Robot-assisted gait training versus treadmill training in patients with Parkinson's disease: a kinematic evaluation with gait profile score.

The purpose of this study was to quantitatively compare the effects, on walking performance, of end-effector robotic rehabilitation locomotor training versus intensive training with a treadmill in Parkinson's disease (PD). Fifty patients with PD were randomly divided into two groups: 25 were assigned to the robot-assisted therapy group (RG) and 25 to the intensive treadmill therapy group (IG). They were evaluated with clinical examination and 3D quantitative gait analysis [gait profile score (GPS) and its constituent gait variable scores (GVSs) were calculated from gait analysis data] at the beginning (T0) and at the end (T1) of the treatment. In the RG no differences were found in the GPS, but there were significant improvements in some GVSs (Pelvic Obl and Hip Ab-Add). The IG showed no statistically significant changes in either GPS or GVSs. The end-effector robotic rehabilitation locomotor training improved gait kinematics and seems to be effective for rehabilitation in patients with mild PD.

Evidence of different spinal pathways for the warmth evoked potentials.

OBJECTIVE: To investigate the presence of multiple spinothalamic pathways for warmth in the human spinal cord. METHODS: Laser evoked potentials to C-fiber stimulation (C-LEPs) were recorded in 15 healthy subjects after warmth stimulation of the dorsal midline at C5, T2, T6, and T10 vertebral levels. This method allowed us to calculate the spinal conduction velocity (CV) in two different ways: (1) the reciprocal of the slope of the regression line was obtained from the latencies of the different C-LEP components, and (2) the distance between C5 and T10 was divided by the latency difference of the responses at the two sites. In particular, we considered the C-N1 potential, generated in the second somatosensory (SII) area, and the late C-P2 response, generated in the anterior cingulate cortex (ACC). RESULTS: The calculated CV of the spinal fibers generating the C-N1 potential (around 2.5m/s) was significantly different (p<0.01) from the one of the pathway producing the P2 response (around 1.4m/s). CONCLUSIONS: Our results suggest that the C-N1 and the C-P2 components are generated by two parallel spinal pathways. SIGNIFICANCE: Warmth sensation is subserved by parallel spinothalamic pathways, one probably reaching the SII area, the other the ACC.

Inhibitory effect of voluntary movement preparation on cutaneous heat pain and laser-evoked potentials.

In our study, preparation of voluntary movement was used to physiologically activate the motor cortex areas and the effect of this activation on CO(2) laser-evoked potentials (LEPs) was explored. LEPs were recorded from 31 scalp electrodes in 10 healthy subjects after painful stimulation of the right C6-C7 skin dermatomes. LEP stimuli were delivered in the time interval between a visual warning stimulus followed after 1 s. by an imperative stimulus. The imperative stimulus triggered: (i) no task in the baseline condition (Pain); (ii) flexion-extension movements of the second finger of the right hand in the movement condition (Pain + Movement); (iii) cognitive task (mathematic computation) in the distraction condition (Pain + Cognition). The experimental conditions were also repeated during application of laser stimuli on the left C6-C7 skin dermatomes. Compared with the baseline condition (no task required), during preparation of right-hand voluntary movement there was a significant reduction in LEP amplitude and subjective pain rating after right- but not after left-hand stimulation, which suggests that the observed effect cannot be attributed to a nonspecific reduction in attention toward painful stimulus. During preparation of a cognitive task, LEP amplitude was reduced compared to baseline. Our results represent the first neurophysiological suggestion that physiological activation of the motor cortex, occurring during movement preparation, inhibits cortical pain processing by a centrifugal mechanism.

Modulation of laser-evoked potentials by experimental cutaneous tonic pain.

The present study aimed to investigate whether tonic cutaneous pain exerts any effect on the cortical processing of nociceptive input and if this effect may involve only body parts in pain. Tonic cutaneous pain was obtained in nine healthy human subjects by infusion of a hypertonic saline (5%) in the s.c. tissue over the hypothenar muscles (10 ml/h for 20 min). Nociceptive cutaneous CO2 laser-evoked potentials were recorded after stimulation of the right hand dorsum, which was adjacent to the painful area, and the right perioral region, corresponding to the adjacent cortical sensory area. Laser-evoked potentials were obtained before saline injection, at the peak pain and 20 min after pain disappeared. During saline infusion, the laser-evoked pain to right hand stimulation was reduced and the vertex laser-evoked potentials (N2a-P2, mean latency 181 ms and 319 ms for the N2a and the P2 potentials, respectively), which are generated in the anterior cingulate cortex, were significantly decreased in amplitude compared with the baseline. Moreover, the topography of these potentials was modified by cutaneous pain, shifting from the central toward the parietal region. Dipolar modeling showed that the dipolar source in the anterior cingulate cortex moved backward during saline infusion. This result suggests that cutaneous pain may modify the relative activities of the anterior and posterior anterior cingulate cortex parts, which are thought to be devoted to encode different aspects of pain sensation. No laser-evoked potential change was observed after stimulation of the right perioral region, suggesting that functional changes in the nociceptive system are selective for the painful regions and not for areas with cortical proximity.

Segmental inhibition of cutaneous heat sensation and of laser-evoked potentials by experimental muscle pain.

The aim of the study was to evaluate the effect of tonic muscle pain evoked by injection of 5% hypertonic saline in the right brachioradialis muscle on the somatosensory sensation of laser-evoked heat pain and laser-evoked potentials. The heat pain pathways were studied in 9 healthy human subjects by recording the scalp potentials evoked by CO(2) laser stimuli delivered on four sites: the skin above the right brachioradialis muscle (ipsilateral local pain), the wrist area where muscle pain was referred in all subjects (ipsilateral referred pain), and two areas on the left arm symmetrical to both local and referred pain (contralateral local pain and contralateral referred pain). Laser-evoked potentials were obtained from 31 scalp electrodes before saline injection, during saline infusion (bolus injection with 0.3 ml saline infused over 20 s, followed by a steady infusion rate of 30 ml/h for the next 25 min), and 20 min after muscle pain had disappeared. While the early N1/P1 component (around 130 ms and 145 ms of latency after stimulation of the skin over the brachioradialis muscle and the wrist, respectively) was not affected by muscle pain, the amplitudes of the later vertex laser-evoked potentials (N2 latency of around 175 ms and 210 ms after stimulation of the skin over the brachioradialis muscle and the wrist, respectively; P2 latency of around 305 ms and 335 ms after stimulation of the skin over the brachioradialis muscle and the wrist, respectively) evoked from ipsilateral local pain, ipsilateral referred pain, and contralateral local pain sites were significantly decreased during muscle pain compared with the baseline recording, while they recovered after pain had disappeared. At the same stimulation sites, the rating of the laser-evoked pain sensation was reduced significantly during muscle pain as compared with the baseline and it recovered after pain had disappeared. On the contrary, muscle pain did not show any effect on both laser-evoked pain and laser-evoked potential amplitude when the contralateral referred pain site was stimulated. The muscle pain inhibitory effect on both heat pain sensation and laser-evoked potential amplitude is probably mediated by an ipsilateral and contralateral segmental mechanism which acts also on the referred pain area, while more general inhibitory mechanisms, such as a distraction effect or a diffuse noxious inhibitory control, are excluded by the absence of any effect of muscle pain on laser-evoked pain and laser-evoked potentials obtained from a remote site, such as the contralateral referred pain area. Since muscle pain induced by hypertonic saline injection is very similar to clinical pain, our results can be useful in understanding the pathophysiology of the somatosensory modifications which can be observed in patients with musculoskeletal pain syndromes.

Reduced habituation to experimental pain in migraine patients: a CO(2) laser evoked potential study.

The habituation to sensory stimuli of different modalities is reduced in migraine patients. However, the habituation to pain has never been evaluated. Our aim was to assess the nociceptive pathway function and the habituation to experimental pain in patients with migraine. Scalp potentials were evoked by CO(2) laser stimulation (laser evoked potentials, LEPs) of the hand and facial skin in 24 patients with migraine without aura (MO), 19 patients with chronic tension-type headache (CTTH), and 28 control subjects (CS). The habituation was studied by measuring the changes of LEP amplitudes across three consecutive repetitions of 30 trials each (the repetitions lasted 5 min and were separated by 5-min intervals). The slope of the regression line between LEP amplitude and number of repetitions was taken as an index of habituation. The LEPs consisted of middle-latency, low-amplitude responses (N1, contralateral temporal region, and P1, frontal region) followed by a late, high-amplitude, negative-positive complex (N2/P2, vertex). The latency and amplitude of these responses were similar in both patients and controls. While CS and CTTH patients showed a significant habituation of the N2/P2 response, in MO patients this LEP component did not develop any habituation at all after face stimulation and showed a significantly lower habituation than in CS after hand stimulation. The habituation index of the vertex N2/P2 complex exceeded the normal limits in 13 out of the 24 MO patients and in none of the 19 CTTH patients (P<0.0001; Fisher's exact test). Moreover, while the N1-P1 amplitude showed a significant habituation in CS after hand stimulation, it did not change across repetitions in MO patients. In conclusion, no functional impairment of the nociceptive pathways, including the trigeminal pathways, was found in either MO or CTTH patients. But patients with migraine had a reduced habituation, which probably reflects an abnormal excitability of the cortical areas involved in pain processing.

Unmyelinated trigeminal pathways as assessed by laser stimuli in humans.

Laser pulses excite superficial free nerve endings innervated by small-myelinated (Adelta) and unmyelinated (C) fibres. Whereas laser-evoked scalp potentials (LEPs) are now reliably used to assess function of the Adelta-fibre nociceptive pathways in patients with peripheral or central lesions, the selective activation of C-fibre receptors and recording of the related brain potentials remain difficult. To investigate trigeminal C-fibre function, we directed laser pulses to the facial skin and studied sensory perception and scalp evoked potentials related to Adelta- or C-fibre activation in healthy humans and patients--one having a bilateral facial palsy, two a trigeminal neuropathy, and two a Wallenberg syndrome. We also measured afferent conduction velocity and, with source analysis, studied the brain generators. Whereas laser pulses of low intensity and small irradiated area elicited pinprick sensations and standard Adelta-LEPs, laser pulses of very-low intensity and large irradiated area elicited warmth sensations and scalp potentials with a latency compatible with C-fibre conduction (negative wave 280 ms, positive wave 380 ms); the estimated conduction velocity was 1.2 m/s. The main waves of the scalp potentials originated from the anterior cingulate gyrus; they were preceded by activity in the opercular region and followed by activity in the insular region. The patient with bilateral facial palsy, who had absent trigeminal-facial reflexes, had normal Adelta- and C-related scalp potentials; the patients with trigeminal neuropathy, characterized by loss of myelinated and sparing of unmyelinated fibres, had absent Adelta- but normal C-related potentials; and the patients with Wallenberg syndrome had absent Adelta- and C-related potentials. We conclude that laser pulses with appropriate characteristics evoke brain potentials related to the selective activation of trigeminal nociceptive Adelta or thermal C fibres. The trigeminal territory yields rewarding LEP findings owing to the high density of thermal receptors and, because the short conduction distance, minimizes the problem of signal dispersion along slow-conducting unmyelinated afferents. The opercular-insular region and the cingulate gyrus are involved in the processing of C-fibre trigeminal inputs. The method we describe may prove useful in patients with lesions affecting the trigeminal thermal pain pathways.

Source generators of the early somatosensory evoked potentials to tibial nerve stimulation: an intracerebral and scalp recording study.

OBJECTIVE: To investigate the location of the cerebral generators of the early scalp somatosensory evoked potentials (SEPs) after tibial nerve stimulation. METHODS: Tibial nerve SEPs were recorded in 15 patients, suffering from Parkinson's disease, who underwent implantation of intracerebral (IC) electrodes in the subthalamic nucleus, in the globus pallidum or in the thalamic ventralis intermediate nucleus. SEPs were recorded both from the scalp surface and from the IC leads. RESULTS: The lemniscal P30 response was recorded by all the electrodes. The IC waveforms included a negative N40IC response, followed by a positive (P50IC) and a negative (N60IC) potential. The N40IC, the P50IC and the N60IC potentials did not differ in latency from the P40, the N50 and the P60 responses recorded by the Cz electrode. In 6 patients, in which SEPs were recorded also during the voluntary movement of the stimulated foot (active gating), an amplitude reduction of the SEP components following the P30 potential was observed during movement at the vertex and in the IC traces. Instead, in the contralateral temporal traces the SEP components (N40temp and P50temp) were not modified by active gating, and in the ipsilateral parietal traces only the positive potentials at about 60ms of latency was decreased. CONCLUSIONS: Two differently oriented generators are active in the contralateral hemisphere at both 40 and 50ms of latency after tibial nerve stimulation. One source is oriented perpendicularly to the mesial hemispheric surface and generates the potentials recorded by the contralateral temporal and the ipsilateral parietal leads; the other dipolar source is radial to the hemispheric convexity, and generates the potentials at the vertex and those recorded by the IC electrodes.

Inhibition of motor system excitability at cortical and spinal level by tonic muscle pain.

OBJECTIVE: To assess whether the motor system excitability can be modified by experimental tonic pain induced either in muscles or in subcutis. METHODS: Transcranial magnetic stimulation of the left primary motor cortex was used to record motor evoked potentials (MEPs) from the right abductor digiti minimi (ADM) muscle. Recordings were made before, during and after experimental pain induced by (1) injection of hypertonic (5%) saline into the right ADM, the right first dorsal interosseum (FDI) and the left ADM muscles, and (2) injection of hypertonic saline in the subcutaneous region of the right ADM. Both MEPs and H-reflex were recorded also from the right flexor carpi radialis (FCR) before, during and after muscle pain. RESULTS: MEPs recorded from the ADM muscle were significantly reduced in amplitude during pain induced in the right ADM and right FDI muscles, but not during pain in the left ADM muscle or during subcutaneous pain. This inhibitory effect was observed during the peak-pain and persisted also after the disappearance of the pain sensation. In the FCR muscle, the MEP inhibition was observed during the peak-pain, while a significant reduction of the H-reflex's amplitude was observed starting 1 min after the peak-pain. CONCLUSIONS: Tonic muscle pain can inhibit the motor system. The motor cortex inhibition observed at an early phase is followed by a reduction of the excitability of both cortical and spinal motoneurones.

Inhibition of biceps brachii muscle motor area by painful heat stimulation of the skin.

ract This study aimed to evaluate whether painful cutaneous stimuli can affect specifically the excitability of the arm proximal muscle motor area. The motor evoked potentials (MEPs), recorded from the right biceps brachii muscle after either transcranial magnetic or electrical anodal stimulation of the left primary motor (MI) cortex, were conditioned by painful CO2 laser stimuli delivered either on the right hand dorsum or on the lateral surface of the right arm. Painful CO2 laser stimuli delivered on the hand skin reduced significantly the amplitude of MEPs evoked by the transcranial magnetic stimulation of the contralateral MI area, while the MEP amplitude was not significantly modified by CO2 laser pulses delivered on the arm skin. The inhibitory effect followed the arrival of the nociceptive inputs to the cerebral cortex. The amplitude of MEPs evoked by anodal electrical stimulation of the motor cortex was not decreased by conditioning painful stimuli delivered on the hand dorsum. Since the magnetic stimulation led to transynaptic activation of pyramidal neurons, while the anodal stimulation activated directly corticospinal axons, our findings suggest that CO2 laser pulses delivered on the hand are able to inhibit the arm proximal muscle motor area.

Characterizing somatosensory evoked potential sources with dipole models: advantages and limitations.

Several methods have been developed to investigate the cerebral generators of scalp somatosensory evoked potentials (SEPs), because simple visual inspection of the electroencephalographic signal does not allow for immediate identification of the active brain regions. When the neurons fired by the afferent inputs are closely grouped, as usually occurs in SEP generation, they can be represented as a dipole, that is, as a linear source with two opposite poles. Several techniques for dipolar source modeling, which use different algorithms, have been employed to build source models of early, middle-latency, and late cognitive SEPs. Modifications of SEP dipolar activities after experimental maneuvers or in pathological conditions have also been observed. Although the effectiveness of dipolar source analysis should not be overestimated due to the intrinsic limitations of the approach, dipole modeling provides a means to assess SEPs in terms of cerebral sources and voltage fields that they produce over the head.

Functional changes of the primary somatosensory cortex in patients with unilateral cerebellar lesions.

Although cerebellar lesions do not cause evident sensory deficits, it has been suggested recently that the cerebellum might play a role in sensory acquisition and discrimination. To determine whether the cerebellum influences the early phases of cortical somatosensory processing, we recorded cortical somatosensory evoked potentials after median nerve stimulation in five patients with unilateral cerebellar damage. We also performed a dipolar source analysis of traces by means of brain electrical source analysis. In all patients, the amplitude of the frontal N24 and parietal P24 components, as well as the strength of the corresponding dipolar sources, were significantly smaller after stimulation of the symptomatic side. These neurophysiological findings indicate that the primary somatosensory cortical processing is altered after contralateral cerebellar damage. They represent the first indication of a possible substrate for the reduction in cerebral blood flow observed in the parietal cortex after cerebellar lesion. Furthermore, the present data allow characterization of the functional influence of the cerebellar input to the primary somatosensory cortex as specifically acting over the inhibitory components of somatosensory processing.

Long-lasting effect evoked by tonic muscle pain on parietal EEG activity in humans.

OBJECTIVE: To explore EEG changes evoked by tonic experimental muscle pain compared to a non-painful vibratory stimulus. METHODS: Thirty-one EEG channels were recorded before, during and after painful and non-painful stimulation. Pain was induced in the left brachioradialis muscle by injection of hypertonic (5%) saline. The vibratory stimulus was applied to the skin area overlying the brachioradialis muscle. The power of the major frequency components of the EEG activity (FFT, fast Fourier transform) was quantified and t-maps between the different experimental conditions were evaluated in frequency domain. RESULTS: The main effect of muscle pain, compared to non-painful stimulation, was a significant and long-lasting increase of delta (1-3 Hz) power and an alpha-1 (9-11 Hz) power increase over the contralateral parietal locus. This finding could suggest a decreased excitability of the primary somatosensory cortex during muscle pain. The main effect of vibration, compared to its unstimulated baseline, consisted in an increase of beta-1 (14-20 Hz) power in the right frontal region. CONCLUSIONS: Our data demonstrate significant and specific topographic EEG changes during tonic muscle pain. Since these modifications differ from those produced by an unstimulated baseline and during non-painful tonic stimulation, they might reflect mechanisms involved in the processing of nociceptive and adverse tonic stimuli.

Unmasking of an early laser evoked potential by a point localization task.

OBJECTIVES: The investigation of the CO(2) laser evoked potential (LEP) modifications following a point localization task. METHODS: LEPs were recorded from 10 healthy subjects in two different conditions. (1) Task condition: laser stimuli were shifted among 3 different locations on the right hand dorsum, and the subjects were asked to identify the stimulated area. The mean error rate in point localization was 4.5%. (2) Non-task condition: laser pulses were delivered on the first intermetacarpal space, and the subject was asked to count the number of stimuli. The mean error rate in counting was 5.8%. RESULTS: In the task condition, the temporal traces contralateral to the stimulation showed an early positive component (eP, mean peak latency 83 ms) preceding the N1 negativity (mean peak latency 144 ms). At the eP peak latency, topographic maps showed a positivity highly focused on the contralateral temporal region. In the non-task recordings no reliable response was identifiable before the N1 potential. CONCLUSIONS: While no LEP component earlier than the middle-latency N1 potential can be recorded in the non-task condition, a positive response (eP) preceding the N1 component is identifiable in the contralateral temporal region during the spatial localization of painful stimuli. The eP scalp distribution is compatible with its origin from a radial source in the second somatosensory (or insular) area, thus suggesting that the opercular cortex is involved not only in the middle-latency (N1 potential), but also in early pain processing.

Dipolar source modeling of somatosensory evoked potentials to painful and nonpainful median nerve stimulation.

Dipolar source modeling might help in clarifying whether somatosensory evoked potentials (SEPs) after electrical stimulation at painful intensity contain any information related to the nociceptive processing. SEPs were recorded after left median nerve stimulation at three different intensities: intense but nonpainful (intensity 2); slightly painful (pain threshold; intensity 4); and moderately painful (intensity 6). Scalp SEPs at intensities 2, 4, and 6 were fitted by a five-dipole model. When the strength modifications of the source activities up to 40 ms were examined across the different stimulus intensities, no significant difference was found. In the later epoch (40-200 ms), a posterior parietal dipole and two bilateral sources probably located in the second somatosensory (SII) areas increased significantly their dipole moments when the stimulus was increased from 2 to 4 and became painful. Since no difference was found when the stimulus intensity was increased from 4 to 6, the observed increase of the dipolar strengths is probably related to a variation of the stimulus quality (nonpainful vs. painful), rather than of the stimulus intensity per se. Our findings lead us to conclude that a large convergence of nociceptive and non-nociceptive afferents probably occurs bilaterally in the SII areas.

Scalp distribution of the earliest cortical somatosensory evoked potential to tibial nerve stimulation: proposal of a new recording montage.

OBJECTIVE: To investigate the most reliable method to record the earliest cortical somatosensory evoked potential (SEP) after tibial nerve stimulation. The 'gating' phenomenon was used to dissociate the overlapping cortical SEP components. METHODS: In 11 subjects we recorded the scalp SEPs at rest, during the voluntary (active gating) and passive (passive gating) foot movement and during the isometric calf muscle contraction (isometric gating). RESULTS: At the vertex the P40 amplitude was reduced in all the gating conditions. Instead, both the P40 response recorded in the parietal region ipsilateral to the stimulation (indicated as P40par) and the fronto-temporal N37 potential were reduced in amplitude only during the passive foot movement. CONCLUSIONS: The same behaviour of the N37 and P40par potentials suggests that they can represent the opposite counterparts of the same dipolar generator. Instead, the real P40 amplitude, which is affected in all the gating conditions, is recorded at the vertex and might be generated by a different source. We conclude that the montage obtained by referring a temporal electrode contralateral to the stimulation to an ipsilateral parietal lead can reliably record the earliest cortical component (N37/P40par) after tibial nerve stimulation.

Somatosensory evoked potentials after multisegmental lower limb stimulation in focal lesions of the lumbosacral spinal cord.

OBJECTIVES: Recording techniques permit the separate analysis of the response from cauda equina roots and the spinal potential that is probably generated by the activation of dorsal horn cells. To improve the functional assessment of focal lesions of the lumbosacral cord, lower limb somatosensory evoked potentials (SEPs) were measured by multisegmental stimulation. METHODS: Common peroneal and tibial nerves SEPs were recorded in 14 patients in whom MRI demonstrated compressive cord damage ranging from T9 to L1 levels. SEPs were recorded in each patient at the lumbar level (cauda equina response), lower thoracic level (spinal response), and from the scalp (cortical response). RESULTS: Abnormalities in spinal response occurred in 50% and 70% of tibial and common peroneal nerve SEPs respectively; these findings were well explained by the radiological compression level, involving in most of the patients lumbar rather than sacral myelomeres. The SEPs were often more effective than the clinical examination in showing the actual extension of damage. CONCLUSIONS: The recording of spinal SEPs after multisegmental lower limb stimulation proved useful in assessing cord dysfunction and determining the cord levels mainly involved by the compression.

Sources of cortical responses to painful CO(2) laser skin stimulation of the hand and foot in the human brain.

OBJECTIVES: To investigate whether the same dipolar model could explain the scalp CO(2) laser evoked potential (LEP) distribution after either hand or foot skin stimulation. METHODS: LEPs were recorded in 14 healthy subjects after hand and foot skin stimulation and brain electrical source analysis of responses obtained in each individual was performed. RESULTS: A 5 dipolar sources model explained the scalp LEP topography after both hand and foot stimulation. In particular, we showed that the co-ordinates of the two earliest activated dipoles were compatible with source locations in the upper bank of the Sylvian fissure on both sides. These sources did not change their location when the stimulation site was moved from the upper to the lower limb. The other 3 dipoles of our model were activated in the late LEP latency range with a biphasic profile and a location compatible with activation of the cingulate gyrus and deep temporo-insular structures. CONCLUSIONS: The dipolar model previously proposed for the hand stimulation LEPs can also satisfactorily explain the LEP distribution obtained after foot stimulation. The earliest activated Sylvian dipolar sources did not change their location when the upper or lower limb was stimulated, as expected from the close projections of hand and foot in the second somatosensory area. No source in the primary somatosensory area was necessary to model the scalp topography of LEPs to hand and foot stimulation.

Effect of movement on dipolar source activities of somatosensory evoked potentials.

The early scalp somatosensory evoked potentials (SEPs) to median and tibial nerve stimulation were recorded at rest and during voluntary movement of the stimulated hand and foot, respectively. Both tibial and median nerve SEP distributions at rest could be explained by four-dipole models, in which one dipole was activated at the same latency as the subcortical far field and the three remaining dipolar sources were located in the perirolandic region contralateral to the stimulated side. Voluntary movement reduced all cortical dipoles in strength, while the subcortical one remained unchanged, suggesting that the effect of movement occurs above the cervicomedullary junction. In animals, cutaneous inputs are suppressed during movement and we therefore interpreted the depression of activity in the primary somatosensory cortex induced by movement as due to selective "gating" of cutaneous afferents. Because the reduction in strength of the cortical dipoles was generally lower during passive than active movement, both centrifugal and centripetal mechanisms probably contribute to the phenomenon of "gating."

Inhibition of the human primary motor area by painful heat stimulation of the skin.

OBJECTIVE: To prove whether painful cutaneous stimuli can affect specifically the motor cortex excitability. METHODS: The electromyographic (EMG) responses, recorded from the first dorsal interosseous muscle after either transcranial magnetic or electric anodal stimulation of the primary motor (MI) cortex, was conditioned by both painful and non-painful CO2 laser stimuli delivered on the hand skin. RESULTS: Painful CO2 laser stimuli reduced the amplitude of the EMG responses evoked by the transcranial magnetic stimulation of both the contralateral and ipsilateral MI areas. This inhibitory effect followed the arrival of the nociceptive inputs to cerebral cortex. Instead, the EMG response amplitude was not significantly modified either when it was evoked by the motor cortex anodal stimulation or when non-painful CO2 laser pulses were used as conditioning stimuli. CONCLUSIONS: Since the magnetic stimulation leads to transynaptic activation of pyramidal neurons, while the anodal stimulation activates directly cortico-spinal axons, the differential effect of the noxious stimuli on the EMG responses evoked by the two motor cortex stimulation techniques suggests that the observed inhibitory effect has a cortical origin. The bilateral cortical representation of pain explains why the painful CO2 laser stimuli showed a conditioning effect on MI area of both hemispheres. Non-painful CO2 laser pulses did not produce any effect, thus suggesting that the reduction of the MI excitability was specifically due to the activation of nociceptive afferents.