DTM™ THERAPY SPINAL CORD STIMULATION

DTM™ SCS is a spinal cord stimulation (SCS) therapy delivered via the Intellis™ SCS platform to treat patients with chronic, intractable pain.

SEE CLINICAL DATA

DTM™ SCS OVERVIEW

Differential Target Multiplexed™ spinal cord stimulation (SCS) is a proprietary therapy supported by preclinical research and clinical research — now with level 1 evidence at 12 months follow up — from an RCT.

Science that matters

beyond the neuron

Decades of basic science research have expanded the understanding of the role of glial cells in the nervous system, which outnumber neurons 12:1 in the spinal cord.1-4

toward a new theory

In preclinical studies, the DTM™ waveform best modulates glial and neuronal gene expression back toward the non-pain state.5-8

 

adapting the science into humans

DTM™ SCS therapy is a proprietary programming option available to treat patients with chronic pain. A randomized trial has shown DTM™ SCS results in superior back pain relief compared to conventional SCS in patients with chronic pain.9

inspired by science

The DTM™ therapy is the first SCS therapy intentionally developed from preclinical science.

proven only

on the

Intellis™

platform

Learn about Intellis™ Platform

evolution of dtm™ scs

hypothesized NOVEL MECHANISM

Glia are electrically responsive cells in the spinal cord and outnumber neurons by 12:1.4 Chronic pain occurs when neuro-glial interactions get out of sync. DTM™ SCS may impact the neuronal-glial interaction.1-3

PRECLINICAL WORK

DTM™ SCS has been studied in animal models, showing statistically significant reversal of pain behaviors compared to either low frequency or high frequency alone.5 In addition, preclinical studies investigating the genome of nerve-injured animals suggests that the DTM™ waveform has a greater impact in the neural-glial interaction than other frequencies alone.5-8

DTM™ SCS Webinar Series

Watch the webinars below to learn more about the evolution of DTM™ SCS and its impact on patients.

1

Milligan ED, Watkins LR. Pathological and protective roles of glia in chronic pain. Nat Rev Neurosci. 2009 Jan;10(1):23-36.

2

Vallejo R, Tilley DM, Vogel L, Benyamin R. The role of glia and the immune system in the development and maintenance of neuropathic pain. Pain Pract. 2010 May-Jun;10(3):167-84.

3

De Leo JA, Tawfik VL, LaCroix-Fralish ML. The tetrapartite synapse: Path to CNS centralization and chronic pain. Pain. 2006; 122:17-21.

4

Ruiz-Sauri A., Orduña-Valls J.M., Blasco-Serra A. et al. Glia to neuron ratio in the posterior aspect of the human spinal cord at thoracic segments relevant to spinal cord stimulation. Journal of Anatomy, vol. 235, no. 5, 2019, pp. 997-1006.

5

Vallejo R, Kelley CA, Gupta A, Smith WJ, Vallejo A, Cedeño DL. Modulation of neuroglial interactions using differential target multiplexed spinal cord stimulation in an animal model of neuropathic pain. Mol Pain. 2020 Jan-Dec;16:1744806920918057.

6

Vallejo R, Smith W, Kelley C, et al. Neuron-glial inflammasome enhanced reversal by DTM-SCS relative to high rate and low rate SCS in a neuropathic pain model. American Society for Regional Anesthesiology and Pain Medicine (ASRA); November 14-17, 2019; New Orleans, LA. Abstract #480 

7

Vallejo R, Kelley C, Smith W, et al. Cell-specific targeting in neural tissue using Differential Target Multiplexed (DTM) SCS. American Society for Regional Anesthesiology and Pain Medicine (ASRA); November 14-17, 2019; New Orleans, LA. Abstract #513

8

Vallejo R, Tilley D, Kelley C, et al. Proteomics of Differential Target Multiplexed-SCS applied to an animal model of neuropathic pain. American Society for Regional Anesthesiology and Pain Medicine (ASRA); November 14-17, 2019; New Orleans, LA. Abstract #509

9

Fishman M, Cordner H, et al. DTM™ SCS RCT 12-month data results. Presented at a Medtronic webinar, jointly supported by the North American Neuromodulation Society (NANS), World Institute of Pain (WIP), and the American Society for Pain and Neuroscience (ASPN). October 19, 2020. Webinar available on society websites.