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M Tinazzi

Publications and source records attributed to M Tinazzi.

45 records · Page 3Linked to original sources

Motor neuron disease with pyramidal tract dysfunction involves the cortical generators of the early somatosensory evoked potential to tibial nerve stimulation.

We evaluated somatosensory evoked potentials (SEPs) to tibial nerve stimulation in 39 patients with sporadic motor neuron disease using multiple scalp derivations (earlobe reference). SEPs were altered in 22 of 29 amyotrophic lateral sclerosis (ALS) patients, whereas they were unaffected in 10 progressive muscular atrophy (PMA) patients. The main changes involved the amplitude and the field distribution of the early P40 and N37 cortical potentials with different modalities varying from a selective loss of the P40 potential (33% of tested sides) to absence of all early cortical SEPs (22% of tested sides). The later components following N50 were generally spared. The commonly used Cz-Fz montage was inadequate for detecting these alterations. Central afferent conduction was slightly affected. The selective loss of cortical SEPs and their close correlation with clinicoelectrophysiologic evidence of central motor system involvement strongly support a cortical origin of the SEP alterations in ALS. We suggest that neuronal loss in the somatosensory cortex may selectively affect the generator sites of the cortical SEPs to lower limb stimulation.

Adult↗

Long-lasting depression of motor-evoked potentials to transcranial magnetic stimulation following exercise.

We used transcranial magnetic stimulation to study the modulation of motor cortex excitability after rapid repetitive movements. Eleven healthy subjects aged 24-32 years were evaluated. Serial motor-evoked potential (MEP) recordings were performed from the right thenar eminence every 5 min for a period of 20 min at rest and for a period of 35 min after repetitive abduction-adduction of the thumb at maximal frequency for 1 min. All subjects presented distinct changes in MEP amplitude after exercise with an approximately 55% mean maximal decrease compared with basal conditions and complete recovery 35 min after the end of the exercise. The time course of MEP amplitude changes presented the following trend: (1) a rapid decrease phase within the first 5 min; (2) a maximal depression phase of 10 min duration (from the 5th to the 15th min); and (3) a slow recovery phase. No significant modifications in post-exercise MEP amplitude were found in ipsilateral non-exercised muscles. In order to determine the level where these changes take place, we recorded the M and F waves induced by median nerve stimulation at the wrist (all subjects) and MEPs in response to transcranial electrical stimulation (five subjects) at rest and during the decrease and maximal depression phases. None of these tests were significantly affected by exercise, indicating that the motor cortex was the site of change. Evaluation of maps of cortical outputs to the target muscle, performed in four subjects, showed an approximately 40% spatial reduction in stimulation sites evoking a motor response during the maximal depression phase. These data prove that exercise induces a reversible, long-standing depression of cortical excitability, probably related to intracortical presynaptic modulation, which transitorily reduces the motor representation area.

Adult↗

Subcortical P30 potential following tibial nerve stimulation: detection and normative data.

Stimulation of the tibial nerve evokes a P30 far-field potential over the scalp which, like the median nerve P14, probably originates in the vicinity of the cervico-medullary junction. Unlike the P14 potential, P30 recording has not been systematically performed in clinical practice, probably because of doubts about the generator of the potential and the possibility of consistently recording it on the scalp after the unilateral stimulation of the tibial nerve. In this study, we tested the reliability of the tibial nerve scalp far-field P30 potential in 34 normal subjects using different montages, of which the Fpz-Cv6 derivation gave the highest signal to noise ratio, making it possible to obtain a P30 potential peaking at 29.2 +/- 1.6 msec in all normal subjects. This suggests that this component should to be included in the routine recording of tibial nerve SEPs in order to evaluate the spinal and intracranial conduction of the somatosensory pathway separately.

Adult↗

Two distinct cervical N13 potentials are evoked by ulnar nerve stimulation.

To investigate the dual nature of the posterior neck N13 potential, we attempted to establish the presence of a latency dissociation between caudal (cN13) and rostral (rN13) potentials on stimulating the ulnar nerve, in view of its lower radicular entry compared to the median nerve. SEPs were evaluated in 24 normal subjects after both median and ulnar nerve stimulation. cN13 was prominent in the lower cervical segments, and rN13 was localized mainly in the upper ones using anteroposterior and longitudinal bipolar montage, respectively. The N9-cN13 interpeak latency did not differ significantly from N9-rN13 when stimulating the median nerve. On the other hand, the N9-rN13 interpeak was significantly longer than the N9-cN13 interpeak when the ulnar nerve was stimulated. The rN13 presented the same latency as P13-P14 far-field potentials in 17 out of 24 ulnar nerves tested. Therefore, the ulnar nerve stimulation evokes two distinct posterior neck N13 potentials. It is widely accepted that the caudal N13 is a postsynaptic potential reflecting the activity of the dorsal horn interneurons in the lower cervical cord. We suggest that the rostral N13 is probably generated close to the cuneate nucleus, which partly contributes to the genesis of P13-P14 far-field potentials.

Adult↗

Assessment of intraspinal and intracranial conduction by P30 and P39 tibial nerve somatosensory evoked potentials in cervical cord, brainstem, and hemispheric lesions.

In routine recordings of tibial nerve somatosensory evoked potentials (SEPs), a global central conduction time is evaluated by measuring the interval between the segmental spinal N22 potential, recorded in the lumbar region, and the cortical P39 potential. In this study, we tested the reliability of the scalp far-field P30 potential, which originates in the vicinity of the cervico-medullary junction, in order to evaluate separately intraspinal and intracranial conduction in normal subjects and patients with cervical cord and intracranial lesions. P30 and cortical P39 potentials were studied in 23 healthy subjects and in 70 patients with cervical cord (n = 47), brainstem (n = 11) or hemispheric lesions (n = 12) selected on the basis of neuroimaging--computed tomography (CT) or magnetic resonance (MR)--findings. Median nerve SEPs were also recorded in all patients. Of the several montages tested to obtain the P30 potential, the Fpz-Cv6 derivation gave the highest signal-to-noise ratio; it permitted to obtain a P30 potential that peaked at 29.2 +/- 1.6 ms in all normal subjects. P30 abnormalities were observed only in patients with cervical or cervico-medullary lesions; these were associated with a normal P39 in only two of 33 abnormal recordings. Conversely, P30 was consistently normal in lesions situated above the cervico-medullary junction whether associated with normal, delayed, or reduced P39. P30 abnormalities were subclinical in 42% of abnormal recordings. All patients with normal tibial and median nerve SEPs on both sides had normal touch, joint, and vibration sensation in the four limbs. There was a strong correlation between tibial nerve P30 and median nerve P14 data in the whole series of patients; both potentials behaved similarly in all cases of intracranial supramedullary lesions. Combined abnormalities of P30 and P39 potentials thus indicate that conduction is impaired at the spinal level and proved to be particularly informative for detecting spinal cord dysfunction in patients with neuroimaging evidence of a narrowed cervical canal. Recording of abnormal N13, P14, or P30 potentials provided evidence of a cervical cord dysfunction in 66% of patients who had a suspected spondylotic myelopathy. Recording of tibial nerve P30 potential has proven to give reliable and useful information when a separate assessment of intraspinal and intracranial somatosensory conduction is needed; it merits inclusion, as does the upper limb N13 potential, in the evaluation of patients whose MR image indicates cervical canal narrowing.

Adolescent↗

Neurophysiological and urodynamic examinations in the functional assessment of the spinal cord below the injury site.

We examined the characteristics of specific components of the evoked electrospinogram (EESG) in response to tibial nerve stimulation in 28 patients with traumatic injury of the dorsal and cervical spinal cord. The data were correlated with clinical, urodynamic and additional neurophysiological findings. In the majority of patients (82%), 11 with complete and 12 with partial spinal cord lesions, the lumbar components of the EESG were normal. In 4 of these patients with complete lesion above T2 the dorsal EESG was absent. In 5 cases (18%), the lumbosacral EESG was altered in the presence of an atypical clinical syndrome characterized by persistent urinary retention associated with lower leg atrophy and reduced tendon jerks. In these cases, MRI provided evidence of an unexpected sacral lesion. Unlike the dorsal EESG reflecting the afferent dorsal column volley, the lumbar components of the EESG are usually unaffected by interruption of the cord pathways; these last events thus originate from segmental neuronal activity, the involvement of which bears witness to additional lumbosacral damage.

Adolescent↗

Dynamic F wave from lower limbs: value and clinical application.

We evaluated changes in F wave from the lower limbs after walking in normals. Twenty-two healthy subjects ranging in age from 24 to 74 years (mean 40.2 SD 15.2) were investigated. The peroneal nerve was examined in 16 subjects and the posterior tibial nerve in 22 subjects on the dominant side. F waves were evaluated at rest and 1 minute and 10 minutes after effort testing consisting in prolonged walking for 15 minutes. F wave minimum, maximum and mean latencies, chronodispersion, duration, persistence and amplitude were evaluated. Only chronodispersion showed a significant decrease for both the peroneal and tibial nerve (p < 0.05) after walking. Moreover we evaluated the F wave after effort in five patients affected by neurogenic claudication: three patients presented a further slowing of proximal conduction, while two patients exhibited a transitory conduction block. In conclusion, F wave changes observed in dynamic conditions in normals probably reflect a synchronization of motorneuron firing requiring a certain amount of descending facilitation. On the other hand, the marked F wave changes after effort observed in patients increase the sensitivity of this method in the clinical setting and may provide insights into the pathophysiologic basis of neurogenic claudication.

Adult↗

Cortical output modulation after rapid repetitive movements.

Transcranial magnetic stimulation was used to evaluate changes in motor cortex excitability after rapid repetitive movements in five healthy subjects aged 23-30 years, by considering the amplitude of motor evoked potentials (MEPs) at rest and after one minute of maximal frequency repetitive abduction-adduction movements of the thumb. In addition, M and F waves were evaluated by stimulating the median nerve at the wrist. All of the examined subjects showed a clear modification in post-exercise MEP amplitudes, with a mean maximal reduction of 50-60% in comparison with basal values and complete recovery after a period of about 35 minutes. The time course of this phenomenon showed a triphasic pattern: (I) a rapid decrease phase up to the fifth minute; (II) a maximal depression phase for a period of about ten minutes; (III) a slow return to basal values. No significant changes were observed in post-exercise M and F waves. These results show the existence of a reversible modulation of the excitability of the upper motor neuron after rapid repetitive movements. It is likely that this modulation takes place at the level of the motor cortex and that its anatomo-functional substrate is represented by the activation of inhibitory intracortical circuits.

Adult↗

Nerve conduction changes during lower limb lengthening. Somatosensory evoked potentials (SEPs) and F-wave results.

The effect of lower limb lengthening on nerve conduction was investigated in 5 achondroplastic subjects who underwent callotasis on a "cross-over" basis. Somatosensory evoked potentials (SEPs) and F waves from the posterior tibial nerve (PTN) were studied preoperatively and then after removal of the axial fixators. SEPs at the end of lengthening showed that both the latency of the plexus potential (P9) and, albeit to a lesser extent, the interpeak time between the plexus and the spinal cord (N15) potentials were significantly increased. The central conduction time (N15-P33) and the amplitude of the scalp responses were not modified. The latencies of the F waves were much longer at the end of bone distraction than in basal conditions. The increases in both PTN SEPs and F-wave latencies are consistent with a slowing of conduction The extent of these latency shifts correlated closely with the degree of limb lengthening. We calculated that, on average, each cm of lengthening could produce 0.21 msec and 0.22 msec delays respectively, suggesting a similar effect of the stretching on both sensory and motor fibers. Our findings indicated that the damage could be widely distributed along the whole length of the nerve, affecting both the peripheral (trunk) and proximal (plexus and root) segments. The electrophysiological changes were not associated with any persistent clinical complaint.

Achondroplasia↗