortex to sound stimuli with different frequencies.

The characteristics of the averaged evoked potentials (AEP) (experiments with awake non-paralysed animals), of the evoked potentials (EP) and of the responses of single sensorimotor cortical neurons (acute experiments) of cats to tone-bursts with frequencies within 0.1-6.0 kHz were studied. Response selectivity to the tone-burst frequencies which are energetically pronounced in some biologically significant sounds for the cat was observed. The averaged curve of the dependence of the amplitude of AEP in the somatosensory cortical region (S1) on the tone-burst frequency has reliable maximum values at the frequencies of 0.8, 1.6 and 2.0-3.0 kHz. Most pronounced changes in the heart rhythm were observed within the tone-burst frequency ranges in which the AEP of the highest amplitudes were recorded. The amplitude of the AEP was found to increase during the conditioned reflex elaboration. The curve of the dependence of the probability of the EP occurrence on the frequency at equal sound pressure levels had maximum values at the frequencies of 1.6 and 3.2 kHz. The highest amplitude values of EP were found at frequencies of 0.8, 1.6 and 3.2 kHz. More than half of the recorded neurons revealed the lowest values of the response thresholds and the maximum values of the occurrence probability under suprathreshold stimulation at frequencies close to 0.8, 1.6, and 3.2 kHz. It is supposed that the above mentioned feature of the input frequency organization in sensorimotor cortex is connected with the selectivity as to the biological significance of acoustic stimuli.     

Changes in extracellular space volume and geometry induced by cortical spreading depression in immature and adult rats

Changes in extracellular space (ECS) diffusion parameters, DC potentials and extracellular potassium concentration were studied during single and repeated cortical spreading depressions (SD) in 13-15 (P13-15), 21 (P21) and 90-day-old (adult) Wistar rats. The real-time iontophoretic method using tetramethylammonium (TMA+)-selective microelectrodes was employed to measure three ECS parameters in the somatosensory cortex: the ECS volume fraction alpha (alpha = ECS volume/total tissue volume), ECS tortuosity lambda (increase in diffusion path length) and the nonspecific TMA+ uptake k'. SD was elicited by needle prick. SD was significantly longer at P13-15 than at P21 and in adults. During SD, alpha in all age groups decreased from 0.21-0.23 to 0.05-0.09; lambda increased from 1.55-1.65 to 1.95-2.07. Ten minutes after SD, alpha (in adults) and lambda (all age groups) increased compared to controls. This increase persisted even 1 hour after SD. When SD was repeated at 1 hour intervals, both alpha and lambda showed a gradual cumulative increase with SD repetition. Our study also shows that cortical SD is, as early as P13, accompanied by severe ECS shrinkage and increased diffusion path length (tortuosity) with values similar to adults, followed by a long-lasting increase in ECS volume and tortuosity when compared to pre-SD values.     

Role of the Prostaglandin E2 EP1 Receptor in Traumatic Brain Injury

Brain injuries promote upregulation of so-called proinflammatory prostaglandins, notably prostaglandin E₂ (PGE₂), leading to overactivation of a class of its cognate G-protein-coupled receptors, including EP1, which is considered a promising target for treatment of ischemic stroke. However, the role of the EP1 receptor is complex and depends on the type of brain injury. This study is focused on the investigation of the role of the EP1 receptor in a controlled cortical impact (CCI) model, a preclinical model of traumatic brain injury (TBI). The therapeutic effects of post-treatments with a widely studied EP1 receptor antagonist, SC-51089, were examined in wildtype and EP1 receptor knockout C57BL/6 mice. Neurological deficit scores (NDS) were assessed 24 and 48 h following CCI or sham surgery, and brain immunohistochemical pathology was assessed 48 h after surgery. In wildtype mice, CCI resulted in an obvious cortical lesion and localized hippocampal edema with an associated significant increase in NDS compared to sham-operated animals. Post-treatments with the selective EP1 receptor antagonist SC-51089 or genetic knockout of EP1 receptor had no significant effects on cortical lesions and hippocampal swelling or on the NDS 24 and 48 h after CCI. Immunohistochemistry studies revealed CCI-induced gliosis and microglial activation in selected ipsilateral brain regions that were not affected by SC-51089 or in the EP1 receptor-deleted mice. This study provides further clarification on the respective contribution of the EP1 receptor in TBI and suggests that, under this experimental paradigm, the EP1 receptor would have limited effects in modulating acute neurological and anatomical pathologies following contusive brain trauma. Findings from this protocol, in combination with previous studies demonstrating differential roles of EP1 receptor in ischemic, neurotoxic, and hemorrhagic conditions, provide scientific background and further clarification of potential therapeutic application of prospective prostaglandin G-protein-coupled receptor drugs in the clinic for treatment of TBI and other acute brain injuries.     

Comparison of visual and objective quantification of elbow and shoulder movement in children with obstetric brachial plexus palsy

Background

Animal studies have demonstrated complex cortical reorganization following peripheral nerve lesion. Central projection fields of intact nerves supplying skin areas which border denervated skin, extended into the deafferentiated cortical representation area. As a consequence of nerve lesions and subsequent reorganization an increase of the somatosensory evoked potentials (SEPs) was observed in cats when intact neighbouring nerves were stimulated. An increase of SEP-components of patients with nerve lesions may indicate a similar process of posttraumatic plastic cortical reorganization.

Methods

To test if a similar process of post-traumatic plastic cortical reorganization does occur in humans, the SEP of intact neighbouring hand nerves were recorded in 29 patients with hand nerve lesions. To hypothetically explain the observed changes of SEP-components, SEP recording following paired stimulation of the median nerve was performed in 12 healthy subjects.

Results

Surprisingly 16 of the 29 patients (55.2%) showed a reduction or elimination of N35, P45 and N60. Patients with lesions of two nerves showed more SEP-changes than patients with a single nerve lesion (85.7%; 6/7 nerves; vs. 34.2%; 13/38 nerves; Fisher's exact test, p < 0.05). With paired stimulation a suppression of the amplitude of N20, P25 and P45 (p < 0.05; sign test), and a marked increment of N35 (p < 0.05; sign test) and N60 (not significant; sign test) of the second response could be observed.

Conclusion

The results of the present investigation do not provide evidence of collateral innervation of peripherally denervated cortical neurons by neurons of adjacent cortical representation areas. They rather suggest that secondary components of the excitatory response to nerve stimulation are lost in cortical areas, which surround the denervated region.