Brain–computer interface (BCI) is a novel communication method between brain and machine. It enables signals from the human brain to influence or control external devices. Currently, much research interest is focused on the BCI-based neural rehabilitation of patients with motor and cognitive diseases. Over the decades, BCI has become an alternative treatment for motor and cognitive rehabilitation. Previous studies demonstrated the usefulness of BCI intervention in restoring motor function and recovery of the damaged brain. Electroencephalogram (EEG)-based BCI intervention could cast light on the mechanisms underlying neuroplasticity during upper limb recovery by providing feedback to the damaged brain. BCI could act as a useful tool to aid patients with daily communication and basic movement in severe motor loss cases like amyotrophic lateral sclerosis (ALS). Furthermore, recent findings have reported the therapeutic efficacy of BCI in people suffering from other diseases with different levels of motor impairment such as spastic cerebral palsy, neuropathic pain, etc. Besides motor functional recovery, BCI also plays its role in improving the behavior of patients with cognitive diseases like attention-deficit/hyperactivity disorder (ADHD). The BCI-based neurofeedback training is focused on either reducing the ratio of theta and beta rhythm, or enabling the patients to regulate their own slow cortical potentials, and both have made progress in increasing attention and alertness. With summary of several clinical studies with strong evidence, we present cutting edge results from the clinical application of BCI in motor and cognitive diseases, including stroke, spinal cord injury, ALS, and ADHD.
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Cervical spondylotic myelopathy (CSM) is a chronic compression injury of the spinal cord, with potentially reversible conditions after surgical decompression, and a unique model of incomplete spinal cord injury. Several animal studies showed pathological changes of demyelination, axon loss and neuron apoptosis in rats with chronic spinal cord compression. However, there is a limited understanding of the neurological change in the spinal cord after surgical decompression. The aim of this study was to validate the neurorestoratology of myelopathic lesions in the spinal cord in a rat model.
A total of 16 adult Sprague-Dawley rats were divided into four groups: sham control (group 1); CSM model with 4-week chronic compression (group 2), 2 weeks (group 3) and 4 weeks (group 4) after surgical decompression of CSM model. The compression and decompression were verified by magnetic resonance imaging (MRI) test. Neurological function was evaluated by Basso, Beattie, and Bresnahan (BBB) locomotor rating scale, ladder rung walking test and somatosensory-evoked potentials (SEPs). Neuropathological change was evaluated by histological examinations.
MRI confirmed the compression of the cervical spinal cord as well as the reshaping of cord morphology after decompression. After decompression, significant changes of neurological function were observed in BBB scores (p < 0.01, F = 10.52), ladder rung walking test (p < 0.05, F = 14.21) and latencies (p < 0.05, F = 5.76) and amplitudes (p < 0.05, F = 3.8) of SEP. Neuronal degeneration was obvious in the ventral horn with gradual restoration. After decompression, the motor neuron number in the ventral horn did not show significant changes (p > 0.05). However, increasing trend of myelin area and staining intensity were observed in all columns of the white matter (p < 0.05) after decompression, especially in the compressed lateral column.
The established rat model is able to simulate histopathological characteristics of cervical myelopathy in human beings. The neuropathological change demonstrated that neurorestoratology in the myelopathic spinal cord would probably attribute to axonal remyelination of the white matter, but there would be an incapability of neuronal regeneration.
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Editorial
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Non-invasive neuroimaging plays a crucial role in the assessment of the human spinal cord, but it is quite challenging. Magnetic resonance imaging (MRI) is an important modality to obtain both high-resolution anatomical and functional information concerning the spinal cord. Besides conventional MRI, advanced MRI techniques could provide novel information about the microstructure and neural function of the spinal cord, thereby enhancing the understanding of spinal cord neurology and pathology of various spinal disorders.
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Original Research
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Cervical spondylotic myelopathy (CSM) is a degenerative disorder that can chronically damage the spinal cord. The aim of this study was to investigate the column-specific degeneration in the cervical cord with CSM and explore the structure-function relationship by diffusion tensor imaging (DTI) and functional magnetic resonance imaging (fMRI).
DTI and blood-oxygen-level-dependent (BOLD) fMRI were obtained from 14 healthy controls and six patients with CSM at 3 T. The fractional anisotropy (FA) value of anterior, lateral, and posterior column and the BOLD signal in response to somatosensory stimulation were compared among three groups: the average value of levels from C3 to C8 in the control and CSM groups and the value at maximal compression site in the CSM (CSM-mc) group. The correlation between FA value and BOLD signal was used to assess the structure-function relationship.
The FA value in CSM-mc was lower than control-ave in all the columns (P<0.01) and lower than CSM-ave in the lateral and posterior column (P<0.05). The BOLD signal in CSM was significantly higher than that in the control (P<0.001). In the posterior column, a significant correlation between BOLD signal and FA value was found (P<0.05).
This study demonstrated that the microstructural damage in CSM was correlated with functional changes. DTI combined with fMRI reveals the relationship between structural damage and neural activity, which might provide a promising method to reveal the underlying pathomechanism of CSM.
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