Showing papers by "Fortunato Battaglia published in 2000"
TL;DR: A substantial increase in visual cortex excitability was demonstrated after a short period of light deprivation, which may underlie behavioral gains reported in humans and animals associated with light deprivation.
Abstract: Long-term deprivation of visual input for several days or weeks leads to marked changes in the excitability and function of the occipital cortex. The time course of these changes is poorly understood. In this study, we addressed the question whether a short period of light deprivation (minutes to a few hours) can elicit such changes in humans. Noninvasive transcranial magnetic stimulation (TMS) of the human occipital cortex can evoke the perception of flashes or spots of light (phosphenes). To assess changes in visual cortex excitability following light deprivation, we measured the minimum intensity of stimulation required to elicit phosphenes (phosphene threshold) and the number of phosphenes elicited by different TMS stimulus intensities (stimulus-response curves). A reduced phosphene threshold was detected 45 min after the onset of light deprivation and persisted for the entire deprivation period (180 min). Following re-exposure to light, phosphene thresholds returned to predeprivation values over 120 min. Stimulus-response curves were significantly enhanced in association with this intervention. In a second experiment, we studied the effects of light deprivation on functional magnetic resonance imaging (fMRI) signals elicited by photic stimulation. fMRI results showed increased visual cortex activation after 60 min of light deprivation that persisted following 30 min of re-exposure to light. Our results demonstrated a substantial increase in visual cortex excitability. These changes may underlie behavioral gains reported in humans and animals associated with light deprivation.
233 citations
TL;DR: Evaluated the reproducibility of intracortical inhibition (ICI) and facilitation studied with paired‐pulse focal transcranial magnetic stimulation with high variability, which may have implications for planning future studies.
Abstract: We have evaluated the reproducibility of intracortical inhibition (ICI) and facilitation (ICF) studied with paired-pulse focal transcranial magnetic stimulation. Three investigators studied the same subjects (n = 4) in three different sessions. A high variability was shown across subjects [coefficient of variation, (cv) 67.3% for ICI and 21.2% for ICF]. Intersession variability was up to 37.1% for ICI and 22.7% for ICF. Interinvestigator variability was 17.3% for ICI and negligible for ICF. Our results may have implications for planning future studies.
104 citations
TL;DR: Recruitment curves of FDI and TA showed significant facilitation during voluntary teeth clenching indicating an overall enhancement in the motor system excitability and an intracortical site of enhancement for the hand.
84 citations
TL;DR: Abnormalities of brain stem interneurons which are responsible for oligosynaptic exteroceptive suppression reflexes occur specifically in ST, and these findings further support the relevance of sensory inputs in the determinism of focal dystonias.
23 citations
TL;DR: A peripheral nerve injury can induce a rearrangement of reciprocal inhibition circuits at the spinal cord level and therefore predispose to the development of a focal dystonia, however, it is likely that another, yet unknown, factor is required to alter the intracortical circuits and produce a clinically evident dySTONia.
Abstract: Objective: To evaluate whether ulnar neuropathy could induce changes in spinal cord and motor cortex excitability and therefore predispose to development of focal dystonia. Background: A high incidence of ulnar neuropathy has been observed in patients with musician’s cramp. Polygraphic electromyograph recordings in patients with entrapment of the ulnar nerve at the elbow have demonstrated long-duration bursts of co-contraction in antagonistic muscles, similar to those observed in focal dystonia. Methods: All control subjects and 12 patients with ulnar neuropathy underwent an electrophysiologic protocol consisting of polygraphic recordings of a repetitive tapping task of the fourth finger, assessment of reciprocal inhibition in forearm muscles, and investigation of motor cortex excitability after paired transcranial magnetic stimulation. Results: Eleven of 12 patients with ulnar neuropathy showed a loss of alternation and of well-formed bursts in both flexor and extensor muscles. Evaluation of reciprocal inhibition in these patients revealed a reduction in the amount of inhibition in the disynaptic and presynaptic phases. None of the patients presented with a clinically evident dystonia of the upper limb. The study of intracortical excitability after paired shocks did not reveal any difference in the amount of intracortical inhibition and facilitation compared with the control group. Conclusions: A peripheral nerve injury can induce a rearrangement of reciprocal inhibition circuits at the spinal cord level. These changes might predispose to the development of a focal dystonia. However, it is likely that another, yet unknown, factor is required to alter the intracortical circuits and produce a clinically evident dystonia.
16 citations