Non-Pharmacological Approaches

**137**

**Chapter 9**

**Abstract**

or its accessories.

**1. Introduction**

spinal cord stimulation

Bench to Bedside

*Laura Tyler Perryman*

Wireless Neuromodulation: From

Spinal cord stimulation (SCS), as a neuromodulation therapy, has rapidly evolved over the past few decades to become the treatment of choice for many chronic pain syndromes. However, many equipment-related limitations such as the bulk of the equipment, an implantable pulse generator (IPG), the limited therapeutic stimulation frequency utilized, and the potential adverse events have restricted SCS applications. Recently, advanced nanotechnology and minimally invasive surgical techniques have shown promising options to expand the indications due to reduced surgical trauma/hospital time/costs. We describe the basis for nanotechnology neuromodulation and the preliminary experience with wireless SCS in the treatment of chronic pain conditions. The equipment utilizes a miniature stimulator with microelectronics, percutaneously placed at the appropriate stimulation target, with wireless control to provide the desired stimulation, and then moderated by the clinician and the patient. The wireless device reduces the bulk of the SCS equipment to a single electrode (with embedded sensors), using the new improved neuralelectric interface. This wireless neuromodulation (WNM) has been clinically used in several chronic pain conditions, including failed back surgery syndrome, facial pain, chronic regional pain syndrome, and postherpetic neuralgia, with encouraging outcome, without the complications of a traditional SCS resulting from the IPG

**Keywords:** neuromodulation, wireless, nanotechnology, chronic pain,

implanted pulse generator (IPG) to provide power.

Therapeutic modulation of excitable neural tissues in the body by electrical stimulation has become an important intervention to manage chronic disabling conditions like pain, involuntary movements, extrapyramidal syndromes, chronic peripheral vascular disease, and cardiac arrhythmias [1–9]. Devices are being implanted to deliver stimulatory signals to the target tissue, record vital signs or action potentials, perform electric cardiac pacing, and control drug release, as well as interface with auditory systems for assisted hearing or even image formation for visual prosthesis. All these systems utilize a subcutaneous battery-operated

Spinal cord stimulation (SCS) has been utilized for over five decades to provide therapeutically effective pain relief from chronic conditions like failed back surgery syndrome (FBSS), regional pain syndromes, and neuralgias, reducing the need for opioids. Several measurable outcomes like pain scores, disability scores, and quality

#### **Chapter 9**

## Wireless Neuromodulation: From Bench to Bedside

*Laura Tyler Perryman*

#### **Abstract**

Spinal cord stimulation (SCS), as a neuromodulation therapy, has rapidly evolved over the past few decades to become the treatment of choice for many chronic pain syndromes. However, many equipment-related limitations such as the bulk of the equipment, an implantable pulse generator (IPG), the limited therapeutic stimulation frequency utilized, and the potential adverse events have restricted SCS applications. Recently, advanced nanotechnology and minimally invasive surgical techniques have shown promising options to expand the indications due to reduced surgical trauma/hospital time/costs. We describe the basis for nanotechnology neuromodulation and the preliminary experience with wireless SCS in the treatment of chronic pain conditions. The equipment utilizes a miniature stimulator with microelectronics, percutaneously placed at the appropriate stimulation target, with wireless control to provide the desired stimulation, and then moderated by the clinician and the patient. The wireless device reduces the bulk of the SCS equipment to a single electrode (with embedded sensors), using the new improved neuralelectric interface. This wireless neuromodulation (WNM) has been clinically used in several chronic pain conditions, including failed back surgery syndrome, facial pain, chronic regional pain syndrome, and postherpetic neuralgia, with encouraging outcome, without the complications of a traditional SCS resulting from the IPG or its accessories.

**Keywords:** neuromodulation, wireless, nanotechnology, chronic pain, spinal cord stimulation

#### **1. Introduction**

Therapeutic modulation of excitable neural tissues in the body by electrical stimulation has become an important intervention to manage chronic disabling conditions like pain, involuntary movements, extrapyramidal syndromes, chronic peripheral vascular disease, and cardiac arrhythmias [1–9]. Devices are being implanted to deliver stimulatory signals to the target tissue, record vital signs or action potentials, perform electric cardiac pacing, and control drug release, as well as interface with auditory systems for assisted hearing or even image formation for visual prosthesis. All these systems utilize a subcutaneous battery-operated implanted pulse generator (IPG) to provide power.

Spinal cord stimulation (SCS) has been utilized for over five decades to provide therapeutically effective pain relief from chronic conditions like failed back surgery syndrome (FBSS), regional pain syndromes, and neuralgias, reducing the need for opioids. Several measurable outcomes like pain scores, disability scores, and quality

of life scales have shown consistent improvement with SCS in patients with back pain and leg pain [1–3].

Outcomes following SCS therapy have demonstrated superior results compared to conservative medical treatment for patients with FBSS in several studies [2, 4], and SCS was also shown to be more cost-effective over the long term due to a decrease in follow-up visits, diagnostic tests, and overall consumption of healthcare facilities [4, 5]. Historically, on the other hand, SCS has not been devoid of complications and limitations in its conventional form utilizing an IPG, since the device options have had a long history of severe adverse events primarily related to the IPG [6, 7]. A large percentage of patients, reportedly as high as 50%, have failed the trial period utilizing conventional SCS devices [6–8], while additional failures came from equipment complications caused by the migration/fracture of the electrodes as well as IPG failures and complications in recharging or reimplantation. Postsurgical complications like infection, hemorrhage, and painful operative wounds were frequently seen associated with IPG and its extension wires. Additionally, SCS in its conventional form is incapable of reaching some anatomical locations to provide targeted therapeutic localized pain relief [6, 8–12].

Several modifications have been introduced to the SCS equipment over the past few years, which have reduced adverse events while promoting the efficacy of the modality, thereby increasing the number of clinical indications [13]. Percutaneous techniques, smaller compact batteries, rechargeable batteries, increased life of the IPG, and improved anchoring methods are some of these modifications currently in use. Part of the refinement also comes from the advancements in the technology of nanomaterials and wireless power transfer techniques.

#### **2. Nanoelectrodes and wireless technology for neuromodulation**

An advancement in this field is the new miniature pulse generator (mini PG) with wireless access (WPG) utilizing a dipole antenna for electric field coupling. This is accomplished with "microwaves", which are very short wavelength pulsed electromagnetic waves at gigahertz (GHz) frequencies. This device (Stimwave Technologies, Florida, USA), instead of using lower frequencies of 100 – 500 kHz of the inductive range operational in most of the present-day implanted medical devices, is powered by a radiative electric field coupling through tissues at microwave frequencies that enable smaller-sized implants to be placed at a significant tissue depth through a percutaneous technique. It also affords minimal power loss, since the higher frequency allows a much better energy transfer to a smaller implant [14]. The principle behind the frequency changes in relation to the wavelength was elaborated earlier by Feynman: "If you build a corresponding circuit on a small scale, its natural frequency goes up, since the wave length goes down as the scale; but the skin depth only decreases with the square root of the scale ratio, and so resistive problems are of increasing difficulty. Possibly we can beat resistance through the use of superconductivity if the frequency is not too high, or by other tricks [15]."

**Figure 1.**

*MRI compatible electrode with nanostimulator and microcircuit to contact wireless pulse generator. This is the only implantable component required for WSCS.*

**139**

*Wireless Neuromodulation: From Bench to Bedside DOI: http://dx.doi.org/10.5772/intechopen.85501*

**stimulator (INS)**

**pulse generator**

ing the neural tissue (**Figure 1**).

signals based on the stimulus feedback.

procedures like laminectomy or laminotomy.

6 mm apart with a combined surface area of 0.8 to 60 mm2

series with one or more electrodes.

The micro-implant WPG is capable of delivering clinically appropriate stimula-

The INS has an enclosure housing the stimulating electrode array, designed to apply electrical pulses to the target tissue and antenna-1 and configured to receive electric energy input from an external antenna-2 through electrical radiative

coupling. The antenna-2, physically separated from the INS lead, is connected to the antenna-1 by electric circuits configured to generate electrical pulses for stimulat-

The INS is without any power source and stays in contact with the excitable neural tissue with passive components capable of receiving an external input signal at a frequency between 300 MHz and 8 GHz. A controller module, positioned in proximity to the patient body, to generate the input signals, sends them to the antenna-2; the latter transmits the input signal to the first dipole antenna placed within the INS through electrical radiative coupling, and antenna-1 extracts the stimulus feedback signal from signals received by the antenna-2 to adjust the parameters of the input

The electrical pulses from the activated stimulating electrode, however, result in zero net charge within the patient's body. The electrodes can be selectively marked as a stimulating return electrode or an inactive one. It can have one capacitor in

INS is designed to be placed in the patient through an introducer or a needle with

. The lead can also be a

electrodes (**Figure 2**) that include a semicylindrical array of electrodes/contacts made up of platinum, or platinum-iridium, or gallium-nitride, or titanium-nitride, or iridium-oxide or similar combinations. The contacts can be 2–16 in number having a length of 1 to 6 mm and 0.4 to 3 mm in width. They are spaced 1 to

paddle type, deliverable through a 14-gauge needle. The enclosure has an external

At present, several therapeutic intra-body electrical stimulation techniques are available to manage neuropathic pain. However, they utilize a bulky, heavy, subcutaneous IPG connected to the implantable wired leads and have many failures or adverse events like mechanical dislodgement, impingement of the lead extension cables, and infection, along with IPG-related discomfort, pain, and irritation. The lead configuration includes cylindrical percutaneous or paddle leads. Cylinders are usually 1.3 mm in diameter and contain several circular electrodes, which are used for trial testing, later followed by permanent placement by minimally invasive, percutaneous approach. Paddles contain electrodes with a wider surface area directionally targeted for control over neural excitation and require invasive surgical

tion with dimensions of 800–1350 μm diameter, a significantly miniature size compared to the conventional SCS-IPG. This is equal to the size of a standard lead body that also incorporates the nanoelectronics within the device itself. It also can be integrated with a variety of lead types carrying four or eight contacts, either in a percutaneous or a paddle-type electrode, and the receiver wire has circuits in the

stimulator device internally with wireless access (**Figure 1**).

**3. The implantable wireless lead or the implantable neural**

**4. The nanoelectronic substrate of the miniature wireless**

*Wireless Neuromodulation: From Bench to Bedside DOI: http://dx.doi.org/10.5772/intechopen.85501*

*From Conventional to Innovative Approaches for Pain Treatment*

targeted therapeutic localized pain relief [6, 8–12].

nanomaterials and wireless power transfer techniques.

pain and leg pain [1–3].

of life scales have shown consistent improvement with SCS in patients with back

Outcomes following SCS therapy have demonstrated superior results compared to conservative medical treatment for patients with FBSS in several studies [2, 4], and SCS was also shown to be more cost-effective over the long term due to a decrease in follow-up visits, diagnostic tests, and overall consumption of healthcare facilities [4, 5]. Historically, on the other hand, SCS has not been devoid of complications and limitations in its conventional form utilizing an IPG, since the device options have had a long history of severe adverse events primarily related to the IPG [6, 7]. A large percentage of patients, reportedly as high as 50%, have failed the trial period utilizing conventional SCS devices [6–8], while additional failures came from equipment complications caused by the migration/fracture of the electrodes as well as IPG failures and complications in recharging or reimplantation. Postsurgical complications like infection, hemorrhage, and painful operative wounds were frequently seen associated with IPG and its extension wires. Additionally, SCS in its conventional form is incapable of reaching some anatomical locations to provide

Several modifications have been introduced to the SCS equipment over the past few years, which have reduced adverse events while promoting the efficacy of the modality, thereby increasing the number of clinical indications [13]. Percutaneous techniques, smaller compact batteries, rechargeable batteries, increased life of the IPG, and improved anchoring methods are some of these modifications currently in use. Part of the refinement also comes from the advancements in the technology of

**2. Nanoelectrodes and wireless technology for neuromodulation**

An advancement in this field is the new miniature pulse generator (mini PG) with wireless access (WPG) utilizing a dipole antenna for electric field coupling. This is accomplished with "microwaves", which are very short wavelength pulsed electromagnetic waves at gigahertz (GHz) frequencies. This device (Stimwave Technologies, Florida, USA), instead of using lower frequencies of 100 – 500 kHz of the inductive range operational in most of the present-day implanted medical devices, is powered by a radiative electric field coupling through tissues at microwave frequencies that enable smaller-sized implants to be placed at a significant tissue depth through a percutaneous technique. It also affords minimal power loss, since the higher frequency allows a much better energy transfer to a smaller implant [14]. The principle behind the frequency changes in relation to the wavelength was elaborated earlier by Feynman: "If you build a corresponding circuit on a small scale, its natural frequency goes up, since the wave length goes down as the scale; but the skin depth only decreases with the square root of the scale ratio, and so resistive problems are of increasing difficulty. Possibly we can beat resistance through the use of superconductivity if the frequency is not too high, or by other

*MRI compatible electrode with nanostimulator and microcircuit to contact wireless pulse generator. This is the*

**138**

**Figure 1.**

*only implantable component required for WSCS.*

tricks [15]."

The micro-implant WPG is capable of delivering clinically appropriate stimulation with dimensions of 800–1350 μm diameter, a significantly miniature size compared to the conventional SCS-IPG. This is equal to the size of a standard lead body that also incorporates the nanoelectronics within the device itself. It also can be integrated with a variety of lead types carrying four or eight contacts, either in a percutaneous or a paddle-type electrode, and the receiver wire has circuits in the stimulator device internally with wireless access (**Figure 1**).

#### **3. The implantable wireless lead or the implantable neural stimulator (INS)**

The INS has an enclosure housing the stimulating electrode array, designed to apply electrical pulses to the target tissue and antenna-1 and configured to receive electric energy input from an external antenna-2 through electrical radiative coupling. The antenna-2, physically separated from the INS lead, is connected to the antenna-1 by electric circuits configured to generate electrical pulses for stimulating the neural tissue (**Figure 1**).

#### **4. The nanoelectronic substrate of the miniature wireless pulse generator**

The INS is without any power source and stays in contact with the excitable neural tissue with passive components capable of receiving an external input signal at a frequency between 300 MHz and 8 GHz. A controller module, positioned in proximity to the patient body, to generate the input signals, sends them to the antenna-2; the latter transmits the input signal to the first dipole antenna placed within the INS through electrical radiative coupling, and antenna-1 extracts the stimulus feedback signal from signals received by the antenna-2 to adjust the parameters of the input signals based on the stimulus feedback.

The electrical pulses from the activated stimulating electrode, however, result in zero net charge within the patient's body. The electrodes can be selectively marked as a stimulating return electrode or an inactive one. It can have one capacitor in series with one or more electrodes.

At present, several therapeutic intra-body electrical stimulation techniques are available to manage neuropathic pain. However, they utilize a bulky, heavy, subcutaneous IPG connected to the implantable wired leads and have many failures or adverse events like mechanical dislodgement, impingement of the lead extension cables, and infection, along with IPG-related discomfort, pain, and irritation. The lead configuration includes cylindrical percutaneous or paddle leads. Cylinders are usually 1.3 mm in diameter and contain several circular electrodes, which are used for trial testing, later followed by permanent placement by minimally invasive, percutaneous approach. Paddles contain electrodes with a wider surface area directionally targeted for control over neural excitation and require invasive surgical procedures like laminectomy or laminotomy.

INS is designed to be placed in the patient through an introducer or a needle with electrodes (**Figure 2**) that include a semicylindrical array of electrodes/contacts made up of platinum, or platinum-iridium, or gallium-nitride, or titanium-nitride, or iridium-oxide or similar combinations. The contacts can be 2–16 in number having a length of 1 to 6 mm and 0.4 to 3 mm in width. They are spaced 1 to 6 mm apart with a combined surface area of 0.8 to 60 mm2 . The lead can also be a paddle type, deliverable through a 14-gauge needle. The enclosure has an external

**Figure 2.**

*Minimally invasive approach to place the wireless implantable neural stimulator in the spinal epidural space.*

biocompatible coating of polymethyl methacrylate (PMMA), polydimethylsiloxane (PDMS), perylene, polyurethane, polytetrafluoroethylene (PTFE), polycarbonate, or a silicone elastomer.

The antenna-1 within the INS enclosure has 2 to 8 contacts, configured to couple with each other as well as the circuit, and these contacts are located proximally relative to the electrode inside the enclosure. These contacts are 1 to 6 mm in length, 1 to 2.5 mm in width, and spaced 30 to 80 mm apart. One antenna is constructed as a conductive trace contained on the circuits and can be fabricated as a conductive wire connected to the circuits, which are flexible with a bend radius of 0.5 mm and located proximal in the enclosure with a waveform conditioning circuit.

#### **5. Remote control of power or polarity selection for a neural stimulator**

The dipole antenna receives input signals containing polarity assignment information and electrical energy, the former designating the polarities for the electrode contacts. The circuits are configured to control an electrode interface so that these electrode contacts have polarities designed by the polarity assignment information to create electrical pulses from the electrical energy contained in the input signal. These electrical pulses reach the contacts according to the polarities assigned.

#### **6. The remote radiofrequency power system with a low-profile transmitting antenna**

The antenna for this wireless system includes a metal signal layer with radiating surface, a feed port, a wave guide surrounding the antenna, and a configuration to guide electromagnetic (EM) energy transmitted from the radiating surface in a direction away from the antenna. It also has a controller module connected to the feed port to drive the antenna to transmit EM energy from the radiating surface, while the antenna, wave guide, and controller module are configured to match a reception characteristic of an implantable device, so that the latter can produce electrical pulses of sufficient amplitude to stimulate the target neural tissue utilizing the EM energy received from the antenna-2, located up to 10 cm away.

Adverse events related to the IPG, due to excessive absorption of EM energy, include burning of tissue, creation of undesirable blood clots, and skin irritation

**141**

neural tissue.

band.

**Figure 4.**

**Figure 3.**

**7. Wireless energy supply**

*Wireless Neuromodulation: From Bench to Bedside DOI: http://dx.doi.org/10.5772/intechopen.85501*

*Remote access by wireless antenna (experimental setting).*

because of adhesions between the implant and tissues. A wireless device, on the other hand, has the antenna located outside the body with a controller module con-

*Neurostimulator receiver. The contacts on the electrodes are managed by independently integrated, circuits that are application specific. The circuitry system within the device produces charge-balanced waveforms.*

The antenna has a dielectric lens filling the wave guide, protruding outward from an opening of the wave guide to narrow the transmitted EM energy and direct it away from the transmitting surface. It also has a return loss cutoff frequency associated with the wave guide; the dielectric lens lowers the return loss of cutoff frequency. The antenna operates within 500 MHz to 4 GHz frequency

The INS receives energy by a wireless method, which includes radiating EM energy from the surface on an antenna located up to 10 cm away, inside the patient, so that the implanted device creates appropriate electrical pulses to stimulate the target neural tissue, using the received EM energy, even during sleep. The radiating surface of the antenna can be placed 1 to 6 feet away from the INS and can be adjusted to increase the EM energy provided to the latter (**Figure 3**). The interface is facilitated by a link between the programmable module and the controller module so that the stimulation pulses created at the implantable device are transmitted as data-encoded parameters from the programming module to the controller module, thus effectively stimulating the

A dipole antenna receiver intercepts the high-frequency microwave EM energy coming from outside the body to produce an oscillating electric field. Frequencies in

necting the implantable device with the antenna (**Figures 3** and **4**).

*Wireless Neuromodulation: From Bench to Bedside DOI: http://dx.doi.org/10.5772/intechopen.85501*

**Figure 3.** *Remote access by wireless antenna (experimental setting).*

**Figure 4.**

*From Conventional to Innovative Approaches for Pain Treatment*

or a silicone elastomer.

**Figure 2.**

polarities assigned.

**transmitting antenna**

biocompatible coating of polymethyl methacrylate (PMMA), polydimethylsiloxane (PDMS), perylene, polyurethane, polytetrafluoroethylene (PTFE), polycarbonate,

*Minimally invasive approach to place the wireless implantable neural stimulator in the spinal epidural space.*

with each other as well as the circuit, and these contacts are located proximally relative to the electrode inside the enclosure. These contacts are 1 to 6 mm in length, 1 to 2.5 mm in width, and spaced 30 to 80 mm apart. One antenna is constructed as a conductive trace contained on the circuits and can be fabricated as a conductive wire connected to the circuits, which are flexible with a bend radius of 0.5 mm and

**5. Remote control of power or polarity selection for a neural stimulator**

The dipole antenna receives input signals containing polarity assignment information and electrical energy, the former designating the polarities for the electrode contacts. The circuits are configured to control an electrode interface so that these electrode contacts have polarities designed by the polarity assignment information to create electrical pulses from the electrical energy contained in the input signal. These electrical pulses reach the contacts according to the

located proximal in the enclosure with a waveform conditioning circuit.

**6. The remote radiofrequency power system with a low-profile**

ing the EM energy received from the antenna-2, located up to 10 cm away.

Adverse events related to the IPG, due to excessive absorption of EM energy, include burning of tissue, creation of undesirable blood clots, and skin irritation

The antenna for this wireless system includes a metal signal layer with radiating surface, a feed port, a wave guide surrounding the antenna, and a configuration to guide electromagnetic (EM) energy transmitted from the radiating surface in a direction away from the antenna. It also has a controller module connected to the feed port to drive the antenna to transmit EM energy from the radiating surface, while the antenna, wave guide, and controller module are configured to match a reception characteristic of an implantable device, so that the latter can produce electrical pulses of sufficient amplitude to stimulate the target neural tissue utiliz-

The antenna-1 within the INS enclosure has 2 to 8 contacts, configured to couple

**140**

*Neurostimulator receiver. The contacts on the electrodes are managed by independently integrated, circuits that are application specific. The circuitry system within the device produces charge-balanced waveforms.*

because of adhesions between the implant and tissues. A wireless device, on the other hand, has the antenna located outside the body with a controller module connecting the implantable device with the antenna (**Figures 3** and **4**).

The antenna has a dielectric lens filling the wave guide, protruding outward from an opening of the wave guide to narrow the transmitted EM energy and direct it away from the transmitting surface. It also has a return loss cutoff frequency associated with the wave guide; the dielectric lens lowers the return loss of cutoff frequency. The antenna operates within 500 MHz to 4 GHz frequency band.

#### **7. Wireless energy supply**

The INS receives energy by a wireless method, which includes radiating EM energy from the surface on an antenna located up to 10 cm away, inside the patient, so that the implanted device creates appropriate electrical pulses to stimulate the target neural tissue, using the received EM energy, even during sleep. The radiating surface of the antenna can be placed 1 to 6 feet away from the INS and can be adjusted to increase the EM energy provided to the latter (**Figure 3**). The interface is facilitated by a link between the programmable module and the controller module so that the stimulation pulses created at the implantable device are transmitted as data-encoded parameters from the programming module to the controller module, thus effectively stimulating the neural tissue.

A dipole antenna receiver intercepts the high-frequency microwave EM energy coming from outside the body to produce an oscillating electric field. Frequencies in the range of GHz were found to be more energy efficient [16]. Typically, the antenna within the device lumen can be anywhere from 2 to 8cm long and can be modified depending upon the indications and the depth at which the device is implanted, since the EM field energy is dissipated across the tissue layers of the skin, fat, muscle, blood vessels, and bone. The deeper the placement, the longer the antenna should be to receive adequate power. Each contact on the electrodes is provided with independent power, a part of an "application-specific" integrated circuit; the embedded circuitry within the device enables production of charge-balanced waveforms. This is managed by internalized addressing systems within the device (**Figure 4**). It is important to note that microwave fields are safe, since these high frequencies fail to activate cell membranes and thus nervous tissue damage is unlikely.

#### **8. Wireless pulse generator (WPG)**

The WPG employs standard cellular phone technology, with an average pulse output power of up to 1 W, depending upon the stimulation parameters and according to the requirements of the target tissue. A radiofrequency (RF) transmitter placed inside the WPG encodes stimulus waveforms into the signal according to the program settings. A microprocessor inside this transmitter controls the data communications and settings (**Figures 3** and **4**). Clinicians as well as patients communicate with the WPG via a controller that uses Bluetooth technology (**Figure 5**) and also can be accessed by a software application (app) on a mobile phone [14].

**Figure 5.** *External wireless pulse generator.*

#### **9. Discussion**

The traditional SCS (TSCS) system has electrodes in a catheter enclosure attached to a long extension cable(s) that connects the electrodes to an IPG that is placed inside the patient's body, inheriting the complications due to failure or malfunction of any of these components. Efforts have been ongoing to reduce the bulk of the implanted material and yet improve the efficiency of the system. Reduction in size has a challenge from the battery life expectancy with the conventional energy settings. Thus, TSCS equipment requires implantation of electrodes, extension cables, and the battery inside the body, requiring multiple incisions along with long segment tunnels under the skin, producing considerable tissue trauma with pain and hemorrhage.

**143**

*Wireless Neuromodulation: From Bench to Bedside DOI: http://dx.doi.org/10.5772/intechopen.85501*

**neuromodulation technology**

incisions/tissue trauma, and hospital visits.

tional SCS has a structure as follows:

body

The wireless SCS system with nanotechnology has been clinically used for SCS, dorsal root ganglia (DRG) stimulation, and peripheral nerve stimulation (PNS) throughout Europe and the USA for several years, and multiple trials have shown encouraging results. The capabilities of this system enabled its utility to be tested in a variety of chronic pain syndromes. Poon et al. [16, 17] demonstrated that in a biological media, the operating frequency for wireless-powered devices was in GHz range as opposed to the MHz, which could have potential advantages. At this frequency range, the size reduction of the receiver has been demonstrated in the subsequent studies by Tyler Perryman et al., while the tissue depth relationship to the energy transmission were further elaborated [17, 18]. Tyler Perryman et al. conducted studies in animals and verified the tissue depths at which the wireless stimulation could achieve effective current density [18]. The dipole antenna of the wireless system (at 915 MHz) could energize the stimulators implanted at a depth of 12 cm in porcine models, especially efficient with a 4.3 cm antenna. Successful stimulation has been observed to provide significant pain relief in patients with back and leg pain with FBSS [19, 20], post herpetic neuralgia [21], refractory craniofacial pain [22], occipital neuralgia [23], and CRPS [24]. Patients undergo implantation of the INS with integrated microcircuits enabling coupling with a pulse generator, while the wireless pulse generator circuit excludes surgical implantation of the IPG, thus eliminating complications related to multiple surgical incisions and interventions for failed IPG or its extension cables. Consequently, there is reduced operating time, minimal consumables, and increased comfort to the patient. In the long run, this should decrease

the costs of SCS and reduce overall healthcare budget in neuromodulation.

**10. Financial implications and economic benefits with the wireless**

as the inventions arrive into the clinical practice. For easy understanding, tradi-

Conversely, wireless neuromodulation with nanotechnology utilizes only implantable stimulating electrodes and an implantable receiver placed in a microincision pocket. Because of the reduced bulk of the implants, wireless technology has much more to offer other than the costs alone. It reduces surgical trauma, operating time, con-sumables, anesthesia, complications secondary to multiple

Compared to the wireless neuromodulation, TSCS was reported to be more expensive (**Table 1**). There have been limited reports on the costs and long-term maintenance

2.External controller (for the patient as well as the clinician)

**11. Costs involved with nanotechnology wireless SCS**

The initial implantation of the wireless stimulator 18,000 Euros IPG costs: Zero (0) Annual maintenance of the neuromodulation cost 1500 Euros/3

Every innovation carries financial burden, and there are economic repercussions

1.Electrodes + connection cables + implantable pulse generator inside the patient

*Wireless Neuromodulation: From Bench to Bedside DOI: http://dx.doi.org/10.5772/intechopen.85501*

*From Conventional to Innovative Approaches for Pain Treatment*

branes and thus nervous tissue damage is unlikely.

**8. Wireless pulse generator (WPG)**

the range of GHz were found to be more energy efficient [16]. Typically, the antenna within the device lumen can be anywhere from 2 to 8cm long and can be modified depending upon the indications and the depth at which the device is implanted, since the EM field energy is dissipated across the tissue layers of the skin, fat, muscle, blood vessels, and bone. The deeper the placement, the longer the antenna should be to receive adequate power. Each contact on the electrodes is provided with independent power, a part of an "application-specific" integrated circuit; the embedded circuitry within the device enables production of charge-balanced waveforms. This is managed by internalized addressing systems within the device (**Figure 4**). It is important to note that microwave fields are safe, since these high frequencies fail to activate cell mem-

The WPG employs standard cellular phone technology, with an average pulse output power of up to 1 W, depending upon the stimulation parameters and according to the requirements of the target tissue. A radiofrequency (RF) transmitter placed inside the WPG encodes stimulus waveforms into the signal according to the program settings. A microprocessor inside this transmitter controls the data communications and settings (**Figures 3** and **4**). Clinicians as well as patients communicate with the WPG via a controller that uses Bluetooth technology (**Figure 5**) and also can be accessed by a software application (app) on a mobile phone [14].

The traditional SCS (TSCS) system has electrodes in a catheter enclosure attached to a long extension cable(s) that connects the electrodes to an IPG that is placed inside the patient's body, inheriting the complications due to failure or malfunction of any of these components. Efforts have been ongoing to reduce the bulk of the implanted material and yet improve the efficiency of the system. Reduction in size has a challenge from the battery life expectancy with the conventional energy settings. Thus, TSCS equipment requires implantation of electrodes, extension cables, and the battery inside the body, requiring multiple incisions along with long segment tunnels under the skin, producing considerable tissue trauma

**142**

**9. Discussion**

*External wireless pulse generator.*

**Figure 5.**

with pain and hemorrhage.

The wireless SCS system with nanotechnology has been clinically used for SCS, dorsal root ganglia (DRG) stimulation, and peripheral nerve stimulation (PNS) throughout Europe and the USA for several years, and multiple trials have shown encouraging results. The capabilities of this system enabled its utility to be tested in a variety of chronic pain syndromes. Poon et al. [16, 17] demonstrated that in a biological media, the operating frequency for wireless-powered devices was in GHz range as opposed to the MHz, which could have potential advantages. At this frequency range, the size reduction of the receiver has been demonstrated in the subsequent studies by Tyler Perryman et al., while the tissue depth relationship to the energy transmission were further elaborated [17, 18]. Tyler Perryman et al. conducted studies in animals and verified the tissue depths at which the wireless stimulation could achieve effective current density [18]. The dipole antenna of the wireless system (at 915 MHz) could energize the stimulators implanted at a depth of 12 cm in porcine models, especially efficient with a 4.3 cm antenna. Successful stimulation has been observed to provide significant pain relief in patients with back and leg pain with FBSS [19, 20], post herpetic neuralgia [21], refractory craniofacial pain [22], occipital neuralgia [23], and CRPS [24]. Patients undergo implantation of the INS with integrated microcircuits enabling coupling with a pulse generator, while the wireless pulse generator circuit excludes surgical implantation of the IPG, thus eliminating complications related to multiple surgical incisions and interventions for failed IPG or its extension cables. Consequently, there is reduced operating time, minimal consumables, and increased comfort to the patient. In the long run, this should decrease the costs of SCS and reduce overall healthcare budget in neuromodulation.

#### **10. Financial implications and economic benefits with the wireless neuromodulation technology**

Every innovation carries financial burden, and there are economic repercussions as the inventions arrive into the clinical practice. For easy understanding, traditional SCS has a structure as follows:

Conversely, wireless neuromodulation with nanotechnology utilizes only implantable stimulating electrodes and an implantable receiver placed in a microincision pocket. Because of the reduced bulk of the implants, wireless technology has much more to offer other than the costs alone. It reduces surgical trauma, operating time, con-sumables, anesthesia, complications secondary to multiple incisions/tissue trauma, and hospital visits.

#### **11. Costs involved with nanotechnology wireless SCS**

Compared to the wireless neuromodulation, TSCS was reported to be more expensive (**Table 1**). There have been limited reports on the costs and long-term maintenance

#### *From Conventional to Innovative Approaches for Pain Treatment*

#### **Table 1.**

*Literature on TSCS cost.*

*HF SCS therapy was similar to TSCS in its costs and complications. USD\*, US dollar; CAD\*, Canadian dollar; UKS\*, United Kingdom Sterling Pound.*

#### **Table 2.**

*Reported costs of traditional SCS (TSCS) and the wireless SCS (WSCS).*

#### **Table 3.**

*Costs for lead revision/repositioning in TSCS.*

of TSCS in the literature. Detailed report on follow-up costs, complications, and replacement charges for reimplantation has not been forthcoming. However, the natural course of TSCS with its multiple implant components leading to their inherent complications could be expected as reported in a few of the studies (**Tables 1–3**). Wireless neuromodulation is evolving, and only limited experience has been reported so far. However, large-scale multicenter studies have been initiated to improve our understanding about the efficacy and acceptable long-term results in the form of improved quality of life, reduced complications, reduction in healthcare costs, and better cosmetic results.

#### **12. Conclusions**

Nanoelectronics have contributed to the development of miniature implants for therapeutic purposes, and wireless technology coupled with mini WPG appears

**145**

**Author details**

Laura Tyler Perryman

provided the original work is properly cited.

Stimwave Technologies, Inc., Pompano Beach, Florida, USA

\*Address all correspondence to<EMAIL_ADDRESS>
*Wireless Neuromodulation: From Bench to Bedside DOI: http://dx.doi.org/10.5772/intechopen.85501*

with improved cosmetic and functional results.

2.US9254393B2. Wearable antenna assembly

5.US8849412B2. Microwave field stimulator

7.US9409030B2. Neural stimulator system

9.US9522270B2. Circuit for an implantable device

3.US9220897B2. Implantable lead

**Copyright information**

stimulator

exiting spinal nerves

from the patent applications.

to enhance the quality of neuromodulation in the field of functional neurosurgery and pain management therapies. Wireless neuromodulation, so far applied as SCS, DRG, and PNS, has provided efficient pain relief in cases of FBSS, neuralgic pain, CRPS, and facial pain syndromes. The results observed in small case series or case illustrations are comparable to traditional SCS methods and devoid of many of the complications of TSCS, primarily related to IPG/battery accessories. Further wireless neuromodulation experience may demonstrate improved quality of life associated with significant reduction in cost as well as reduction in complications,

Authors hold the following patents. Information in the chapter includes material

1.US9409029B2. Remote RF power system with low profile transmitting antenna

4.US9199089B2. Remote control of power or polarity selection for a neural

6.US8903502B2. Methods and devices for modulating excitable tissue of the

8.US15228715. Remote rf power system with low profile transmitting antenna

Author has copyrights on the publications referenced [18, 19, 22, 23].

© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium,

*Wireless Neuromodulation: From Bench to Bedside DOI: http://dx.doi.org/10.5772/intechopen.85501*

to enhance the quality of neuromodulation in the field of functional neurosurgery and pain management therapies. Wireless neuromodulation, so far applied as SCS, DRG, and PNS, has provided efficient pain relief in cases of FBSS, neuralgic pain, CRPS, and facial pain syndromes. The results observed in small case series or case illustrations are comparable to traditional SCS methods and devoid of many of the complications of TSCS, primarily related to IPG/battery accessories. Further wireless neuromodulation experience may demonstrate improved quality of life associated with significant reduction in cost as well as reduction in complications, with improved cosmetic and functional results.

#### **Copyright information**

*From Conventional to Innovative Approaches for Pain Treatment*

**Author Journal Year No. of**

of TSCS in the literature. Detailed report on follow-up costs, complications, and

1. Repositioning of electrode €360 \$2700 2. Replacement €1530 \$5450 3. Reimplantation following infection €6192 \$19,600

**Procedure TSCS USD\* TSCS CAD\* TSCS**

*Reported costs of traditional SCS (TSCS) and the wireless SCS (WSCS).*

Implantation 32,882 21,595 15,081 €18,000 Complication cost 9649 5191 576 NA Revision cost 5450 5339 (lead) €2500 **IPG cost 13,150 10,591 7243 0 Maintenance 5071 (4 years) 3539 (4 years) NA 1500 (3 years)** *HF SCS therapy was similar to TSCS in its costs and complications. USD\*, US dollar; CAD\*, Canadian dollar;*

1. Manca et al. [25] European J Pain 2008 52 CAD 19,486, Euro 12,653 2. Kumar et al. [10] J Neurosurg Spine 2006 160 CAD 23,205 3. Kumar and Bishop [26] J Neurosurg Spine 2009 197 CAD 21,595, USD 32,882 4. Hornberger et al. [27] Clin J Pain 2008 NA USD 26,005 (nonrechargeable)

5. Babu et al. [28] Neuromodulation 2013 4536 USD 30,200 (percutaneous)

6. Annemans et al. [29] J LTE Med Implants 2014 Model UK£ 15,056 (HF SCS)

**UKS\***

**patients**

**Stimwave WSCS**

**American experience [31]**

**Cost**

USD 35,109 (rechargeable)

4536 USD 29,963 (paddle electrodes)

replacement charges for reimplantation has not been forthcoming. However, the natural course of TSCS with its multiple implant components leading to their inherent complications could be expected as reported in a few of the studies (**Tables 1–3**). Wireless neuromodulation is evolving, and only limited experience has been reported so far. However, large-scale multicenter studies have been initiated to improve our understanding about the efficacy and acceptable long-term results in the form of improved quality of life, reduced complications, reduction in healthcare costs, and better cosmetic results.

**European experience [30]**

Nanoelectronics have contributed to the development of miniature implants for therapeutic purposes, and wireless technology coupled with mini WPG appears

**144**

**12. Conclusions**

*UKS\*, United Kingdom Sterling Pound.*

*Costs for lead revision/repositioning in TSCS.*

**Table 2.**

**Table 3.**

**Table 1.**

*Literature on TSCS cost.*

Authors hold the following patents. Information in the chapter includes material from the patent applications.

Author has copyrights on the publications referenced [18, 19, 22, 23].

#### **Author details**

Laura Tyler Perryman Stimwave Technologies, Inc., Pompano Beach, Florida, USA

\*Address all correspondence to<EMAIL_ADDRESS>
© 2019 The Author(s). Licensee IntechOpen. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/ by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

### **References**

[1] Turner JA, Loeser JD, Bell KG. Spinal cord stimulation for chronic low back pain: A systematic literature synthesis. Neurosurgery. 1995;**37**:1088-1096

[2] Kumar K, Taylor RS, Jacques L, et al. The effects of spinal cord stimulation in neuropathic pain are sustained: A 24-month follow-up of the prospective randomized controlled multicenter trial of the effectiveness of spinal cord stimulation. Neurosurgery. 2008;**63**:762-770

[3] Kapural L, Yu C, Doust M, et al. Novel 10-kHz high-frequency therapy (HF10 therapy) is superior to traditional low-frequency spinal cord stimulation for the treatment of chronic back and leg pain the SENZA-RCT randomized controlled trial. Anesthesiology. 2015;**123**:851-860

[4] Deer TR, Mekhail N, Provenzano D, et al. The appropriate use of neurostimulation of the spinal cord and peripheral nervous system for the treatment of chronic pain and ischemic diseases: The neuromodulation appropriateness consensus committee. Neuromodulation. 2014;**17**:515-550

[5] Mekhail NA, Aeschbach A, Stanton-Hicks M. Cost benefit analysis of neurostimulation for chronic pain. The Clinical Journal of Pain. 2004;**20**:462-468

[6] Turner JA, Loeser JD, Deyo RA, Sanders SB. Spinal cord stimulation for patients with failed back surgery syndrome or complex regional pain syndrome: A systematic review of effectiveness and complications. Pain. 2004;**108**:137-147

[7] Mekhail NA, Mathews M, Nageeb F, Guirguis M, et al. Retrospective review of 707 cases of spinal cord stimulation: Indications and complications. Pain Practice. 2011;**11**:148-153

[8] Cameron T. Safety and efficacy of spinal cord stimulation for the treatment of chronic pain: A 20-year literature review. Journal of Neurosurgery. 2004;**100**:254-267

[9] Krishna K, Jefferson RW, Gupta S. Complications of spinal cord stimulation, suggestions to improve outcome, and financial impact. Journal of Neurosurgery. 2006;**5**:191-203

[10] Kumar K, Hunter G, Demeria D. Spinal cord stimulation in treatment of chronic benign pain: Challenges in treatment planning and present status, a 22-year experience. Neurosurgery. 2006;**58**:481-496

[11] North RB, Kidd DH, Zahurak M, et al. Spinal cord stimulation for chronic, intractable pain: Experience over two decades. Neurosurgery 1993;**32**:384-394; discussion 394-395.

[12] Pineda A. Complications of dorsal column stimulation. Journal of Neurosurgery. 1978;**48**:64-68

[13] Slavin KV. Spinal stimulations for pain: Future applications. Neurotherapeutics. 2014;**11**:535-542

[14] Yearwood TL, Perryman LT. Peripheral neurostimulation with a microsize wireless stimulator. In: Slavin KV, editor. Stimulation of the Peripheral Nervous System. The Neuromodulation Frontier. Progress in Neurological Surgery. Basel, Switzerland: Karger Publishing; 2016. pp. 168-191

[15] Feynman RP. There's plenty of room at the bottom. CalTech, Pasedena CA: Presentation to the American Physical Society; 1959

[16] Poon AS, O'Driscoll S, Meng TH. Optimal operating frequency in wireless power transmission for implantable devices. In: Conf Proc IEEE Eng Med

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> neuralgia: Case illustrations. Journal of Neurology & Stroke. 2017;**6**:00213

[24] Herschkowitz D, Kubias J. Wireless peripheral nerve stimulation for complex regional pain syndrome type I of the upper extremity: A case illustration introducing a novel technology. Scandinavian Journal of Pain. July

[25] Manca A, Kumar K, Taylor RS, Jacques L, Eldabe S, Meglio M, et al. Quality of life, resource consumption and costs of spinal cord stimulation versus conventional medical management in neuropathic pain patients with failed back surgery syndrome (PROCESS trial). European Journal of Pain. 2008;**12**:1047-1058

[26] Kumar K, Bishop S. Financial impact of spinal cord stimulation on the health care budget: A comparative analysis of costs in Canada and the United States. Journal of Neurosurgery:

Spine. 2009;**10**:564-573

2008;**24**:244-252

2013;**16**:418-427

Implants. 2014;**24**:173-183

[27] Hornberger J, Kumar K,

Verhulst E, Clark MA, Hernandez J. Rechargeable spinal cord stimulation versus non-rechargeable system for patient with failed back surgery syndrome: A cost consequences analysis. The Clinical Journal of Pain.

[28] Babu R, Hazzard MA, Huang KT, Ugiliweneza B, Patil CG, Boakye M, et al. Outcomes of percutaneous and paddle lead implantation for spinal cord stimulation: A comparative analysis of complications, reoperation rates, and health-care costs. Neuromodulation.

[29] Annemans L, Van Buyten JP, Smith T, Al-Kaisy A. Cost effectiveness of a novel 10 kHz high-frequency spinal cord stimulation system in patients with failed back surgery syndrome (FBSS). Journal of Long-Term Effects of Medical

2018:555-560

Biol Soc; Lyon, France. 2007. pp.

[17] Poon A, O'Driscoll, Meng TH. Optimal frequency for wireless power transmission into dispersive tissue. IEEE Transactions on Antennas and Propagation. 2010;**58**:1739-1750

[18] Tyler Perryman L, Larson P, Glaser J. Tissue depth study for a fully implantable, remotely powered and programmable wireless neural stimulator. International Journal of Nano Studies and Technology.

[19] Weiner RL, Yeung A, Garcia CM, Perryman LT, Speck B. Treatment of FBSS low back pain with a novel percutaneous DRG wireless stimulator:

Pilot and feasibility study. Pain Medicine. 2016;**17**:1911-1916

[20] Billet B, Wynendaele R, Vanquathem N. Wireless

[21] Billet B, Wynendaele R, Vanquathem N. A novel minimally invasive wireless technology for neuromodulation via percutaneous intercostal nerve stimulation (PNS) for post-herpetic neuralgia: A case report with short term follow up. Pain Practice.

[22] Weiner RL, Garcia CM, Vanquathem N. A novel miniature wireless neurostimulator in the

management of chronic craniofacial pain: Preliminary results from a prospective pilot study. Scandinavian Journal of Pain.

[23] Perryman LT, Speck B, Weiner RL. A novel wireless minimally invasive neuromodulation device for the

treatment of chronic intractable occipital

Archives. 2017;**5**:1-8

2018;**3**:374-379

2017:350-354

neuromodulation by a minimally invasive technique for chronic

refractory pain. Report of preliminary observations. Medical Research

2016;**S2**(001):1-6

5674-5679

*Wireless Neuromodulation: From Bench to Bedside DOI: http://dx.doi.org/10.5772/intechopen.85501*

Biol Soc; Lyon, France. 2007. pp. 5674-5679

[17] Poon A, O'Driscoll, Meng TH. Optimal frequency for wireless power transmission into dispersive tissue. IEEE Transactions on Antennas and Propagation. 2010;**58**:1739-1750

[18] Tyler Perryman L, Larson P, Glaser J. Tissue depth study for a fully implantable, remotely powered and programmable wireless neural stimulator. International Journal of Nano Studies and Technology. 2016;**S2**(001):1-6

[19] Weiner RL, Yeung A, Garcia CM, Perryman LT, Speck B. Treatment of FBSS low back pain with a novel percutaneous DRG wireless stimulator: Pilot and feasibility study. Pain Medicine. 2016;**17**:1911-1916

[20] Billet B, Wynendaele R, Vanquathem N. Wireless neuromodulation by a minimally invasive technique for chronic refractory pain. Report of preliminary observations. Medical Research Archives. 2017;**5**:1-8

[21] Billet B, Wynendaele R, Vanquathem N. A novel minimally invasive wireless technology for neuromodulation via percutaneous intercostal nerve stimulation (PNS) for post-herpetic neuralgia: A case report with short term follow up. Pain Practice. 2018;**3**:374-379

[22] Weiner RL, Garcia CM, Vanquathem N. A novel miniature wireless neurostimulator in the management of chronic craniofacial pain: Preliminary results from a prospective pilot study. Scandinavian Journal of Pain. 2017:350-354

[23] Perryman LT, Speck B, Weiner RL. A novel wireless minimally invasive neuromodulation device for the treatment of chronic intractable occipital neuralgia: Case illustrations. Journal of Neurology & Stroke. 2017;**6**:00213

[24] Herschkowitz D, Kubias J. Wireless peripheral nerve stimulation for complex regional pain syndrome type I of the upper extremity: A case illustration introducing a novel technology. Scandinavian Journal of Pain. July 2018:555-560

[25] Manca A, Kumar K, Taylor RS, Jacques L, Eldabe S, Meglio M, et al. Quality of life, resource consumption and costs of spinal cord stimulation versus conventional medical management in neuropathic pain patients with failed back surgery syndrome (PROCESS trial). European Journal of Pain. 2008;**12**:1047-1058

[26] Kumar K, Bishop S. Financial impact of spinal cord stimulation on the health care budget: A comparative analysis of costs in Canada and the United States. Journal of Neurosurgery: Spine. 2009;**10**:564-573

[27] Hornberger J, Kumar K, Verhulst E, Clark MA, Hernandez J. Rechargeable spinal cord stimulation versus non-rechargeable system for patient with failed back surgery syndrome: A cost consequences analysis. The Clinical Journal of Pain. 2008;**24**:244-252

[28] Babu R, Hazzard MA, Huang KT, Ugiliweneza B, Patil CG, Boakye M, et al. Outcomes of percutaneous and paddle lead implantation for spinal cord stimulation: A comparative analysis of complications, reoperation rates, and health-care costs. Neuromodulation. 2013;**16**:418-427

[29] Annemans L, Van Buyten JP, Smith T, Al-Kaisy A. Cost effectiveness of a novel 10 kHz high-frequency spinal cord stimulation system in patients with failed back surgery syndrome (FBSS). Journal of Long-Term Effects of Medical Implants. 2014;**24**:173-183

**146**

*From Conventional to Innovative Approaches for Pain Treatment*

[8] Cameron T. Safety and efficacy of spinal cord stimulation for the treatment of chronic pain: A 20-year literature review. Journal of Neurosurgery. 2004;**100**:254-267

[9] Krishna K, Jefferson RW, Gupta S.

[10] Kumar K, Hunter G, Demeria D. Spinal cord stimulation in treatment of chronic benign pain: Challenges in treatment planning and present status, a 22-year experience. Neurosurgery.

[11] North RB, Kidd DH, Zahurak M, et al. Spinal cord stimulation for chronic, intractable pain: Experience over two decades. Neurosurgery 1993;**32**:384-394; discussion 394-395.

[12] Pineda A. Complications of dorsal column stimulation. Journal of

[13] Slavin KV. Spinal stimulations for pain: Future applications. Neurotherapeutics. 2014;**11**:535-542

[14] Yearwood TL, Perryman LT. Peripheral neurostimulation with a microsize wireless stimulator. In: Slavin KV, editor. Stimulation of the Peripheral Nervous System. The Neuromodulation Frontier. Progress in Neurological Surgery. Basel, Switzerland: Karger Publishing; 2016. pp. 168-191

[15] Feynman RP. There's plenty of room at the bottom. CalTech, Pasedena CA: Presentation to the American Physical

[16] Poon AS, O'Driscoll S, Meng TH. Optimal operating frequency in wireless power transmission for implantable devices. In: Conf Proc IEEE Eng Med

Society; 1959

Neurosurgery. 1978;**48**:64-68

Complications of spinal cord stimulation, suggestions to improve outcome, and financial impact. Journal of Neurosurgery. 2006;**5**:191-203

2006;**58**:481-496

[1] Turner JA, Loeser JD, Bell KG. Spinal cord stimulation for chronic low back pain: A systematic literature synthesis. Neurosurgery. 1995;**37**:1088-1096

[2] Kumar K, Taylor RS, Jacques L, et al. The effects of spinal cord stimulation in neuropathic pain are sustained: A 24-month follow-up of the prospective randomized controlled multicenter trial of the effectiveness of spinal cord stimulation. Neurosurgery.

[3] Kapural L, Yu C, Doust M, et al. Novel 10-kHz high-frequency therapy (HF10 therapy) is superior to traditional low-frequency spinal cord stimulation for the treatment of chronic back and leg pain the SENZA-RCT randomized controlled trial. Anesthesiology.

[4] Deer TR, Mekhail N, Provenzano D,

neurostimulation of the spinal cord and peripheral nervous system for the treatment of chronic pain and ischemic diseases: The neuromodulation appropriateness consensus committee. Neuromodulation. 2014;**17**:515-550

et al. The appropriate use of

[5] Mekhail NA, Aeschbach A,

Stanton-Hicks M. Cost benefit analysis of neurostimulation for chronic pain. The Clinical Journal of Pain.

[6] Turner JA, Loeser JD, Deyo RA, Sanders SB. Spinal cord stimulation for patients with failed back surgery syndrome or complex regional pain syndrome: A systematic review of effectiveness and complications. Pain.

[7] Mekhail NA, Mathews M, Nageeb F, Guirguis M, et al. Retrospective review of 707 cases of spinal cord stimulation: Indications and complications. Pain

2008;**63**:762-770

**References**

2015;**123**:851-860

2004;**20**:462-468

2004;**108**:137-147

Practice. 2011;**11**:148-153

[30] Kemler MA, Furnee CA. Economic evaluation of spinal cord stimulation for chronic reflex sympathetic dystrophy. Neurology. 2002;**59**:1203-1209

[31] Bell GK, Kidd D, North RB. Costeffectiveness analysis of spinal cord stimulation in treatment of failed back surgery syndrome. Journal of Pain and Symptom Management. 1997;**13**:286-295

**149**

pain management

**1. Introduction**

status (**Figure 1**).

**Chapter 10**

**Abstract**

Resolution

*has the disease".*

*myoActivation*: A Structured

Process for Chronic Pain

*Gillian Lauder, Nicholas West and Greg Siren*

to all clinicians that manage people living with chronic pain.

**Keywords:** pain, chronic pain, paediatric pain, mobility dysfunction, fascia, myofascial trigger points, timeline of lifetime trauma, physical trauma, scars, palpation, catenated cycles, structured assessment, non-pharmaceutical,

Pain is defined by the International Association for the Study of Pain (IASP) as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage" [1]. Pain is a highly subjective sensation influenced by: degree of tissue damage, response to medications, diet, age, sex, genetics, cultural background, and psychosocial factors including attention, emotion, cognition, beliefs, expectations, and socioeconomic

Chronic pain is a significant burden in all societies. The myofascial origins of chronic pain are often unrecognized but play a major role in chronic pain generation. Myofascial release has been shown to be effective and can augment the limited number of therapeutic tools available to manage chronic pain. However, there is no standardized approach that allows for comparative analysis of this technique. *myoActivation*® is a unique therapeutic system, which targets active myofascial trigger points, fascia in tension, and scars in patients with chronic pain. Targets for intervention are determined through obtaining a history of lifetime trauma and a structured, reproducible posture, and movement assessment. Catenated cycles of movement tests, palpation, and needling are used to achieve the goal of pain resolution through restoration of soft tissue integrity. This chapter describes the distinctive features of *myoActivation* from the important key elements of the patient's clinical history, through to the aftercare instructions. Relevant evidence for each component will be presented. Case studies will be used to illustrate some important concepts and the effectiveness of *myoActivation*. This chapter is relevant

*"The good physician treats the disease; the great physician treats the patient who*

*Sir William Osler, 1849–1919*

#### **Chapter 10**

*From Conventional to Innovative Approaches for Pain Treatment*

[30] Kemler MA, Furnee CA. Economic evaluation of spinal cord stimulation for chronic reflex sympathetic dystrophy.

[31] Bell GK, Kidd D, North RB. Costeffectiveness analysis of spinal cord stimulation in treatment of failed back surgery syndrome. Journal of Pain and Symptom Management. 1997;**13**:286-295

Neurology. 2002;**59**:1203-1209

**148**

## *myoActivation*: A Structured Process for Chronic Pain Resolution

*Gillian Lauder, Nicholas West and Greg Siren*

*"The good physician treats the disease; the great physician treats the patient who has the disease".*

*Sir William Osler, 1849–1919*

#### **Abstract**

Chronic pain is a significant burden in all societies. The myofascial origins of chronic pain are often unrecognized but play a major role in chronic pain generation. Myofascial release has been shown to be effective and can augment the limited number of therapeutic tools available to manage chronic pain. However, there is no standardized approach that allows for comparative analysis of this technique. *myoActivation*® is a unique therapeutic system, which targets active myofascial trigger points, fascia in tension, and scars in patients with chronic pain. Targets for intervention are determined through obtaining a history of lifetime trauma and a structured, reproducible posture, and movement assessment. Catenated cycles of movement tests, palpation, and needling are used to achieve the goal of pain resolution through restoration of soft tissue integrity. This chapter describes the distinctive features of *myoActivation* from the important key elements of the patient's clinical history, through to the aftercare instructions. Relevant evidence for each component will be presented. Case studies will be used to illustrate some important concepts and the effectiveness of *myoActivation*. This chapter is relevant to all clinicians that manage people living with chronic pain.

**Keywords:** pain, chronic pain, paediatric pain, mobility dysfunction, fascia, myofascial trigger points, timeline of lifetime trauma, physical trauma, scars, palpation, catenated cycles, structured assessment, non-pharmaceutical, pain management

#### **1. Introduction**

Pain is defined by the International Association for the Study of Pain (IASP) as "an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage" [1]. Pain is a highly subjective sensation influenced by: degree of tissue damage, response to medications, diet, age, sex, genetics, cultural background, and psychosocial factors including attention, emotion, cognition, beliefs, expectations, and socioeconomic status (**Figure 1**).

#### *From Conventional to Innovative Approaches for Pain Treatment*

#### **Figure 1.**

*The biopsychosocial contributors to chronic pain.*

 In acute pain, this sensory output is important to protect the organism from further harm during the healing phase, and, is usually associated with a nociceptive stimulus.

Chronic pain is quite different; although it is typically considered to refer to pain lasting longer than 3 months, such a time limit seems to be reductive, and it more properly refers to "pain that extends beyond the expected period of healing" [2]. The overall prevalence of chronic pain conditions is estimated to be in the order of 35–51% of the adult population [3] and the incidence of widespread chronic pain estimated to be 10–15% [4]. Chronic pain occurs across the lifespan, including children [5] and the elderly [6]. The frequency of visits to physicians, emergency departments, and other healthcare providers is significantly increased in the presence of chronic pain [7]. Currently, the burden of chronic pain has a huge impact on quality of life in the lives of people with chronic pain [8, 9]. The economic burden of chronic pain in terms of healthcare costs is substantial, but pales in significance compared to the costs of lost productivity due to job redundancy and sick days [9].

#### **1.1 Background**

Chronic pain is a complex biopsychosocial phenomenon that requires a multidisciplinary approach to management. This usually includes return to physical function [10], graded return to work/school, medications to help with pain, mood and sleep, as well as non-pharmacological techniques to address the psychosocial components of pain [9, 11, 12]. The weakest link in this therapeutic process is the pharmacological approach, especially the overreliance on the use of *opioid* medications. The prescription of opioids for chronic non-cancer pain increased fourfold in USA from the early 1990s up to 2011 [13, 14]. Opioids contribute only modest relief of chronic pain. They have limited effects on improvement in function but cause significant opioid side effects [15]. Opioid substance abuse and opioid-related death are major issues associated with prescription of opioids for chronic pain. Review of opioid-related deaths demonstrates that the majority had a diagnosis of chronic pain in their last year of life [16]. Prescription of opioid medications has gradually decreased since 2011, but the opioid-related overdose death rate continues to rise exponentially [17]. This current opioid crisis constitutes a critical public health issue in USA and Canada [13]. Even though the prescription of opioid drugs does not appear to be causally

**151**

*myoActivation: A Structured Process for Chronic Pain Resolution*

with chronic musculoskeletal pain are prescribed opioids [19].

cant contributor to a chronic pain issue presenting many years later.

of the originating tissue to a normal anatomical state [41].

Chronic pain occurs from various combined sources, including nociceptive, inflammatory, neuropathic, myofascial, as well as peripheral and central sensitisation. *Musculoskeletal* (*MSK*) conditions are a predominant source of chronic pain worldwide [29]. The clinical and etiological characteristics of myofascial pain have been poorly investigated. The subsequent lack of evidence has led to undertraining of health care professionals, and poor recognition of the clinical importance of *myofascial pain syndromes* (a group of painful conditions that affect muscles and connective tissues) [30, 31]. Myofascial pain syndromes are characterized by pain, *myofascial trigger points* (*MTPs*) (palpable nodules in taut bands of muscle fibres), referred pain, coupled pain, and autonomic changes. Chemical changes within the muscle may also lead to peripheral sensitization. MTPs can generate continual nociceptive traffic to induce central sensitization, cortical re-organization, and alterations in descending inhibitory pain pathways [32–36]. MTPs are associated with muscles in sustained contraction causing limited movement across joints [37]. The MSK system is symmetrical; a muscle in sustained contraction on one side will cause compensatory MSK issues to occur on the other. Therefore, a patient with MSK imbalance may proceed to have many different myofascial areas affected from one previous injury or insult. It is important to note that *palpable pain points* (*PPPs*) exist, not only in skeletal muscle, but also in fascia and scars. One of the components of MSK pain is *coupled pain*, which is distinct from referred pain. Referred pain is pain perceived at a location other than the site of the painful stimulus or origin of pain. Referred pain results from neuronal stimulation within a dermatome (a localized area of skin that has its sensation via a single nerve, from a single nerve root of the spinal cord). In coupled pain, the source of pain is distant, not dermatomal, from the localized area of pain. Examples include shoulder pain or knee pain originating from strained ipsilateral external oblique muscle, or lower quadrant abdominal pain originating from an ipsilateral quadratus lumborum muscle in sustained contraction [38–40]. This distant site has no direct muscular or neurological connection, yet the coupled pain is resolved by restoration

related to overdose deaths, it is clear that their prescription is one pathway to longterm use: 5.3% of opioid naïve adults prescribed opioids will still be on opioids 1 year later [18]. Increased numbers of opioids prescribed on the first prescription predicts a lower likelihood of opioid discontinuation [18]. It is notable that 20% of children

Up to 22.5% of chronic pain patients develop their chronic pain condition after surgery [20]. *Persistent postsurgical pain* (*PPSP*) represents a significant clinical problem, occurring after 10–50% of surgeries and resulting in severe chronic pain in 2–10% of these patients [21]. PPSP is considered to be primarily neuropathic (nerve damage during surgery) where the incidence depends on various perioperative factors, including genetic predisposition, preoperative anxiety, depression, preoperative pain, the extent of the surgical insult, surgical technique, length of surgery, and the quality of acute postoperative pain management [21, 22]. In 27% of patients receiving chronic opioid therapy, treatment for pain after surgery was the reason for opioid initiation [23]. There is 5.9–6.5% incidence of new persistent opioid use after surgery, not only after major surgery but also after minor surgical procedures [24]. Multiple traumas have a cumulative effect on chronic pain [25], independent of post-traumatic distress disorder symptoms [26]. Increased risk of physical ill-health is associated with exposure to a single traumatic event but accrues as more events are experienced [27]. It is not clear what characteristics of past traumatic experiences (type, duration, severity, earlier onset) influence the strength of the relationship between accumulative traumatic events and subsequent medical conditions [28]. Contemporary clinical history taking often neglects distant trauma as signifi-

*DOI: http://dx.doi.org/10.5772/intechopen.84377*

#### *myoActivation: A Structured Process for Chronic Pain Resolution DOI: http://dx.doi.org/10.5772/intechopen.84377*

*From Conventional to Innovative Approaches for Pain Treatment*

Pain is a sensory output from the brain when the brain is on alert. In acute pain, this sensory output is important to protect the organism from further harm during

Chronic pain is quite different; although it is typically considered to refer to pain lasting longer than 3 months, such a time limit seems to be reductive, and it more properly refers to "pain that extends beyond the expected period of healing" [2]. The overall prevalence of chronic pain conditions is estimated to be in the order of 35–51% of the adult population [3] and the incidence of widespread chronic pain estimated to be 10–15% [4]. Chronic pain occurs across the lifespan, including children [5] and the elderly [6]. The frequency of visits to physicians, emergency departments, and other healthcare providers is significantly increased in the presence of chronic pain [7]. Currently, the burden of chronic pain has a huge impact on quality of life in the lives of people with chronic pain [8, 9]. The economic burden of chronic pain in terms of healthcare costs is substantial, but pales in significance compared to the costs of lost productivity due to job redundancy and sick days [9].

Chronic pain is a complex biopsychosocial phenomenon that requires a multidisciplinary approach to management. This usually includes return to physical function [10], graded return to work/school, medications to help with pain, mood and sleep, as well as non-pharmacological techniques to address the psychosocial components of pain [9, 11, 12]. The weakest link in this therapeutic process is the pharmacological approach, especially the overreliance on the use of *opioid* medications. The prescription of opioids for chronic non-cancer pain increased fourfold in USA from the early 1990s up to 2011 [13, 14]. Opioids contribute only modest relief of chronic pain. They have limited effects on improvement in function but cause significant opioid side effects [15]. Opioid substance abuse and opioid-related death are major issues associated with prescription of opioids for chronic pain. Review of opioid-related deaths demonstrates that the majority had a diagnosis of chronic pain in their last year of life [16]. Prescription of opioid medications has gradually decreased since 2011, but the opioid-related overdose death rate continues to rise exponentially [17]. This current opioid crisis constitutes a critical public health issue in USA and Canada [13]. Even though the prescription of opioid drugs does not appear to be causally

the healing phase, and, is usually associated with a nociceptive stimulus.

**150**

**1.1 Background**

**Figure 1.**

*The biopsychosocial contributors to chronic pain.*

related to overdose deaths, it is clear that their prescription is one pathway to longterm use: 5.3% of opioid naïve adults prescribed opioids will still be on opioids 1 year later [18]. Increased numbers of opioids prescribed on the first prescription predicts a lower likelihood of opioid discontinuation [18]. It is notable that 20% of children with chronic musculoskeletal pain are prescribed opioids [19].

Up to 22.5% of chronic pain patients develop their chronic pain condition after surgery [20]. *Persistent postsurgical pain* (*PPSP*) represents a significant clinical problem, occurring after 10–50% of surgeries and resulting in severe chronic pain in 2–10% of these patients [21]. PPSP is considered to be primarily neuropathic (nerve damage during surgery) where the incidence depends on various perioperative factors, including genetic predisposition, preoperative anxiety, depression, preoperative pain, the extent of the surgical insult, surgical technique, length of surgery, and the quality of acute postoperative pain management [21, 22]. In 27% of patients receiving chronic opioid therapy, treatment for pain after surgery was the reason for opioid initiation [23]. There is 5.9–6.5% incidence of new persistent opioid use after surgery, not only after major surgery but also after minor surgical procedures [24].

Multiple traumas have a cumulative effect on chronic pain [25], independent of post-traumatic distress disorder symptoms [26]. Increased risk of physical ill-health is associated with exposure to a single traumatic event but accrues as more events are experienced [27]. It is not clear what characteristics of past traumatic experiences (type, duration, severity, earlier onset) influence the strength of the relationship between accumulative traumatic events and subsequent medical conditions [28]. Contemporary clinical history taking often neglects distant trauma as significant contributor to a chronic pain issue presenting many years later.

Chronic pain occurs from various combined sources, including nociceptive, inflammatory, neuropathic, myofascial, as well as peripheral and central sensitisation. *Musculoskeletal* (*MSK*) conditions are a predominant source of chronic pain worldwide [29]. The clinical and etiological characteristics of myofascial pain have been poorly investigated. The subsequent lack of evidence has led to undertraining of health care professionals, and poor recognition of the clinical importance of *myofascial pain syndromes* (a group of painful conditions that affect muscles and connective tissues) [30, 31].

Myofascial pain syndromes are characterized by pain, *myofascial trigger points* (*MTPs*) (palpable nodules in taut bands of muscle fibres), referred pain, coupled pain, and autonomic changes. Chemical changes within the muscle may also lead to peripheral sensitization. MTPs can generate continual nociceptive traffic to induce central sensitization, cortical re-organization, and alterations in descending inhibitory pain pathways [32–36]. MTPs are associated with muscles in sustained contraction causing limited movement across joints [37]. The MSK system is symmetrical; a muscle in sustained contraction on one side will cause compensatory MSK issues to occur on the other. Therefore, a patient with MSK imbalance may proceed to have many different myofascial areas affected from one previous injury or insult. It is important to note that *palpable pain points* (*PPPs*) exist, not only in skeletal muscle, but also in fascia and scars.

One of the components of MSK pain is *coupled pain*, which is distinct from referred pain. Referred pain is pain perceived at a location other than the site of the painful stimulus or origin of pain. Referred pain results from neuronal stimulation within a dermatome (a localized area of skin that has its sensation via a single nerve, from a single nerve root of the spinal cord). In coupled pain, the source of pain is distant, not dermatomal, from the localized area of pain. Examples include shoulder pain or knee pain originating from strained ipsilateral external oblique muscle, or lower quadrant abdominal pain originating from an ipsilateral quadratus lumborum muscle in sustained contraction [38–40]. This distant site has no direct muscular or neurological connection, yet the coupled pain is resolved by restoration of the originating tissue to a normal anatomical state [41].

Myofascial release can be effective but lacks a standardized approach and therefore prevents good quality comparative analysis.

Given the societal burden of pain and overuse of opioid medications, it is clear that clinicians require a different and more effective model of assessment and treatment that minimizes opioid prescriptions and realizes myofascial components of pain [19, 42]. This chapter will outline the importance of surgical scars and myofascial dysfunction as other important determinants of a chronic pain presentation. *myoActivation* is one component of the multimodal approach to patient care that helps to accurately determine and treat the myofascial components of chronic pain without the need for prescription medications.

#### **1.2 Aim**

The aim of this chapter is to describe a system of standardized assessment and treatment for chronic pain called *myoActivation®*. We will comprehensively describe the distinctive features of this system, from the patient's clinical history to after-care management. We will present evidence for the scientific background and individual component techniques of *myoActivation*, where it exists, and outline future approaches for gathering evidence of the effectiveness and efficiency of the *myoActivation* treatment programme as a whole.

This chapter is practically orientated to enable clinicians to understand what *myoActivation* means. Three case studies will illustrate the effectiveness of *myoActivation*. Then, the next steps in the development and evaluation of *myoActivation* will be discussed. Barriers to integrative care (including alternative therapies) are awareness, availability, accessibility, and affordability [43]; these will be discussed in relation to *myoActivation* as well as the need to establish a firm basis of clinical evidence for this treatment system.

Finally, we must emphasize that *myoActivation* should be seen as one component of multidisciplinary care, i.e., part of a multimodal approach to care, which includes focus on eventual return to physical function and work/school, improving recovery from opioid dependency, weaning prescription drug use as well treating the psychosocial components of pain.

#### **1.3** *myoActivation* **overview**

*myoActivation* is a unique structured system of assessment and treatment designed to reduce myofascial components of chronic pain. A key principle of *myoActivation* is to understand that the site of pain is often not the source of pain [38–41, 44]. For example, spasm of the quadratus lumborum muscle mimics appendicitis and low back pain may originate from the abdominal wall musculature [38, 39, 45]. Myofascial pain is characterised by the presence of myofascial trigger points. Myofascial trigger points develop in response to many different insults such as trauma, injury, surgery, repetitive microtrauma, poor posture, muscle overuse, or overload [46, 47]. Myofascial trigger points that cause pain can originate in scars, skeletal muscle, and/or fascia.

The *myoActivation* assessment is distinguished by recognition of the importance of lifetime trauma and the mechanisms of any injuries identified. Postural observations during systematized, ordered, movement tests identify the true origin of pain in soft tissues. The most painful or restricted movement on core tests distinguishes the most important tissues to treat first. Careful inspection and palpation of these tissues identifies the myofascial source of pain. Treatment entails refined trigger point injections, using micro-aliquots of physiological saline, to restore anatomic integrity to injured tissues. Fine gauge hypodermic needles are inserted into trigger points

**153**

*myoActivation: A Structured Process for Chronic Pain Resolution*

tion, scars, fascial lines of tension, and the interstitial space).

that compromise function of muscle, ligament, tendon, subcutaneous fascia, scar tissue, and the peripheral nerves of the skin. After each individual myofascial area is treated, movement tests are repeated to demonstrate immediate change and direct the clinician to the next most important target area. Several cycles occur during each *myoActivation* session. The purpose of these catenated cycles (see **Figure 6**) is to help unravel multiple sources that contribute to the full myofascial pain presentation.

Immediate treatment responses occur, which include reduction in pain, increased flexibility, and improved fluidity of movement. After-care instructions require the patient to change posture frequently but to refrain from exertional activity for 5 days following every *myoActivation* session. To understand how this technique might be useful in everyday care of patients with chronic pain, it is important to understand the essential components of myofascial pain (skeletal muscle in sustained contrac-

Myofascial pain syndrome is characterized by multisite pain, referred pain, coupled pain, and peripheral and central sensitisations. A component of myofascial pain is due to MTPs associated with muscles in sustained contraction causing limitation of movement across joints [37]. The mechanisms of myofascial pain have

A 2007 review identified 19 different descriptions of diagnostic criteria for myofascial trigger points and associated pain but found lack of consensus or standard

A trigger point is a hyperirritable spot in fascia or surrounding skeletal muscle.

Microdialysis techniques demonstrate unique biochemical changes in the region of trigger points, which include low pH, increased concentrations of bradykinin, calcitonin gene-related peptide, substance P, tumour necrosis factor (TNF), interleukins, serotonin, and norepinephrine. These are also associated with decreased local blood flow, reduced oxygen content, and increased reactive oxygen species. These nociceptive neuropeptides and inflammatory markers may be the source of peripheral nociception potentially initiating and maintaining central sensitization

The veracity of myofascial trigger points representing true pathologic entities have been questioned and debated [54]. However, leading experts in myofascial

A systematic MSK exam can distinguish patients with MTPs and chronic pain from subjects with no pain [56]. One of the main problems with medical community acceptance of MTPs has been the lack of objective imaging techniques to corroborate examination findings and to assess treatment outcomes [57]. Imaging techniques that have been reported to establish the presence of muscle MTPs include: *magnetic resonance elastography* (MRE) [58], and *sonoelastography* (SEG) (**Figure 2**) [59]. MRE couples MRI with cyclic shear waves to assess tissue stiffness in myofascial taut bands. Stiffness in taut bands was found to be 50% greater than adjacent normal muscle tissue. SEG is a non-invasive method that combines

Muscular trigger points are associated with palpable nodules in taut bands of muscle fibres. Compression of a trigger point may elicit local tenderness, referred pain, coupled pain, autonomic symptoms, or a local twitch response. The *local twitch response* (*LTR*) is recognized as a spinal reflex [50]. An LTR when the MTP is

needled or activated is considered a positive response to intervention [51].

*DOI: http://dx.doi.org/10.5772/intechopen.84377*

**2. Scientific background**

definition [49].

**2.1 Skeletal muscle in sustained contraction**

been reviewed by Jafri [31] and Shah et al. [48].

in myofascial pain syndrome [48, 52, 53].

techniques consider this to be a biased view [55].

*myoActivation: A Structured Process for Chronic Pain Resolution DOI: http://dx.doi.org/10.5772/intechopen.84377*

that compromise function of muscle, ligament, tendon, subcutaneous fascia, scar tissue, and the peripheral nerves of the skin. After each individual myofascial area is treated, movement tests are repeated to demonstrate immediate change and direct the clinician to the next most important target area. Several cycles occur during each *myoActivation* session. The purpose of these catenated cycles (see **Figure 6**) is to help unravel multiple sources that contribute to the full myofascial pain presentation.

Immediate treatment responses occur, which include reduction in pain, increased flexibility, and improved fluidity of movement. After-care instructions require the patient to change posture frequently but to refrain from exertional activity for 5 days following every *myoActivation* session. To understand how this technique might be useful in everyday care of patients with chronic pain, it is important to understand the essential components of myofascial pain (skeletal muscle in sustained contraction, scars, fascial lines of tension, and the interstitial space).

#### **2. Scientific background**

*From Conventional to Innovative Approaches for Pain Treatment*

therefore prevents good quality comparative analysis.

without the need for prescription medications.

*myoActivation* treatment programme as a whole.

evidence for this treatment system.

psychosocial components of pain.

**1.3** *myoActivation* **overview**

skeletal muscle, and/or fascia.

**1.2 Aim**

Myofascial release can be effective but lacks a standardized approach and

The aim of this chapter is to describe a system of standardized assessment and treatment for chronic pain called *myoActivation®*. We will comprehensively describe the distinctive features of this system, from the patient's clinical history to after-care management. We will present evidence for the scientific background and individual component techniques of *myoActivation*, where it exists, and outline future approaches for gathering evidence of the effectiveness and efficiency of the

This chapter is practically orientated to enable clinicians to understand what *myoActivation* means. Three case studies will illustrate the effectiveness of *myoActivation*. Then, the next steps in the development and evaluation of *myoActivation* will be discussed. Barriers to integrative care (including alternative therapies) are awareness, availability, accessibility, and affordability [43]; these will be discussed in relation to *myoActivation* as well as the need to establish a firm basis of clinical

Finally, we must emphasize that *myoActivation* should be seen as one component of multidisciplinary care, i.e., part of a multimodal approach to care, which includes focus on eventual return to physical function and work/school, improving recovery from opioid dependency, weaning prescription drug use as well treating the

*myoActivation* is a unique structured system of assessment and treatment designed to reduce myofascial components of chronic pain. A key principle of *myoActivation* is to understand that the site of pain is often not the source of pain [38–41, 44]. For example, spasm of the quadratus lumborum muscle mimics appendicitis and low back pain may originate from the abdominal wall musculature [38, 39, 45]. Myofascial pain is characterised by the presence of myofascial trigger points. Myofascial trigger points develop in response to many different insults such as trauma, injury, surgery, repetitive microtrauma, poor posture, muscle overuse, or overload [46, 47]. Myofascial trigger points that cause pain can originate in scars,

The *myoActivation* assessment is distinguished by recognition of the importance of lifetime trauma and the mechanisms of any injuries identified. Postural observations during systematized, ordered, movement tests identify the true origin of pain in soft tissues. The most painful or restricted movement on core tests distinguishes the most important tissues to treat first. Careful inspection and palpation of these tissues identifies the myofascial source of pain. Treatment entails refined trigger point injections, using micro-aliquots of physiological saline, to restore anatomic integrity to injured tissues. Fine gauge hypodermic needles are inserted into trigger points

Given the societal burden of pain and overuse of opioid medications, it is clear that clinicians require a different and more effective model of assessment and treatment that minimizes opioid prescriptions and realizes myofascial components of pain [19, 42]. This chapter will outline the importance of surgical scars and myofascial dysfunction as other important determinants of a chronic pain presentation. *myoActivation* is one component of the multimodal approach to patient care that helps to accurately determine and treat the myofascial components of chronic pain

**152**

#### **2.1 Skeletal muscle in sustained contraction**

Myofascial pain syndrome is characterized by multisite pain, referred pain, coupled pain, and peripheral and central sensitisations. A component of myofascial pain is due to MTPs associated with muscles in sustained contraction causing limitation of movement across joints [37]. The mechanisms of myofascial pain have been reviewed by Jafri [31] and Shah et al. [48].

A 2007 review identified 19 different descriptions of diagnostic criteria for myofascial trigger points and associated pain but found lack of consensus or standard definition [49].

A trigger point is a hyperirritable spot in fascia or surrounding skeletal muscle. Muscular trigger points are associated with palpable nodules in taut bands of muscle fibres. Compression of a trigger point may elicit local tenderness, referred pain, coupled pain, autonomic symptoms, or a local twitch response. The *local twitch response* (*LTR*) is recognized as a spinal reflex [50]. An LTR when the MTP is needled or activated is considered a positive response to intervention [51].

Microdialysis techniques demonstrate unique biochemical changes in the region of trigger points, which include low pH, increased concentrations of bradykinin, calcitonin gene-related peptide, substance P, tumour necrosis factor (TNF), interleukins, serotonin, and norepinephrine. These are also associated with decreased local blood flow, reduced oxygen content, and increased reactive oxygen species. These nociceptive neuropeptides and inflammatory markers may be the source of peripheral nociception potentially initiating and maintaining central sensitization in myofascial pain syndrome [48, 52, 53].

The veracity of myofascial trigger points representing true pathologic entities have been questioned and debated [54]. However, leading experts in myofascial techniques consider this to be a biased view [55].

A systematic MSK exam can distinguish patients with MTPs and chronic pain from subjects with no pain [56]. One of the main problems with medical community acceptance of MTPs has been the lack of objective imaging techniques to corroborate examination findings and to assess treatment outcomes [57]. Imaging techniques that have been reported to establish the presence of muscle MTPs include: *magnetic resonance elastography* (MRE) [58], and *sonoelastography* (SEG) (**Figure 2**) [59]. MRE couples MRI with cyclic shear waves to assess tissue stiffness in myofascial taut bands. Stiffness in taut bands was found to be 50% greater than adjacent normal muscle tissue. SEG is a non-invasive method that combines

**Figure 2.** *Sonography of muscle trigger points (reproduced from Sikdar et al. [59], with permission from Elsevier).*

ultrasound with simultaneously applied external vibration to distinguish ultrasound colour variance with tissue stiffness. Muscle trigger points identified as palpable painful nodules in muscle appear as focal, elliptical shaped, hypoechogenic areas. Localized regions of low entropy in symptomatic muscle make the tissue macroscopically more heterogeneous than a normal muscle that has relatively uniform echotexture. Texture analysis of SEG images can distinguish between painful muscle trigger points compared to normal muscle [60, 61].

#### *2.1.1 Muscle activation*

Muscle activation is the term used to describe when a muscle in sustained contraction is restored to a normal relaxed state, through manipulative therapies or needling techniques [62]. When a needling technique is used, there is no difference in outcomes between dry needling compared to a liquid injectate (such as lidocaine) [63–65]. Muscle activation is associated with reduction in pain, and improved flexibility, fluidity and range of movement. There is no consensus on the most effective needling techniques for different pain presentations [66]. Elicitation of an LTR has classically been required for effective muscle activation [51]. Recent work disputes that an LTR is necessary, but acknowledges more research is required [67]. Decreased spontaneous electrical activity and acetylcholine levels are seen at active myofascial trigger points after dry needling in rats [68].

Vascular, chemical, endocrine, neural, and central changes have been demonstrated following needling techniques [68–86]. Interestingly, dry needling also appears to be associated with activation of diffuse noxious inhibitory control reducing pain sensitivity in remote areas to the site of needling. This may be mediated through endogenous opioid mechanisms [69, 79–84].

**155**

*2.2.1 Scars*

*myoActivation: A Structured Process for Chronic Pain Resolution*

There are a number of papers in support of the treatment effects, beyond the placebo effect, of myofascial release [51, 62, 66, 87–99]. Recent reviews have concluded that better quality studies with standardized interventions and outcomes are required to show that myofascial release is an effective intervention in the different types of myofascial pain syndromes [100–102]. Despite this, it is clear that myofascial trigger points in skin, fascia, and muscles play an important role in myofascial

MTPs and their referral patterns have been eloquently outlined in two volumes by Travell and Simons, the first volume for the upper body and the second for the lower half of the body [46, 47]. Unfortunately, the publication of these volumes did not translate into everyday use in common clinical practice due to a number of factors: lack of basic scientific evidence around the aetiology of MTPs, no gold standard to identify clinical MTPs, failure to include reproducible assessment and examination of MTPs in medical curricula, complexity and diagnostic uncertainty from the interaction of more than one MTP on perceived pain, co-occurrence of myofascial pain with other disorders such as arthritis, and under-recognition of

The skin is one of the largest organs in the body and is naturally exposed to external stimuli. The skin provides a crucial interface between the body and its environment. Skin has different functions and connections, which include connections to the nervous system through the autonomic nervous system and the locomotor apparatus [103]. The autonomic nervous system constitutes the most important connection between the skin, the fascia, and the body [39]. There is continual nervous activity, in afferent and efferent mode, between the skin and central

There is an independent central emotional connection principally between the anterior cingulate cortex and the skin whereby a sympathetic electrical signal can be detected in the skin in response to viewing emotionally charged images [105]. The skin is also a primary site of small fibre nociceptive endings [106]. It is not difficult to speculate that any restriction or impact on the skin, like a scar, will have an impact

When the skin is breached by surgery or injury, a healing process occurs. There are four stages to healing: haemostasis, inflammation, proliferation, and remodelling [109]. The remodelling process can take many years and depends on the size and nature of the initial wound. During remodelling, type 3 collagen is replaced by a stronger type 1 collagen, but not in an ordered manner. Scar tissue is therefore strong but not as elastic or flexible as normal tissue [109]. There is an increase in nerves and neuropeptides in scar tissue especially hypertrophic scars [110]. In patients asked to move actively, electrical activity from a scarred area is higher than

on normal homeostasis and function and hold emotional memory [107, 108].

that from normal tissue in the same patient doing the same movement [111].

Mechanoreceptors and mechanosensitive nociceptors in scarred areas sense an alteration from normal and send non-physiological signals creating a pathological reflex arc [39]. Scars can limit normal movement and flexibility of skin, and underlying fascia and muscles. For example, an ankle scar will alter the gait dynamics through maldistribution of myofascial loads [39]. Patients with scars in the abdominal region often have low back pain related to impaired mobility of the soft tissues [111, 112]. Scars also have an impact on the distribution of forces

*DOI: http://dx.doi.org/10.5772/intechopen.84377*

myofascial components in chronic pain [30].

nervous system to maintain normal homeostasis [39, 104].

**2.2 Skin and the impact of scars**

chronic pain presentations.

*myoActivation: A Structured Process for Chronic Pain Resolution DOI: http://dx.doi.org/10.5772/intechopen.84377*

There are a number of papers in support of the treatment effects, beyond the placebo effect, of myofascial release [51, 62, 66, 87–99]. Recent reviews have concluded that better quality studies with standardized interventions and outcomes are required to show that myofascial release is an effective intervention in the different types of myofascial pain syndromes [100–102]. Despite this, it is clear that myofascial trigger points in skin, fascia, and muscles play an important role in myofascial chronic pain presentations.

MTPs and their referral patterns have been eloquently outlined in two volumes by Travell and Simons, the first volume for the upper body and the second for the lower half of the body [46, 47]. Unfortunately, the publication of these volumes did not translate into everyday use in common clinical practice due to a number of factors: lack of basic scientific evidence around the aetiology of MTPs, no gold standard to identify clinical MTPs, failure to include reproducible assessment and examination of MTPs in medical curricula, complexity and diagnostic uncertainty from the interaction of more than one MTP on perceived pain, co-occurrence of myofascial pain with other disorders such as arthritis, and under-recognition of myofascial components in chronic pain [30].

#### **2.2 Skin and the impact of scars**

The skin is one of the largest organs in the body and is naturally exposed to external stimuli. The skin provides a crucial interface between the body and its environment. Skin has different functions and connections, which include connections to the nervous system through the autonomic nervous system and the locomotor apparatus [103]. The autonomic nervous system constitutes the most important connection between the skin, the fascia, and the body [39]. There is continual nervous activity, in afferent and efferent mode, between the skin and central nervous system to maintain normal homeostasis [39, 104].

There is an independent central emotional connection principally between the anterior cingulate cortex and the skin whereby a sympathetic electrical signal can be detected in the skin in response to viewing emotionally charged images [105]. The skin is also a primary site of small fibre nociceptive endings [106]. It is not difficult to speculate that any restriction or impact on the skin, like a scar, will have an impact on normal homeostasis and function and hold emotional memory [107, 108].

#### *2.2.1 Scars*

*From Conventional to Innovative Approaches for Pain Treatment*

ultrasound with simultaneously applied external vibration to distinguish ultrasound colour variance with tissue stiffness. Muscle trigger points identified as palpable painful nodules in muscle appear as focal, elliptical shaped, hypoechogenic areas. Localized regions of low entropy in symptomatic muscle make the tissue macroscopically more heterogeneous than a normal muscle that has relatively uniform echotexture. Texture analysis of SEG images can distinguish between painful

*Sonography of muscle trigger points (reproduced from Sikdar et al. [59], with permission from Elsevier).*

Muscle activation is the term used to describe when a muscle in sustained contraction is restored to a normal relaxed state, through manipulative therapies or needling techniques [62]. When a needling technique is used, there is no difference in outcomes between dry needling compared to a liquid injectate (such as lidocaine) [63–65]. Muscle activation is associated with reduction in pain, and improved flexibility, fluidity and range of movement. There is no consensus on the most effective needling techniques for different pain presentations [66]. Elicitation of an LTR has classically been required for effective muscle activation [51]. Recent work disputes that an LTR is necessary, but acknowledges more research is required [67]. Decreased spontaneous electrical activity and acetylcholine levels are seen at active

Vascular, chemical, endocrine, neural, and central changes have been demonstrated following needling techniques [68–86]. Interestingly, dry needling also appears to be associated with activation of diffuse noxious inhibitory control reducing pain sensitivity in remote areas to the site of needling. This may be mediated

muscle trigger points compared to normal muscle [60, 61].

myofascial trigger points after dry needling in rats [68].

through endogenous opioid mechanisms [69, 79–84].

*2.1.1 Muscle activation*

**Figure 2.**

**154**

When the skin is breached by surgery or injury, a healing process occurs. There are four stages to healing: haemostasis, inflammation, proliferation, and remodelling [109]. The remodelling process can take many years and depends on the size and nature of the initial wound. During remodelling, type 3 collagen is replaced by a stronger type 1 collagen, but not in an ordered manner. Scar tissue is therefore strong but not as elastic or flexible as normal tissue [109]. There is an increase in nerves and neuropeptides in scar tissue especially hypertrophic scars [110]. In patients asked to move actively, electrical activity from a scarred area is higher than that from normal tissue in the same patient doing the same movement [111].

Mechanoreceptors and mechanosensitive nociceptors in scarred areas sense an alteration from normal and send non-physiological signals creating a pathological reflex arc [39]. Scars can limit normal movement and flexibility of skin, and underlying fascia and muscles. For example, an ankle scar will alter the gait dynamics through maldistribution of myofascial loads [39]. Patients with scars in the abdominal region often have low back pain related to impaired mobility of the soft tissues [111, 112]. Scars also have an impact on the distribution of forces

that pass through the body following motor vehicle accident (MVA) or injury [39]. It has also been suggested that the skin can keep a memory of trauma [107, 108]. It is clinically important to consider this when releasing scars associated with a particular emotional traumatic event. More research is required to ascertain the characteristics of scars that make a significant contribution to a chronic pain presentation.

#### *2.2.2 Scar release*

Scar release can be achieved with soft tissue mobilization techniques or subcision [107, 111, 113]. *Subcision*, or microneedling, also known as percutaneous collagen induction therapy, is a minimally invasive minor surgical procedure used for treating depressed cutaneous scars and wrinkles. Subcision is performed using a hypodermic needle inserted through a puncture in the skin surface [114] or dermaroller. First described in 1995 [115], subcision is a safe, and effective microneedling technique used as an aesthetic treatment for several different dermatological conditions including scars, rhytids, and striae [114, 116, 117]. Microneedling has been shown to induce new collagen formation via platelet and neutrophil release of growth factors (TGFβ, platelet derived growth factor, connective tissue growth factor, connective tissue activating protein), resulting in increased production of collagen, elastin, and glycosaminoglycans [118]. The penetration of a needle through skin has been shown to produce other physiological effects such as activation of the diffuse noxious inhibitory control systems [119], as well as oxytocin mediated peripheral stimulation that inhibits c-fibre discharge to suppress experimental behavioural nociception in rats [120].

Currently, the immediate relief of chronic pain following needling of surgical scars is limited to case reports [110], and to date, there is insufficient evidence to advise on the right time to treat scars after surgery [121]. It will be seen later that scar identification and release is an integral part of *myoActivation* therapy for chronic pain.

#### **2.3 Fascial lines of tension**

*Fascia* is described as "dense irregular connective tissue, this tissue surrounds and connects every muscle, even the tiniest myofibril, and every single organ of the body. It forms a true continuity throughout our whole body" [122, 123]. Fascia has traditionally been named according to the region in which it invests, for example, thoracolumbar fascia or the iliotibial band. This regional focus is considered to be a barrier to the understanding the whole-body interconnectivity of fascia [124]. Fascia has both loose and hard fibrous connective tissue components. Loose fascia functions to help slide and glide between structures and dense fascia exerts a tensile strength in tissues like tendons. Fascia is a complex structure. It contains cells (fibroblasts, fasciocytes, myofibroblasts, and telocytes), an extracellular matrix (fibres, hyaluronan, and water), nerve elements (proprioceptors, interoceptors, and nociceptors), and a system of microchannels (the primovascular system) [125]. The contractile elements may contribute to spasms, dysfunction, and pain [39]. The fasciocytes produce hyaluronan in response to shear stresses [125]. The fascial fibroblasts produce collagen in response to load and stretching. Telocytes are probably important in regeneration [126]. Fascia is rich in proprioceptors and is an essential integrative component in the locomotor apparatus in assessment and control of human posture and movement organization [70]. Fascia has been nicknamed our organ of form [39, 127, 128]. Techniques are currently being developed to improve imaging of fascia [129].

**157**

*myoActivation: A Structured Process for Chronic Pain Resolution*

Fascia flexibility is reduced following injury and subsequent immobility; this worsens with time and persists even with restoration of movement [130]. Stretching, however, reduces thickness of inflammatory lesions, reduces migration of neutrophils, and increases concentration of pro-resolving mediators (resolvins) [130–134]. It is becoming increasingly clear that fascia has an extremely important role to play in molecular biology, functional anatomy, exercise, sport science, repair mechanisms, as well as therapeutic modalities [135]. As *myoActivation* is associated with improvements in flexibility and posture, it may well be that one of its effects is mediated through fascial mechanisms that enable movement and stretch in a more

*Proposed myofascial chains (reproduced from Wilke et al. [136], with permission from Elsevier).*

*Biotensegrity* is a structural design concept that defines the relationship between parts of an organism and the mechanical system that integrates them into a functional unit. Humans are described as tension-dependent organisms with myofascial chains (**Figure 3**) [136]. These myofascial chains enable three-dimensional movement while continually providing information on balance, stability, and mobility. These chains often have an opposing chain to help achieve this balance within the MSK system; for example, a posterior myofascial chain pairs with an anterior myofascial chain.

These chains may well help to explain how some pain presentations at distant sites, and how myofascial release at distant sites (or opposite sides of the body) resolve coupled pain presentations. For example, release of the external oblique muscle in sustained contraction will help shoulder pain, release of tension around the coccyx will help with neck pain, and/or release of the gastrocnemius/soleus

The interstitial space is a major fluid compartment present in many parts of the body. It contains dynamically compressible and distensible sinuses through which interstitial fluid flows around the body. It is distinct from, but drains into, the lymphatic system. In the average human, up to 15 L of extracellular fluid are normally housed in the extracellular interstitial space. *Interstitial fluid* (ISF) and flow is an important element of normal tissue function; it bathes and surrounds cells, delivers nutrients, and removes metabolic waste [137]. ISF also affects cell signalling, differentiation, remodelling, and migration (giving directional cues to cells) [138]. The ISF only flows under conditions of low hydraulic resistance. Blockage of these channels in pigs induces hyperalgesia [139]. Release of tight tissues, following *myoActivation*, may help to restore interstitial fluid flow and promote the delivery of

muscles in sustained contraction relieves occipital headaches.

nutrients and removal of metabolic waste of surrounding tissues.

*DOI: http://dx.doi.org/10.5772/intechopen.84377*

normal anatomical manner.

**Figure 3.**

**2.4 The interstitial space**

*myoActivation: A Structured Process for Chronic Pain Resolution DOI: http://dx.doi.org/10.5772/intechopen.84377*

*From Conventional to Innovative Approaches for Pain Treatment*

presentation.

chronic pain.

**2.3 Fascial lines of tension**

to improve imaging of fascia [129].

*2.2.2 Scar release*

behavioural nociception in rats [120].

that pass through the body following motor vehicle accident (MVA) or injury [39]. It has also been suggested that the skin can keep a memory of trauma [107, 108]. It is clinically important to consider this when releasing scars associated with a particular emotional traumatic event. More research is required to ascertain the characteristics of scars that make a significant contribution to a chronic pain

Scar release can be achieved with soft tissue mobilization techniques or subcision [107, 111, 113]. *Subcision*, or microneedling, also known as percutaneous collagen induction therapy, is a minimally invasive minor surgical procedure used for treating depressed cutaneous scars and wrinkles. Subcision is performed using a hypodermic needle inserted through a puncture in the skin surface [114] or dermaroller. First described in 1995 [115], subcision is a safe, and effective microneedling technique used as an aesthetic treatment for several different dermatological conditions including scars, rhytids, and striae [114, 116, 117]. Microneedling has been shown to induce new collagen formation via platelet and neutrophil release of growth factors (TGFβ, platelet derived growth factor, connective tissue growth factor, connective tissue activating protein), resulting in increased production of collagen, elastin, and glycosaminoglycans [118]. The penetration of a needle through skin has been shown to produce other physiological effects such as activation of the diffuse noxious inhibitory control systems [119], as well as oxytocin mediated peripheral stimulation that inhibits c-fibre discharge to suppress experimental

Currently, the immediate relief of chronic pain following needling of surgical scars is limited to case reports [110], and to date, there is insufficient evidence to advise on the right time to treat scars after surgery [121]. It will be seen later that scar identification and release is an integral part of *myoActivation* therapy for

*Fascia* is described as "dense irregular connective tissue, this tissue surrounds and connects every muscle, even the tiniest myofibril, and every single organ of the body. It forms a true continuity throughout our whole body" [122, 123]. Fascia has traditionally been named according to the region in which it invests, for example, thoracolumbar fascia or the iliotibial band. This regional focus is considered to be a barrier to the understanding the whole-body interconnectivity of fascia [124]. Fascia has both loose and hard fibrous connective tissue components. Loose fascia functions to help slide and glide between structures and dense fascia exerts a tensile strength in tissues like tendons. Fascia is a complex structure. It contains cells (fibroblasts, fasciocytes, myofibroblasts, and telocytes), an extracellular matrix (fibres, hyaluronan, and water), nerve elements (proprioceptors, interoceptors, and nociceptors), and a system of microchannels (the primovascular system) [125]. The contractile elements may contribute to spasms, dysfunction, and pain [39]. The fasciocytes produce hyaluronan in response to shear stresses [125]. The fascial fibroblasts produce collagen in response to load and stretching. Telocytes are probably important in regeneration [126]. Fascia is rich in proprioceptors and is an essential integrative component in the locomotor apparatus in assessment and control of human posture and movement organization [70]. Fascia has been nicknamed our organ of form [39, 127, 128]. Techniques are currently being developed

**156**

**Figure 3.** *Proposed myofascial chains (reproduced from Wilke et al. [136], with permission from Elsevier).*

Fascia flexibility is reduced following injury and subsequent immobility; this worsens with time and persists even with restoration of movement [130]. Stretching, however, reduces thickness of inflammatory lesions, reduces migration of neutrophils, and increases concentration of pro-resolving mediators (resolvins) [130–134]. It is becoming increasingly clear that fascia has an extremely important role to play in molecular biology, functional anatomy, exercise, sport science, repair mechanisms, as well as therapeutic modalities [135]. As *myoActivation* is associated with improvements in flexibility and posture, it may well be that one of its effects is mediated through fascial mechanisms that enable movement and stretch in a more normal anatomical manner.

*Biotensegrity* is a structural design concept that defines the relationship between parts of an organism and the mechanical system that integrates them into a functional unit. Humans are described as tension-dependent organisms with myofascial chains (**Figure 3**) [136]. These myofascial chains enable three-dimensional movement while continually providing information on balance, stability, and mobility. These chains often have an opposing chain to help achieve this balance within the MSK system; for example, a posterior myofascial chain pairs with an anterior myofascial chain.

These chains may well help to explain how some pain presentations at distant sites, and how myofascial release at distant sites (or opposite sides of the body) resolve coupled pain presentations. For example, release of the external oblique muscle in sustained contraction will help shoulder pain, release of tension around the coccyx will help with neck pain, and/or release of the gastrocnemius/soleus muscles in sustained contraction relieves occipital headaches.

#### **2.4 The interstitial space**

The interstitial space is a major fluid compartment present in many parts of the body. It contains dynamically compressible and distensible sinuses through which interstitial fluid flows around the body. It is distinct from, but drains into, the lymphatic system. In the average human, up to 15 L of extracellular fluid are normally housed in the extracellular interstitial space. *Interstitial fluid* (ISF) and flow is an important element of normal tissue function; it bathes and surrounds cells, delivers nutrients, and removes metabolic waste [137]. ISF also affects cell signalling, differentiation, remodelling, and migration (giving directional cues to cells) [138]. The ISF only flows under conditions of low hydraulic resistance. Blockage of these channels in pigs induces hyperalgesia [139]. Release of tight tissues, following *myoActivation*, may help to restore interstitial fluid flow and promote the delivery of nutrients and removal of metabolic waste of surrounding tissues.

More research is required to determine exactly which component (muscle, biomechanics, the interstitium, fascia, skin, scars or a combination of these) is the major contributor to a chronic pain presentation. The rest of this chapter will outline the specific details of the basics of *myoActivation*, which provides the muchneeded standardized process to correctly identify and treat MTPs in priority order, to reduce chronic pain.

#### **3.** *myoActivation***: detailed methods**

#### **3.1 Clinical history**

As with all chronic pain presentations, it is important to define the clinical problem, the main site of perceived pain, with its transition over time, as well as the goals of treatment for the patient. The focus of a *myoActivation* history frames the clinical problem as the *Timeline of Lifetime Trauma* (TiLT) and the mechanisms of any injuries reported. TiLT requires careful questioning to determine if there have been any motor vehicle accidents, fractures, sprains, falls, tailbone injury, major surgery, minor surgery, burns, bites, or other scars (e.g., chicken pox or acne). The associated healing process of any scar is essential to determine their significance in the pain presentation. Infection during a healing process or injuries and scars sustained at a young age appear to have significant impact. Recreational and occupational activities with any associated injuries are important components that need to be asked. An important enquiry in the *myoActivation* history is to ask the patient what they consider to be their greatest physical trauma. All these details will be synthesized with the subsequent examination findings to help determine the true source of pain.

#### *3.1.1 Investigations*

Routine imaging investigations are typically not useful to guide *myoActivation* treatment. However, reports on imaging studies that are provided with a referral or by the patient should be reviewed and acknowledged in the encounter documentation.

#### *3.1.2 Examination*

Optimally, the patient has as much skin exposed as possible to allow easier evaluation of postural asymmetries, fascial lines of tension, skin creases, and forgotten scars. Initially, the patient is asked to identify the location of their perceived pain; this point helps direct the examination and is used as an index for subsequent treatment effect. Where the patient identifies the perceived origin of pain is rarely the tissue that is responsible for the true origin of pain. Then, core Biomechanical Assessment and Symmetry Evaluation (BASE) tests are administered (**Figure 4**). In execution of all tests, the clinician is always looking for postural asymmetries.

#### *3.1.3 Balance*

The first BASE test is balance. The talus has no muscular attachments and functions as a ball and socket joint around which the skeleton sways depending on the distribution of myofascial forces (**Figure 5**). The centre of the body mass is normally located anterior to the S2 vertebrae in humans. In an erect stance where there is no significant anatomical postural distortion, the centre of mass or gravity will be evenly distributed between the feet and over each plantar surface. Therefore, if one

**159**

**Figure 5.**

**Figure 4.**

*myoActivation: A Structured Process for Chronic Pain Resolution*

*The core biomechanical assessment and symmetry evaluation (BASE) tests.*

foot feels heavier than the other, then there is a shift of the centre of mass or gravity towards that side of the body. For example, if weight is perceived to be more on the right foot, then there is likely contracted musculature in the right leg "pulling" the pelvis to the right and shifting the centre of mass to the right. At this time, the patient is asked to report about the distribution of weight on their feet (i.e., right or

At the time of the balance test, the clinician observes postural and position between the right and left sides reviewing; feet (e.g., pronated, elevated little toe, clawed toes), knees (e.g., hyperextended or hyperflexed), level of the hips, shoulder height, any pelvic rotation or tilt, as well as any tilt of the torso or the head. No

This will be the first time the clinician touches the patient and a verbal consent

left predominance, towards heels or balls, outside of feet or inside).

abnormality detected (NAD) should also be documented.

prior to examination of any asymmetries is pertinent.

*Muscle groups that play a part in balancing the upright skeleton.*

*DOI: http://dx.doi.org/10.5772/intechopen.84377*

**Figure 4.**

*From Conventional to Innovative Approaches for Pain Treatment*

to reduce chronic pain.

**3.1 Clinical history**

*3.1.1 Investigations*

documentation.

*3.1.2 Examination*

*3.1.3 Balance*

**3.** *myoActivation***: detailed methods**

More research is required to determine exactly which component (muscle, biomechanics, the interstitium, fascia, skin, scars or a combination of these) is the major contributor to a chronic pain presentation. The rest of this chapter will outline the specific details of the basics of *myoActivation*, which provides the muchneeded standardized process to correctly identify and treat MTPs in priority order,

As with all chronic pain presentations, it is important to define the clinical problem, the main site of perceived pain, with its transition over time, as well as the goals of treatment for the patient. The focus of a *myoActivation* history frames the clinical problem as the *Timeline of Lifetime Trauma* (TiLT) and the mechanisms of any injuries reported. TiLT requires careful questioning to determine if there have been any motor vehicle accidents, fractures, sprains, falls, tailbone injury, major surgery, minor surgery, burns, bites, or other scars (e.g., chicken pox or acne). The associated healing process of any scar is essential to determine their significance in the pain presentation. Infection during a healing process or injuries and scars sustained at a young age appear to have significant impact. Recreational and occupational activities with any associated injuries are important components that need to be asked. An important enquiry in the *myoActivation* history is to ask the patient what they consider to be their greatest physical trauma. All these details will be synthesized with the subsequent examination findings to help determine the true source of pain.

Routine imaging investigations are typically not useful to guide *myoActivation* treatment. However, reports on imaging studies that are provided with a referral or by the patient should be reviewed and acknowledged in the encounter

Optimally, the patient has as much skin exposed as possible to allow easier evaluation of postural asymmetries, fascial lines of tension, skin creases, and forgotten scars. Initially, the patient is asked to identify the location of their perceived pain; this point helps direct the examination and is used as an index for subsequent treatment effect. Where the patient identifies the perceived origin of pain is rarely the tissue that is responsible for the true origin of pain. Then, core Biomechanical Assessment and Symmetry Evaluation (BASE) tests are administered (**Figure 4**). In execution of all tests, the clinician is always looking for postural asymmetries.