The majority of first-line and second-line pain medications aim to either decrease the formation of PGE2 or decrease the transmission for pain in the posterior horn via pre-synaptic or post-synaptic inhibition. However, there is growing evidence that other factors may lead to chronic pain syndromes, including an imbalance in the autonomic nervous system (ANS).
The ANS provides a balance between the sympathetic and parasympathetic nervous systems. The sympathetic nervous system (SNS) is designed to prepare the body to “fight or flight” while the parasympathetic nervous system (PNS) has the opposite effect, essentially maintaining homeostasis. ANS controls three physiological processes that have been linked to chronic musculoskeletal (MSK) diseases or chronic pain syndromes:1-3
- muscle blood flow
- muscle contractility
- sensory motor control
Working theory suggests that central sensitization resulting in over activation of the SNS causes whole body vasoconstriction, decreasing blood flow to muscles, muscle activation (spasm), and hyperalgesia and allodynia. There is also a decrease in parasympathetic activity, which would normally bring the body back into homeostasis. Additionally, the imbalance in SNS and PNS activity can affect other systems, including cardiac, respiratory, and gastrointestinal. This alteration in ANS has been linked to several chronic pain syndromes including:4
- rheumatoid arthritis (RA)
- complex regional pain syndrome (CRPS)
- fibromyalgia syndrome (FMS)
Amplified Musculoskeletal Pain Syndrome (AMPS)
AMPS is a term used to describe a continuum of diffuse or limited chronic non-inflammatory pain syndromes in children. Subsets of AMPS include CRPS, FMS, and widespread pain that does not fit diagnostic criteria for a specific syndrome.5
Sherry et al reported that 80% of patients aged 12 to 16 (509 female, 127 male), between 2015 and 2019, with AMPS are female, 79% Caucasian, 91% non-Hispanic.5,6Additionally, only 35% of research participants met the American College of Rheumatology (ACR) fibromyalgia diagnostic criteria.5,7 There is a psychological component associated with AMPS in many patients, including anxiety (45%) and depression (27%). The presence of psychological co-factors may be associated with the type of pain (limited or diffuse) and duration of symptoms.5,6,8 External factors that could impact pain levels include high socioeconomic status, controlling parents, and academically high achieving children.6,9
Etiology for AMPS is unknown, however, it is theorized that central sensitization resulting in over activation of the SNS is involved, similar to adult chronic pain syndromes.
Treatment for AMPS became more medicalized between 2008 and 2014, including an increase in the average number of medications used, therapies tried, and providers seen. Without a significant change in pain score or duration. Pharmacological approaches alone were not demonstrated to be successful in treating AMPS.10
Thus, current treatments focus on re-establishing functional movement through intense exercise or “re-setting” the nerves using sensory level electrostimulation. Sherry et al also reported a 90% success rate utilizing high-intensity therapy consisting of a combination of physical, occupational, and aquatic therapies along with desensitization of affected areas as needed.9
The treatment program includes 6 to 8 hours of exercise per day for 2 to 3 weeks. This regimen is followed by a high-intensity home exercise programs. Treatment is often coupled with psychological interventions when appropriate. However, patients may not be able to complete the program due to activating the intense pain. More recently, Calmare electrotherapy treatment has shown some success in treating AMPS.11 However, this therapy is currently only available in specialty clinics.
Another possible approach to treatment is to decrease sympathetic nervous system activity. The SNS utilizes chain ganglions, which are all connected and run parallel to the spine. The three cervical chain ganglions connect to the cardiac and pulmonary plexuses, which affects the heart, lungs, and blood vessel circumference.
The stellate ganglion (SG) is the middle of the three cervical ganglions and is a common site for nerve blocks. SG blocks have been used to treat CRPS, FMS pain, herpes zoster infection affecting the head, neck, arm, or upper chest,12and PTSD.13 An SG block consists mainly of analgesic medications, however, photobiomodulation or light therapy, has been successfully used to block the SG to relieve pain and cause a sympatholytic response.14
We propose treating the SG with PBM to inhibit the overactive sympathetic nervous system, which is proposed to be causing AMPS. PBM is biphasic and either stimulatory (low dose) or inhibitory (high dose).15 A high dose of PBM to the SG should cause a sympatholytic response, thereby decreasing symptoms caused by the overactive SNS.
Case Report: Using SG Block to Decrease AMPS Symptoms
Patient is a 13-year-old-male. The patient has a history of a knee fracture, which he fully recovered to within normal limits and ADLs. The patient was playing at a trampoline park and developed the following symptoms: tachycardia, dyspnea, vertigo, migraine, nausea, global weakness, dim vision, low blood pressure, profuse sweating, syncope, unable to stand or walk, severe global pain, and reporting having an “out of body experience.” The patient was treated at the ED twice. However, the following diagnostic tests failed to determine the cause of symptoms: MRI, CT scan, X-Rays, ECG, and EEGs. The patient was told to rest, stay hydrated, exercise to tolerance, and eat well. However, the patient continued to have symptoms.
Based on the wide array of symptoms related to the ANS, it was determined that the patient could be suffering from AMPS. PBM treatment was given using a 25 W emitter containing super pulses laser (905 nm), infrared (875 nm), and red (660 nm) diodes. The SG is a deep structure, so to ensure enough photons were on target for inhibition, PBM was applied for 10 minutes bi-laterally (see Figure 1 example) with a dose of 60 J per side. The prescribed course of treatment consisted of 12 treatments over 4 weeks.
The patient reported a positive treatment response after the first session and complete resolution of symptoms after the fourth session. PBM treatments were slowly withdrawn to monitor the patient’s response and to prevent a possible relapse. PBM was reduced to 1 treatment per week for 6 weeks with no relapse in symptoms. The treatments were then reduced to 1 treatment every 2 weeks for 2 months, again with no return of symptoms.
The patient currently receives 1 PBMT per month due to parental concern around returning symptoms. The patient’s mother reported the patient has been symptom-free for 14 months and able to fully participate in all activities of daily living including soccer and playing at the trampoline park.
Based on the presented case, low-level laser therapy or photobiomodulation to the stellate ganglion may be an effective nonpharmacological and non-invasive treatment for pediatric patients with AMPS. It is possible that PBM treatments to the SG may also be effective for treating adult chronic pain syndromes associated with an overactive SNS. More research needs to be completed to determine the appropriate frequency of treatments for specific cases.
In the presented case, it is unclear whether the patient’s symptoms would have returned if we stopped low-laser light therapy after the fourth treatment when all of the symptoms were resolved, or how frequently the patient may need a maintenance treatment. Therefore, a double-blind RCT should be conducted to determine the efficacy of this treatment and the best treatment protocol. Ideally, the study would include a comparison of the intense exercise protocol, PBMT to the stellate ganglion, and a combination of PBMT and exercise. There is evidence supporting a synergistic effect of PBMT and exercise for treating fibromyalgia syndrome in adults.16