Biomedical subjects

A Fiaschi

Publications and source records attributed to A Fiaschi.

At least 37 records · Page 2Linked to original sources

PubMed2001

Intravenous clomipramine decreases excitability of human motor cortex. A study with paired magnetic stimulation.

Several recent reports suggest the possibility of monitoring pharmacological effects on brain excitability through transcranial magnetic stimulation (TMS). In these studies, paired magnetic stimulation has been used in normal subjects and on patients who were taking different antiepileptic drugs. The aim of our study was to investigate motor area excitability on depressed patients after intravenous administration of a single dose of clomipramine, a tricyclic antidepressant. Motor cortex excitability was studied by single and paired transcranial magnetic stimulation (TMS) before and after 4, 8 and 24 h from intravenous administration of 25 mg of clomipramine. Cortical excitability was measured using different TMS parameters: motor threshold (MT), motor evoked potential (MEP) amplitude, duration of cortical silent period (CSP), intracortical inhibition (ICI) and intracortical facilitation (ICF). Spinal excitability and peripheral nerve conduction was measured by F response and M wave. A temporary but significant increase of motor threshold and intracortical inhibition and a decrease of intracortical facilitation were observed 4 h following drug administration. MEP amplitude, cortical silent period, F response and M wave were not significantly affected by drug injection. Our findings suggest that a single intravenous dose of clomipramine can exert a significant but transitory suppression of motor cortex excitability in depressed patients. TMS represents a useful research tool in assessing the effects of motor cortical excitability of neuropsychiatric drugs used in psychiatric disease.

Adult↗

PubMed2001

Somatosensory disinhibition in dystonia.

Despite the fact that somatosensory processing is inherently dependent on inhibitory functions, only excitatory aspects of the somatosensory feedback have so far been assessed in dystonic patients. We studied the recovery functions of spinal N13, brainstem P14, parietal N20, P27, and frontal N30 somatosensory evoked potentials (SEPs) after paired median nerve stimulation in 10 patients with dystonia and in 10 normal subjects. The recovery functions were assessed (conditioning stimulus: S1; test stimulus: S2) at interstimuls intervals (ISIs) of 5, 20, and 40 ms. SEPs evoked by S2 were calculated by subtracting the SEPs of the S1 only response from the SEPs of the response to the paired stimuli (S1 + S2), and their amplitudes were compared with those of the control response (S1) at each ISI considered. This ratio, (S2/S1)*100, investigates changes in the excitability of the somatosensory system. No significant difference was found in SEP amplitudes for single stimulus (S1) between dystonic patients and normal subjects. The (S2/S1)*100 ratio at the ISI of 5 ms did not significantly differ between dystonic patients and normal subjects, but at ISIs of 20 and 40 ms, this ratio was significantly higher in patients than in normals for spinal N13 and cortical N20, P27, N30 SEPs. These findings suggest that in dystonia there is an impaired inhibition at spinal and cortical levels of the somatosensory system which would lead to an abnormal sensory assistance to the ongoing motor programs, ultimately resulting in the motor abnormalities present in this disease.

Adult↗

PubMed2001

Cutaneomotor integration in human hand motor areas: somatotopic effect and interaction of afferents.

The aim of this study was to elucidate sensorimotor integration in human hand motor areas, its time course, somatotopy and the interaction of sensory fields arising from two different fingers. We studied the influence of different intensities of electrical digital stimulation of two different fingers on motor-evoked potentials elicited in hand muscles by transcranial magnetic stimulation (TMS). Single conditioning electrical stimuli were applied to the right second (D2) and fifth fingers (D5) individually and also to both fingers (D2+D5) simultaneously in six normal volunteers. Magnetic tests, adjusted to produce a response in the abductor digiti minimi muscle of the right hand, were delivered using a circular and a focal coil. The digital stimuli were delivered to the finger at the sensory threshold (ST), at 3 and 5 times the ST, and over the pain threshold at interstimulus intervals (ISIs) ranging from 10 to 100 ms. In order to define the anatomical level of the sensorimotor interactions, the effect of the digital stimulation on TMS was compared to the effect on transcranial electrical stimulation. When the peripheral stimulation was delivered at the ST a small inhibitory effect was found only when stimulating both fingers. At 3 times the ST we detected a topographic distribution of motor-evoked potential inhibition, which partially disappeared at higher intensity (5 times the ST); two types of convergence effects took place at different ISIs. When conditioning stimuli were painful, somatotopy and convergence were lost. Sensorimotor integration shows somatotopy and interaction of afferents at different sites. The intensity of the conditioning stimulus plays an important role in topography and sensory convergence. The importance of these mechanisms in physiology and physiopathology is discussed.

Afferent Pathways↗

PubMed2000

Neuroplastic changes related to pain occur at multiple levels of the human somatosensory system: A somatosensory-evoked potentials study in patients with cervical radicular pain.

Studies suggest that pain may play a major role in determining cortical rearrangements in the adult human somatosensory system. Most studies, however, have been performed under conditions whereby pain coexists with massive deafferentation (e.g., amputations). Moreover, no information is available on whether spinal and brainstem changes contribute to pain-related reorganizational processes in humans. Here we assess the relationships between pain and plasticity by recording somatosensory-evoked potentials (SEPs) in patients who complained of pain to the right thumb after a right cervical monoradiculopathy caused by compression of the sixth cervical root, but did not present with clinical or neurophysiological signs of deafferentation. Subcortical and cortical potentials evoked by stimulation of digital nerves of the right thumb and middle finger were compared with those obtained after stimulation of the left thumb and middle finger and with those obtained in a control group tested in comparable conditions. Amplitudes of spinal N13, brainstem P14, parietal N20 and P27, and frontal N30 potentials after stimulation of the painful right thumb were greater than those of the nonpainful left thumb and showed a positive correlation with magnitude of pain. This right-left asymmetry was absent after stimulation of the patients' middle fingers and in control subjects. Results suggest that chronic cervical radicular pain is associated with changes in neural activity at multiple levels of the somatosensory system. The absence of correlation between the amplitude of spinal, brainstem, and cortical components of SEPs suggests that enhancement of cortical activity is not a simple amplification of subcortical enhancement.

Adult↗

PubMed2000

Abnormal central integration of a dual somatosensory input in dystonia. Evidence for sensory overflow.

Several observations suggest impaired central sensory integration in dystonia. We studied median and ulnar nerve somatosensory evoked potentials (SEPs) in 10 patients who had dystonia involving at least one upper limb (six had generalized, two had segmental and two had focal dystonia) and in 10 normal subjects. We compared the amplitude of spinal N13, brainstem P14, parietal N20 and P27 and frontal N30 SEPs obtained by stimulating the median and ulnar nerves simultaneously (MU), the amplitude value being obtained from the arithmetic sum of the SEPs elicited by stimulating the same nerves separately (M + U). Throughout the somatosensory system, the MU : (M + U) ratio indicates the interaction between afferent inputs from the two peripheral nerves. No significant difference was found between SEP amplitudes and latencies for individually stimulated median and ulnar nerves in dystonic patients and normal subjects, but recordings in patients yielded a significantly higher percentage ratio [MU : (M + U)x100] for spinal N13 brainstem P14 and cortical N20, P27 and N30 components. The SEP ratio of central components obtained in response to stimulation of the digital nerves of the third and fifth fingers was also higher in patients than in controls but the difference did not reach a significant level. The possible contribution of subliminal activation was ruled out by recording the ratio of SEPs in six normal subjects during voluntary contraction. This voluntary contraction did not change the ratio of SEP suppression. These findings suggest that the inhibitory integration of afferent inputs, mainly proprioceptive inputs, coming from adjacent body parts is abnormal in dystonia. This inefficient integration, which is probably due to altered surrounding inhibition, could give rise to an abnormal motor output and might therefore contribute to the motor impairment present in dystonia.

Adult↗

PubMed2000

Early and late intracortical inhibition in juvenile myoclonic epilepsy.

PURPOSE: We investigated 15 patients with juvenile myoclonic epilepsy (JME) by subjecting them to single and paired transcranial magnetic stimulation to test the hypothesis that motor cortical inhibition may be abnormal in this form of benign epilepsy. METHODS: Different conditioning paradigms of paired transcranial magnetic stimulation were used with interstimulus intervals (ISIs) of varying lengths (1 to 400 milliseconds) to investigate changes in balance between excitatory and inhibitory intracortical circuits. RESULTS: Motor evoked potential (MEP) inhibition at ISIs of 1 to 4 milliseconds was significantly lower in JME patients than in age-matched healthy controls (p < 0.001), whereas no significant differences in MEP inhibition were noted at long ISIs (100 to 150 milliseconds). This pattern was observed in both hemispheres in seven of seven patients studied bilaterally and was present in both treated and untreated patients. There were no group differences between JME patients and controls in intracortical facilitation, motor threshold, MEP amplitude, and cortical silent period. CONCLUSIONS: We documented a different pattern of MEP inhibition in JME patients, suggesting impaired functioning of inhibitory interneuronal circuits, which may account for the hyperexcitability of the motor system in this form of epilepsy.

Adult↗

PubMed1999

Intracoronary serotonin release after high-pressure coronary stenting.

It is known that platelet-derived serotonin at the site of coronary angioplasty induces an increase in coronary tone and plays a role in vasoconstriction after balloon angioplasty. The goal of the present investigation was to compare local release of serotonin with changes in coronary tone after coronary stenting and coronary angioplasty. Twenty patients with significant stenosis (> or =50% diameter narrowing) of the left anterior descending coronary artery were referred to traditional coronary angioplasty (10 patients; group 1) or high-pressure coronary stenting (10 patients; group 2). An additional 16 patients with similar angiographic characteristics were referred to the coronary angioplasty group (8 patients; group 1a) or stenting group (8 patients; group 2a) after pretreatment with ketanserin. Serotonin plasma levels in coronary sinus and coronary cross-sectional area distal to the site of dilatation were measured before and after bath revascularization procedures. In groups 1 and 1a, plasma serotonin levels in coronary sinus increased from basal values of 3.2+/-0.8 and 3.2+/-0.5 ng/ml to 29.5+/-13 and 25.6+/-9 ng/ml after ballooning (p <0.001 vs baseline). In groups 2 and 2a, plasma serotonin levels in coronary sinus increased from basal values of 3.5+/-0.3 and 3.5+/-0.7 ng/ml to 114.6+/-34 and 113+/-29 ng/ml after stenting (p <0.001 vs baseline and vs postangioplasty values in groups 1 and 1a). Coronary cross-sectional area distal to the site of dilatation significantly decreased after angioplasty in group 1 (from 4.33+/-0.4 to 3.32+/-0.3 mm2; p <0.001), and after stenting in group 2 (from 4.27+/-0.3 to 2.86+/-0.2 mm2; p <0.001 vs baseline, and p <0.02 vs values after coronary angioplasty in group 1). Pretreatment with ketanserin significantly reduced distal coronary vasoconstriction after angioplasty and stenting. It is concluded that the higher local serotonin release after coronary stenting may explain the more marked coronary constriction observed after prosthesis deployment with respect to traditional coronary angioplasty. Ketanserin is able to significantly attenuate the increase in distal coronary tone induced by both revascularization procedures.

Angioplasty, Balloon, Coronary↗

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↗

PubMed1999

Cortical excitability in patients after loading doses of lamotrigine: a study with magnetic brain stimulation.

PURPOSE: Transcranial magnetic stimulation (TMS) of the brain allows the pharmacologic effects of anti-convulsant drugs (AEDs) on the excitability of motor corticospinal pathways to be evaluated in patients with epilepsy and normal subjects. However, no study has yet documented the changes in motor excitability in patients treated with lamotrigine (LTG). We aimed to study the effects of loading doses of LTG on TMS recordings in patients with epilepsy at the beginning of their treatment. METHODS: We investigated single-pulse TMS in six patients with complex partial seizures. The TMS recordings were performed in five sessions before and during 5 weeks of treatment. Motor threshold, motor-evoked potential (MEP) amplitude, cortical silent period, and peripheral conduction velocity were used as parameters of evaluation. LTG was started with a dosage of 25 mg/day until a daily maintenance dosage of 200 mg/day was reached. RESULTS: The motor threshold activation of thenar muscles was significantly increased by LTG after 2 weeks of treatment and was increased in a parallel way to the loading dose of the drug at week 3 and 5 of treatment. The MEP size recorded from the thenar muscles did not show significant changes at high- or low-intensity stimulation. The cortical silent period remained unchanged at low- and high-intensity stimulation. The absolute latency of MEPs after cortical and cervical stimulation was unchanged, as was the central motor conduction time. CONCLUSIONS: Our study documents that loading doses of LTG, administered as monotherapy, progressively increases patients' motor thresholds over short periods.

Action Potentials↗

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

Spike topography and functional magnetic resonance imaging (fMRI) in benign rolandic epilepsy with spikes evoked by tapping stimulation.

We performed a spike topography study and a functional magnetic resonance imaging (fMRI) in a female patient with benign rolandic epilepsy presenting single high-amplitude evoked spikes in response to somatosensory peripheral stimulation. The stimulus was delivered to the first finger of the right hand using a tendon hammer, which evoked a single spike followed by a slow wave, showing the maximal amplitude over the left central regions. fMRI showed that the contralateral sensory cortices (S1 and S2) and the motor cortex (M I) were activated during tapping stimulation. In 3 normal subjects, tapping stimulation produced no fMRI activation. This fMRI study documents a highly focal activation of sensorimotor areas related to subclinical evoked spikes in benign rolandic epilepsy.

Acoustic Stimulation↗

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↗