Spinal Cord Stimulation Prevents Autonomic Dysreflexia in Individuals with Spinal Cord Injury: A Case Series

Figures

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  Figure 1. Demographics, blood pressure responses, epidural implant location and stimulation configuration, including active anodic and cathodic electrodes on the implants in three individuals with SCI. Anatomical placement of the 16-electrode array: conventional radiography of the thoracic and lumbar spines displays the position of the 16-electrode array. Stimulation configurations: red identifies anodes and black identifies cathodes. Cathodes were the caudal electrodes in all participants. Abbreviations: ABPM, ambulatory blood pressure monitoring; AD, autonomic dysreflexia; AIS, American Spinal Injury Association Impairment Scale; BP, blood pressure; C, cervical; DBP, diastolic blood pressure; Hz: hertz; SBP, systolic blood pressure; us, microseconds; V, volts.

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  Figure 2. Effect of eSCS on AD during DARS in three individuals with SCI. (a) Cardiovascular responses during DARS with eSCS OFF (grey shading) and eSCS ON (blue shading). The first vertical black dotted line (1) shows the start of DARS (i.e., insertion of index finger into the rectum), and the second vertical black dotted line (2) shows the completion of DARS (i.e., removal of finger). (b) Changes in SBP, DBP and HR during DARS with (blue symbols) and without (black symbols) eSCS in each participant. During DARS without eSCS, all participants showed an elevation in SBP greater than the 20-mmHg threshold for AD diagnosis (gray dotted lines). However, DARS with eSCS consistently reduced changes in SBP, keeping it below the threshold for AD diagnosis (grey dotted lines). (c) Scalogram showing wavelet power (yellow color) at low frequencies (0.05–0.15 Hz, y-axis) over time (x-axis). Wavelet power scalogram shows increased low frequency power during DARS without eSCS. However, with eSCS, all participants showed a decrease in wavelet power following the start of DARS (white dotted vertical line 1). (d) The elevation in low frequency power following DARS was prevented with eSCS ON compared to…

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  Figure 3. Potential mechanism of epidural spinal cord stimulation for mitigating autonomic dysreflexia. This figure shows the effect of eSCS at the caudal lumbosacral spinal segments (S2–S4) on visceral stimuli in the intact and injured spinal cord, at or above T6. (a) Without eSCS, visceral inputs by anorectal distention activate excitatory interneurons (red) through afferent fibers. The excitatory inputs polysynaptically ascend to thoracolumbar spinal segments (T6–L2), likely via long propriospinal neurons in the dorsal gray commissure (DGC) [16]. The ascending inputs activate sympathetic preganglionic neurons (SPNs, orange) via glutamatergic synapses (e.g., vesicular–glutamate transporter positive (Vglut2+) synapses), increasing vasculature of the sympathetic nervous system activity, leading to autonomic dysreflexia [13,14]. (b) With eSCS, primary afferent inputs (gray with myelination) potentially activate inhibitory interneurons (e.g., GABAergic interneurons, green) [56,57]. The inhibitory interneurons may inhibit the activation of excitatory interneurons (red), which results in no excitation of SPNs to prevent vasoconstriction related to visceral inputs from S2 to S4.