Median nerve somatosensory evoked potentials. Apomorphine-induced transient potentiation of frontal components Clin. Parkinson's disease and in parkinsonism

Somatosensory evoked potentials (SEPs) to median nerve stimulation have been recorded from parietal and frontal districts Clin. 43 parkinsonians, 17 patients with parkinsonism and 35 healthy controls matched for age and sex. Latency/ amplitude characteristics of the parietal P14-N20-P25 and of the frontal P20-N30-P40 wave complexes before and after (10, 20, 30 and 60 min) subcutaneous administration of apomorphine chloride were evaluated Clin. all the 60 patients and Clin. 3 controls. The frontal waves N30 and P40 were either absent or significantly smaller than normal Clin. 31 patients with Parkinson's disease (PD) (72.1%) and Clin. 9 with parkinsonism Clin. baseline records (56.3%). Following apomorphine, the parietal deflections did not significantly vary Clin. amplitude. On the contrary, the frontal complex showed a significant amplitude increase Clin. 27 PD and 8 parkinsonisms (respectively 62.8 and 47.1%): 79.1% of PD and 35.3% of parkinsonisms were improved clinically. Amplitude increase was evident at 10 min after apomorphine, Clin. parallel with clinical improvement, and vanished nearly Clin. coincidence with the end of the clinical effect.     

Enhanced amplitude reduction of somatosensory evoked potentials by voluntary movement in the elderly

We studied the effects of aging on modification of the median nerve somatosensory evoked potentials (SEPs) by voluntary movement in 17 aged (66.5±8.9 years, mean±SD) and 12 young normal humans (27.5±5.0 years). The amplitudes of cortical SEP components were generally larger in the aged group than in the young group. Following isometric contraction of the thenar muscle, the aged group showed significant attenuation of the prerolandic P22-N28-P45 and the postrolandic P24-N30-P45, while the young group only demonstrated significant reduction of the prerolandic P22-N28 amplitude. In the prerolandic N28-P45 and the postrolandic P24-N30 and N30-P45, amplitudes reduced by voluntary movement (gated amplitude) significantly correlated with amplitudes at rest (resting amplitude) and with the age of subjects. The effects of stimulus intensity and frequency on gating supported the correlative changes between gated and resting amplitudes. These results suggest that the magnitude of gating depends on SEP amplitudes at rest, and that augmented gating in the aged group is a result of enlarged SEPs. Since the cervical and Erb's potentials were not changed by movement, and passive movement did not significantly affect the SEPs, a centrifugal mechanism is probably responsible for gating in this study.     

Effect of manipulation and fractionated finger movements on subcortical sensory activity in man

Previous studies have shown that the somatosensory evoked potentials (SEPs) recorded from the scalp are modified or gated during motor activity in man. Animal studies show corticospinal tract terminals in afferent relays, viz. dorsal horn of spinal cord, dorsal column nuclei and thalamus. Is the attenuation of the SEP during movement the result of gating in subcortical nuclei? This study has investigated the effect of manipulation and fractionated finger movements of the hand on the subcortically generated short latency SEPs in 9 healthy subjects. Left median nerve SEPs were recorded with electrodes optimally placed to record subcortical activity with the least degree of contamination. There was no statistically significant change in amplitude or latency of the P9, N11, N13, P14, N18 and N20 potentials during rest or voluntary movement of the fingers of the left hand or manipulation of objects placed in the hand. The shape of the N13 wave form was not modified during these 3 conditions. It is concluded that in man attenuation of cortical waves during manipulation is not due to an effect of gating in the subcortical sensory relay nuclei.     

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.     

Entacapone Reduces Cortical Activation in Parkinson's Disease with Wearing-Off: A f-MRI Study

Background and Purpose

Wearing-off is one of the most frequent problems encountered by levodopa-treated patients. Entacapone, a peripheral inhibitor of catechol-O-methyltransferase (COMT), reduces this motor complication by prolonging the effect of levodopa. We sought to understand the impact of COMT-inhibition on movement execution in PD patients with wearing-off by comparing functional magnetic resonance imaging (f-MRI) activation patterns prior to and during entacapone treatment. Our hypothesis was to determine whether changes in cortical activation are associated to COMT-inhibitor treatment.

Methods

Nine levodopa-treated non-demented PD patients with wearing-off were prospectively studied in two f-MRI session, prior to and during entacapone treatment. A group of control subjects were also studied for comparison.

Results

The patients significantly improved under COMT-inhibitor treatment based on home diaries. F-MRI results showed that at baseline the patients presented a bilateral activation of the primary motor, controlateral premotor cortex and supplementary motor area, as well as ipsilateral cerebellum. During treatment with entacapone, PD patients showed reductions in the activations of these cortical areas and a decreased activation in the ipsilateral cerebellum.

Conclusions

Our preliminary findings indicate that f-MRI is able to detect cortical activation changes during long-term modulation of dopaminergic treatment in PD patients with wearing-off, and thus, this technique could be further investigated in advanced PD patients.     

Bit-mapped somatosensory evoked potentials and muscular reflex responses in man: comparative analysis in different experimental protocols

Bit-colour maps of somatosensory evoked potentials (SEPs) and muscular responses from forearm and hand muscles were simultaneously recorded after median nerve stimulation. Subjects were asked either to relax totally (A), or to contract the examined muscle continuously and isometrically at 10–20% (B) and 80–100% (C) of the maximal strength. Isotonic contractions ipsilateral (D) and contralateral to the stimulus (E) were also examined. Both SEPs and EMG responses were elicited by individual near-motor threshold pulses delivered at 0.2/sec to the median nerve at the elbow. SEPs were maximal in amplitude during complete relaxation, whilst all the components following the parietal N20 were depressed by muscle contraction. Such decrements affected predominantly the parietal and frontal peaks of positive polarity during condition B, whilst the frontal negative component (wave N30) dropped remarkably in conditions C and D. Early EMG responses (V1 = spinal circuitry) were usually absent in condition A; they were present together with later components (= V2 possibly long-loop, transcortical circuitry) in C and D, whilst they were alone recordable in B and E. The amplitudes of the frontal wave N30 in SEPs and of V2 in LLRs were inversely correlated. This observation is consistent with the hypothesis that a change in the reactivity of the sensorimotor brain areas to afferent impulses is coupled to LLR elicitation in forearm and hand muscles.     

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.     

Peri-rolandic and fronto-parietal components of scalp-recorded giant SEPs in cortical myoclonus

Scalp topography of giant SEPs to median nerve stimulation was studied in 4 patients with cortical myoclonus of various etiology. The positive peak (P30) at the contralateral parietal area was simultaneously accompanied by a negative peak at the frontal area (N30), and at least one of these two peaks was enhanced in 2 patients. Another positive peak (P25) and a negative peak (N35) were also identified at the peri-rolandic area with different latency from P30 and N30, respectively, in all patients. N35 was enhanced in 3 patients, and P25 in 2 patients. It is concluded that, as seen in normal subjects, tangential (P30-N30) and radial (P25 and N35) components of SEPs are most likely distinguishable in giant SEPs, and that either one or both of those components is enhanced in different ways depending on the patients.     

Sensory Attenuation Assessed by Sensory Evoked Potentials in Functional Movement Disorders

Background

Functional (psychogenic) movement disorders (FMD) have features associated with voluntary movement (e.g. distractibility) but patients report movements to be out of their control. One explanation for this phenomenon is that sense of agency for movement is impaired. The phenomenon of reduction in the intensity of sensory experience when movement is self-generated and a reduction in sensory evoked potentials (SEPs) amplitude at the onset of self-paced movement (sensory attenuation) have been linked to sense of agency for movement.

Methods

We compared amplitude of SEPs from median nerve stimulation at rest and at the onset of a self-paced movement of the thumb in 17 patients with FMD and 17 healthy controls.

Results

Patients showed lack of attenuation of SEPs at the onset of movement compared to reduction in amplitude of SEPs in controls. FMD patients had significantly different ratios of movement onset to rest SEPs than did healthy controls at each electrode: 0.79 in healthy controls and 1.35 in patients at F3 (t = -4.22, p<0.001), 0.78 in healthy controls and 1.12 at patients C3 (t = -3.15, p = 0.004) and 0.77 in healthy controls and 1.05 at patients P3 (t = -2.88, p = 0.007).

Conclusions

Patients with FMD have reduced sensory attenuation as measured by SEPs at onset of self-paced movement. This finding can be plausibly linked to impairment of sense of agency for movement in these patients.     

Abnormalities of short-latency somatosensory evoked potentials in parkinsonian patients

Twenty-two patients (16 affected by parkinsonian syndromes, 6 by other neurological diseases) and 12 age-matched controls were examined. Short-latency somatosensory evoked potentials were recorded from 30 scalp electrodes in the 45–52 msec following separate left and right median nerve stimulation at the wrist. Bit-colour maps were generated on a 4096 pixel matrix via quadratic interpolation. Peak latencies and amplitudes of the parietal, central and frontal components were evaluated. Moreover, the amplitude ratios between parietal and frontal components on the same hemiscalp and between peaks on homologous right and left scalp districts were taken into account. The unique significant difference between parkinsonians and controls was represented by a depressed frontal N₃₀ wave. This peak was absent in 3 and reduced in 7 out of 16 parkinsonians, with an overall abnormality rate of 47% of the examined arms. Average maps pooling data of parkinsonians and controls confirmed the presence of reduced evoked activity for the whole duration of wave N₃₀ on those mid- and parasgittal frontal districts where this peak is maximally represented in normals. A similar abnormality was found in 1 of the 6 non-parkinsonian neurological patients suffering from a meningioma of the falx compressing the left supplementary motor area. Possible pathophysiology of such wave N₃₀ abnormalities in parkinsonians is discussed.     

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.     

Recovery function of somatosensory evoked potentials in juvenile myoclonic epilepsy*

Abstract

Objective: We analysed the recovery function of somatosensory evoked potentials (SEPs) in juvenile myoclonic epilepsy (JME) patients. We hypothesized that there may be disinhibition in the recovery of SEPs at 20–100?ms intervals in JME patients.

Methods: We recorded SEPs and SEP recovery in 19 consecutive patients with JME admitted for a routine follow-up examination, and in a control group composed of 13 healthy subjects who were similar to the patient group regarding age and sex. The recovery function of SEPs was examined using paired stimuli at 30, 40, 60, and 100?ms intervals.

Results: The amplitudes of N20-P25 and P25-N33 components were higher in patients with JME. Ten patients had high-amplitude SEPs. By paired stimulation, there was inhibition of SEPs in both groups. The mean recovery percentages of N20-P25 and P25-N33 components at 30, 40, 60, and 100?ms were not different between healthy subjects and patients with JME.

Conclusions: The recovery function of SEP is normal in JME even in the presence of high-amplitude SEPs.     

SEPs in two patients with localized lesions of the postcentral gyrus

Scalp distributions of median nerve SEPs were studied in normal controls and 2 patients with localized lesions of the postcentral gyrus. In controls, parieto-occipital electrodes registered N20-P27 while frontal electrodes registered P20-N27. Other small components, parieto-occipital P22 and frontal N22, were recognized in about half of the control records. The wave forms at a frontal and a parieto-occipital electrode, both distant from the central region, formed exact mirror images of each other concerning N20-(P22)-P27 and P20-(N22)-N27. Electrodes near the central region contralateral to the stimulation registered cP22-cN30 (central P22 and central N30). When the postcentral gyrus was damaged, N20/P20-P27/N27 and cP22-cN30 were eliminated and the only remaining components were a frontal negative wave (frN) and a contralateral parieto-occipital positive wave (poP). Digital nerve stimulation also evoked poP and frN in both cases. In case 2, poP coincided with P22 of the non-affected side. The following generators were proposed; N20/P20-P27/N27: area 3b, cP22-cN30: areas 1 and 2, poP/early frN (= P22/N22): area 4 at the anterior wall of the central sulcus (due to direct thalamic inputs to motor cortex), late frN: uncertain (SMA?, SII?).     

Giant central N20-P22 with normal area 3b N20-P20: an argument in favour of an area 3a generator of early median nerve cortical SEPs?

Generators of early cortical somatosensory evoked potentials (SEPs) still remain to be precisely localised. This gap in knowledge has often resulted in unclear and contrasting SEPs localisation in patients with focal hemispheric lesions. We recorded SEPs to median nerve stimulation in a patient with right frontal astrocytoma, using a 19-channel recording technique. After stimulation of the left median nerve, N20 amplitude was normal when recorded by the parietal electrode contralateral to the stimulation, while it was abnormally enhanced in traces obtained by the contralateral central electrode. The amplitude of the frontal P20 response was within normal limits. This finding suggests that two dipolar sources, tangential and radial to the scalp surface, respectively, contribute concomitantly to N20 generation. The possible location of the N20 radial source in area 3a is discussed. The P22 potential was also recorded with increased amplitude by the central electrode contralateral to the stimulation, while N30 amplitude was normal in frontal and central traces. We propose that the radial dipolar source of P22 response is independent from both N20 and N30 generators and can be located either in 3a or in area 4. This report illustrates the usefulness of multichannel recordings in diagnosing dysfunction of the sensorimotor cortex in focal cortical lesions.     

Somatosensory evoked potentials during long-term isometric muscle contraction

The effect of sustained isometric contraction on somatosensory evoked potentials (SEPs) was studied. An attenuation of early SEP components N20--P30, P30--N35) was observed during the last minute of the endurance time. The late components (P45--N55, N55--P100) showed a significant increase of the amplitude during the first minute of the contraction. The amplitude of N35--P45 did not change during voluntary contraction, although it was decreased immediately after the contraction. An increase of the integrated EMG of forearm flexors was observed in the last minute of the endurance time. The maximal voluntary contraction was decreased immediately after the sustained contraction. The observed changes in SEPs could be attributed to possible changes in sensory information and motor command due to motor task.     

Upper limb H reflexes and somatosensory evoked potentials modulated by movement.

In the human lower limb, the magnitudes of both Hoffmann (H) reflexes and primary somatosensory evoked potentials (SEPs) from scalp electrodes, are reduced by active and/or passive movement. We surmised that similar effects occur for the upper limb and specifically hypothesised that amplitudes of median nerve induced flexor carpii radialis H reflexes and cortical SEPs are reduced with passive movement about the wrist or elbow. The results showed (P<0. 05) that either movement significantly attenuated mean magnitudes of SEPs elicited from stimulation at elbow or wrist and that reflex magnitudes attenuated with wrist movement. Thus, the upper limb shows similar movement-induced modulation to the lower limb. These attenuations of fast conducting sensory paths consequent to movement per se, may be a basic level of motor control, initiated from muscle mechanoreceptor discharge. Upon this basic level, more complex modulations then may be laid as appropriate for the particular characteristics of active motor tasks.     

Somatosensory cortex excitability changes due to differences in instruction conditions of motor imagery

Purpose Vivid motor imagery appears to be associated with improved motor learning efficiency. However, the practical difficulties in measuring vivid motor imagery warrant new analytical approaches. The present study aimed to determine the instruction conditions for which vividness in motor imagery could be more easily seen and the excitability of the sensory cortex as it relates to the motor image. Materials and methods In total, 15 healthy, right-handed volunteers were instructed to imagine grasping a rubber ball under a verbal-only instruction condition (verbal condition), a verbal?+?visual instruction condition (visual condition), and a verbal?+?execution (physically grasping a real ball) condition (execution condition). We analyzed motor imagery-related changes in somatosensory cortical excitability by comparing somatosensory-evoked potentials in each condition with the rest (control) condition. We also used a visual analogue scale to measure subject-reported vividness of imagery. Results We found the N33 component was significantly lower in the execution condition than in the rest condition (p?Conclusions These data suggest that experiencing a movement through actual motor execution immediately prior to performing mental imagery of that movement enhances the excitability of motor-related cortical areas. It is suggested that the excitability of the motor-related region increased as a result of the motor imagery in the execution condition acting on the corresponding somatosensory cortex.     

Dermatomal and mixed nerve somatosensory evoked potentials in the diagnosis of neurogenic thoracic outlet syndrome

To evaluate the diagnostic utility of dermatomal and mixed nerve somatosensory evoked potentials (SEPs) in patients with thoracic outlet syndrome (TOS) and to compare their value with routine electrodiagnostic methods, we studied a group of 44 patients with neurogenic TOS and 30 healthy controls. In addition to bilateral median and ulnar SEPs, evoked potentials were recorded after stimulation of C6 and C8 dermatomes from the first and fifth digits, respectively. The patients were classified into 3 groups according to the nature of their clinical condition. The abnormality rate for both ulnar and C8 dermatomal SEPs was 100% in a small group of patients with severe neurological signs like atrophy. In groups of patients with lesser degrees of neurogenic damage, abnormality rates for ulnar and C8 dermatomal SEPs on affected limb(s) were 67 and 50%, respectively. Same abnormality rates were 25 and 18% in patients with only subjective symptoms. In patients with objective neurological signs, the major increase in sensitivity was with electromyography (EMG). Abnormalities of routine nerve conduction studies and F-wave latency were observed in patients with severe neurogenic damage. We concluded that the most useful tests in the diagnosis of neurogenic TOS are needle EMG and ulnar SEPs.     

Mapping somatosensory evoked potentials to finger stimulation at intervals of 450 to 4000 msec and the issue of habituation when assessing early cognitive components

Somatosensory evoked potentials (SEPs) to mild electric stimulation of two fingers of the left hand were studied at regular interstimulus intervals (ISIs) of 450, 800, 1400, 2500 and 4000 msec. Habituation was evaluated while the subject was reading a novel so as to virtually ignore the finger stimuli while maintaining steady vigilance levels. Brain SEPs recorded from 25 scalp electrodes were assessed by scatter displays, electronic subtraction, bit-mapped potentials fields, and by calculating theZ estimator and dilation factor. Similar results were obtained with randomly varying ISIs. The P14 farfield and cortical N20 did not change with ISIs. The parietal P27–P45 decreased at ISIs of 800 and 450 msec, but showed no significant habituation at ISIs of 1400, 2500 or 4000 msec. This validated the control conditions used for assessing the early cognitive P30 and P40 to attended target stimuli. The frontal N30 also decremented at the shorter ISIs but still habituated up to ISIs of 2500 msec. The clear dissociation between frontal N30 and parietal P27 at the larger ISIs suggests that they involve at least in part distinct neural generators.     

SEPs to finger joint input lack the N20-P20 response that is evoked by tactile inputs: contrast between cortical generators in areas 3b and 2 in humans

A method using a DC servo motor is described to produce brisk angular movements at finger interphalangeal joints in humans. Small passive flexions of 2° elicited sizable somatosensory evoked potentials (SEPs) starting with a contralateral positive P34 parietal response thought to reflect activation of a radial equivalent dipole generator in area 2 which receives joint inputs. By contrast, electric stimulation of tactile (non-joint) inputs from the distal phalanx evoked the usual contralateral negative N20 reflecting a tangential equivalent dipole generator in area 3b. Finger joint inputs also evoked a precentral positivity equivalent to the P22 of motor area 4, and a large frontal negativity equivalent to N30. It is suggested that natural stimulation allows human SEP components to the differentiated in conjunction with distinct cortical somatotopic projections.