From the neurophysiological frustrations described above arose PNfS and HS. PNfS enjoys as its almost sole audience the subcutaneous sensory fibers, which synapse at the dorsal horn. In the majority of cases, there exist no other electrically active neural fibers nearby. There exist three separate approaches to stimulation of the axial back and neck: (1) direct peripheral nerve stimulation, which is stimulation of a target nerve, such as the cluneal or thoracic intercostal nerves for stimulation of pain within that neural watershed; (2) PNfS which is defined as stimulation of the subcutaneous tissues by placing an electrode array wholly under the skin in the area of pain within the local watershed; and (3) hybrid stimulation defined as cross-talking electrical stimulation from electrodes at a distance from each other, be it electrical circuit from periphery to periphery [11], or between the spinal cord and the periphery. The use of PNfS and HS is based on the concept that the delivery of current to a specific peripheral nerve or DRG will affect transmission of pain influencing the firing of the A-delta and C fibers, as well as possibly change the neurotransmitters in the tissue. Although the exact mechanism of PNfS is unknown, it is thought to rely on the “gate-control theory” put forth by Melzack and Wall [12]. This theory proposed that the activation of low-threshold myelinated primary afferent fibers decreases the response of dorsal horn neurons to unmyelinated nociceptors through competitive inhibition.

The placement of a PNfS lead, while appearing easy, is dependent on the area of target pain. Pain outside the area of paresthesia will not be influenced, so the aim is to produce a net of depolarizing current, which will serve to depolarize the A-beta fibers and competitively inhibit A-delta and C fibers at the dorsal horn. Electrodes should be placed to frame the painful area, casting the net either within the periphery itself or between the spinal canal/cord and the periphery. Having the patient mark the painful areas on the skin is additionally very helpful, especially if done over the days preceding the trial (see Figs. 18.4 and 18.6).

Flank pain following spinal fusion might be trialed as seen in Fig. 18.3, one lead overlying the spinal cord, one lead in the gutter, overlying the post-ganglionic afferent dorsal root entry zone fibers, one PNfS lead superior to the painful area, and one inferior, one anterior. The trial patient seen in Fig. 18.3 was implanted with two leads in the canal and two in the periphery, one posteriorly, one anteriorly.

Posterior, high axial cervical and complex thoracic pain following attempted keyhole and cervical laminoplasty might be trialed in the following manner: SCS lead over the posterior dorsal columns in the low cervical region, and then one lead superficially just near the area of maximal pain in cervical area and a second lead in the area of maximal pain in thoracic spine, as can be seen in Figs. 18.4 and 18.5. Since the density of paresthesia is divisible by the area stimulated, the decision to sacrifice the right, low thoracic midline 7-8/10 pain was made to likely capture the midthoracic pain seen surrounding the lead placement there. Additionally, as can be seen in Fig. 18.4, asking the patient to make a dermatographic representation of the existing pain aids planning of lead placement significantly (Fig. 18.6).

Focal, axial spinal pain, perhaps the most demanding to treat with SCS alone, is often well treated with SCS leads in conjunction with overlying PNfS leads, forming an HS field of paresthesia programmed to place either cathode or anode in the canal with the corresponding electrode in the periphery overlying the pain (see Figs. 18.7, 18.8, and 18.9). Interestingly, it has been the observation of the authors and others that with HS programming, even if one anesthetizes the skin and periphery with local anesthetic around the peripherally placed lead, one can still cross-talk program to obtain principally axial paresthesia—indicating that neither the peripheral cutaneous nerves nor the ascending dorsal sensory tracts are likely the primarily depolarized neural tissue, as the peripheral nerves are chemically impeded and the dorsal tracts represent primarily radicular projections to areas where patients do not typically report paresthesia. They rather report axial paresthesia—indicating depolarization of either DREZ, DRG, or large, axial peripheral nerves.

PNS is neither new nor experimental. PNS was the first tested and reported invasive neuromodulatory device used to treat pain in 1967 when Wall and Sweet published their sentinel, “Temporary abolition of pain in man” [13]. Since that time, significant case studies have demonstrated effect and technique, but to date PNS and PNfS lack the scientific effort seen to substantiate SCS. Several case series have suggested PNfS as effective for truncal pain. Paicus et al. [14] first reported a case series of six patients, five of whom had undergone previous surgery, and all noting at least 50 % pain relief. Verrills et al. [15] reported a consecutive case series of patients with PNfS in which 85 % reported at least 50 % pain relief. Discographically confirmed cervical discogenic pain was treated with 100 % improvement with PNfS at 9-month follow-up [16]. At least two case series have described pain relief with concurrent use of PNfS and SCS hybrid stimulation [17, 18]. Bernstein et al. [18] chronicled a series of 20 patients with combined SCS/PNfS with the majority of patients reporting a preference of the combined stimulation over either modality alone.