The modulation of short and long-latency interhemispheric inhibition during bimanually coordinated movements

Author(s):  
Harry T. Jordan ◽  
Miriam Schrafl-Altermatt ◽  
Winston D. Byblow ◽  
Cathy M. Stinear
2013 ◽  
Vol 109 (12) ◽  
pp. 2955-2962 ◽  
Author(s):  
Soumya Ghosh ◽  
Arpan R. Mehta ◽  
Guan Huang ◽  
Carolyn Gunraj ◽  
Tasnuva Hoque ◽  
...  

Transcranial magnetic stimulation (TMS) of the human primary motor cortex (M1) at suprathreshold strength results in inhibition of M1 in the opposite hemisphere, a process termed interhemispheric inhibition (IHI). Two phases of IHI, termed short-latency interhemispheric inhibition (SIHI) and long-latency interhemispheric inhibition (LIHI), involving separate neural circuits, have been identified. In this study we evaluated how these two inhibitory processes interact with each other. We studied 10 healthy right-handed subjects. A test stimulus (TS) was delivered to the left M1, and motor evoked potentials (MEPs) were recorded from the right first dorsal interosseous (FDI) muscle. Contralateral conditioning stimuli (CCS) were applied to the right M1 either 10 ms or 50 ms prior to the TS, inducing SIHI and LIHI, respectively, in the left M1. The effects of SIHI and LIHI alone, and SIHI and LIHI delivered together, were compared. The TS was adjusted to produce 1-mV or 0.5-mV MEPs when applied alone or after CCS. SIHI and LIHI were found to be additive when delivered together, irrespective of the strength of the TS. The interactions were affected neither by varying the strength of the conditioning stimulus producing SIHI nor by altering the current direction of the TS. Small or opposing interactions, however, may not have been detected. These results support previous findings suggesting that SIHI and LIHI act through different neural circuits. Such inhibitory processes may be used individually or additively during motor tasks and should be studied as separate processes in functional studies.


2013 ◽  
Vol 109 (3) ◽  
pp. 659-665 ◽  
Author(s):  
Jie-Yuan Li ◽  
Ping-Hong Lai ◽  
Robert Chen

Recent studies in normal subjects suggested that callosal motor fibers pass through the posterior body of the corpus callosum (CC), but this has not been tested in patients with callosal infarction. The objective of this study is to define the pathways involved in transcallosal inhibition by examining patients with infarctions in different subregions of the CC. We hypothesized that patients with lesions in the posterior one-half of the CC would have greater reduction in transcallosal inhibition between the motor cortices. Twenty-six patients with callosal infarction and 14 healthy subjects were studied. The callosal lesions were localized on sagittal MRI and were attributed to one of five segments of the CC. Transcranial magnetic stimulation was used to assess ipsilateral silent period (iSP) and short- and long-latency interhemispheric inhibition (SIHI and LIHI, respectively) originating from both motor cortices. The results showed that the iSP areas and durations were markedly reduced bilaterally in patients with callosal infarction compared with normal subjects. Patients with callosal infarctions also had less IHI bidirectionally compared with normal subjects. iSP areas and durations were lower in patients with lesions than in patients without lesions in segment 3 (posterior midbody) of the CC. Lesion burden in the posterior one-half of the CC negatively correlated transcallosal inhibition measured with iSP and SIHI. Our study suggests that callosal infarction led to reduced transcallosal inhibition, as measured by iSP, SIHI, and LIHI. Fibers mediating transcallosal inhibition cross the CC mainly in the posterior one-half.


1977 ◽  
Vol 40 (3) ◽  
pp. 626-646 ◽  
Author(s):  
C. K. Knox ◽  
S. Kubota ◽  
R. E. Poppele

1. Responses of DSCT neurons to random electrical stimulation of peripheral nerves of the hindleg at group I intensity were studied using cross-correlation analysis of the output spike train with the stimulus. Three types of response were found: type 1 was due to monosynaptic activation of DSCT cells, type 2 resulted from inhibition of those cells, and type 3 was due to a long-latency excitation that was probably polysynaptic. 2. Most of the units studied responded to stimulation of both proximal and distal flexor and extensor nerves. The extensive convergence of afferent input on DSCT cells is much greater than has been observed previously, with type 2 and type 3 responses totaling 80% of the observed responses. We attribute this to the sensitivity of the analysis in detecting small changes in postsynaptic excitability. 3. The results of the study, particularly the derivation of postsynaptic excitability changes, generally confirm those of earlier work employing intracellular recording. 4. By varying stimulus rate and stimulus intensity in the group 1 range and simulating the resulting correlations, we conclude that excitability changes in DSCT cells are the net result of complex interactions involving excitation and inhibition. A summary of these findings is presented as a model for the minimum circuitry necessary to account for the observed behavior.


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