Investigation of the primary visual cortex using short-interval paired-pulse transcranial magnetic stimulation (TMS)

Sparing, Roland; Dambeck, Nina; Stock, K. F.; Meister, Ingo G.; Huetter, Dorothee; Boroojerdi, Babak

doi:10.1016/j.neulet.2005.03.036

Cited by 30 publications

(24 citation statements)

References 30 publications

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“…The observation demonstrates one more physiological difference between the reaction of motor cortex and visual cortex to magnetic stimulation, since in the motor system with increasing stimulation intensity the number of evoked I-waves and thus the duration of the cortical responses increase. It is in line with the observation that the visual system does not generate short interval intracortical inhibition (SICI) applying paired-pulse stimuli in the intensity sequence subthreshold-suprathreshold, as has been shown both in humans (Sparing et al, 2005) and cats (Moliadze et al, 2005). The present study is the seventh on phosphenes from our laboratory.…”

Section: Discussionsupporting

confidence: 87%

“…With double pulses at a SOA of 50 ms phosphene thresholds decreased to 0.7 of single pulse thresholds both in healthy subjects and in migraine patients. Sparing et al (2005) investigated phosphene detection rates with double pulses of different intensities at SOAs between 2 and 12 ms. They searched for an equivalent of short-interval intracortical inhibition (SICI) known from the motor system (Kujirai et al, 1993;Ilic et al, 2002) expecting an increase in phosphene threshold with double pulses in the sequence sub threshold -supra threshold stimulation intensity.…”

Section: Introductionmentioning

confidence: 99%

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Phosphene thresholds evoked with single and double TMS pulses

Kammer

Baumann

2010

Clinical Neurophysiology

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Section: Discussionsupporting

confidence: 87%

Section: Introductionmentioning

confidence: 99%

Phosphene thresholds evoked with single and double TMS pulses

Kammer

Baumann

2010

Clinical Neurophysiology

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“…Four subjects were unable to perceive phosphenes even at maximum stimulator output. Such a failure rate is in accordance with previous studies of phosphene elicitation (22,29,30). However, all subjects who were not able to perceive phosphenes had a MT in the normal range.…”

Section: Subjectssupporting

confidence: 91%

“…Boroojerdi and coworkers (5) found involvement of GABAergic inhibition and NMDA receptor activation in rapid processes of human visual cortex plasticity by using PT as a measurement of V1 excitability. On the contrary, it has been shown that the mechanisms underlying phosphene induction in V1 are probably different from those underlying intracortical inhibition and facilitation in M1 (29).…”

Section: Possible Pathophysiological Mechanisms Of Hv On Neuronal Excmentioning

confidence: 95%

Excitability of human motor and visual cortex before, during, and after hyperventilation

Sparing¹,

Dafotakis²,

Buelte³

et al. 2007

Journal of Applied Physiology

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Sparing R, Dafotakis M, Buelte D, Meister IG, Noth J. Excitability of human motor and visual cortex before, during, and after hyperventilation. J Appl Physiol 102: 406 -411, 2007. First published September 21, 2006; doi:10.1152/japplphysiol.00770.2006.-In humans, hyperventilation (HV) has various effects on systemic physiology and, in particular, on neuronal excitability and synaptic transmission. However, it is far from clear how the effects of HV are mediated at the cortical level. In this study we investigated the effects of HV-induced hypocapnia on primary motor (M1) and visual cortex (V1) excitability. We used 1) motor threshold (MT) and phosphene threshold (PT) and 2) stimulus-response (S-R) curves (i.e., recruitment curves) as measures of excitability. In the motor cortex, we additionally investigated 3) the intrinsic inhibitory and facilitatory neuronal circuits using a short-interval paired-pulse paradigm. Measurements were performed before, during, and after 10 min of HV (resulting in a minimum end-tidal PCO2 of 15 Torr). HV significantly increased motor-evoked potential (MEP) amplitudes, particularly at lower transcranial magnetic stimulation (TMS) intensities. Pairedpulse stimulation indicated that HV decreases intracortical inhibition (ICI) without changing intracortical facilitation. The results suggest that low PCO 2 levels modulate, in particular, the intrinsic neuronal circuits of ICI, which are largely mediated by neurons containing ␥-aminobutyric acid. Modulation of MT probably resulted from alterations of Na ϩ channel conductances. A significant decrease of PT, together with higher intensity of phosphenes at low stimulus intensities, furthermore suggested that HV acts on the excitability of M1 and V1 in a comparable fashion. This finding implies that HV also affects other brain structures besides the corticospinal motor system. The further exploration of these physiological mechanisms may contribute to the understanding of the various HV-related clinical phenomenona. partial pressure of carbon dioxide; phosphenes; threshold; pairedpulse transcranial magnetic stimulation; intracortical facilitation; intracortical inhibition HYPERVENTILATION (HV) (or hyperpnea) is the state of breathing faster or deeper than necessary, thereby reducing the CO 2 concentration of the blood below normal. What is usually referred to as HV is, in fact, hypocapnia. Since a reduction of arterial PCO 2 (Pa CO 2 ) below the normal level (40 Torr) is obtained by increasing the alveolar ventilation, HV became synonymous with hypocapnia (32). HV is known to have various effects on human physiology (for a review, see Ref. 6).For instance, a reduction in Pa CO 2 increases the excitability of sensory and motor axons in the peripheral nervous system (21,23,28).The aim of the present study was to investigate further the neural mechanisms of the HV-induced changes in cortical excitability. As measures of primary motor cortex (M1) excitability, motor threshold (MT), stimulus-response (S-R) curves (i.e., recruitment curves), intra...

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“…Similar patterns of inhibition and facilitation can be induced in motor (Maeda, Gangitano, Thall, & Pascual-Leone, 2002), prefrontal (Oliveri, Caltagirone, et al, 2000;Oliveri, Rossini, et al, 2000) and parietal (Oliveri, Caltagirone, et al, 2000;Oliveri, Rossini, et al, 2000) cortex. In the visual cortex such reversing patterns of excitation and inhibition have not been observed (Kammer & Baumann, 2010;Moliadze, Giannikopoulos, Eysel, & Funke, 2005;Sparing et al, 2005) and little is known about the effects of longer ISIs (for an exception see Ray, Meador, Epstein, Loring, & Day, 1998).…”

Section: Introductionmentioning

confidence: 99%