Ko HY. Korean J Neurotrauma. 2018 Oct;14(2):47-54. https://doi.org/10.13004/kjnt.2018.14.2.47

Background: To observe brain activation induced by functional electrical stimulation, voluntary contraction, and the combination of both using functional magnetic resonance imaging (fMRI). Methods: Nineteen healthy young men were enrolled in the study. We employed a typical block design that consisted of three sessions: voluntary contraction only, functional electrical stimulation (FES)-induced wrist extension, and finally simultaneous voluntary and FES-induced movement. MRI acquisition was performed on a 3.0 T MR system. To investigate activation in each session, one-sample t-tests were performed after correcting for false discovery rate (FDR; p < 0.05). To compare FES-induced movement and combined contraction, a two-sample t-test was performed using a contrast map (p < 0.01). Results: In the voluntary contraction alone condition, brain activation was observed in the contralateral primary motor cortex (MI), thalamus, bilateral supplementary motor area (SMA), primary sensory cortex (SI), secondary somatosensory motor cortex (SII), caudate, and cerebellum (mainly ipsilateral). During FES-induced wrist movement, brain activation was observed in the contralateral MI, SI, SMA, thalamus, ipsilateral SII, and cerebellum. During FES-induced movement combined with voluntary contraction, brain activation was found in the contralateral MI, anterior cingulate cortex (ACC), SMA, ipsilateral cerebellum, bilateral SII, and SI. The activated brain regions (number of voxels) of the MI, SI, cerebellum, and SMA were largest during voluntary contraction alone and smallest during FES alone. SII-activated brain regions were largest during voluntary contraction combined with FES and smallest during FES contraction alone. The brain activation extent (maximum t score) of the MI, SI, and SII was largest during voluntary contraction alone and smallest during FES alone. The brain activation extent of the cerebellum and SMA during voluntary contraction alone was similar during FES combined with voluntary contraction; however, cerebellum and SMA activation during FES movement alone was smaller than that of voluntary contraction alone or voluntary contraction combined with FES. Between FES movement alone and combined contraction, activated regions and extent due to combined contraction was significantly higher than that of FES movement alone in the ipsilateral cerebellum and the contralateral MI and SI. Conclusions: Voluntary contraction combined with FES may be more effective for brain activation than FES-only movements for rehabilitation therapy. In addition, voluntary effort is the most important factor in the therapeutic process.

One of the pathophysiologies of post-stroke spasticity (PSS) is the imbalance of the reticulospinal tract (RST) caused by injury to the corticoreticular pathway (CRP) after stroke. We investigated the relationship between injuries of the CRP and PSS using MR diffusion tensor imaging (DTI). The subjects were divided into spasticity and control groups. We measured the ipsilesional fractional anisotropy (iFA) and contralesional fractional anisotropy (cFA) values on the reticular formation (RF) of the CRP were on the DTI images. We carried out a retrospective analysis of 70 patients with ischemic stroke. The cFA values of CRP in the spasticity group were lower than those in the control group (p = 0.04). In the sub-ROI analysis of CRP, the iFA values of pontine RF were lower than the cFA values in both groups (p < 0.05). The cFA values of medullary RF in the spasticity group were lower than the iFA values within groups, and also lower than the cFA values in the control group (p < 0.05). This results showed the CRP injury and that imbalance of RST caused by CRP injury was associated with PSS. DTI analysis of CRP could provide imaging evidence for the pathophysiology of PSS.

To compare the urodynamic study variables at the onset of vesicoureteral reflux (VUR) between the overactive and underactive bladders in patients with spinal cord injury who presented with VUR. A total of 28 (13 cases of detrusor overactivity and 15 detrusor underactivity) men were enrolled. We compared the urodynamic variables between the two groups; detrusor pressure and bladder compliance, the infused volume at the onset of VUR measured on a voiding cystourethrography and cystometric capacity, maximum detrusor pressure, and bladder compliance during filling cystometry were recorded. At the onset of VUR, the bladder volume and compliance, except for the detrusor pressure, showed a significant difference between the two groups. The detrusor pressure, bladder volume, and bladder compliance relative to the cystometric capacity showed a significant difference between the two groups. The detrusor pressure, bladder volume, and bladder compliance at the onset of VUR relative to the cystometric bladder capacity did not show any significant difference between the two groups. There were differences in some variables at the onset of VUR depending on the type of neurogenic bladder. The VUR occurred at a lower capacity in neurogenic bladder with detrusor overactivity than in neurogenic bladder with detrusor underactivity at the same pressure. VUR occurred at a lower intravesical pressure compared to that known as the critical detrusor pressure (≥40 cm H2O) required for the development of VUR. The results of our study demonstrate that the detrusor pressure should be maintained lower than the well known effective critical detrusor pressure for the prevention and treatment of VUR.