Abstract
Spinal cord stimulation is an effective therapy for the management of chronic pain with historical origins dating back to the 1960s. The therapy consists of electrical stimulation of the spinal cord to ‘mask’ pain. One effect of stimulation is generation of tingling paresthesia in the patient, and overlap of the paresthesia with the pain is important to successful therapy. Clinical and anatomical challenges to successful and durable concordant paresthesia include: contact impedance changes, lead migration, clinical programming time requirements, unknown anatomic variables, and optimal lead design. In this chapter we review these challenges, the principles guiding engineering solutions and trade-offs, and the use of computational tools to guide design of system components. Topics include a historical overview, stimulation waveform and clinical effects of waveform parameters such as pulse width, voltage vs. current control, multiple-source systems, real-time programming methods, contact size and spacing, use of field potentials for electrical imaging, modeling methods, and others.
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Notes
- 1.
The failure of the Gate Theory to adequately explain the incomplete response of chronic pain patients to SCS led investigators to explore other aspects of the chronic pain condition [2, 3]. Most animal and clinical studies of neuropathic pain have focused on the individual ‘signatures’ of the disease: changing homeostasis (local blood flow, neurotransmitter release, and regulation) [2], perceptual sensation (pain quality, paresthesia), and behavior (disturbed sleep, depression) [4]. In 2005, Ronald Melzack revisited the ‘gate theory’ [5] and replaced the ‘gate’ with a more system-oriented concept, which he termed the ‘neuromatrix.’ He defined the neuromatrix as ‘an array of neural circuit elements (genetically programmed) to perform a specific function as interconnected and to produce awareness and action.’ He proposed that pain is ‘a multidimensional experience produced by characteristic “neurosignature” patterns of nerve impulses generated by a widely distributed neural network – the “body-self neuromatrix” – in the brain.’ Therefore, chronic pain is likely produced by a combination of neural activities – perceptual, homeostatic, and behavioral programs – and activated by the ‘body-self neuromatrix.’ In future assessments, SCS might be better understood as a therapy that modulates the output patterns of this neuromatrix by electrically activating a few key components of the matrix (e.g., the dorsal columns, the dorsal roots, etc.).
- 2.
- 3.
Commercial implementations of FBC include Medtronic TargetStim™, St. Jude Medical Dynamic MultiStim™, and Boston Scientific area balancing in the Precision™ system.
- 4.
Commercial implementation of FS includes Boston Scientific i-Sculpt™ in the Precision™ system.
- 5.
In the model described by Lee et al., the spinal cord geometry (Fig. 18) was based on a histological cross section [116] and the dorsal root trajectory A1 from Struijk et al. with the dorsal root mother fiber branching into two thinner daughter fibers upon entering the spinal cord [29]. DC fibers have a straight trajectory in the rostro-caudal direction. The voltage data from the finite element model (FEM) along corresponding fibers in three-dimensional space were applied to the non-linear axon models with different fiber diameters [117].
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Moffitt, M.A., Lee, D.C., Bradley, K. (2009). Spinal Cord Stimulation: Engineering Approaches to Clinical and Physiological Challenges. In: Greenbaum, E., Zhou, D. (eds) Implantable Neural Prostheses 1. Biological and Medical Physics, Biomedical Engineering. Springer, New York, NY. https://doi.org/10.1007/978-0-387-77261-5_5
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