Functional Reorganization of the Brain in Humans Following Spinal Cord Injury: Evidence for Underlying Changes in Cortical Anatomy

Abstract

Loss of somatosensory drive results in functional reorganization of the primary somatosensory cortex (SI). While the phenomenon of functional cortical reorganization is well established, it remains unknown whether in humans, functional reorganization results from changes in brain anatomy, or simply reflects an unmasking of already existing dormant synapses. In 20 subjects with complete thoracic spinal cord injuries (SCIs) and 23 controls, we used functional and structural magnetic resonance imaging to determine whether SI reorganization was associated with changes in SI anatomy. SCI resulted in a significant SI reorganization, with the little finger representation moving medially toward the lower body representation (i.e., area of sensory loss). Furthermore, although SCI was associated with gray matter volume loss in the lower body representation, this loss was minimized as reorganization increased. That is, the greater the medial shift in little finger representation, the greater the gray matter preservation in the lower body representation. In addition, in the region of greatest SI reorganization (little finger), fractional anisotropy was correlated with SI reorganization. That is, as SI reorganization increased, the extent of aligned structures decreased. Finally, although thalamocortical fibers remained unchanged, the ease and direction of water movement within the little finger representation was altered, being directed more toward the midline in SCI subjects. These data show that SI reorganization following SCI is associated with changes in SI anatomy and provide compelling evidence that SI reorganization in humans results from the growth of new lateral connections, and not simply from the unmasking of already existing lateral connections.

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

“…29 Patients with complete SCI exhibit morphological changes such as reduced gray matter volume in the primary motor, medial prefrontal, cingulate, and cerebellar cortices, as well as diffusion tensor imaging changes in cortical and brainstem motor areas. 14,22,41 With the advent of functional imaging, various reorganization patterns were recognized. In a review by Kokotilo et al, 29 nearly half of the included studies documented a significant increase in activation magnitude in motor areas.…”

Pain and Plasticity: Is Chronic Pain Always Associated with Somatosensory Cortex Activity and Reorganization?

“…Since this initial report, many investigators have reported functional reorganization of human S1 following various forms of deafferentation, such as limb amputation and complete spinal cord injury (Kaas, 1991;Flor et al, 1995Flor et al, , 1997Maihöfner et al, 2003;Wrigley et al, 2009;Henderson et al, 2011). Despite these findings, close inspection reveals that, in some individuals, deafferentation is not associated with significant cortical plasticity, whereas in others, a seemingly identical injury results in a significant change in cortical representations.…”

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.…”