Differential Effect of Spinal Cord Injury and Functional Impairment on Human Brain Activation

Abstract

Reorganization of human brain function after spinal cord injury (SCI) has been shown in electrophysiological studies. However, it is less clear how far changes of brain activation in SCI patients are influenced by the extent of SCI (neuronal lesion) or the consequent functional impairment. Positron emission tomography ([15O]-H2O-PET) was performed during an unilateral hand movement in SCI patients and healthy subjects. SCI patients with paraplegia and normal hand function were compared to tetraplegic patients with impaired hand movements. Intergroup comparison between paraplegic patients and healthy subjects showed an increased activation of contralateral sensorimotor cortex (SMC), contralateral thalamus, ipsilateral superior parietal lobe, and bilateral cerebellum. In contrast to this, tetraplegic patients with impaired upper limb function revealed only a significant activation of supplementary motor area (SMA). Correlational analysis in the tetraplegic patients showed that the strength of hand movement was related to the activation of contralateral SMC. However, the severity of upper limb sensorimotor deficit was related to a reduced activation of contralateral SMA and ipsilateral cerebellum. The findings suggest that in paraplegic patients with normal hand function the spinal neuronal lesion itself induces a reorganization of brain activation unrelated to upper limb function. Compared to this, in tetraplegic patients changes of brain activation are related to the impaired upper limb function. Therefore, in patients with SCI a differential impact of spinal lesion and functional impairment on brain activation can be shown. The effect of impaired afferent feedback and/or increased compensatory use of non-impaired limbs in SCI patients needs further evaluation.

Delayed pain decrease following M1 tDCS in spinal cord injury: A randomized controlled clinical trial

“…tDCS mechanisms are related to its influence on sodium and calcium channels opening and NMDA receptors excitability [50], while longlasting effects are analogous to activity-dependent synaptic plasticity, namely long-term potentiation (LTP) and long-term depression (LTD) [51][52][53]. Structural, functional and connectivity alterations at the cortical level have been described in patients with SCI, especially in the somatosensory cortex, consequently to the injury itself, as well as a result of the lack of sensory and motor inputs [54][55][56]; these changes being related to neuropathic pain [57]. Therefore, it is possible that patients with SCI sustain a decline in plasticity mechanisms as compared to those observed in healthy subjects, and therefore, tDCS related neuroplastic mechanisms may occur in a delayed manner.…”

Functional cortical reorganization in cases of cervical spondylotic myelopathy and changes associated with surgery

“…35 Not many studies have correlated the postoperative motor improvement with plasticity. 19 Some studies have shown adaptive changes in bilateral primary motor cortex (M1), supplementary motor area (SMA), premotor area (PMA), cingulate motor area, parietal cortex, and contralateral primary somatosensory cortex (S1) in cases of SCI [8][9][10][11][27][28][29]33,40 and cervical compressive myelopathy due to spondylosis. 13,14,23,38 In this study we aimed to understand the cortical changes that occur due to CSM and following CSM surgery and to correlate these changes with functional recovery by using functional MRI (fMRI).…”

Transcranial Magnetic Stimulation to Investigate Motor Cortical Circuitry and Plasticity in Spinal Cord Injury

“…SCI is associated with complete or incomplete damage to ascending sensory and/or descending motor pathways [3,4] and may ultimately lead to alterations within neural circuits of M1 [5][6][7]. In controls, experimentally induced differentiation reduces inhibitory, GABAergic cortical activity in sensory motor cortices [8] and is a mechanism proposed to mediate rapid cortical plasticity [9].…”