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472 D. Lewis et al.

neuropathy, nonsurgical refractory low back pain, visceral, and peripheral nerve

pain [2]. There exists a paucity of information in the literature speciﬁcally focusing

on the perioperative management and essential considerations relevant to patients

with implanted pain devices presenting for surgery. In many cases, contacting an

individual device manufacturer may represent the optimal method to obtain relevant

guideline and labeling information.

2 Mechanism of Action

Spinal cord stimulation functions via the delivery of various waveforms and frequen-

cies to modulate pain signaling and decrease pain symptomology. With this variety

in electrical stimulation delivery, there are many theories that attempt to explain how

this signaling leads to modulation of pain sensation. The most common form of spinal

cord stimulation remains dorsal column stimulation, although other variations such

as dorsal root ganglion stimulation, do exist [3]. The original, and still leading, theory

describing pain modulation via spinal cord stimulation is the gate control theory. This

theory hypothesizes that stimulation of the dorsal column-medial lemniscus pathway

results in opening of downstream electrochemical gates and activation of GABA and

cholinergic spinal interneurons. Subsequent increased activity in descending anal-

gesic pathways ultimately results in inhibition of pain signal transmission along the

lateral spinothalamic tract.

These devices all contain similar componentry: the electrodes or leads, insulated

wires connecting the leads to the implantable pulse generator (IPG) or battery, and

the charging and reprogramming equipment. Leads that are cylindrical can be placed

percutaneously with image guidance, whereas paddle leads require a laminotomy/

laminectomy for placement. The type of lead can easily be distinguished with ﬂuo-

roscopy or x-ray. While older forms of SCS included leads with 4 electrodes, new

generations of percutaneous arrays commonly contain 8–16 electrodes with paddle

arrays containing 16–32, improving stimulation selectivity and programming options

[4, 5].

Notably,it is common for patients to either have a single paddle array or 2 percuta-

neous leads placed. These electrodes in the form of metal contacts, create an electric

ﬁeld, modulating neurons via the software of the speciﬁc device [1]. Prior to perma-

nent implantation, most patients undergo a trial with a percutaneous temporary SCS

for 5–7 days and must have signiﬁcant pain relief before proceeding. During perma-

nent implantation, the wires connected to the electrodes are then tunneled subcuta-

neously and connected to an implanted pulse generator, commonly in the posterior

ﬂank.

Peripheral nerve stimulators work in a similar fashion via both central and periph-

eral mechanisms. Central mechanisms include inhibition of pain signals via the

aforementioned gate control theory, modulation of wide dynamic range neurons

on the dorsal horn, and reduction of neural impulses via the medial lemniscal

pathway. Peripheral PNS mechanisms include disruption of nociceptive afferent

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Perioperative Management of Pumps and Stimulators 473

ﬁbers and alteration of the local microenvironmental milieu including downregula-

tion of inﬂammatory mediators. Combined CNS and PNS mechanisms may improve

both central and peripheral sensitization of pain. One speciﬁc device has been shown

to provide sustained relief at 12 months, following only a 60 day period of peripheral

stimulation before the temporary externalized leads were removed. These devices

involve percutaneous leads delivered along peripheral nerves, with wires connected

to internal pulse generators that are, similar to SCS, implanted in the subcutaneous

tissue and anchored to fascia, either directly connected to a power source or connected

to an external power source transcutaneously that is worn in a harness overlying the

battery [2].

Intrathecal pain pump devices allow for the continuous, with or without bolus,

delivery of therapeutic agents directly to the intrathecal space, bypassing ﬁrst pass

metabolism and acting directly on spinal cord ion channels and receptors. This mech-

anism allows for the utilization of molecules that cannot cross the blood brain barrier,

for much smaller doses to be used to achieve therapeutic beneﬁt, and a decreased

risk of signiﬁcant adverse effects [6]. These devices have demonstrated beneﬁt in

patients with intractable terminal pain, chronic nonmalignant pain, and an expanding

collection of other diagnoses. The only medications FDA-approved for intrathecal

administration include morphine and ziconotide for chronic pain and baclofen for

spasticity, although many other therapeutic agents are used in an off-label fashion

either as monotherapy or combination therapy, including local anesthetics and adren-

ergic agonists such as clonidine. These devices consist of an integrated battery and

implanted pump with a reﬁllable reservoir that is connected to a catheter that delivers

medication into the intrathecal space. The most common type of intrathecal pump is

the Medtronic SynchroMed

II, introduced in 2004. This device consists of a metal

housing that holds a bellow containing the drug, which is surrounded by pressurized

gas that exerts pressure on both the bellow and the drug. The drug is then delivered

via a battery-powered peristaltic pump which has rollers to compress the catheter

tubing and advance the drug forward. Notably, differences in temperature and pres-

sure/altitude will affect pump gas pressures and thus medication dosage delivered. In

2012, the Prometra

Flowonix pump received FDA approval for their device which

features a dosing chamber that mitigates, but does not eliminate, the dosing vari-

ability caused by changes in pressure and temperature. The dosing is managed by

an external programming device. Similar to SCS, the intrathecal catheter is tunneled

percutaneously to the pump system which is surgically implanted into a subcutaneous

pocket, commonly in the posterior ﬂank or lower lateral abdomen. These systems do

require medication withdrawal and reﬁll either before medication runs out or expires.

Similar to SCS, most patients undergo a trial period, often a single shot of medication

into the intrathecal space with monitored therapeutic response prior to permanent

pump placement [7].

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474 D. Lewis et al.

3 Perioperative Concerns

Similar to AICD and pacemaker devices, it is advisable for implanted pain devices

to be interrogated and reprogrammed to turn the device off or to the lowest possible

setting/amplitude prior to a planned surgical procedure. Patients with implanted

intrathecal pain pumps will likely have a higher opioid tolerance and may require

elevated opioid doses in the perioperative phase of care to maintain hemodynamics

and address postoperative pain complaints. It is recommended that devices be inter-

rogated post-operatively to ensure proper functioning or delivery of medication.

Regarding SCS or intrathecal pump device removal, dural leak is a known compli-

cation and the development of signs and symptoms suggesting postdural puncture

headache symptomology should prompt further evaluation. If either type of device

must be removed intraoperatively, the SCS leads or intrathecal pump catheter may be

done via gentle traction after cutting sutures anchoring to the supraspinous fascia and

disconnecting the wires from the IPG or catheter from the pump. Collaboration with

the device representative on the day of surgery, either by phone or directly in-person,

is recommended [1].

4 Magnetic Resonance Imaging (MRI)

Certain implanted devices have demonstrated safety for use in MRI, however, this

is not the case for all. These devices may malfunction during or after MRI, leading

to dosing errors. In patients with implanted stimulators, broken devices or circuit

disruptions, could generate heat when exposed to the magnetic ﬁeld and injure the

patient [1]. Discussions with the device representative is paramount prior to ordering

imaging. Most manufacturers will state if their device is MRI compatible, or more

commonly the parameters in which the device is MRI conditional. It is important

to consider if the patient’s medication can be suspended or delivered via a different

route of administration during the MRI. In general, the magnetic ﬁeld created by the

scanner will temporarily suspend the pump, pausing drug delivery, and restarting once

MRI exposure has ended. It is recommended to interrogate the device 20–30 minutes

after the scan to ensure it has restarted automatically. This is particularly important

in patients with intrathecal baclofen pumps as withdrawal can be life-threatening.

Notably, if the patient has an older SCS, the battery or IPG may be exchanged for a

newer model, making the device MRI compatible/conditional [7].

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Perioperative Management of Pumps and Stimulators 475

5 Electrocautery

The use of monopolar electrocautery during surgery may affect electrical conduc-

tance posing an increased risk to both the patient and their device. When exposed

to monopolar electrocautery, patients have previously described lancinating sensa-

tions the location of which is impacted by lead placement. If monopolar electro-

cautery is deemed necessary, implanted stimulation devices need to be turned off

and checked for impedance after the procedure. Intraoperative monopolar cautery

utilization should be limited to the lowest effective setting and the grounding pad

should be placed as far away from the implanted device as possible.

Bipolar electrocautery is preferrable and may present with less risk to the patient.

Bipolar devices do not require a dispersive return electrode pad because both the

active and return electrodes are integrated in the energy delivery forceps to a smaller

focused area [1].

Care should be taken to not touch any part of the SCS device with active cautery

as this could cause thermal damage along the tract of the lead or damage the insulated

coat of the wire, making the device nonfunctional and/or stimulating/shocking the

patient [3].

6 Device Complications for Spinal Cord Stimulators

and Intrathecal Pumps

Following intrathecal pump placement, and less commonly SCS placement, dural

leak is a known complication occurring in as many as 20% of cases [8]. To prevent

this, some providers place a purse-string suture into the dura at the time of placement.

Many of these can be managed conservativelywith activity modiﬁcation, positioning,

caffeine, OTC headache medication, and ﬂuid resuscitation. If conservative measures

fail, the leak must be sealed with blood patch or primary closure. If an intrathecal

pump must be explanted, the decision may be made to leave the tied off catheter in

place.

Infections can range from superﬁcial, to pocket infection, to fulminant epidural or

intrathecal spread in less than 1% of cases [9]. Management of superﬁcial infections

may include culture-guided antibiotic administration alone, whereas deeper infec-

tions may require device removal, irrigation, and debridement. Most commonly,

pathogens are Staphylococcus or gram-negative bacteria. Notably, approximately

1:4 of infected devices are culture-negative. The site most commonly infected is the

pocket containing the pump or IPG. Thorough neurological examination, as well as

accompanying imaging, should be performed to evaluate for signs and symptoms of

meningitis, epidural abscess, and intrathecal infection [10].

Mechanical device complications are known to occur in up to 20% of patients

with implanted pumps [8] and less commonly with spinal cord stimulators [10].

Known mechanical failures include catheter/lead migration, dislocation, breakage,

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476 D. Lewis et al.

granuloma formation at the catheter tip, and pump failure. These complications

should be diagnosed with device interrogation, plain radiographs (with contrast for

pumps), and CT imaging (following intracatheter contrast administration for pumps).

Neuraxial injury, including paralysis, has been reported after both SCS and

intrathecal pump placement. Thankfully, this has been reported in less than 1% of

cases for intrathecal catheter [2] and SCS placement [11]. Injury can be a result of

direct needle or hardware trauma, hematoma formation, or infection. If the patient’s

history or physical examination s uggests a spinal cord injury, appropriate imaging

is indicated to elucidate reversible causes [12–14].

7 Management

Prior to any procedure in a patient with an implanted pump, the age of device,

time of last evaluation, medication dosing, and date of next reﬁll should be deter-

mined by the care team. If possible, communication with the healthcare professional

responsible for pump-management is encouraged, as well as communication with

and ensuring availability of the device representative. It is also important to review the

speciﬁc device’s manufacturer guidelines for perioperative management. As previ-

ously mentioned, careful titration of intraoperative and postoperative opiate dosing is

required in patients with implanted pumps containing opioids. In these patients, the

addition of procedure-related opioids may induce unwanted respiratory depression.

In those r eceiving intrathecal baclofen, addition of opioids may have a greater-than

expected response due to the synergistic nature of the drugs. Further complicating the

clinical management of these patients is the lack of a reliable method for converting

intrathecal opioid dosages to intravenous equivalents. For example, estimates for

an equianalgesic dose of oral to intrathecal morphine ranges from 12:1 to 300:1.

Careful consideration of patient positioning must account for the location of all device

components. Most intrathecal pumps are located in the lower abdomen in a location

avoiding contact with the pelvis, ribs, and patient’s waist or belt-line. In patients with

a larger body habitus, the device may be implanted in the posterior ﬂank. Regarding

the catheter, care must be taken to avoid excessive twisting and bending as this may

result in catheter damage, kinking, occlusion, or dislodgement. Neuraxial analgesia

is not absolutely contraindicated in these patients, but cautious care must be taken

to avoid damage to the catheter through needle contact and entry must be made at a

level different than that of the catheter. Imaging modalities, such as ultrasound, may

be helpful in certain circumstances to identify the location of leads or catheter tubing

as they course to either their IPG or reservoir. As previously mentioned, temperature

of the patient can affect dosing delivered by older pumps, so the recommendation

is to maintain patient body temperature below 39 °C, with a lower limit to be kept

within the normal physiologic range. In the event that deﬁbrillation is indicated,

the ﬁrst concern is obviously the termination of aberrant arrhythmias and patient

survival. If possible, deﬁbrillation pad placement away from implanted devices is

desirable. As for diathermy, it is not absolutely contraindicated. The primary concern

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Perioperative Management of Pumps and Stimulators 477

with diathermy is device heating, which as previously mentioned may alter infusion

rates. Shortwave diathermy is not recommended for use within 30 cm of the pump

or catheter for this reason. The use of electroconvulsive therapy has not been estab-

lished, but there is concern regarding alteration in pump operation and ﬂow rate.

There is limited data on lithotripsy, but manufacturers do recommend the focus of

the beam be at least 15 cm away from the pump. As for radiation therapy, caution

should be used as permanent damage can occur. Manufacturer recommendations are

to not direct high radiation sources at the pump, or a shield be placed over the pump

if necessary. Notably, there is one study of 39 patients in which 12 received radiation

with either the pump or the catheter in the ﬁeld, and all devices were found to be in

working order following completion of treatment. Radiofrequency and microwave

ablation in the presence of a pump are not well documented, with the primary concern

being overdose due to device heating [7].

A number of the aforementioned complications can occur perioperatively, leading

to over- or under-dosing of intrathecal medication. It is imperative to recognize and

promptly treat these complications.

Signs of morphine withdrawal include malaise, anxiety, myalgia, insomnia, fever,

and worsening pain. Investigation of the catheter with a dye study may be warranted,

along with interrogation of the pump. In contrast to withdrawal, morphine overdose

can be rapidly life-threatening. Overdose symptoms include confusion, sedation,

respiratory arrest, and seizures. The ﬁrst priority should be to provide airway support

and administer naloxone. Notably, intrathecal morphine has a much longer half-life

than naloxone and therefore attentive monitoring is required to assess for the need

for either repeat naloxone dosing or continuous infusion.

Signs and symptoms of baclofen withdrawal include increased spasticity,

pruritis, hypotension, tachycardia, paresthesia, muscle rigidity, fever, hallucina-

tions, delirium, delusions and paranoia. Patients with a spinal cord injury at T6

or higher have an increased risk of autonomic dysreﬂexia, malignant hyperthermia,

and neuroleptic malignant syndrome. Baclofen withdrawal treatment includes expe-

dited pump repair and oral baclofen supplementation. Unfortunately, oral baclofen

administration may not effectively replace intrathecal baclofen dosing and drugs with

similar properties such as propofol and benzodiazepines may also be required. With

insufﬁcient data, dantrolene and cyproheptadine may also address the development

of signiﬁcant withdrawal symptoms. Signs of baclofen overdose include drowsiness,

lightheadedness, somnolence, dizziness, respiratory depression, and coma. After

necessary breathing and circulatory support are provided, a physician experienced

with intrathecal baclofen should be consulted to interrogate the pump and determine

potential overdose etiologies. The treatment of baclofen overdose includes a tempo-

rary pump interruption for no more than 48 hours to minimize the occurrence of

pump damage, CSF aspiration through the pump side port can be considered with

careful consideration of the amount of CSF aspirated, and physostigmine adminis-

tration for symptomatic relief. It is worth mentioning that if a catheter dye study is

considered for diagnostic reasons, the pump side port should be aspirated for at least

the volume of the catheter to avoid bolusing the patient with more medication [7].

https://t.me/med1917

478 D. Lewis et al.

Ziconotide overdose management can include dose reduction if mild symptoms

are encountered (nausea, dizziness, weakness, somnolence, vision changes) and

termination of drug delivery in the setting of severe symptoms (psychosis, suicidal

ideation, deep sedation, confusion) [7].

8 Conclusion

An increasing number of patients with implantable stimulators and intrathecal pumps

are presenting for surgery. It is critically important to be familiar with the relevant

anatomy, device componentry, mechanism of action, and complications associated

with these devices in order to optimize the analgesic and anesthetic care of these

patients.

Key Takeaways

1. Prior to any procedure in a patient with an implanted pump, device age, time of

last evaluation, medication dosing, and date of next reﬁll should be determined

by the care team. It is advisable to turn the device off or to the lowest possible

setting prior to a planned surgical procedure.

2. Patients with implanted pain pumps will likely have a higher opioid tolerance and

may require elevated opioid doses in the perioperative phase of care to maintain

hemodynamics and address postoperative pain complaints.

3. It is important to be familiar with device manufacturer recommendations

regarding MRI capability. When in doubt, contact the local device representative.

4. Intraoperative monopolar cautery utilization should be limited to the lowest effec-

tivesetting and the grounding pad should be placed as far away from the implanted

device as possible. Bipolar electrocautery is preferable and may present with less

risk to the patient. Care should be taken to not touch any part of an SCS device

with active cautery as this could cause thermal damage along the tract of the lead

or damage the insulated coat of the wire, making the device nonfunctional and/

or stimulating/shocking the patient.

5. It is recommended that devices be interrogated post-operatively to ensure proper

functioning or delivery of medication.

References

1. Daniels A, McDonald C, Basques B, Hershman S. Perioperative management of spinal cord

stimulators and intrathecal pain pumps. J Am Acad Orthop Surg. 2022;30(17):e1095–105.

https://doi.org/10.5435/JAAOS-D-22-00053.

2. Abd-Elsayed A, D’Souza RS. Peripheral nerve stimulation: the evolution in pain

medicine. Biomedicines. 2021;10(1):18. https://doi.org/10.3390/biomedicines10010018.

PMID: 35052698; PMCID: PMC8773238.

https://t.me/med1917

Perioperative Management of Pumps and Stimulators 479

3. Harned ME, Gish B, Zuelzer A, Grider JS. Anesthetic Considerations and perioperative

management of spinal cord stimulators: literature review and initial recommendations. Pain

Physician. 2017;20(4):319–29. PMID: 28535554.

4. Lempka SF, Patil PG. Innovations in spinal cord stimulation for pain. Curr Opin Biomed

Eng. 2018;8:51–60. https://doi.org/10.1016/j.cobme.2018.10.005. Epub 2018 Nov 12. PMID:

30911705; PMCID: PMC6430588.

5. Hasoon J, Berger A, Urits I, Orhurhu V, Viswanath O, Aner M. Spinal cord stimulation for the

treatment of chronic pelvic pain after Tarlovcyst surgery in a 66-year-old woman: a case report.

Case Rep Women’s Health. 2020;25: e00171. https://doi.org/10.1016/j.crwh.2020.e00171.

6. Nelson AM, Jericho BG, Anitescu M. Pump IT up-perioperative care of patients with intrathecal

drug delivery systems. Anesth Analg. 2022;134(1):32–4. https://doi.org/10.1213/ANE.000000

0000005821. PMID: 34908544.

7. Nadherny W, Anderson B, Abd-Elsayed A. Perioperative and periprocedural care of patients

with intrathecal pump therapy. Neuromodulation. 2019;22(7):775–80. https://doi.org/10.1111/

ner.12880. Epub 2018 Oct 31. PMID: 30378724.

8. Knight KH, Brand FM, Mchaourab AS, Veneziano G. Implantable intrathecal pumps for

chronic pain: highlights and updates. Croat Med J. 2007;48(1):22–34. PMID: 17309136;

PMCID: PMC2080496.

9. Esquer Garrigos Z, Farid S, Bendel MA, Sohail MR. Spinal cord stimulator infection: approach

to diagnosis, management, and prevention. Clin Infect Dis. 2020;70(12):2727–35. https://doi.

org/10.1093/cid/ciz994. PMID: 31598641.

10. Deer T, Stewart D (2008). Complications of spinal cord stimulation: identiﬁcation, treatment,

and prevention. Pain Med. 2008;9(1):S93–S101.

11. Labaran L, Jain N, Puvanesarajah V, Jain A, Buchholz AL, Hassanzadeh H. A retrospective

database review of the indications, complications, and incidence of subsequent spine surgery

in 12,297 spinal cord stimulator patients. Neuromodulation. 2020;23:634–8.

12. Aprili D, Bandschapp O, Rochlitz C, Urwyler A, Ruppen W. Serious complications asso-

ciated with external intrathecal catheters used in cancer pain patients. Anesthesiology.

2009;111:1346–55.

13. D’Souza RS, Warner MA, Olatoye OO, et al. Perioperative opioid consumption and clinical

outcomes in surgical patients with a pre-existing opioid-based intrathecal drug delivery system.

Anesth Analg. 2022;134:35–43.

14. Graham RD, Sankarasubramanian V, Lempka SF. Dorsal root ganglion stimulation for chronic

pain: hypothesized mechanisms of action. J Pain. 2022;23(2):196–211. https://doi.org/10.1016/

j.jpain.2021.07.008. Epub 2021 Aug 20. PMID: 34425252; PMCID: PMC8943693.

https://t.me/med1917

Peripheral Nerve Stimulation for Acute

Postoperative Pain

John J. Finneran IV and Brian M. Ilfeld

Abstract The use of electric stimulation for pain control (“neuromodulation”) has

ancient origins. Although studied more extensively for chronic pain, percutaneous

peripheral nerve stimulation, especially when combined with a single injection local

anesthetic based peripheral nerve block, has the potential to provide weeks of pain

relief following painful orthopedic surgeries. In contrast to nerve blocks with local

anesthetic, nerve stimulation produces analgesia with minimal sensory, propriocep-

tive, or motor deﬁcits. Percutaneous stimulation of the brachial plexus and femoral

and sciatic nerves has been utilized for analgesia following orthopedic surgery.

This chapter will examine the history and mechanism of action of neuromodula-

tion, its application in acute postoperative pain management, as well as associated

contraindications and potential complications.

Keywords Neuromodulation

· Peripheral nerve stimulation · Gate control theory ·

Percutaneous lead · Ultrasound-guidance · Peripheral nerve block · Lead fracture

1 History of Neuromodulation

Electrical stimulation for the treatment of pain, or neuromodulation, has been

utilized for thousands of years. Ancient Greeks and Romans described using living

torpedo ﬁsh, which can generate up to 220 V, for the treatment of maladies including

gout and headache [1]. During the eighteenth and nineteenth centuries, many descrip-

tions of the physiologic effects of application of electricity to various tissues were

published, the ﬁrst of these by Benjamin Franklin in 1774. The nineteenth century

witnessed the development of technology that could create, store, and harness electric

current; and the popularization of this knowledge is evident in works such as Mary

J. J. Finneran IV · B. M. Ilfeld (

)

University of California, San Diego, USA

e-mail: bilfeld@health.ucsd.edu

J. J. Finneran IV

e-mail: jﬁnneran@health.ucsd.edu

A. Abd-Elsayed and K. Schroeder (eds.), Perioperative Pain Management,

https://doi.org/10.1007/978-3-031-67648-2_31

481

https://t.me/med1917

482 J. J. Finneran IV and B. M. Ilfeld

Shelley’s Frankenstein, published in 1818. In the early twentieth century, many elec-

tric devices were marketed for the treatment of pain along with nearly every other

conceivable ailment [2]. However, the use and marketing of these devices had little or

no scientiﬁc support. In 1910, the Carnegie Foundation published the Flexner Report,

which called on medical schools to improve standards in admission, graduation, and

teaching of scientiﬁcally backed clinical practice and recommended the exclusion of

electrotherapy from clinical practice [3]. Concomitantly, death by electrocution was

becoming a common method for execution in the United States, possibly contributing

to a decline in public interest in medical devices employing electric current.

Modern use of peripheral nerve stimulation to treat pain can be traced to

1967, when neurosurgeons Sweet and Hall [4] reported successfully treating pain

in a series of 8 patients using surgically implanted peripheral nerve stimulators.

Unfortunately, the application of such devices required relatively large incisions

and extensive surgical dissection, precluding use for acute surgical or traumatic

pain. Over subsequent decades, percutaneous leads that could be passed through the

skin were developed and transcutaneous neuromuscular stimulation–direct stimu-

lation of large muscles–was described for various chronic pain conditions [5]. The

advent of ultrasound-based localization of peripheral nerves and real-time guidance

of needles towards those nerves offered the possibility of highly targeted stimulation

of peripheral nerves without surgical exposure. Huntoon and Burgher [6] were the

ﬁrst to describe peripheral nerve stimulation for treatment of chronic neuropathic

pain using a percutaneously inserted lead placed with ultrasound guidance in 2009.

In the following years, various lead placement systems were developed and found

to be beneﬁcial for treatment of chronic pain. However, at the time of this writing

there is only one percutaneous peripheral nerve stimulator lead system cleared by

the United States Food and Drug Administration (USFDA) for treatment of acute

pain [7].

2 Mechanism of Analgesia

Many hypotheses about how electric stimulation produces analgesia have been

posited. The most commonly accepted explanation is the “Gate Control Theory,”

ﬁrst described by Melzack and Wall [8]. This theory suggests that the activation of

large diameter sensory afferent ﬁbers, those carrying primarily touch and pressure

sensation, within peripheral nerves activates a region of the spinal cord, the substantia

gelatinosa. Axons from the substantia gelatinosa project to and inhibit signaling via

small diameter afferent ﬁbers, those transmitting pain signals. Applying the “Gate

Control Theory” to electric neuromodulation, the activation of large diameter ﬁbers

(touch) by electrical stimulation closes the “gate” for small diameter ﬁbers (pain).

Thus, peripheral nerve stimulation produces a (usually pleasant) touch sensation

while inhibiting the transmission of pain signals from the periphery to the brain

(Fig. 1).

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