Biomedical subjects

M Tinazzi

Publications and source records attributed to M Tinazzi.

At least 37 records · Page 2Linked to original sources

PubMed1999

Temporal discrimination of somesthetic stimuli is impaired in dystonic patients.

Clinical and experimental evidence documents abnormal somatosensory functions in dystonia. Despite the fact that somatosensory processing is inherently temporal, mainly spatial aspects of somatosensory functions have so far been assessed in dystonic patients. Seven patients with idiopathic dystonia and nine healthy controls were given pairs of non-noxious electrical stimuli separated by different time intervals and asked to report if they perceived single or double stimuli. Somesthetic temporal discrimination thresholds (STDT) were obtained by computing the shortest time interval at which stimuli, applied to the left or the right hand, were perceived as separate. STDT were significantly higher in dystonic than in controls thus showing for the first time that temporal and not only spatial somatosensory processing is altered in dystonia.

Adult↗

PubMed1999

Parkinson's disease and lower limb somatosensory evoked potentials: apomorphine-induced relief of the akinetic-rigid syndrome and vertex P37-N50 potentials.

We evaluated brainstem P30, vertex-central P37-N50 and contralateral frontal N37 somatosensory evoked potentials (SEPs) from the tibial nerve in 14 patients affected by Parkinson's disease (PD) with akinetic-rigid syndrome. In seven patients SEPs were recorded after administration of apomorphine. The cortical P37-N50 complex was either absent (five patients, eight tested sides) or significantly smaller in patients as compared to the control group (n = 18). There was a relationship between abnormalities of early vertex potentials and degree of motor impairment. Administration of apomorphine was followed by an increase in amplitude of P37-N50 response, which was maximal after 15-30 min and then progressively returned to basal values in parallel with clinical improvement. Amplitude of brainstem P30 and frontal N37 responses was within normal values and did not vary following drug administration. These results suggest that the P37-N50 complex arises from independent cortical generators, probably located in the pre-rolandic cortex, which may be selectively affected by basal ganglia dysfunction. Amplitude decrease of the P37-50 complex may reflect an abnormal processing of somatosensory inputs within the pre-central cortex due to defective modulation exerted by basal ganglia circuitry on cortical excitability. SEP potentiation following apomorphine, besides indicating that this dysfunction is partly reversible, might suggest objective method to measure therapeutic efficacy.

Aged↗

PubMed1999

Evidence for an abnormal cortical sensory processing in dystonia: selective enhancement of lower limb P37-N50 somatosensory evoked potential.

We evaluated brain stem P30, contralateral frontal N37, and the vertex-ipsilateral central P37, N50 somatosensory evoked potentials (SEPs) obtained in response to stimulation of the tibial nerve in 10 patients with idiopathic dystonia. Results were compared with those obtained in 10 healthy subjects matched for age and sex. The amplitude of the brain stem P30 potential and of the contralateral frontal N37 response in dystonic patients was not significantly different from that recorded in normal subjects. The vertex- ipsilateral central P37-N50 complex, which is thought to originate in the pre-rolandic cortex, was significantly enhanced in patients compared with the control group. These results suggest the enhancement of the vertex-ipsilateral central P37-N50 complex might reflect an abnormal response to somatosensory inputs of a precentral cortex which is excessively activated because of a disorder of the basal ganglia. Such inefficient sensory processing in motor areas might contribute to motor impairment in dystonia.

Adult↗

PubMed1998

Inhibitory action of forearm flexor muscle afferents on corticospinal outputs to antagonist muscles in humans.

1. To find out whether muscle afferents influence the excitability of corticospinal projections to antagonist muscles, we studied sixteen healthy subjects and one patient with a focal brain lesion. 2. Using transcranial magnetic and electrical brain stimulation we tested the excitability of corticomotoneuronal connections to right forearm muscles at rest after conditioning stimulation of the median nerve at the elbow. Somatosensory potentials evoked by median nerve stimulation were also recorded in each subject. 3. Test stimuli delivered at 13-19 ms after median nerve stimulation significantly inhibited EMG responses elicited in forearm extensor muscles by transcranial magnetic stimulation, but did not inhibit responses to electrical stimulation. In contrast, magnetically and electrically elicited responses in forearm flexor muscles were suppressed to the same extent. 4. The higher the intensity of the test shocks, the smaller was the amount of median nerve-elicited inhibition. Inhibition in extensor muscles was also smaller during tonic wrist extension, or if the induced electrical stimulating current in the brain flowed from posterior to anterior over the motor strip rather than vice versa. Test responses evoked by magnetic transcranial stimulation in the first dorsal interosseous and in brachioradialis muscles were not inhibited after median nerve stimulation at the elbow. Stimulation of digital nerves failed to inhibit motor potentials in extensor muscles. 5. Test stimuli delivered at 15 and 17 ms after radial nerve stimulation significantly inhibited EMG responses elicited in forearm flexor muscles by magnetic transcranial stimulation. 6. In the patient with a focal thalamic lesion, who had dystonic postures and an absent N20 component of the somatosensory-evoked potentials but normal strength, median nerve stimulation failed to inhibit magnetically evoked responses in forearm extensor muscles. 7. We propose that activation of median nerve muscle afferents can suppress the excitability of cortical areas controlling the antagonist forearm extensor muscles acting on the hand. The inhibitory effect occurs at short latency and might assist spinal pathways mediating reciprocal inhibition by contrasting the co-activation of antagonistic pools of corticospinal cells.

Adult↗

PubMed1998

Modulation of ipsilateral motor cortex in man during unimanual finger movements of different complexities.

To understand the role of the ipsilateral motor cortex in the control of unimanual movements, we evaluated changes in cortical motor evoked potentials (MEP) from the left abductor pollici brevis (APB) to transcranial magnetic stimulation (TMS) of the right hemisphere in nine normal subjects during execution of right finger movements of different complexities. The motor tasks were (a) repetitive opposition movement (thumb tapping the 3rd finger); (b) isolated finger movements in a 'usual' sequence (thumb tapping fingers 2, 3, 4 and 5) and (c) in an 'unusual' sequence (thumb tapping fingers 3, 5, 2 and 4). Subjects were trained before the study up to disappearance of EMG synkinetic activity in the left APB. As compared to the rest condition, MEP amplitude was enhanced in all subjects during paradigm (b) and even more during (c), but remained unchanged during paradigm (a). The MEP increase disappeared in four out of the nine subjects undergoing overtraining. No significant modifications in MEP amplitude were found in the left proximal muscle (biceps, five subjects). The H reflex induced by left median nerve stimulation at the elbow (four subjects) and MEPs from the left APB to transcranial electrical stimulation (three subjects) were not significantly affected by any of the motor paradigms, indicating that the motor cortex was the site of change. These results provide evidence of an increased excitability of cortical motor outputs targeting the unmoving hand muscles during contralateral sequential finger movements which disappears with overtraining. We conclude that during motor learning there is an interhemispheric transfer of information, possibly in order to inhibit the opposite hemisphere from interfering when a fine unimanual movement is required.

Adult↗

PubMed1998

Scalp topography and source analysis of interictal spontaneous spikes and evoked spikes by digital stimulation in benign rolandic epilepsy.

OBJECTIVES: We report the analysis of scalp topography and dipole modeling of the rolandic spikes in 6 patients suffering of benign rolandic epilepsy of childhood with extremely high amplitude SEP by tapping stimulation of the finger of the hand. METHODS: EEG and BESA analysis were performed for both rolandic spontaneous interictal spikes and high amplitude scalp activity evoked by tapping and electrical stimulation of the first finger of the right hand. RESULTS: The evoked responses showed a morphology characterized by a rapid phase (spike) followed by a slow phase (slow wave). The spike presented an early small positive component followed by a main negative component. Similar morphology, dipole configuration and source localization were observed for both rolandic spikes and evoked high amplitude scalp responses. Dipole localization showed an overlap of spatial coordinates between rolandic and evoked spikes. CONCLUSIONS: These findings suggest that the extremely high amplitude SEPs could be evoked spikes which probably had the same cortical generators of the spontaneous rolandic spikes.

Brain Mapping↗

PubMed1998

Influence of somatosensory input on paroxysmal activity in benign rolandic epilepsy with 'extreme somatosensory evoked potentials'.

We studied six patients suffering from benign rolandic epilepsy of childhood with central temporal spikes who presented so-called 'extreme somatosensory evoked potentials (SEPs)' following peripheral somatosensory stimulation. Stimuli were delivered to the fingers of one hand using both a triggered tendon hammer and low-intensity electrical stimulation. The electrical stimulation was delivered in sequences in different conditions (i.e. random order, 1, 3 and 10 Hz). Both tapping and electrical stimulation produced scalp evoked potentials in all subjects, characterized by a spike followed by a slow wave, similar in morphology and scalp distribution to the spontaneously occurring spikes. This paroxysmal activity was sensitive to stimulus rate; the number of evoked spikes was inversely related to the frequency of stimulation, being maximal at 1 Hz and disappearing at high frequencies (10 Hz). Spontaneous spikes disappeared during high-frequency stimulation but were present during low-frequency stimulation. Averaged SEPs at 3-Hz stimulation showed a late high-amplitude component, identical in morphology and distribution to the single evoked spike. We therefore conclude that, in these subjects, the so-called 'extreme SEPs' are evoked spikes and that evoked and spontaneous spikes share common cortical sensorimotor generators. The evidence that these generators can be influenced by afferent input provides important information regarding the functional mechanisms involved in modulating cortical excitability in benign rolandic epilepsy. Moreover, we suggest that peripheral electrical stimulation can be used as an additional activation test in this kind of epilepsy.

Age of Onset↗

PubMed1998

Neurophysiological evidence of neuroplasticity at multiple levels of the somatosensory system in patients with carpal tunnel syndrome.

The human somatosensory cortex (S1) is capable of modification after partial peripheral deafferentation, but it is not known whether spinal and brainstem changes contribute to this process. We recorded spinal, brainstem and cortical somatosensory evoked potentials following ulnar nerve stimulation in patients affected by unilateral carpal tunnel syndrome with EMG evidence of chronic alterations in median nerve sensorimotor conduction at the wrist lasting at least 4 weeks, and compared them with those from the unaffected hand and with those obtained in a control group. Amplitudes of spinal N13 and brainstem P14 potentials following stimulation of the ulnar nerve ipsilateral to the deafferented median nerve were greater than those following stimulation of the contralateral ulnar nerve. Side-to-side amplitude differences in N13 and P14 were greater in patients than in the control group. Parietal N20 and P27 potentials, supposedly generated in S1, were also significantly increased. The present results suggest that a chronic pathological modification of peripheral sensorimotor inputs is associated with changes in neural activity at multiple sites of the somatosensory system. Changes in spinal and brainstem structures could contribute to the mechanisms subserving changes in the S1. Changes in synaptic strength and unmasking inputs secondary to disconnection of the normally dominant inputs to the 'median nerve' cortex may be the mechanisms underlying ulnar nerve SEP changes.

Adult↗

PubMed1998

Effects of voluntary contraction on tibial nerve somatosensory evoked potentials: gating of specific cortical responses.

We evaluated vertex-parietal P37, N50, and contralateral N37 somatosensory evoked potentials (SEPs) to posterior tibial nerve stimulation during weak (20 to 30%) and strong (80 to 90%) ipsilateral gastrocnemius-soleus contraction. The results were compared with data obtained during full relaxation. P37 and N50 were attenuated significantly during weak contraction and then abolished during strong contraction, whereas the contralateral N37 was not. The N37 potential spreads over the vertex and over the ipsilateral parietal region during strong contraction. The Cz'-F3 montage was not appropriate for detecting these SEP patterns. These findings suggest that thalamic or cortical gating mechanisms affect specific cortical responses. P37 and N50 could reflect the arrival of the afferent volley into the motor areas from thalamic and cortical (subareas 1 and 2 of S1) projections. N37 could be generated in subarea 3b. Differential analysis of N37 and P37 is required in clinical practice, mainly in those conditions that involve the motor system and in those conditions in which tonic muscular activity is increased.

Adult↗

PubMed1997

Transient deafferentation in humans induces rapid modulation of primary sensory cortex not associated with subcortical changes: a somatosensory evoked potential study.

Human somatosensory cortex (S1) is capable of rapid modification after temporary peripheral deafferentation but it is not known whether subcortical changes contribute to this modulation. We recorded spinal, brainstem and cortical somatosensory evoked potentials (SEPs) to median nerve stimulation following anaesthetic block of the ipsilateral ulnar nerve. Spinal N13 and subcortical P14, N18 potentials remained unchanged during the experiment. N20/P20, P27 and N30 cortical potentials, which are generated in different subareas of the S1 (N20/P20, N30 in area 3b; P27 in area 1), showed different increases in amplitude during the anaesthesia, which were more marked for N20/P20 and N30 than for P27 potentials. These results suggest that changes in S1 neural activity induced by transient deafferentation may be primarily intracortical in origin and appear to be segregated within the different subareas of the somatosensory cortex. Unmasking of pre-existing thalamo-cortical projections from median nerve territories, induced by ipsilateral ulnar nerve deafferentation, may be the mechanism underlying cortical SEP enhancement.

Adult↗

PubMed1997

Binocular interaction in normal vision studied by pattern-reversal visual evoked potential (PR-VEPS).

Monocular and binocular visual evoked potentials (VEPs) in response to different check size (15-21-38-84 minutes or arc) were studied in 14 subjects with normal visual acuity and stereopsis. The binocular VEP amplitude is slightly higher than the VEP amplitude on stimulation of the "better eye" and significantly higher than the VEP amplitude on stimulation of the "worse eye"; this effect is observed using small checks and almost exclusively involved N75-P100. Both the N75 and P100 peaks occur earlier after binocular than monocular stimulation. The shortening of the N75 mean latency is significantly greater than that of the P100 mean latency when larger check sizes are used. The mean latency of the N145 potential is not significantly different in monocular and binocular stimulus conditions. The slight summation effect and latency shortening in the binocular VEPs are not consistent with the hypothesis that it is the sum of separate monocular signals originating from the visual cortex that gives rise to the response. The early components of both monocular and binocular VEPs are thought to be of post-synaptic origin (outside layer 4c of area 17), where the inputs become mixed so that most cells receive information from both eyes. The amplitude enhancement of binocular VEPs, which mainly occurs when using small checks, may be related to the increase in the total amount of cortical activity representing the macular region; this may account for binocular superiority in fine spatial resolution. The latency shortening in binocular conditions can be explained by considering that the critical determinant of the latency is the fundamental spatial frequency of the pattern. When coarse patterns are used, their effectiveness in parafoveal stimulation may affect the VEPs, with a significant contribution coming from the more peripheral retina. The enlargement of the visual field when the eyes see simultaneously may therefore further reduce the latency of the response when using the larger checks suitable for eccentric stimulation.

Adult↗

PubMed1997

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.

Adult↗

PubMed1997

Crossed and direct effects of digital nerves stimulation on motor evoked potential: a study with magnetic brain stimulation.

We studied the influence of contralateral and ipsilateral cutaneous digital nerve stimulation on motor evoked potentials (MEPs) elicited in hand muscles by transcranial magnetic stimulation (TMS). We tested the effect of different magnetic stimulus intensities on MEPs recorded from the thenar eminence (TE) muscles of the right hand while an electrical conditioning stimulus was delivered to the second finger of the same hand with an intensity four times above the sensory threshold. Amplitude decrement of conditioned MEPs as a function of magnetic stimulus intensity was observed. The lowest TMS stimulus intensity produced the largest decrease in conditioned MEPs. Moreover, we investigated the effects of ipsilateral and contralateral electrical digital stimulation on MEPs elicited in the right TE and biceps muscle using an intensity 10% above the threshold. Marked MEP inhibition in TE muscles following both ipsilateral and contralateral digital stimulation is the main finding of this study. The decrease in conditioned MEP amplitude to ipsilateral stimulation reached a level of 50% of unconditioned MEP amplitude with the circular coil and 30% with the focal coil. The amplitude of conditioned MEPs to contralateral digital stimulation showed a decrease of 60% with the circular coil and more than 50% with the focal coil. The onset of the inhibitory effect of contralateral stimulation using the focal coil occurred at a mean of 15 ms later than that of ipsilateral stimulation. No MEP inhibition was observed when recording from proximal muscles. Ipsilateral and contralateral digital stimulation had no effect on F wave at appropriate interstimulus intervals, where the main MEP suppression was noted. We stress the importance of selecting an appropriate test stimulus intensity to evaluate MEP inhibition by digital nerves stimulation. Spinal and cortical sites of sensorimotor integration are adduced to explain the direct and crossed MEP inhibition following digital nerves stimulation.

Adult↗

PubMed1997

Reversible changes of motor cortical outputs following immobilization of the upper limb.

We mapped the cortical representations of the abductor pollicis brevis, flexor carpi radialis, biceps and deltoid muscles in six subjects with unilateral wrist fractures, immediately after the removal of the splint. This was repeated 1 month later in three out of the six subjects. Duration of immobilization was 1 month. Muscle maps were obtained by delivering four focal magnetic pulses for each scalp position (1 cm apart with reference to Cz) over the contralateral hemisphere. Motor evoked potentials (MEPs) were averaged off-line and expressed as a percentage of the motor action potential evoked by supramaximal peripheral nerve stimulation. Volume, area and threshold of the motor maps showed no significant hemispheric differences within each muscle in 10 control subjects. In the first recording session the volume of each immobilized muscle was distinctly higher when compared to that of controls in terms of absolute value and side-to-side ratio. This finding disappeared 1 month later. Moreover, MEP amplitude difference recorded from hand muscle could be reversed during a small tonic voluntary contraction. Immobilization had no significant effect on the threshold for activation of the target muscles and on the area of the motor map. The increase in MEP amplitudes occurred without changes in spinal excitability as tested by the F wave. These findings suggest that immobilization of the upper limb induces a reversible enhancement of the excitability of structures along the corticomotoneuronal pathway. Sustained restriction of volitional movements and reduction in somatic sensory inputs might promote this functional modulation of the motor system.

Adult↗

PubMed1997

Amplitude changes of tibial nerve cortical somatosensory evoked potentials when the ipsilateral or contralateral ear is used as reference.

We performed topographical mapping of somatosensory evoked potentials (SEPs) to the posterior tibial nerve using earlobe references both ipsilateral and contralateral to the stimulation side. The voltage of the frontal contralateral N37 and P50 components was enhanced, while the voltage of the parietal ipsilateral P37 and N50 components was reduced when the contralateral earlobe was substituted by the ipsilateral earlobe reference. Maps of the same data documented concomitant changes in negative and positive potential fields, showing an expansion of the pre-Rolandic N37 toward the centrotemporal contralateral regions, and a tendency of the parietal ipsilateral P37, N50 components to be more focally distributed at the vertex. SEPs recorded at each earlobe (Cv6 reference) provided an explanation of these results: The contralateral earlobe detected a negative potential corresponding to the N37 potential recorded over the scalp, followed by a P50 potential that attenuated the contralateral responses and enhanced the ipsilateral ones. The ipsilateral earlobe had no significant effects on scalp SEPs, since it detected only a large N33 negativity. Current source density (CSD) maps were, of course, not influenced by the ear used as reference. Our results suggest that the ipsilateral ear reference is better than the contralateral one for recording "genuine" cortical SEPs. Therefore, it can be recommended in the clinical domain for mapping studies of lower-limb cortical SEPs.

Adult↗

PubMed1996

'Direct' and 'crossed' modulation of human motor cortex excitability following exercise.

Rapid repetitive movements of the thumb (1 min duration) produce a reversible decrease in the activated primary motor cortex (MI) excitability to transcranial magnetic stimulation (TMS) with recovery within 35-40 min. In the present study we investigated (1) the role of peripheral sensory feedback in inducing such decrease and (2) possible effects of exercise on the non-activated MI. Stimulation of peripheral Ia afferent fibres, induced by 1 min vibration of thenar muscles and 2 Hz electrical stimulation of the median nerve at the wrist, have no effect on motor evoked potential (MEP) amplitude to TMS suggesting no role for sensory feedback to produce MI excitability modulation. Exercise produces a significant (P < 0.01) decrease of MEPs for homologous non-exercised muscles with concomitant contraction of corresponding motor cortical output maps, suggesting that changes in MI excitability also occur in the nonactivated hemisphere. This 'crossed' effect might relate to an interhemispheric transfer of information, via homotopic connections of the corpus callosum.

Adult↗

PubMed1996

Neural generators of tibial nerve P30 somatosensory evoked potential studied in patients with a focal lesion of the cervicomedullary junction.

The tibial nerve P30 potential was studied in 6 patients with focal lesions located in the vicinity of the cervicomedullary junction. P30 potential was unaffected while cortical P39 was abnormal in the patients with a supramedullary lesion affecting the somatosensory pathway just above its decussation. Conversely, P30 was abnormal in the presence of a lesion situated caudally to the cervicomedullary junction affecting the lower limb sensory fibers just below their decussation. Median nerve P14 behaved similarly to the P30 potential in these cases. These clinical observations suggest that P30 potential, as P14 of median nerve somatosensory evoked potentials, is generated in the lower brain stem probably before the decussation of the sensory fibers; nucleus gracilis and medial lemniscus fibers in the lower brain stem are probably the anatomical structures generating P30 potential. This suggests that P30 potential may be used to study intraspinal and intracranial conduction times separately in the afferent somatosensory pathways.

Adult↗

PubMed1996

Effect of stimulus rate on the cortical posterior tibial nerve SEPs: a topographic study.

We performed topographical mapping of somatosensory evoked potentials (SEPs) in response to posterior tibial nerve stimulation delivered at 2, 5 and 7.5 Hz in 15 healthy subjects. P37 was significantly attenuated at 5 and 7.5 Hz and the N50 component attenuated only at 5 Hz, its amplitude remaining stable for further increases in stimulus frequency. Frontal N37 and P50 potentials showed no significant decrease when the stimulus repetition frequency was changed from 2 to 7.5 Hz. P60 showed an attenuation of the amplitude only at 7.5 Hz. Latency and scalp topographies of all cortical components examined remained unchanged for the 3 stimulus rates tested. The optimal stimulus rate for mapping of tibial nerve SEPs was lower than 5 Hz. The distinct recovery function of the contralateral. N37-P50 and ipsilateral P37-N50 responses suggests that these potentials arise from separate generators.

Adult↗