Access to the PPM Journal and newsletters is FREE for clinicians.
12 Articles in Volume 16, Issue #1
A New Look at Sphenopalatine Ganglion Blocks for Chronic Migraine
Can Weight Loss Help Reduce Psoriatic Arthritis Symptoms?
Chronic Back and Neck Pain in America 2015 Survey Results
Efficacy of Acupressure Plus Manipulation for Lumbar Disc Herniation: A Clinical Report
Is Tapentadol a Glorified Tramadol?
Letters to the Editor: Naloxone, Opioid Tolerance, Polyarthropathy
New Research Into Psoriatic Arthritis
New Technique Shows Promise as Adjunct In Chronic Pain Management
Pharmacogenetic Testing in Pain Management: Where Do We Stand?
Reinventing IM and Procedural Injections: The Sota Omoigui Short Needle Technique
Timely- versus Delayed-Use of TNFi’s: Which Approach Is Better?
Undiagnosed Atlas Subluxation in Patient with Pain and Poor Myofascial Function

New Technique Shows Promise as Adjunct In Chronic Pain Management

The Bio-Acoustical Utilization Device (BAUD), a biofeedback device, has shown promise in the management of patients with central sensitization.

Chronic pain is one of the most difficult problems to treat, especially when central sensitization (CS) has occurred. There are a number of articles in the literature that suggest that poorly managed pain leads to CS, which worsens with anxiety and lack of sleep.1,2

Long-term potentiation (LTP) causes a pain circuit to become hyperaroused. It literally becomes “stuck” in a high-volume firing state. LTP maintains pain even after an injury heals, causing pain to become a chronic self-perpetuating illness.

It is important to differentiate CS from central pain syndrome, which was formerly known as thalamic pain syndrome or Dejerine-Roussy syndrome. Although central pain syndrome involves both CS and chronic pain, it is further characterized by actual damage to the central nervous system, through spinal cord ischemia or stroke, for example. The chronic pain cases used in this presentation involve only CS.


New Research Focuses on Brain Plasticity

Fortunately for the millions of patients who suffer from chronic pain, pioneering research is driving the development of new treatments focused on brain plasticity, with the more promising developments based on modulating activity in the limbic system. Since maladaptive brain plasticity creates chronic pain (ie, CS), it makes sense to address this process directly.

Stress and the release of stress hormones play a role in the development of CS because they generate hyperalgesia and chronic pain through both peripheral and central mechanisms. Peripherally, catecholamines secreted by the adrenal medulla cause hyperalgesia. CS causes spinal neuroinflammation, decreasing the mechanical nociceptor threshold, and increasing sensory hypersensitivity and long-lasting anxiety-induced hyperalgesia.3-5

The various components of CS are muscle pain, dyesthesia, hyperpathia, allodynia, shooting pain, circulatory pain that mimics circulatory insufficiency, and peristaltic pain in the visceral organs,6,7 which makes this a challenging disorder to treat. Many people who have CS are sensitive to bright lights, loud noises, medications, temperature, and may have hypersensitivity to touch and mechanical pressure.8

Role of Limbic System

Recent studies are clarifying the role that the brain and limbic system play in the experience of chronic pain.9-11 A clear example of maladaptive plasticity in the brain is phantom limb pain, where the physical pain and emotional trauma of an accident has created a memory circuit in the brain that continues to register pain signals from a limb that is no longer attached to the body.12

It is well established that trauma creates potentiated or sensitized neural circuits in the limbic system, especially the amygdala, that perpetuate problematic emotions.13,14 The amygdala receives sensory input of all types, including nociceptive information in the latero-capsular portion of the central nucleus.15 In the amygdala, emotional feelings of threat or helplessness are integrated with nociceptive pain sensations. Together, this establishes neural memories of fear and pain, which can lead to the development of chronic pain, as described previously.15

This subconscious helplessness can promote maladaptive plasticity and an aberration of memory.16,17 The pain memory circuits fire and the patient feels pain as if the injury is still there, much like the amputee with phantom pain.

Attention Deficit Disorder Treatment Used for Pain

The Bio-Acoustical Utilization Device (BAUD, Insight NeuroSystems, Olathe, KS) is a sound-based treatment that was originally developed for the treatment of attention deficit disorder (ADD)/attention deficit hyperactivity disorder (ADHD) and was subsequently discovered to be useful in the treatment of stress and negative emotional symptoms.18 Initial functional magnetic resonance imaging (fMRI) research suggests it works by disrupting reorganization of long-term processing memory circuits in the limbic system.19

Since BAUD has been successful in reducing negative emotional perceptions, we reasoned that it might have a similar effect on pain due to the close relationship of those circuits in the amygdala. If so, we hypothesized that it could be a safe and effective adjunct treatment for chronic pain.20 To test that theory, we tested the device on 3 patients with chronic pain.

How it Works

BAUD is a FDA-approved class II biofeedback device that emits 2 adjustable frequency tones that intersect to create a third binaural beat, producing an acoustical neuromodulation (Figure 1). This stimulation appears to affect the amygdala and the hippocampus of the limbic system by theta wave stimulation. Theta activity has been established as essential to both the consolidation and reconsolidation of all memories, including pain memories.21,22

The BAUD instrument produces a square wave, perceived by the patient to be unpleasant. The sound resembles that created by a swarm of angry bees. Kumar et al postulated that adverse sound has an arousal effect on the amygdala through the medial geniculate nucleus via the thalamus23 (Figure 2).The result creates both a stimulation and temporary disruption of a sensitized circuit, which stimulates a neural ‘reset’ courtesy of the brain’s ability to self-regulate. Research has shown that once a memory circuit is activated, it can be modified.24

During treatment, the patient is given earphones and asked to set the volume controls to a moderately loud level in each ear. The patient is instructed to focus on the area(s) of pain. The pitch of the sound is adjusted such that the person feels the sound connect to the body’s location of his or her pain. For example, if the person’s pain is in the shoulder, the sound feels like it resonates there.

Therefore, in the first step—tuning the base frequency—the patient will feel some change in the pain sensation. Even though the stimulation is to the brain, it is felt in the connected body area. This has most often been described as a feeling of resonance or vibration likened to a slight stimulation, or intensification of the pain, or other individual sensations. But note that this is a neurological response to the sound input, so the actual sensation varies with individuals. In this step, we are looking for any change in sensation that indicates the chosen frequency is affecting the pain circuit. This type of attentional modulation has been shown to increase neural activity of pain circuits.25

In our protocol, lower pitch frequencies are used for pain in the lower body and low back, whereas high pitch frequencies are used for upper body areas. The reasons why this works are not fully known, and come mostly from observation and patient reports. G. Frank Lawlis, MD, a medical psychologist and inventor of the BAUD settled on these frequencies after reviewing research about resonance frequencies of the human body, and fine-tuned the frequencies in his clinical practice. BAUD shares frequencies in common with most-used TENS frequencies from 0 up to 250 Hz.18

In the second step, the disruptor knob is slowly advanced, producing a binaural pulse that, again, directly affects the amygdala. When properly set (almost always in the 4-8 Hz theta range), the disruptor has the effect of weakening or reducing the target symptom. This is felt almost immediately as a marked reduction in the pain sensation. In this way, we use the brain as the monitor (and the patent’s sensations) to adjust the BAUD’s input. The unit is left on for 15 to 20 minutes, with the person focusing on the areas of pain to maintain the level necessary for acoustical neutralization.

BAUD is more than a momentary distraction, however, since brain imaging (EEG) shows positive neural changes both during the BAUD session and persisting long after (EEG, fMRI and LORETA). Patients also report enduring relief. We believe that disrupting the active pain circuit also interferes with its reconsolidation, thereby reducing even persistent chronic pain.

People with chronic pain and CS sensitization are excellent candidates for BAUD therapy, provided they are not overly sensitive to loud, noxious noises. People with auditory sensitivity are more prone to agitation and a worsening of their symptoms when this therapy is employed.

Case Studies

Case 1

A 58-year-old veteran presented with a 10-year history of constant thoraco lumbar pain and intermittent lower extremity paresthesias. His past medical history included a diagnosis of fibromyalgia, post-traumatic stress disorder, substance abuse, bilateral carpal tunnel syndrome, and left knee arthroscopic debridement of a medial meniscus tear.

His medication regimen included atenolol (Tenormin, others), hydrochlorothiazide (Microzide, others), fluoxetine (Prozac, others), amitriptyline, and simvastatin (Zocor, others). In addition, he had a home transcutaneous electrical nerve stimulator (TENS) unit and an Alpha Stim (Electro Medical Products, Mineral Wells, Tx) unit, which he used daily for anxiety. His physical evaluation is outlined in Table 1.

His initial treatment plan included iontophoresis with acetic acid for the anti-inflammatory effect, therapeutic ultrasound, thoracic-lumbar decompression, and a mobility exercise program. After 4 treatments, the patient was unchanged with respect to pain or function.

BAUD therapy was added to his treatment plan and after 4 more treatments he was able to stand for 2 hours, walk for 2 miles, cut wood with a chainsaw, and sleep through the night. His lumbar flexion returned to 90 degrees without pain, and extension was 25 degrees without pain. He also reported that he was able to sleep better and think more clearly.26 No further treatments have been required in over a year.

Case 2

A 47-year-old woman who was diagnosed with post-traumatic heterotrophic ossifications in both hips and lower legs and required bilateral axillary crutches for the previous 10 years, presented to our clinic. Because of her method of locomotion, she developed cervical pain that was greater on the right side (Verbal Pain Scale, [VPS], 7 out of 10), with trapezius, levator scapula, and rhomboid hypertonus. An MRI confirmed a herniated nucleus pulposus of C 5-6.

Her medical history was significant. She had difficulty turning her head, sleeping, and had 5 to 6 headaches a week. She had undergone trigger point injections and occipital nerve blocks with some pain relief (5 out of 10 VPS). She admitted to being hypersensitive to many medications as well as to bright lights.

Her current medication regimen included ibuprofen (Advil, Motrin, others) 600 mg PRN, hydrocodone/acetaminophen (Norco, Lortab, others) 5/325 mg QID, and monthly pamidronate infusions. She reported being allergic to gabapentin (Neurontin, Gralise, others) and ondansetron (Zofran, Zuplenz, others). Her physical evaluation results are outlined in Table 1.

She had been seen in physical therapy previously, receiving electrical stimulation, therapeutic ultrasound, soft-tissue massage, laser treatment, and mobility exercises, with little symptomatic change after 5 treatments. BAUD therapy was added to her treatment plan, and she noticed a reduction of headaches and cervical hypertonus with easier cervical mobility after 4 more treatments (VPS, 3 out of 10). Her range of motion improved globally by between 25% and 30% of initial measurements. She required additional treatments 6 months later due to a return of symptoms.

Case 3

The third clinic case is a 61-year-old woman who had been in a severe head-on motor vehicle accident when she was 17 years old. She sustained a fractured left femur and multiple fractures of the right ankle, necessitating a triple arthrodesis. She had had chronic back, right foot, and left knee pain, which had been unrelieved by oral analgesics and over-the-counter ibuprofen, since her accident 44 years previously.

She had undergone physical therapy after her accident, but had no formal treatment since then except for exercises after an arthroscopic left knee debridement of a loose body 10 years previously. She admitted to being sensitive to medications, bright lights, and loud noises since her accident.

BAUD therapy was attempted, but the patient could not tolerate the noxious sound, even at the lowest setting. She reported a feeling of agitation afterwards that lasted for 2 days. Her treatment plan was changed to a hands-on approach using the Associative Awareness Technique (AAT),27 and the patient reported an immediate improvement in her symptoms. Theoretically, AAT is designed to change conditioned negative association by creating new positive sensory and cognitive awareness.

The therapist uses 5 types of safe sensory input of scratching, tapping, vibration, deep pressure, and light touch to the patient’s extremities. These sensations are designed to affect the sensory nerve endings and mechanoreceptors in the skin, which are the primary barrier between the environment and the nervous system. During AAT treatment, the patient is instructed to avoid focusing on the areas of pain in order to change the current negative associations of helplessness and stress.


The addition of BAUD therapy can be a useful addition to the overall treatment regimen of people who have experienced chronic pain caused by sensitization of the neural circuits of the amygdala. The addition of BAUD therapy can help improve function, as illustrated in case 1 and case 2, and decrease pain, as shown in case 2. Theoretically, this treatment would be the non-pharmaceutical treatment of choice in people who are hypersensitive to touch, such as autistic patients with known tactile sensitivities.

The last case illustrates that importance of patient selection when using BAUD therapy noise having a noxious effect in some circumstances. AAT uses various non-noxious tactile inputs to the extremities to effect a neural reset.

AAT works by having the patient avoid focusing on the pain; BAUD biofeedback, on the other hand, requires the patient to actively focus on the area and intensity of pain. More studies are needed to confirm these findings.


Last updated on: February 9, 2016
Continue Reading:
Chronic Back and Neck Pain in America 2015 Survey Results

Join The Conversation

Register or Log-in to Join the Conversation
close X