Non-stimulated Hemisphere Research Articles

Theta burst stimulation induces after‐effects on contralateral primary motor cortex excitability in humans

Interhemispheric interactions between the primary motor cortices (M1) have been described with a variety of TMS methods. Here we give a detailed description of the interhemispheric interactions of a period of theta burst simulation (TBS), a rapid method of producing long lasting after-effects on the excitability of the stimulated M1. A total of 18 right handed healthy subjects participated. In most experiments, continuous and intermittent TBS (cTBS and iTBS) were delivered over the right M1 using a coil orientated to induce antero-posterior followed by postero-anterior (AP-PA) currents in the brain. The intensity of stimulation was 80% of active motor threshold (AMT), and a total of 600 pulses were applied. The effects on the amplitude of motor evoked potentials (MEPs), short interval intracortical inhibition (SICI) and intracortical facilitation (ICF) were evaluated in the left and right M1 before and at three different times after TBS. We also tested long-interval intracortical inhibition (LICI) in right M1 and interhemispheric inhibition (IHI) from right to left M1. Finally, to explore the effect of different polarities of cTBS over dominant and non-dominant hemisphere we delivered AP-PA and postero-anterior followed by antero-posterior (PA-AP) cTBS over either right or left M1 and tested MEPs in both hemispheres. In the stimulated hemisphere, cTBS reduced MEPs and SICI whereas iTBS increased MEPs and SICI. In the non-stimulated hemisphere cTBS increased MEPs and reduced SICI, while iTBS reduced MEPs and increased SICI. There were no effects on ICF, LICI or IHI. Although both AP-PA cTBS and PA-AP cTBS reduced MEPs in the stimulated M1, the former increased MEPs from non-stimulated M1 whereas the latter did not. There was no difference in the effect of cTBS on the dominant or non-dominant hemisphere.

Acute Remapping within the Motor System Induced by Low-Frequency Repetitive Transcranial Magnetic Stimulation

Repetitive transcranial magnetic stimulation (rTMS) of human primary motor cortex (M1) changes cortical excitability at the site of stimulation and at distant sites without affecting simple motor performance. The aim of this study was to explore how rTMS changes regional excitability and how the motor system compensates for these changes. Using functional brain imaging, activation was mapped at rest and during freely selected finger movements after 30 min of 1 Hz rTMS. rTMS increased synaptic activity in the stimulated left M1 and induced widespread changes in activity throughout areas engaged by the task. In particular, movement-related activity in the premotor cortex of the nonstimulated hemisphere increased after 1 Hz rTMS. Analyses of effective connectivity confirmed that the stimulated part of M1 became less responsive to input from premotor and mesial motor areas. Conversely, after rTMS our results were consistent with increased coupling between an inferomedial portion of left M1 and anterior motor areas. These results are important for three reasons. First, they show changes in motor excitability to central inputs from other cortical areas (as opposed to peripheral or exogenous inputs used in previous studies). Second, they suggest that maintenance of task performance may involve activation of premotor areas contralateral to the site of rTMS, similar to that seen in stroke patients. Third, changes in motor activations at the site of rTMS suggest an rTMS-induced remodeling of motor representations during movement. This remapping may provide a neural substrate for acute compensatory plasticity of the motor system in response to focal lesions such as stroke.

Effect of hemisphere-selective repetitive magnetic brain stimulation on middle cerebral artery blood flow velocity

The changes of cerebral hemodynamics following repetitive hemisphere-selective magnetic stimulation over the motor cortex were investigated in 8 healthy volunteers. Bilateral simultaneous monitoring of middle cerebral artery blood flow velocity was done using transcranial Doppler ultrasonography during magnetic stimulation with single, double and triple stimuli with interstimulus intervals of 100 msec. Magnetic cortex stimulation was followed by a significant increase of ipsilateral flow velocity ranging from 5.3% ± 2.7% for single stimuli up to 8.5% ± 4.1% for triple stimuli and by a smaller increase of contralateral flow velocity. The ipsilateral increases are comparable to those measured previously during voluntary finger movements and indicate a physiological cortex stimulation. In parallel, the average sum of the baseline to peak hand motor response amplitudes increased from 1.5 ± 0.7 mV (single stimuli) to 4.5 ± 3.2 mV (triple stimuli). The increase of flow velocity in the non-stimulated hemisphere occurred during the absence of motor responses and might reflect a transcallosal activation of inhibitory neuronal structures. The occurrence of maximum velocity responses within 2–3 heartbeats following the first cortex stimulus points to a fast adjustment of cerebral perfusion in response to transcranial brain stimulation. No significant change of flow velocity was observed following motor responses evoked by unilateral magnetic stimulation of the brachial plexus or following acoustic artifacts of the coil discharge.

Lasting influence of amygdaloid kindling on cholinergic neurotransmission

Possible biochemical changes in cholinergic systems were investigated in nine brain regions of rats kindled by daily amygdaloid stimulation. Choline acetyltransferase (CAT) activity in the kindled animals was significantly decreased bilaterally in the frontal cortex, amygdala, and hippocampus. No such bilateral changes were found in specific muscarinic cholinergic receptor binding. In the stimulated hemisphere, muscarinic cholinergic receptor binding was decreased in the frontal cortex but increased in the amygdala. In the nonstimulated hemisphere, that receptor binding increased in the pyriform cortex. These results imply persistent effects of amygdaloid kindling on cholinergic neurotransmission.