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Richard loves sports. He really enjoyed football and played throughout high school. During a typical game in high school he suffered an injury to his back. What he did not know is that this would change the course of his life forever.
In 1960, under the crunching leaves of a crisp fall New England day, Richard was playing center during a yearly high school football game against the freshman of the University of Vermont football team. When the play began, a 240lb football player kneed Richard in the lower back and they both went down. He had sudden severe back pain and spasms so he left the game. Richard was sent to the hospital for further evaluation and imaging found fractures of the right L4 and L5 transverse processes and an L4-5 disc herniation. He was done for the season and spent a lot of time in bed which was the standard of care at time.
In college, Richard felt fit enough to return to sport but was re-injured during a pickup rugby game in 1963. He returned to the hospital and spent three months in a hard and uncomfortable plastic turtle shell to treat L4-5 level spinal instability and again spent a good deal of time in bed.
By 1966, Richard recovered and began to water skiing competitively. Once during this time, he lost the ability to weight bear on his right leg. This began to happen more episodically but did not impact his lifestyle.
He moved his family to California in 1970 to open a new company office. Richard noticed that he was having more episodes of severe pain while placing pressure on his right leg. He felt like it was akin to stepping on an electrified wire which in some cases caused him to collapse. Richard contacted the head of neurosurgery at the Hospital for Joint Diseases in New York City and was referred to Huntington Hospital in Santa Monica California where he had an L4-5 level laminectomy and discectomy. The surgery was somewhat helpful.
He returned to New York City in 1972 and consulted with the orthopedic surgery department at Columbia Presbyterian Hospital as he was again having increasing right leg pain and weakness as well as new left leg pain with severe muscle cramping. Richard underwent an emergency L4-S1 lumbar spine fusion. This was followed by several inpatient stays for weeks of therapy at the Rusk Rehabilitation Center at NYU, where he spent weeks in a wheelchair unable to walk. He continued to have severe pain in his right lower back that radiated all the way down his right leg. Further imaging and nerve tests were done which did not show any new changes in his lower back or to the nerves that came out of his lower back.
Richard’s searing pain had to be treated, so he was prescribed pain medications to allow him to perform everyday activities. He had the usual side effects such as severe constipation and drowsiness so he began to spend more and more time in bed, sometimes for weeks at a time. For years he continued to take the pain medications (hydromorphone in the 1980s, morphine shots, and oxycodone/acetaminophen) until he developed a severe allergy to the opioids he was taking. To treat his itching, the doctor gave him diphenhydramine which caused even more drowsiness. Richard felt like he was sleeping most of the day. He felt like life was slipping away, so he decided to discontinue his pain medications and try to limit the activities which caused pain. He also learned how to hypnotize himself to help with the pain. Yet he still spent hours sitting in a chair or days lying in bed.
Over the next 40 years, Richard consulted with many types of physicians at NYU, Columbia and Cornell who tried all kinds of medications and procedures. He tried every injection and therapy known with little success. Physical therapy often exacerbated his pain. Meditation and relaxation had no effect although it made him more resilient to the pain. He had many ketorolac injections in the ER, ten lumbar epidural steroid injections and 21 trigger point injections which helped temporarily. For years Richard relied on these types of procedures to allow him to function temporarily for several days to weeks, although never normally.
Richard’s cardiologist believes that his pain caused an enlarged heart and cardiac arrhythmia. He had an implantable pacemaker implanted in 2002 and eventually he had to undergo life threatening cardiac ablation surgery with a 30% chance of death. Luckily, he survived and did well, but his cardiologist warned him about the possibility of this life threatening arrhythmia returning if his pain remained untreated.
When I met Richard, I was the co-director of the Spine Center at NewYork-Presbyterian Hospital. Every step he took to get into the examination room made childbirth look like a walk in the park. With every single step his eyes would squeeze tight and his face would turn bright red. He would sweat as though he just finished a marathon and the process of walking ten feet look like a climb up Mount Everest.
We did the usual physical therapy, epidural steroid injections and trigger point injections which continued to help temporarily. He remained uninterested in using regular pain medications. A CT scan did not show any new fractures, new disc herniations or instability at the lumbar fusion site. We could not do an MRI due to his implantable pacemaker.
Over the years, we found that he did best for several weeks with ultrasound guided trigger point injections. During one of these injections, we noticed the medication disappearing within the thoracolumbar fascial plane. Although fascia is connective tissue that separates the muscles, a cavity is not known to commonly exist in this region.
We decided to proceed with an ultrasound-guided platelet rich plasma infiltration into the cavity in hopes of gluing the cavity together. We did this in February of 2014 and within three months, Richard was 100% pain-free. Not only is he pain-free getting out of bed and walking any distance, but he is not limited in his ability to do any activity. Richard now regularly does yard work, shovels snow, climbs ladders and walks unlimited distances; things that he could not imagine ever doing again.
Although the treatment appears to be deceptively simple as well as incredibly successful, the great challenge was trying to identify the exact source of his pain. The reason this was challenging is that x-ray, MRI, and CT scans could not identify this tear. Even using ultrasound imaging did not demonstrate significant tissue damage. The tear or separation was only noticeable while injecting fluid within the region during a trigger point injection which is commonly done into the muscle belly.
So Richard now lives pain free and is active. He does not live in the fear of this horrible pain returning. He has been given the precious opportunity to do things that he never thought possible to recapture the life that was taken from him so many years ago.
I am humbled by this experience but it taught me a profound lesson. If we can identify the source of pain, the pain can be treated even half a century later. So there is a chance for hope in people who live with chronic back pain.
Low back pain is one of the most prevalent musculoskeletal disorders, affecting up to 85% of the adult chronic pain population. Up to 40% of patients remain in pain at 6 months and 62% suffer a relapse within one year. (Von Korff 1993). Also up to 75% of patients will continue to experience pain one year after onset (Becker, 2010). Yet with this epidemic, a precise patho-anatomical diagnosis cannot be determined in up to 85% of patients with low back pain (Airaksinen, 2006).
The spine is made of a column of individual cylindrical bones called vertebral bodies which are connected via flexible collagen spacers called intervertebral discs. If these discs were not present then we would not be able to bend forwards or backwards which would greatly limit our activities. With motion carries the additional risk of injury at each disc level. There are also thick collagen fibers that connect the outer bones called ligaments that stabilize the spine in the same way that the rigging of a ship stabilizes the mast. The spine is controlled by parallel layers of back muscles called the erector spinae. The small ones that are next to the spine are call the interspinalis and progressing laterally in order are the multifidi, longissimus and iliocostalis respectively. To keep the muscles in place, they are covered in a thick collagen called the thoracolumbar fascia.
The thoracolumbar fascia transfers the load from the arms and torso to the legs and vice versa. The thoracolumbar fascia is assumed to connect the latissimus dorsi muscles and abdominal muscles to the spine and iliac crests as well as the gluteal muscles in the buttocks. Through this expansive reach, an internal ectoskeletal corset is created that allows force to move up and down between the arms and legs and also provides a flexible structure that stabilizes the bones to provide the incredible strength with different movements that we have come to rely on (Willard, 2012).
Additional functions of the thoracolumbar fascia include:
In this patient’s case, the original blunt force and fracture may have resulted in local soft tissue injury in addition to the fractures which resulted in progressive L4-5 instability. This injury was not apparent enough to be seen with conventional imaging. In addition, the weeks spent lying in bed or immobile created increased stiffness within the thoracolumbar fascia which lost its flexibility, so with every step there was an increasing tug on the tightened tissue along with weakened muscle which had greater difficulty supporting the forces through the back.
We trialed trigger point injections with different preparations and concentrations of corticosteroids and anesthetic with only moderate improvement which ruled out an intrinsic injury or spasm to the muscle as a source of his pain. Although there is excellent literature that discusses the biochemical milieu within trigger points of muscles (Shah, 2008), there is lack of research that assess the biochemical milieu of the adjacent thoracolumbar fascia which most likely has a greater density of sensory innervations. In research assessing delayed onset muscle soreness (DOMS), an injection of hypertonic saline within the fascia was found to result in more pain than a similar injection into the muscle itself (Gibson, 2009) suggesting that the fascia is the primary pain generating tissue outside of direct muscle injury.
Fortuitously, during one of the trigger point injections we noticed that we had placed the injectate within a sagittal cavity. As the injection proceeded we did not see the typical enlarging circular cavity that is usually found while injecting into tissue.
This suggested that a fascial tear or separation was created which would most likely develop friction with motion. This sensitized of the free nerve endings and encapsulated mechanoreceptors within the thoracolumbar fascia (Yahia, 1992). He had tremendous improvement after the corticosteroid injection within the fascial plane which suggested that we had found the pain generator, although it was temporarily helpful
Long-lasting sensitization to mechanical and chemical stimulation in the deeper tissues can occur if nerve growth factor is injected into the erector spinae (Deising, 2012). This does not cause sensitization on the skin which results in the absence of symptoms to guide physicians during a physical examination. Some researchers believe that this may contribute to chronic back pain.
Ingrowth of nociceptive fibers have been well documented in the intervertebral disc (Hirsch, 1963) and this process has also been documented in patients with nociceptive fibers invading the fascia with patellofemoral malalignment (Sanchis-Alfonso , 2000). This suggests that a similar process can occur within the thoracolumbar fascia as well.
Research into the histological structure of fascia has been done using tissue close to the spinous process of the vertebral body. This fascia has been found to be composed of three layers:
The primary sensory fibers found in the thoracolumbar fascia are the peptidergic calcitonin gene-related peptide (CGRP) and substance P containing fibers (a subpopulation of the CGRP fibers). They can cause neurogenic inflammation-vasodilation and increased blood vessel permeability and and invade the nerve endings antidromically (against the normal direction of propagation) (Mense, 1996). Also, 2/3 of the of thoracolumbar fascia innervation is efferent and primarily composed of sympathetic, post ganglionic fibers. This may explain why psychological stressors can significantly worsen low back pain (Brage, 2007). This can contribute to the fact that most practitioners have great difficulty identifying the source of pain and agreeing on whether it is back pain (McCombe, 1989). Thus, the thoracolumbar fascia is possibly a more important pain source than the low back muscles and other soft tissues
Corticosteroids are the workhorse of medicine. They are very helpful for severe inflammatory conditions. The anti-inflammatory action of corticosteroids is mediated by the inhibition of phospholipaseA2, which which is the enzyme responsible for the breakdown phospholipid from the cell membrane to arachidonic acid thus inhibiting the synthesis of leukotrienes, prostaglandins and thromboxanes resulting in:
Since inflammation is important in the healing process, the anti-inflammatory action of corticosteroids could be detrimental for complete tissue healing (Fadale, 1994).
Central sensitization is amplification of the neural signaling within the central nervous system that causes pain hypersensitivity including increased brain activity (Roussel, 2013). This patient not only had severe pain for decades, but he also developed cardiac manifestations so it would have been expected that central sensitization played a key role in his pain experience. It may be also possible that central sensitization was encouraged by peripheral pain and once resolved, the central sensitization also resolved.
Platelet-rich plasma is unique as it has the unique ability to enhance tissue healing. The alpha-granules in platelets contain many growth factors that are responsible for the initiation and maintenance of the healing response. The growth factors that are released include PDGF, TGF-beta, VEGF and FGF. The platelets begin secreting their proteins within 10 minutes of clotting with more than 95% of the growth factors secreted within one hour and continue secreting additional proteins for the remainder of their 5-10 day lifespan. A fibrin matrix forms also has an additional stimulatory effect on healing by trapping platelets and providing an initial matrix for fibroblast migration. (Kuffler DP, 2013) , (Lana, 2014), Platelet-rich plasma has also been shown to heal nerve injury in experimental animal models (Küçük,2014). Unfortunately, very little is known about acute fascial healing (Lau, 2014), and I could not find research that reviewed long-term fascial tissue healing.
This is the first article to document a thoracolumbar fascial tear as a source of back pain as well as a successful treatment using regenerative medicine. A search of the English literature in Pubmed did not yield any articles addressing the thoracolumbar fascia as a cause of chronic back pain or of its successful treatment.