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FC45.2 Inhibitory effect on cortical silent period following transcranial magnetic stimulation over the cerebellum
Oral Communications / Clinical Neurophysiology 117 (2006) S49–S111
by dipping them into icewater. Simultaneously to these interventions the subject was asked to turn its attention (i) to the right, (ii) to the left or (iii) to neither hand. Dipole source reconstruction was based on a 96-channel arrangement. The location and the 3D-distance of the sources representing the primary somatosensory area of D1 and D5 were analysed. Results: After anesthesia as well as the application of pain to digit D2–D4 a significant enlargement of the 3D-distance of digit D1–D5 could be shown. In particular the cortical representation of the thumb shifted towards the front, along the gyrus postcentralis. Directing attention to the stimulated limb, respectively, the site of the intervention did not yield to an additional effect. Conclusion: The present results give evidence for short term cortical plasticity of the primary somatosensory cortex derived by interventions to the limb contralateral to the stimulus in median nerve SEP. These effects are most probably mediated by transcallosal disinhibition as has been hypothesized from animal data. This alteration seems not to be additionally affected by spatial attention to the stimuli, presumably due to a saturation of the system by the intervention itself. doi:10.1016/j.clinph.2006.06.148
FC45.2 Inhibitory effect on cortical silent period following transcranial magnetic stimulation over the cerebellum Y. Nakamura, I. Yamada, H. Sakamoto Sakai Hospital, Kinki University School of Medicine, Japan Background: Transcranial magnetic cerebellar stimulation (cerebellar TMS) can make early inhibition (ISIs of 4–10 ms) of motor cortex. However, there is less study on late intracortical inhibition. Our experiment aims to clarify the effect of late intracortical inhibition on cerebellar TMS. Methods and patients: Seven normal subjects and twelve ataxic patients (MSA 7, CCA 5) were enrolled. For CSP, TMS over the hand motor area was done during muscle contraction. The paradigm of double magnetic stimulation was used; the first stimulation of cerebellum (condition) following the second stimulation (test) of motor cortex. The first stimulation intensity was 90% active threshold with double-cone coil on ipsilateral cerebellar hemisphere. Test stimulation was done on hand motor area with 150% active threshold intensity. Stimulation paradigm was composed of two conditions: one was test stimulus alone, and another was condition-test stimuli. The CSP and amplitude of MEP were measured. CSP and amplitude of MEP were expressed as a percentage of unconditioned response. Results: CSP for test stimulus alone in normal subjects, MSA and CCA was 80.2 ± 22.6, 91.0 ± 41.0 and
S109
114.1 ± 59.1 ms, respectively. After cerebellar TMS, the percentage of CSP in normal subjects, MSA, and CCA was significantly decreased (77.1 ± 18.7%, 77.1 ± 18.7% and 90 ± 11.4%, respectively). The amplitude of MEP in normal subjects, MSA, and CCA after cerebellar TMS was not decreased (104.4 ± 11.4%, 98.6 ± 11.3% and 112.5 ± 14.4%, respectively). Discussion: Cerebellar TMS can have significant decrease of CSP in normal subjects and patients with ataxia, but there was no significant change of amplitude of MEP. Patients with ataxia had been known to be no early inhibition of motor cortex followed by cerebellar TMS. However, CSP could be produced by late intracortical inhibition, our finding suggests that cerebellar TMS could inhibit intracortical inhibition in both normal subjects and patients with ataxia. doi:10.1016/j.clinph.2006.06.149
FC45.3 Effect of paired associative stimulation (PAS) on the interaction between afferent stimulation and long interval intracortical inhibition (LICI) S. Meunier, H. Russmann, M. Hallett NINDS/NIH, HMCS, USA Background: After paired-associative stimulation (PAS) corticospinal excitability is increased for 30–60 min. Short intracortical inhibition, which is mediated by GABAA, is normal after PAS, but the cortical silent period (SP) is shortened. The SP is a product of both spinal and cortical (presumably GABAB) inhibition. Objective: To investigate the effect of PAS intervention on long intracortical inhibition (LICI), a GABAB inhibitory circuit, and its interaction (I) with peripheral stimulation that induces long afferent inhibition (LAI). Methods: We studied 12 control subjects. rget muscle was the flexor pollicis brevis (FPB). LICI was tested by pairing 2 suprathreshold TMS pulses (ISI 90 ms). Interaction between LICI and LAI was tested by comparing LICI with and without a median nerve stimulation (med) applied 240 ms before the test stimulus (i.e., 150 ms before the conditioning TMS). I was calculated as follows: [LICI with med LICI without med]/LICI without med. PAS was induced by pairing median nerve stimulation and TMS targeting FPB (0.2 Hz, 25 ms interstimulus interval). Subjects were monitored before PAS intervention (t0), immediately after PAS (t1) and 45 min after PAS (t2). Results: At t0, LICI [conditioned MEP/test MEP 1] was 54%. Immediately after PAS LICI was decreased (t1: 39%) and even further decreased 45 min after the end of PAS (t2: 25%). A strong inhibitory interaction was found between LICI and LAI at t0, but this was not significantly modified by PAS.
by dipping them into icewater. Simultaneously to these interventions the subject was asked to turn its attention (i) to the right, (ii) to the left or (iii) to neither hand. Dipole source reconstruction was based on a 96-channel arrangement. The location and the 3D-distance of the sources representing the primary somatosensory area of D1 and D5 were analysed. Results: After anesthesia as well as the application of pain to digit D2–D4 a significant enlargement of the 3D-distance of digit D1–D5 could be shown. In particular the cortical representation of the thumb shifted towards the front, along the gyrus postcentralis. Directing attention to the stimulated limb, respectively, the site of the intervention did not yield to an additional effect. Conclusion: The present results give evidence for short term cortical plasticity of the primary somatosensory cortex derived by interventions to the limb contralateral to the stimulus in median nerve SEP. These effects are most probably mediated by transcallosal disinhibition as has been hypothesized from animal data. This alteration seems not to be additionally affected by spatial attention to the stimuli, presumably due to a saturation of the system by the intervention itself. doi:10.1016/j.clinph.2006.06.148
FC45.2 Inhibitory effect on cortical silent period following transcranial magnetic stimulation over the cerebellum Y. Nakamura, I. Yamada, H. Sakamoto Sakai Hospital, Kinki University School of Medicine, Japan Background: Transcranial magnetic cerebellar stimulation (cerebellar TMS) can make early inhibition (ISIs of 4–10 ms) of motor cortex. However, there is less study on late intracortical inhibition. Our experiment aims to clarify the effect of late intracortical inhibition on cerebellar TMS. Methods and patients: Seven normal subjects and twelve ataxic patients (MSA 7, CCA 5) were enrolled. For CSP, TMS over the hand motor area was done during muscle contraction. The paradigm of double magnetic stimulation was used; the first stimulation of cerebellum (condition) following the second stimulation (test) of motor cortex. The first stimulation intensity was 90% active threshold with double-cone coil on ipsilateral cerebellar hemisphere. Test stimulation was done on hand motor area with 150% active threshold intensity. Stimulation paradigm was composed of two conditions: one was test stimulus alone, and another was condition-test stimuli. The CSP and amplitude of MEP were measured. CSP and amplitude of MEP were expressed as a percentage of unconditioned response. Results: CSP for test stimulus alone in normal subjects, MSA and CCA was 80.2 ± 22.6, 91.0 ± 41.0 and
S109
114.1 ± 59.1 ms, respectively. After cerebellar TMS, the percentage of CSP in normal subjects, MSA, and CCA was significantly decreased (77.1 ± 18.7%, 77.1 ± 18.7% and 90 ± 11.4%, respectively). The amplitude of MEP in normal subjects, MSA, and CCA after cerebellar TMS was not decreased (104.4 ± 11.4%, 98.6 ± 11.3% and 112.5 ± 14.4%, respectively). Discussion: Cerebellar TMS can have significant decrease of CSP in normal subjects and patients with ataxia, but there was no significant change of amplitude of MEP. Patients with ataxia had been known to be no early inhibition of motor cortex followed by cerebellar TMS. However, CSP could be produced by late intracortical inhibition, our finding suggests that cerebellar TMS could inhibit intracortical inhibition in both normal subjects and patients with ataxia. doi:10.1016/j.clinph.2006.06.149
FC45.3 Effect of paired associative stimulation (PAS) on the interaction between afferent stimulation and long interval intracortical inhibition (LICI) S. Meunier, H. Russmann, M. Hallett NINDS/NIH, HMCS, USA Background: After paired-associative stimulation (PAS) corticospinal excitability is increased for 30–60 min. Short intracortical inhibition, which is mediated by GABAA, is normal after PAS, but the cortical silent period (SP) is shortened. The SP is a product of both spinal and cortical (presumably GABAB) inhibition. Objective: To investigate the effect of PAS intervention on long intracortical inhibition (LICI), a GABAB inhibitory circuit, and its interaction (I) with peripheral stimulation that induces long afferent inhibition (LAI). Methods: We studied 12 control subjects. rget muscle was the flexor pollicis brevis (FPB). LICI was tested by pairing 2 suprathreshold TMS pulses (ISI 90 ms). Interaction between LICI and LAI was tested by comparing LICI with and without a median nerve stimulation (med) applied 240 ms before the test stimulus (i.e., 150 ms before the conditioning TMS). I was calculated as follows: [LICI with med LICI without med]/LICI without med. PAS was induced by pairing median nerve stimulation and TMS targeting FPB (0.2 Hz, 25 ms interstimulus interval). Subjects were monitored before PAS intervention (t0), immediately after PAS (t1) and 45 min after PAS (t2). Results: At t0, LICI [conditioned MEP/test MEP 1] was 54%. Immediately after PAS LICI was decreased (t1: 39%) and even further decreased 45 min after the end of PAS (t2: 25%). A strong inhibitory interaction was found between LICI and LAI at t0, but this was not significantly modified by PAS.