New evidence for preserved somatosensory pathways in complete spinal cord injury: A fMRI study

Abstract

Trauma to the spinal cord rarely results in complete division of the cord with surviving nerves sometimes remaining silent or failing to function normally. The term motor or sensory discomplete has been used to describe this important but unclassified subgroup of complete SCI. Importantly, silent motor or sensory pathways may contribute to aversive symptoms (spasticity, pain) or improved treatment success. To demonstrate more objectively the presence of subclinical preserved somatosensory pathways in clinically complete SCI, a cross-sectional study using functional MRI (fMRI) was undertaken. The presence of brain activation following innocuous brushing of an insensate region belowinjury (great toe) was analyzed in 23 people (19 males (83%), mean 6 SD age 43 6 13 years) with clinically complete (AIS A) SCI with (n 5 13) and without (n 5 10) below-level neuropathic pain and 21 people without SCI or pain (15 males (71%); mean 6 SD age 41 6 14 years). Location appropriate, significant fMRI brain activation was detected in 48% (n 5 11/23) of subjects with clinically complete SCI from below-injury stimulation. No association was found between the presence of subclinical sensory pathways transmitting innocuous mechanical stimuli (dorsal column medical lemniscal) and belowlevel neuropathic pain (v 2 5 0.034, P 5 0.9). The high prevalence of sensory discomplete injuries ( 50% complete SCI) strengthens the case to explore inclusion of this category into the international SCI taxonomy (ISNCSCI). This would ensure more widespread inclusion of discomplete SCI in ongoing pain and motor recovery research. Neurophysiological tests such as fMRI may play a role in this process. Hum Brain Mapp 39:588-598, 2018.

Does galvanic vestibular stimulation decrease spasticity in clinically complete spinal cord injury?

“…However, the reported changes in spasticity after GVS in two out of seven SCI patients reported here are in contrast to the lower prevalence of medium latency responses in the erector spinae muscles below the level detected by Iles et al (2004) in only two of nine patients or the presence of vestibular-evoked myogenic potentials reported by Squair et al (2016) in two of 16 AIS-A patients. Thus, the accumulated evidence is consistent with broader neuro-physiological observations suggesting traces of somato-sensory (Finnerup et al, 2004;Awad et al, 2015;Wrigley et al 2018) and motor preservation (Sherwood et al, 1992;McKay et al, 2004;Dimitrijević et al, 2015;Mayr et al, 2016) is patients classified as having the AIS-A injury, which is also supported by the autopsy studies (Kakulas and Kaelan, 2015).…”

Neuropathic Pain After Spinal Cord Injury: Challenges and Research Perspectives

“…However, mechanisms that contribute solely to below-level withdrawal responses may be relevant to development of spasticity and/or autonomic dysreflexia and merit further consideration. Additionally, up to 50% of patients with complete SCI have fMRI activation of the somatosensory cortex in response to below-level brush stimulation despite absence of conscious perception of the stimulus [86], indicating that unperceived below-level sensory inputs could contribute to the ongoing below-level pain. Therefore, neuropathic SCI pain can arise as a consequence of altered sensory processing at any point along the path from peripheral sensation to conscious perception either at or below the level of injury.…”

Augmenting Quadriplegic Hand Function Using a Sensorimotor Demultiplexing Neural Interface

“…The participant’s severe C5 SCI functionally blocks communication with the hand, but a clinically complete SCI does not necessarily equate to an anatomically complete SCI. Recent study demonstrates that residual sub-perceptual sensory information from below the lesion is transmitted to sensory areas of the brain, even following severe clinically complete SCI 11 . Our findings support the hypothesis that there is some anatomical sparing of spinal tissue even after severe AIS-A SCI, allowing sensory information transmission from below the lesion to M1, at sufficient levels for enabling new sensory related BCI capabilities.…”

“…Sensory function can potentially be augmented using a BCI that can decipher residual sensory neural activity from the impaired hand and dynamically translate this into closed-loop sensory feedback that the user can perceive. Intriguingly, recent study demonstrates that residual sub-perceptual sensory information from below the lesion is transmitted to sensory areas of the brain, even following severe clinically complete SCI 11 . M1 may encode sensory and touch-related signals following severe clinically complete SCI, although it has not yet been reported.…”