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68. Defective Motor Cortex Plasticity in juvenile myoclonic epilepsy
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Abstracts / Clinical Neurophysiology 127 (2016) e323–e341
Repeated measures ANOVA showed a trend to significance in MEP amplitude increase in T20 and T30 (p = 0.066 and 0.057 respectively) and a significant increase in T60 (p = 0.047) in patients without Riluzole. In patients assuming Riluzole, no significant change in MEP amplitude was found. Riluzole could impair sensory-motor integrative circuits, as evaluated by PAS protocol. doi:10.1016/j.clinph.2016.10.079
68. Defective Motor Cortex Plasticity in juvenile myoclonic epilepsy—C. Pizzamiglio, G. Strigaro, L. Falletta, G. Tondo, P. Barbero, C. Varrasi, R. Cantello (Novara, Italy)
Abnormal cortical plasticity has been hypothesized to play a crucial role in the pathogenesis of juvenile myoclonic epilepsy (JME). We used an excitatory paired associative stimulation (PAS) paradigm to study motor cortex plasticity in patients with JME. Twelve adult patients with JME were compared with 13 healthy subjects (HS) of similar age and sex. PAS consisted of 180 electrical stimuli of the right median nerve paired with a single transcranial magnetic stimulation (TMS) stimulus over the hotspot of right abductor pollicis brevis (APB) at an ISI of 25 ms (PAS25). We measured motor evoked potentials (MEPs) before and after each intervention for up to 30 min. Data entered repetitive measure ANOVAs. In HS the PAS25 protocol was followed by a significant increase of the MEP amplitude (p<0.001). In patients with JME, the MEP amplitude did not change. We suggest that a defective motor cortex plasticity may play a role in the pathogenesis of JME and it may be involved in the development of myoclonus in these patients. doi:10.1016/j.clinph.2016.10.080
69. Impaired spike timing dependent cortico-cortical plasticity in Alzheimer’s Disease patients—F. Di Lorenzo, A. Martorana, V. Ponzo, S. Bonní, G. Koch (Roma, Italy)
Mechanisms of cortical plasticity have been widely investigated in Alzheimer’s Disease (AD) patients with transcranial magnetic stimulation (TMS) protocols as Theta Burst Stimulation, showing a clear impairment of Long-Term Potentiation (LTP) cortical-like plasticity and a relative sparing of Long Term Depression (LTD) mechanisms. Recently a new TMS protocol, investigating the connections between posterior parietal cortex (PPC) and primary motor cortex (M1), elicited in a bidirectional way LTP and LTD effects. The aim of our study is to investigate mechanisms of spike-timing dependent plasticity in Alzheimer’s disease patients and furthermore to investigate the effects of the modulation of PPC-M1 pathway on cholinergic transmission, greatly impaired in AD patients. Twelve AD patients and eight age-matched healthy subjects were evaluated. We used bifocal TMS to repeatedly activate the connection between the PPC and M1 of the left-dominant hemisphere. Left PPC TMS preceded or followed the M1 stimulation by 5 ms, respectively PAS +5 and PAS 5. To best activate the ipsilateral PPC‑‘M1 connection, the conditioning stimulus was applied over the left PPC at an intensity of 90% of the ipsilateral resting motor threshold. For the PAS protocol, 100 pairs of stimuli were continuously delivered at a rate of 0.2 Hz for âˆ1/48.3 min. Motor evoked potentials and central cholinergic pathway, evaluated with Short-latency afferent
inhibition (SAI) protocol, were evaluated before and after PAS (+5 or 5) protocol. As expected HS showed an LTP-like cortical plasticity following PAS 5 protocol and an LTD-like cortical plasticity after PAS +5 protocol, while AD patients didn’t show any significant modification of the amplitude of MEP after repeated activation of PPC-M1 connections. As compared to HS, AD patients showed worst SAI values. Interestingly, after PAS +5 protocol, in AD patients SAI levels were restored. The data here presented confirm that in AD patients there is an altered cortical plasticity, elicited with a new TMS protocol able to investigate the connections between PPC-M1. The central cholinergic pathway as indexed by the amount of SAI, is altered in AD patients, but it is normalized after the application of PAS +5 protocol, suggesting a possible role of PPC-M1 pathway on the modulation of this inhibitory intracortical circuit. PAS protocol is able to investigate the mechanisms of altered cortical plasticity in AD patients. Central cholinergic transmission can be modulated by stimulation of PPC-M1 connections. doi:10.1016/j.clinph.2016.10.081
70. Effects of music reading on motor cortex excitability— F. Giovannelli, S. Rossi, A. Borgheresi, M. Calistri, G. Zaccara, G. Avanzini, M.P. Viggiano, M. Cincotta (Firenze, Italy, Siena, Italy, Milano, Italy)
Neurophysiological studies suggest that reading sheet music facilitates sensorimotor cortex in musicians. The aim of the present study was twofold: to evaluate (1) whether in piano players, reading notes in the bass clef (usually played with the left hand) and in the treble clef (usually played with the right hand) selectively enhances right and left M1 excitability, respectively (inter-hemispheric effect); and (2) whether reading notes played with the thumb or with the little finger selectively modulate the excitability of the abductor pollicis brevis (APB) and abductor digitorum minimi (ADM) muscles, respectively (intra-hemispheric effect). Seven pianists participated to the study. Single pulse TMS was applied to either M1 while subjects alternatively read the bass or the treble clef of five sheets music without any movements. As a baseline condition TMS was delivered during the observation of a blank pentagram. When subjects read the treble clef, the excitability of the left M1 was significantly higher compared to that recorded in the right M1. No significant differences emerged during reading of the bass clef. Moreover, motor-evoked potentials were higher in the ADM muscle regardless the note. These preliminary data support the view that music reading may induce specific inter-hemispheric modulation of the motor cortex excitability. doi:10.1016/j.clinph.2016.10.082
71. Cerebellum modulates defensive response within the peripersonal space—D. Barloscio, L. Parenti, M. Bartolotta, M. Vergari, R. Ferrucci, A. Priori, E. Santarcangelo, A. Di Rollo, G. Carli, F. Sartucci, T. Bocci (Pisa, Italy, Siena, Italy, Milano, Italy)
We evaluated the role of cerebellum in defensive responses, by recording the Hand Blink Reflex (HBR) and modulating cerebellar activity with transcranial Direct Current Stimulation (tDCS). The active electrode was centered on the median line 2 cm below the
Abstracts / Clinical Neurophysiology 127 (2016) e323–e341
Repeated measures ANOVA showed a trend to significance in MEP amplitude increase in T20 and T30 (p = 0.066 and 0.057 respectively) and a significant increase in T60 (p = 0.047) in patients without Riluzole. In patients assuming Riluzole, no significant change in MEP amplitude was found. Riluzole could impair sensory-motor integrative circuits, as evaluated by PAS protocol. doi:10.1016/j.clinph.2016.10.079
68. Defective Motor Cortex Plasticity in juvenile myoclonic epilepsy—C. Pizzamiglio, G. Strigaro, L. Falletta, G. Tondo, P. Barbero, C. Varrasi, R. Cantello (Novara, Italy)
Abnormal cortical plasticity has been hypothesized to play a crucial role in the pathogenesis of juvenile myoclonic epilepsy (JME). We used an excitatory paired associative stimulation (PAS) paradigm to study motor cortex plasticity in patients with JME. Twelve adult patients with JME were compared with 13 healthy subjects (HS) of similar age and sex. PAS consisted of 180 electrical stimuli of the right median nerve paired with a single transcranial magnetic stimulation (TMS) stimulus over the hotspot of right abductor pollicis brevis (APB) at an ISI of 25 ms (PAS25). We measured motor evoked potentials (MEPs) before and after each intervention for up to 30 min. Data entered repetitive measure ANOVAs. In HS the PAS25 protocol was followed by a significant increase of the MEP amplitude (p<0.001). In patients with JME, the MEP amplitude did not change. We suggest that a defective motor cortex plasticity may play a role in the pathogenesis of JME and it may be involved in the development of myoclonus in these patients. doi:10.1016/j.clinph.2016.10.080
69. Impaired spike timing dependent cortico-cortical plasticity in Alzheimer’s Disease patients—F. Di Lorenzo, A. Martorana, V. Ponzo, S. Bonní, G. Koch (Roma, Italy)
Mechanisms of cortical plasticity have been widely investigated in Alzheimer’s Disease (AD) patients with transcranial magnetic stimulation (TMS) protocols as Theta Burst Stimulation, showing a clear impairment of Long-Term Potentiation (LTP) cortical-like plasticity and a relative sparing of Long Term Depression (LTD) mechanisms. Recently a new TMS protocol, investigating the connections between posterior parietal cortex (PPC) and primary motor cortex (M1), elicited in a bidirectional way LTP and LTD effects. The aim of our study is to investigate mechanisms of spike-timing dependent plasticity in Alzheimer’s disease patients and furthermore to investigate the effects of the modulation of PPC-M1 pathway on cholinergic transmission, greatly impaired in AD patients. Twelve AD patients and eight age-matched healthy subjects were evaluated. We used bifocal TMS to repeatedly activate the connection between the PPC and M1 of the left-dominant hemisphere. Left PPC TMS preceded or followed the M1 stimulation by 5 ms, respectively PAS +5 and PAS 5. To best activate the ipsilateral PPC‑‘M1 connection, the conditioning stimulus was applied over the left PPC at an intensity of 90% of the ipsilateral resting motor threshold. For the PAS protocol, 100 pairs of stimuli were continuously delivered at a rate of 0.2 Hz for âˆ1/48.3 min. Motor evoked potentials and central cholinergic pathway, evaluated with Short-latency afferent
inhibition (SAI) protocol, were evaluated before and after PAS (+5 or 5) protocol. As expected HS showed an LTP-like cortical plasticity following PAS 5 protocol and an LTD-like cortical plasticity after PAS +5 protocol, while AD patients didn’t show any significant modification of the amplitude of MEP after repeated activation of PPC-M1 connections. As compared to HS, AD patients showed worst SAI values. Interestingly, after PAS +5 protocol, in AD patients SAI levels were restored. The data here presented confirm that in AD patients there is an altered cortical plasticity, elicited with a new TMS protocol able to investigate the connections between PPC-M1. The central cholinergic pathway as indexed by the amount of SAI, is altered in AD patients, but it is normalized after the application of PAS +5 protocol, suggesting a possible role of PPC-M1 pathway on the modulation of this inhibitory intracortical circuit. PAS protocol is able to investigate the mechanisms of altered cortical plasticity in AD patients. Central cholinergic transmission can be modulated by stimulation of PPC-M1 connections. doi:10.1016/j.clinph.2016.10.081
70. Effects of music reading on motor cortex excitability— F. Giovannelli, S. Rossi, A. Borgheresi, M. Calistri, G. Zaccara, G. Avanzini, M.P. Viggiano, M. Cincotta (Firenze, Italy, Siena, Italy, Milano, Italy)
Neurophysiological studies suggest that reading sheet music facilitates sensorimotor cortex in musicians. The aim of the present study was twofold: to evaluate (1) whether in piano players, reading notes in the bass clef (usually played with the left hand) and in the treble clef (usually played with the right hand) selectively enhances right and left M1 excitability, respectively (inter-hemispheric effect); and (2) whether reading notes played with the thumb or with the little finger selectively modulate the excitability of the abductor pollicis brevis (APB) and abductor digitorum minimi (ADM) muscles, respectively (intra-hemispheric effect). Seven pianists participated to the study. Single pulse TMS was applied to either M1 while subjects alternatively read the bass or the treble clef of five sheets music without any movements. As a baseline condition TMS was delivered during the observation of a blank pentagram. When subjects read the treble clef, the excitability of the left M1 was significantly higher compared to that recorded in the right M1. No significant differences emerged during reading of the bass clef. Moreover, motor-evoked potentials were higher in the ADM muscle regardless the note. These preliminary data support the view that music reading may induce specific inter-hemispheric modulation of the motor cortex excitability. doi:10.1016/j.clinph.2016.10.082
71. Cerebellum modulates defensive response within the peripersonal space—D. Barloscio, L. Parenti, M. Bartolotta, M. Vergari, R. Ferrucci, A. Priori, E. Santarcangelo, A. Di Rollo, G. Carli, F. Sartucci, T. Bocci (Pisa, Italy, Siena, Italy, Milano, Italy)
We evaluated the role of cerebellum in defensive responses, by recording the Hand Blink Reflex (HBR) and modulating cerebellar activity with transcranial Direct Current Stimulation (tDCS). The active electrode was centered on the median line 2 cm below the