Diagnosis & Collaborative Management Between the Chiropractor as the Primary Spine Care Provider and the Neurosurgeon
By: Matt Erickson DC, FSBT
Mark Studin DC, FASBE(C), DAAPM, DAAMLP
John Edwards MD, Neurosurgeon
Clay Wickiser DC
is defined as softening of the spinal cord and can be a result of injury and represents a serious and potentially life-threatening sequella to injury if not treated. According to Zhou, Kim, Vo and Riew (2015), “Cervical myelomalacia is a relatively uncommon finding on MRI, with anoverall prevalence of 4.2% among all patients who underwent cervical MRI. Males had a higher prevalence (5.6%) than the females (3.0%).” (pg. E250)
Zhou et al., (2015) also reported, “There were considerable variations in the prevalence of myelomalacia in patients referred by different specialties/subspecialties. Specialists in spinal cord injury had the highest rate (28.7%), followed by neurological (8.4%) and orthopedic (6.4%) spine surgeons, general neurosurgeons (5.5%), and neurologists (4.2%). Specialists who generally do not treat patients with spine problems had the lowest (1.2%) followed by non-spine orthopedists (1.6%) and primary care doctors (2.1%)” (p. E248).
Myelomalacia is ischemic or hemorrhagic necrosis of the spinal cord that can occur following acute spinal cord injury, and represents extensive damage of the intramedullary spinal vasculature” (pg. 78). According to “In small animal neurology, the term myelomalacia … is normally used to refer to hemorrhagic infarction of the spinal cord that can occur as a sequel to acute injuries, such as that caused by intervertebral disc extrusion. Myelomalacia may occur as a focal lesion or may spread cranially and caudally along the spinal cord, resulting in a diffuse, severe lesion. Histologic lesions of myelomalacia are compatible with ischemic necrosis” (pg. 326).
According to a website article titled, “Myelomalacia” by Foster and Wilborn (2019), “Myelomalacia is a medical condition in which the spinal cord becomes soft. It is caused by the insufficient blood supply to the spinal cord, either as a result of bleeding or because of poor circulation. Myelomalacia most often occurs as a result of the injury” (www.wisegeek.com/what-is-myelomalacia.htm). Foster and Wilborn (2019) added, “Caused by mild to severe spinal cord injury, myelomalacia leads to neurological problems, often related to muscle movement. Often, the onset of the condition is slow and subtle, making it difficult for doctors to catch at an early stage. The condition may present simply as high blood pressure, for example, and may not be diagnosed until after the point at which it has become inoperable. While symptoms vary, they may include loss of motor function in the lower extremities, sudden jerking of the limbs, an inability to sense pain, depression, difficulty breathing, and paralysis. The damage can migrate towards the brain in a condition known as ascending syndrome. Myelomalacia can be fatal if it causes paralysis of the respiratory system (para. 2-3).
, “The exact pathophysiology is poorly understood but it seems to be the result of the concussive effects of trauma, ischemia, and the release of vasoactive substances, oxygen-free radicals and cellular enzymes. When the spinal cord is acutely damaged, cell death in the gray matter may occur within 4 hours, with this area of necrosis expanding for a few days” (pg. 78). This means that many patients can have significant underlying progressive pathology with symptoms that have not yet fully expressed themselves, but the evidence is demonstrative to the trained expert. This further supports the necessity and importance of having a primary spine care provider with trauma qualifications to diagnose the issue early on and coordinate care with the neurosurgeon.
Operative Neurosurgery, “Myelomalacia” (administrator updated) (2018, para. 4), explained, “Gradual cranial migration of the neurological deficits (problems relating to the nervous system), is known as ascending syndrome and is said to be a typical feature of diffuse myelomalacia. Although clinical signs of myelomalacia are observed within the onset (start) of paraplegia, sometimes they may become evident only in the post-operative period, or even days after the onset of paraplegia. Death from myelomalacia may occur as a result of respiratory paralysis when the ascending lesion (abnormal damaged tissue) reaches the motor nuclei of the phrenic nerves (nerves between the C3-C5 region of the spine) in the cervical (neck) region” (https://operativeneurosurgery.com/doku.php?id=myelomalacia).
As such, it is imperative for there to be collaborative case management between the primary spine care expert and the neurosurgeon. The role of the primary spine care provider is an early diagnosis to be able to identify, treat and involve the neurosurgeon when clinically indicated because if left undiagnosed and untreated, myelomalacia can become a seriously debilitating and/or life-threatening injury. Those injuries are from and trauma the spinal cord is exposed to (auto accidents, sports injuries, falls, etc.). Currently, there is a growing body of chiropractors nationally that are primary spine care and trauma qualified and trained in the early detection (diagnosis) and management of this population of patients.
According to Zohrabian and Flanders, Chapter 37: Imaging of trauma of the spine from the Handbook of Clinical Neurology Part II, “MRI is the only available imaging modality that is able to clearly depict the internal architecture of the spine cord, and, as such, has a central role in depicting parenchymal changes resulting from injury” (pg. 760). Further, “It may be difficult to distinguish spinal cord white matter from gray matter, especially in the sagittal plane, due to the similar T1 and T2 relaxation characteristics. Many prior investigations have shown that MRI characteristics of (SCI) Spinal Cord Injury, including presence and extent of cord edema and hemorrhage, are concordant with neurologic impairment at the time of injury and predict recovery” (pg.760).
Zohrabian and Flanders also wrote, “The most common location of posttraumatic spinal cord hemorrhage is the central gray matter of the spinal cord at the point of mechanical impact. The lesion most often represents hemorrhagic necrosis; true hematomyelia is rarely encountered. The lesion appears as a discrete focus of hypointensity on T2-weighted and gradient echo images, developing rapidly after SCI” (pg.760).
Zohrabian and Flanders (2016) stated, “Moreover, the location of cord hemorrhage has been shown to closely correspond to the neurologic level of injury, with frank hemorrhage correlation with poor neurologic recovery” (p. 760).
Zohrabian and Flanders (2016) further added, “Although several MRI classification schemes have been proposed, there are three common imaging observations: spinal cord hemorrhage, spinal cord edema, and spinal cord swelling. Each of these characteristics can be further described by their rostra-caudal (top to bottom) location in the cord and the amount of cord parenchyma they involve” (p. 760).
“Spinal cord edema, colloquially referred to as a cord contusion, can occur with or without hemorrhage. Edema involves a length of the spinal cord above and below the level of injury, with the length of the spinal cord show to be proportional to the degree of initial neurologic deficit. Spinal cord hemorrhage always coexists with spinal cord edema. Cord edema alone usually confers a more favorable prognosis that cord hemorrhage” (pg. 761).
According to D.J. Seidenwurm MD (, “In traumatic myelopathy, the first priority is mechanical stability. Plain radiographs are sometimes useful for this purpose, but CT is more useful when a high probability of bony injury or ligamentous injury is present. In many centers, routine multidetector CT with sagittal and coronal reconstructions has replaced plain radiographs, especially in the setting of multiple trauma” (pg. 1032).
Concerning CT, Foster and Wilborn (2019) reported, “Myelography uses a contrast medium injected into the spine to reveal injuries in x-rays. It is more invasive than an MRI, but can also detect injury in some cases in which MRI cannot. Therefore, myelography is typically used as a follow up to MRI when the latter fails to identify the source of pain or injury.” (para. 4)Finally, Zohrabian and Flanders reported, “Unlike in spinal cord cysts, myelomalacia will not parallel CSF (cerebral spinal fluid) signal intensity and its margins will usually be irregular and ill-defined (Falcone et al., 1994). The cord may be normal in size, although it is frequently atrophic at the site of myelomalacia (Fig. 37.24).” (pg. 763)
Zhou, Kim and Vo (2015) further explain, “Myelomalacia is a radiographical finding on magnetic resonance imaging (MRI) manifested by an ill-defined area of cord signal change, visible on T1- and T2-weighted sequences as hypo- and hyperintense areas, respectively. It is commonly associated with focal cord atrophy. It occurs as a sequel to spinal cord injury (SCI) due to different causes such as cord compression, ischemia, and hemorrhage. It is the most common finding in patients with previous spinal cord injury with a prevalence of 55% among patients with SCI” (p. E248).
Due to the seriousness and progressive nature of myelomalacia, it is important for the Primary Spine Care Provider, to recognize the signs and symptoms associated with myelomalacia and to identify the lesion on MRI and if identified, immediately refer the patient for a neurosurgical consultation. This also underscores why physical therapists, although licensed to treat spine, should never be the first provider to manage a spine case as diagnosing these and other conditions are not within their scope.
Foster and Wilborn (2019, para. 5) also reported, “Unfortunately, neurological damage due to myelomalacia is permanent. It can also worsen, as the nerve damage can cause affected muscles to whither. Treatment is focused on preventing further damage. Possible treatments include spinal cord surgery and medication with steroids, which serves to relax spastic muscles, reduce pain, and reduce swelling of the spinal cord.” Foster and Wilborn (2019, para. 6) also suggested, “Stem cell therapy may be used to repair neurological damage caused by myelomalacia in the future, but the therapy is currently experimental and controversial. Recent technology suggests that adult stem cells, which can be harvested from the patient's own body, show promise in treating neurological damage by allowing new, healthy tissue to grow”(www.wisegeek.com/what-is-myelomalacia.htm).
Zhou, Kim, Vo and Riew (2015) reported, “The presence of myelomalacia in the cervical spinal cord has prognostic value after decompression surgery. Some surgeons consider operative treatment of all patients with myelomalacia based on the assumption that myelomalacia is a relatively uncommon finding.” (p. E248) The authors also reported, “Many patients with myelomalacia are clinically asymptomatic or have only mild myelopathic symptoms and signs. The extent of intramedullary changes on MRI does not always correlate with clinical symptoms. Hence, for patients with asymptomatic or mild myelopathy with myelomalacia on MRI, the appropriate management remains controversial” (p. E249).
Zhou et al (2015) further added, “Several articles have suggested that conservative management is not an unreasonable option for patients with myelomalacia and mild myelopathy. It has been reported that the condition of 56% of patients with mild CSM (cervical spine myelomalacia) had not deteriorated or required surgery after 10 years. However, 2 of 45 (4.4%) patients who were treated nonoperatively with T2 hyperintensities experienced catastrophic neurological deficits with trivial trauma. Early-stage myelomalacia may be reversible, depending on the severity of the initial SCI (spinal cord injury), and may be reversed after decompression surgery” (p. E249).
This is not suggesting surgery for myelomalacia is always required. According to Dr. Mark Kotter (n.d., para. 3) in a website article titled “Myelomalacia” from myelopathy.org,“The presence or absence of myelomalacia should not be used to define when surgery should occur.” Although he further stated, “its presence and extent may be related to prognosis” (http://www.myelopathy.org/myelomalacia.html). Myelomalacia, like any spinal related injury never uses imaging findings exclusively as an arbiter for surgery. That decision is reserved for combining a clinical examination with imaging findings and the surgeon decides if surgery will benefit the patient. It is the role of the primary spine care provider to ensure and early diagnosis and referral to try to develop treatment protocols to surgically decompress the spinal cord to help reverse this pathology and often can be done if damage has been minimized.
Surgery for Myelomalacia
A patient with myelomalacia may require surgery to decompress the spinal cord. Different techniques are used depending on the pathology that may or may not include spinal fusion. Many patients are treated with an anterior approach. The offending material is removed and the spine is reconstructed either with a fusion or an artificial disc replacement. Some patients, especially with multilevel pathology, require posterior decompression with or without fusion.
The primary goal of surgery for myelomalacia is to decompress the spinal cord. Secondary goals include maintaining spinal structural integrity, alignment, and biomechanical function.
The image on the left is courtesy of Jed Weber MD, Neurosurgeon. You can see the severe spinal cord compression creating an hour glass affect secondary to a disc extrusion. Myelomalacia is also present as a white spot in the spinal cord at the compression site.
Concerning surgically balancing the spine, sagittal (front to back) balance is associated with better post-surgical outcomes. Healia.com reported on lectures by Serena Hu, MD, Jean Charles LeHuec, MD, PhD and J.N. Alastair Gibson, MD, FRCS(Ed), FRCS (Tr &Orth), MFSTEd related to outcomes of lumbar spine surgery about sagittal balance. According to Dr. Hu (2016, para 3), “Surgical outcomes for spine surgery are improved when spinal, pelvic and hip alignment is considered in both degenerate and deformity cases, and how we better understand these will help us better improve outcomes for our patients” (https://www.healio.com/spine-surgery/lumbar/news/print/spine-surgery-today/%7B54ac5ca2-7939-407d-96a5-31fa9c0fc904%7D/proper-sagittal-balance-may-correlate-with-better-surgical-outcomes).
Dr. Hu (2016) further reported, “Sagittal imbalance in a patient can negatively affect the outcomes of a surgical procedure. But, how extensive the surgery required is to correct the imbalance must be carefully considered for the individual patient” (para. 4). Dr. LeHuec (2016) added, “Sagittal balance is an active phenomenon for patients. “The best course of action is to strive to achieve sagittal balance in patients” (para. 8).
In a study by
In an article by Yeh, Lee, Chen, Yu, Liu, Peng, Wang, and Wu, (2018) they concluded, “The results of this study support previous findings that functional outcomes are closely associated with sagittal radiographic parameters in the patients with the degenerative thoracolumbar spinal disease who received long-segment fusion. The achievement of global and regional sagittal alignment balance is a crucial factor for improved postoperative functional outcomes” (p. 1361).
The primary care spine provider and the neurosurgeon can work together to best achieve spinal alignment and balance. If the patient has been cleared for mechanical treatment, the primary care spine provider can work to balance the spine (front to back and side to side) before any necessary surgical intervention. The neurosurgeon can work to maintain and improve spinal alignment with surgery. Post-operatively, ongoing chiropractic spinal adjustments can help maintain and continue to improve spinal alignment. This can lead to the best possible surgical outcomes.
Patients with myelomalacia present an ideal opportunity to further the relationship between the Doctor of Chiropractic as the primary care spine provider and the neurosurgeon. The finding of myelomalacia requires surgical consultation. If the chiropractor identifies myelomalacia, he or she can then refer to the neurosurgeon and begin the discussion necessary for further co-management. The chiropractor can ask if surgery is necessary. If so, the Doctor of Chiropractic can ask if mechanical treatment can be done pre-operatively or ask if it should wait until after surgery. If the patient needs close monitoring over time, the astute chiropractor can regularly check on and provide education to the patient under the direction of the neurosurgeon.
In patients with myelomalacia, the ability of the Doctor of Chiropractic to monitor symptoms, prepare a patient for surgery, and manage the spine mechanically after surgery are advantageous to the surgeon, who can spend more of their time performing surgery and also enjoy greater patient satisfaction and outcomes.
Myelomalacia represents a softening of the spinal cord that commonly results from trauma. If myelomalacia is observed on imaging, the advanced trained Doctor of Chiropractic in the capacity of a primary spine care provider, should refer the patient out for a neurosurgical consultation. In the event surgery is not indicated, the chiropractor can create a treatment plan with the surgeon to help axially balance and stabilized the spine, thereby reducing the compressive forces on the spinal cord and maintaining spinal mechanics. If surgery is required, the chiropractor can coordinate conservative care with the surgeon to help biomechanically balance and then manage the patient’s spine to promote a better long term post-surgical outcome. Whether surgical or not, the chiropractor can play an integral role in the patient’s car and should the chiropractor have additional training in MRI Spine Interpretation, Spinal Biomechanical Engineering and/or other advanced spinal knowledge, it provides the basis for better collaboration.
Preventing Spinal Degeneration Through Chiropractic Care
Subluxation Degeneration/Spondylosis Explained via Wolff’s Law
Spondylosis, also known as osteoarthritis of the spine, is rarely appreciated as one of the most sigificant causes of persistent pain and disability in the world today. This form of arthropathy is so universal that it is often regarded as part of the “normal” aging process. “Osteoarthritis is usually progressive and often deforming and disabling” as reported by Gottlieb (1997). “Up to 50% of individuals will experience arthritic back pain at some point in their lives. Despite its high prevalence, there exists limited information (albeit through allopathic medicine) available regarding the factors associated with the development of lumbar spine degeneration” as reported by Weinberg, Liu, Xie, Morris, Gebhart and Gordon (2017). The projected number of older adults with arthritis or other chronic musculoskeletal joint symptoms is expected to nearly double from 21.4 million in 2005 to 41.1 million by 2030 in the United States. The assumption is so will the progression of persistent pain and disability. We see that allopathic medicine has little information to help reduce the progression of this disease process, which is why chiropractic is the only true solution since we view the body from a mechanical perspective. It is the maintenance of the mechanical workings of the spine that is the real approach to preventing degenerative “wear and tear” of the human spine.
Weinberg et. Al (2017) continued by reporting “Certain mechanical causes have been implicated in the development of degenerative joint disease of the lumbar spine, including lumbar lordosis, the length of the transverse processes, disc-space narrowing, and traction spurs. Lately, authors have begun investigating the roles of facet orientation, tropism, and pelvic incidence, although data remains limited. It has recently been suggested that the relationships between pelvic incidence and facet orientation may have profound implications in the development of adjacent segment lumbar degenerative joint disease—this has sparked enthusiastic research better defining the role of sagittal balance in osteoarthritis formation.” Pg. 1593
When we consider spinal osteoarthritis, we must compare normal spinal biomechanics and loading vs. abnormal spinal biomechanics and pathological loading that results. Teichtahl, Wluka, Wijethilake, Wang, Ghasem-Zadeh and Cicuttini (2015) reported “Julius Wolff (1836–1902), a German anatomist and surgeon, theorized that bone will adapt to the repeated loads under which it is placed. He proposed that, if the load to a bone increases, remodeling will occur so that the bone is better equipped to resist such loads. Likewise, he hypothesized that, if the load to a bone decreases, homeostatic mechanisms will shift toward a catabolic state, and bone will be equipped to withstand only the loads to which it is subjected.” Pg. 2
“It is now recognized that remodeling of bone in response to a load occurs via sophisticated mechano-transduction mechanisms. These are processes whereby mechanical signals are converted via cellular signaling to biochemical responses. The key steps involved in these processes include mechano-coupling, biochemical coupling, signal transmission, and cell response.” Pg. 1
“Bone is a dynamic tissue that is tightly regulated by a multitude of homeostatic controls. One key environmental regulator of periarticular bone is mechanical stimulation. Wolff’s law relates to the response of bone to mechanical stimulation and states that bony adaptation will occur in response to a repeated load. It is interesting to consider this in the setting of knee OA, which has a strong biomechanical component to its etiology.” Pg. 1
“When periarticular bone is subjected to increased loading, some bone properties change. These include, but are not limited to, an expanding subchondral bone cross-sectional area, changes in bone mass, and remodeling of the trabeculae network. Although these changes likely represent appropriate homeostatic responses of bone to increased loading, they also appear to inadvertently predate maladaptive responses in other articular structures, most notably cartilage.” Pg. 1
Keorochana, Taghavi, Lee, Yoo, Liao, Fei and Wang reported (2011) “Differences in sagittal spinal alignment between normal subjects and those with low back pain have been reported. Previous studies have demonstrated that changes in sagittal spinal alignment are involved in the development of a spectrum of spinal disorders. It has also been a topic of great interest in the management of lumbar degenerative pathologies, especially when focusing on the role it may play in accelerating adjacent degeneration after spinal fusion and non-fusion procedures such as dynamic stabilization and total disc replacement. Spinal morphology may influence the loading and stresses that act on spinal structures. Alterations in the stress distribution may ultimately influence the occurrence of spinal degeneration. Moreover, changes in sagittal morphology may alter the mechanics of the lumbar spine, affecting mobility.” Pg. 893
Panjabi (2006) reported:
Cramer et al. (2002) reported “One component of spinal dysfunction treated by chiropractors has been described as the development of adhesions in the zygapophysial (Z) joints after hypomobility. This hypomobility may be the result of injury, inactivity, or repetitive asymmetrical movements…one beneficial effect of spinal manipulation may be the “breaking up” of putative fibrous adhesions that develop in hypomobile or “fixed” Z joints. Spinal adjusting of the lumbar region is thought to separate or gap the articular surfaces of the Z joints. Theoretically, gapping breaks up adhesions, thus helping the motion segment reestablish a physiologic range of motion.” (p. 2459)
Evans (2002) reported “On flexion of the lumbar spine, the inferior articular process of a zygapophyseal joint moves upward, taking a meniscoid with it. On attempted extension, the inferior articular process returns toward its neutral position, but instead of re-entering the joint cavity, the meniscoid impacts against the edge of the articular cartilage and buckles, forming a space-occupying "lesion" under the capsule: a meniscoid entrapment. A large number of type III and type IV nerve fibers (nociceptors) have been observed within capsules of zygapophyseal joints. Pain occurs as distension of the joint capsule provides a sufficient stimulus for these nociceptors to depolarize. Muscle spasm would then occur to prevent impaction of the meniscoid. The patient would tend to be more comfortable with the spine maintained in a flexed position, because this will disengage the meniscoid. The extension would therefore tend to be inhibited. This condition has also been termed a "joint lock" or "facet-lock" the latter of which indicates the involvement of the zygapophyseal joint.” Pg. 252
The sagittal spinal misalignments developed after hypo or hypermobility as a result of injury, inactivity, or repetitive asymmetrical movements as reported Cramer, creates mechanoreceptor and nociceptor pathological input, this in turn as reported by Evans creates a mechanical displacement of the zygapophyseal joint and aberrant stimulation to type III and IV nociceptors. This also, according to Panjabi causes a corrupting of neuromuscular transducers (mechanoreceptors and nociceptors) of the spinal muscular system. These combine to create spinal neuro-pathobiomechanics for the spine globally and at each affected motor unit. This is what has been historically called in chiropractic “vertebral subluxation.“ Based upon Wolff’s Law, the persistent biomechanical failure, as perpetuated by the central nervous system being corrupted and attempting to compensate through muscular activity creates premature degeneration of the spine or osteoarthritis or “Subluxation Degeneration.”
Evans (2002) concluded that a high velocity-low amplitude manipulation (chiropractic spinal adjustment) of the joint involving flexion and gapping, reduces the impaction and opens the joint to encourage re-entry of the meniscoid into the joint space and realignment of the joint.” Pg. 253 This activity reduced the irritation or pressure on the nociceptors on the zygapophyseal joints stopping the corruption of the central nervous system and allowing the body to “right itself” and halt the degenerative process of the spine.
It has already been concluded, as reported by Blanchette, Rivard, Dionne, Hogg-Johnson and Steenstra (2017) in a population-based study of 5511 injured workers in Ontario Canada as reported by the Workplace Safety and Insurance Board, a governmental agency reported a comparison of outcomes for back pain among patients seen by three types of providers: medical physicians, chiropractors and physical therapists. The found “The type of first healthcare provider was a significant predictor of the duration of the first episode of compensation only during the first 5 months of compensation. When compared with medical doctors, chiropractors were associated with shorter durations of compensation and physiotherapists with longer ones. Physiotherapists were also associated with higher odds of the second episode of financial compensation.” (pg.392) and “These differences raise concerns regarding the use of physiotherapists as gatekeepers for the worker’s compensation system.” (pg. 382)
Blanchette, Rivard, Dionne, Hogg-Johnson and Steenstra (2017) continued, “The cohort study of American workers with back pain conducted by Turner et al. found that the first healthcare provider was one of the main predictors of work disability after a year. By our findings, workers who first sought chiropractic care were less likely to be work-disabled after 1 year compared with workers who first sought other types of medical care.
Considering that 50% of the population will experience some type of pain and/or potential disability as a result of spinal arthritis, chiropractic, as reported above is positioned as the best first option for spine as an evidence-based solution. This is called Primary Spine Care and chiropractic is best positioned to lead society in the prevention of osteoarthritis/subluxation degeneration through chiropractic care.
Chiropractic Adjustments Increases Maximal Bite Forces Through Effecting Cortical Changes
By: Mark Studin
William J. Owens
Citation: Studin M., Owens W. (2019) Chiropractic Adjustments Increase Maximal Bite Forces Through Effecting Cortical Changes, American Chiropractor, 41 (1) 12, 14, 16
A report on the scientific literature
Chiropractic has been shown in the literature to affect neural plastic changes. According to Wikipedia, “Neuroplasticity, also known as brain plasticity and neural plasticity, is the ability of the brain to change throughout an individual's life, e.g., brain activity associated with a given function can be transferred to a different location, the proportion of grey matter can change, and synapses may strengthen or weaken over time. Research in the latter half of the 20th century showed that many aspects of the brain can be altered (or are "plastic") even through adulthood. However, the developing brain exhibits a higher degree of plasticity than the adult brain. Neuroplasticity can be observed at multiple scales, from microscopic changes in individual neurons to larger-scale changes such as cortical remapping in response to injury.” (https://en.wikipedia.org/wiki/Neuroplasticity) This article focuses on a specific piece of evidence to demonstrably verify the effects of those neuroplastic changes as sequella to a chiropractic “high velocity-low amplitude spinal adjustment.
Haavik, Ozyurt, Naizi, Holt, Nefergaard, Yilmaz and Turker (2018) reported “It has previously been proposed in the literature that chiropractic spinal manipulation has a central neural effect. This is because multiple studies have shown that spinal manipulation of dysfunctional spinal segments can impact somatosensory processing, sensorimotor integration, and motor control.” (pg. 6) Haavik, Naizi, Jochumsen, Sherwin, Flavel and Turker (2017) supported the previous finding by reporting “The result presented are consistent with previous findings that have suggested increases in strength following spinal manipulation were due to descending cortical drive and could not be explained by changes at the level of the spinal cord. Spinal manipulation may therefore be indicated for the patients who have lost tonus of their muscle and/or are recovering from muscle degrading dysfunctions such as stroke or orthopedic operations and/or may also be of interest to sports performers.” (pg. 12)
Lelic, Niazi, Jochumsen, Dremstrup, Velder, Murphy, Drewes and Haavik (2016) also supported the neural plastic changes of a chiropractic spinal adjustment by reporting their “study resulted in two major findings. Firstly, the study reproduced previous findings of somatosensory evoked potential (SEPs) studies that have shown that chiropractic spinal adjusting of dysfunctional spinal segments alters early sensorimotor integration (SMI) of input from the upper limb. The second major finding of this study was that we were able to show, using dipole source localization, that this change in SMI that occurs after spinal manipulation predominantly happens in the prefrontal cortex. The SEP peak showed multiple neural generators including primary sensory cortex, basal ganglia, thalamus, premotor areas, and primary motor cortex. The frontal N30 peak is therefore thought to reflect early SMI.”
Haavik, Ozyurt, Naizi, Holt, Nefergaard, Yilmaz and Turker (2018) also found “The major finding of this study was that chiropractic spinal manipulation (adjustment) increased maximum bite force immediately after the intervention and the increase in bite force remained at 1-week follow-up. This is the first study to show that a single session of chiropractic spinal manipulation can increase jaw bite strength compared to a sham intervention.
This immediate increase in jaw bit force of 11% post spinal manipulation was unlikely to be due to the placebo effect, as all subjects were naïve to chiropractic, and most of the subjects did not know which intervention was real upon questioning after both interventions. The 2.3% decrease in maximum bite force after the sham intervention may have been due to fatigue from maximum biting on the mold, or simply due to random variations in maximum efforts.
The current study now also suggests that cervical spine function can influence maximal bite force. The effort with which the subject’s bite would also influence maximum bite force, and for this reason the study was conducted in Turkey, where chiropractic is relatively unknown, to enable a more effective sham intervention. As no increase in strength occurred following the sham intervention, the effort is unlikely to have been the reason the subjects’ bite force increased after the spinal manipulation.
Increases in lower limb muscle strength in subjects with subclinical pain following chiropractic spinal manipulation has been reported. An increase in lower limb strength in elite athletes that lasted 30 min post spinal manipulation was shown. Chilibeck, et al. reported that in subjects with imbalances in lower limb muscle strength, spinal manipulation resulted in increased muscle strength of hip abductors in their weak leg. Botelho and Andrade reported increases in grip strength in a group of national level judo athletes following spinal manipulation.”
Haavik et. Al continued, “In two of these previous studies that showed lower limb muscle maximum voluntary strength increases after chiropractic spinal manipulation H-reflex excitability and V-waves were also recorded. Both studies showed increases in maximum plantarflexion force and significant increases in the cortical drive to the plantar flexors (i.e., V-wave) following spinal manipulation, and that both these measures significantly decreased after the control intervention… The increase therefore seen following the spinal manipulations was, therefore, most likely because of the increased cortical drive to the muscle.”
“It has previously been proposed in the literature that chiropractic spinal manipulation has a central neural effect. This is because multiple studies have shown that spinal manipulation of dysfunctional spinal segments can impact somatosensory processing, sensorimotor integration, and motor control as mentioned in the introduction. This current study supports this notion, as spinal manipulation appears to alter maximum biting force in this group of subjects. This study, therefore, supports the growing body of research that suggests chiropractic spinal manipulation’s main effect is neuroplastic in nature that affects cortical excitability.”
“Spinal dysfunction, even mild, recurrent spinal dysfunction, has been shown to be associated with maladaptive neural plastic changes, such as alterations in elbow joint position sense, mental rotation ability, and even multisensory integration, suggesting spinal dysfunction can alter the brains inner body schema and maps of the body and the world around us. This may be because spinal manipulation has been shown to change both cerebellum-M1 processing as well as prefrontal cortex processing. In the current study, the subjects’ mild spinal dysfunction may have altered the somatosensory input from the neck to the brain centers involved in sensorimotor integration and motor control of the jaw, and that adjusting these dysfunctional segments therefore impacted on these same central regions altering the maximum bite force the subjects could perform.”
Haavik et. Al concluded “Knowing that spinal function can have an impact on jaw function has functional implications for patient populations. It is possible that chiropractic spinal manipulation may influence the clinical outcomes for patients with TMJ disorders, as has been suggested by individual case studies.” There are also a significant amount of other applications of maximal bite force in our population that would also benefit from a chiropractic spinal adjustment when clinically indicated.
What’s not to be lost in this reporting of the literature as mentioned previously “multiple studies have shown that spinal manipulation of dysfunctional spinal segments can impact somatosensory processing, sensorimotor integration, and motor control.” There is a myriad of signs, symptoms, conditions and disease process that emanate from the malfunction of those centrally controlled functions in the human body. Although we have proven that a chiropractic spinal adjustment positively affects these functions, we are still at the forefront of fully understanding the full extent of how the adjustment influences a patient’s overall health although these authors have seen evidence clinically for almost four decades and chiropractors since 1895 have been reporting the same.
The Legal and Appropriate Use of X-Ray in Chiropractic
To Consider the American Chiropractic Association's “Choose Wisely” X-Ray Recommendations is a Potential Public Risk
[to view any of the author's credentials, please click on their name]
NOTE: After the references is visual evidence of why x-ray should not be limited in chiropractic
Let’s be very clear on who determines the appropriateness and necessity of chiropractic clinical practice including x-ray, it is the state licensure boards of Alabama, Alaska, Arizona, Arkansas, California and all the rest to the 50th state alphabetically through Wyoming. These authors are perplexed as to why a political organization, the American Chiropractic Association (ACA), has deliberately inserted itself between the practicing doctor of chiropractic and their individual state licensure boards which has quickly delivered its negative effects by limiting the diagnostic tools and reimbursement of chiropractors nationally. Additionally, instead of working towards and supporting increased access to chiropractic care they are consuming limited financial and personnel resources and those of other political organizations by pushing an agenda crafted by a distinct minority of the profession. This is despite our state licensure boards laws and regulations that already regulate the appropriate utilization of x-ray in chiropractic.
To think that this doesn’t have a far-reaching negative effect on your practice and reimbursement is Pollyannaish, as these authors predicted in their 2017 article “Should Chiropractic Follow the American Chiropractic Association/American Board of Internal Medicine’s Recommendation on X-Ray? (1), because it has already happened and will continue to happen. To further outline the gravity of the issue and lend objective evidence that the American Chiropractic Association is now cause for limitation of your services and reimbursement, ACA President R. Ray Tuck in an official ACA capacity, wrote to Blue Cross Blue Shield of Illinois the following letter on July 31, 2018:
“I write to you on behalf of the American Chiropractic Association ("ACA") in connection with the above-referenced coverage policy recently adopted by your company. We note that the coverage policy references a "Choosing Wisely" article entitled ‘Five Things Physicians and Patients Should Question and utilizes portions of the article as coverage standards.
Permit me to bring to your attention the following disclaimer appearing on the ‘Choosing Wisely’ web page:
‘Note: Choosing Wisely recommendations should not be used to establish coverage decisions or exclusions. Rather, they are meant to spur conversation about what is an appropriate and necessary treatment. As each patient situation is unique, providers and patients should use the recommendations as guidelines to determine an appropriate treatment plan together.’ (emphasis added)
Conveying information not intended or designed to be coverage standards as such, while at the same time attributing such standards to this association, conveys an unfair and false impression. This action also, in our view, constitutes a violation of the Illinois Unfair Claims Practices Act by knowingly misrepresenting relevant facts relating to coverage issues (215 ILCS 5/154.6(a)).
We, therefore, would request your company's immediate attention to this matter and the withdrawal of all coverage standards derived from the ‘Choosing Wisely’ article from the Chiropractic Services coverage policy.”
To review the American Chiropractic Association’s Choosing Wisely guidelines that were released in 2017, especially in regard to how they relate to imaging our patients in a clinical setting, they state “Do not obtain spinal imaging for patients with acute low-back pain during the six (6) weeks after onset in the absence of red flags.” (2) This controversial recommendation was adopted in conjunction with the American Board of Internal Medicine (ABIM) Foundation and Consumer Reports.
The ACA has continued to support their position by writing articles in support of their own internal decision. Christine Goertz DC, Ph.D. wrote in an article titled Choosing Wisely X-ray Recommendations Reflect Evolving Evidence, Accepted Standards: “This recommendation is not only on ACA’s Choosing Wisely® list; a similar item is also included on the lists of seven other organizations. This includes, among others, the American College of Emergency Physicians, the North American Spine Society and the American College of Physicians. It's also one of the performance measures established by the Centers for Medicare and Medicaid (CMS) under the MIPS Program. Thus, it is a widely accepted standard.” It should be noted, while the three groups that Dr. Goertz cited above, the American College of Emergency Physicians, the North American Spine Society and the American College of Physicians, are all held in high regard, we have to examine this fact at a deeper academic level. Regarding the North American Spine Society, their recommendations specifically state they “Do not recommend advanced imaging (MRI) of the spine within the first six weeks in patients with non-specific acute low back pain in the absence of red flags.” Their recommendations do not include x-ray. (3)The American College of Physicians, as an organization, represent internal medicine physicians and while we recognize they are focused on the diagnosis and management of systemic disease, they do not have advanced training in musculoskeletal or biomechanical spine diagnosis and are not trained as spine specialists.
Dr. John Edwards, a neurosurgeon from Provo, Utah wrote:
December 1, 2018
Dear Dr. Studin,
I would like to commend you for the work you have done to integrate chiropractic into higher education, medical research, and the medical community.
Over the past few years in my neurosurgical practice, I have understood more and more the value of biomechanical testing and treatment as the foundation for spinal care. I have discovered what you have known for years-biomechanical failures in the spine do not respond nearly as well to narcotics, steroids, injections, and surgery, as they do to chiropractic spinal adjusting.
Plain x-ray of the spine is the foundation of biomechanical diagnosing and biomechanical treatment, and supplemented with MRI as needed, enables the chiropractor as a primary spinal provider to triage patient care and initiate treatment as clinically indicated.
I think it is appropriate for the American Board of Internal Medicine to limit the frequency with which their providers are ordering diagnostic spinal tests, but inappropriate to hold this same standard to chiropractors. Internists generally know little about how to diagnose and treat spinal conditions. However, as a well-trained chiropractor, you understand when to order these tests. You can interpret them. You have validated, low cost, low-risk interventions that you can implement for treatment.
I hope the biomechanically trained chiropractor will be valued, validated, and viewed as the most important primary care spinal provider in the future. In our low access, high cost, high-risk health care system, the high access, low cost, low-risk management chiropractors can provide should be embraced by the entire medical community.
Although state licensure boards have spoken loudly in their historical support of doctors of chiropractic having the right to take x-rays within their lawful scope of practice, let’s examine the list of other organizations that have no such x-ray recommendation like the ACA has adopted. These groups are arguably in a better position to provide recommendations as they relate to and represent doctors with advanced training in spinal care and diagnosis. This list includes the American Academy of Orthopedic Surgeons, the American Academy of Physical Medicine and Rehabilitation, the North American Spine Society, the American College of Radiology, the American College of Surgeons, the American Medical Society for Sports Medicine, the American Society for Clinical Pathology, and the American Society of Clinical Oncology. These organizations have far more experience when dealing with x-rays and how they relate to treating patients for spine pain particularly in the diagnosis of spinal disorders. The ACA should have consulted with these groups before providing their recommendations for the Choosing Wisely program. Instead they sided with organizations consisting of non-spine specialties while choosing to ignore those with advanced training.
Plain film radiographs are clinically indicated to both asses anatomical (space occupying lesion, fracture, tumor or infection) and biomechanical pathology directed by thorough clinical evaluation. In the absence of an anatomical source of pathology and spine pain, associated it is critical that aberrant biomechanical motion is assessed. These paradoxical biomechanical diagnoses indicate failure of the surrounding spinal ligaments and/or tendons demonstrating the mechanical source of the ensuing nociceptive, mechanoreceptive and proprioceptive neuropathological cascade. Fedorak, Ashworth, Marshall, and Paull (2003) reported: “This study has shown that the visual assessment of cervical and lumbar lordosis is unreliable. This tool only has fair intra-rater reliability and poor interrater reliability. Visual assessment of spinal posture was previously shown to be inaccurate, and this study has demonstrated that is reliability is poor.” (4). In contrast, the reliability of x-ray in morphology, measurements, and biomechanics has been determined accurate and reproducible. Additionally, Ohara, Miyamoto, Naganawa, Matsumoto, and Shimzu (2006) reported, “Assessment of the sagittal alignment of the spine is important in both clinical and research settings… and it is known that the alignment affects the distribution of the load on the intervertebral discs”(5)
In a recent informal survey of 400 doctors of chiropractic nationally returning 152 responses asking “Does the clinical use of x-rays changes either your diagnosis, prognosis or treatment plan?” Out of 152 respondents, 98.42% of those surveyed, used x-rays in their clinical practices that changed either the diagnosis, prognosis and/or treatment plan for their patients. X-rays, and being able to visualize the biomechanical pathology in the absence of anatomical pathology, is vital to the chiropractic physician and the outcomes of their patients.
Some organizations, such as the American Association of Neurological Surgeons, have published recommendations stating, “Do not obtain spinal imaging for patients with acute “non-specific” low-back pain during the six (6) weeks after onset in the absence of red flags.” (6) Let us examine the term non-specific low back pain and how it relates to the clinical assessment of other professions outside chiropractic. Non-specific low back pain is low back pain without a known anatomical cause, meaning without structural pathology. Simply because there is no anatomical pathology present doesn’t mean the pain is “non-specific.” Doctors of chiropractic have long known the cause of non-specific low back pain, it has gone by various names, neuro-biomechanical lesions, biomechanical lesions, subluxation, vertebral subluxation complex, and spinal fixation.
Gedin et. Al (2018) reported, “it has been estimated that the vast majority of back pain cases is of non-specific origin. (7) The concept of simply focusing on the anatomical component of spine pain patients would render chiropractic no different than any other health profession. When focusing on the “non-specific” nature of spine pain, the focus must be on the biomechanical pathological component since the anatomical correlation is missing or does not correlate. The direction of care should be to the biomechanical compensation and individual motor units of the spine with a particular focus on spinal function and balance. Previous literature has verified that the supposition that “non-specific” is synonymous with “unobjectifiable” is erroneous since definite biomechanical changes in the motor units of the spine cause alterations of spinal balance, therefore resulting in “very specific” biomechanical pathology causing pain syndromes.
Panjabi in 1992, who had led the laboratory-based research into biomechanical spine pain, presented a detailed work explaining how the biomechanical systems within the human spine react to the external environment, how it can become dysfunctional and cause pain. He stated “Presented here is the conceptual basis for the assertion that the spinal stabilizing system consists of three subsystems, the vertebrae, discs, and ligaments constitute the passive subsystem, all muscles and tendons surrounding the spinal column that can apply forces to the spinal column constitute the active subsystem and finally, the nerves and central nervous system comprise the neural subsystem, which determines the requirements for spinal stability by monitoring the various transducer signals [of the nervous system] and directs the active subsystem to provide the needed stability.” He goes on to state, “A dysfunction of a component of any one of the subsystems may lead to one or more of the following three possibilities, an immediate response from other subsystems to successfully compensate, a long-term adaptation response of one or more subsystems or an injury to one or more components of any subsystem.” (8)
Panjabi continues, “It is conceptualized that the first response results in normal function, the second results in normal function but with an altered spinal stabilizing system, and the third leads to overall system dysfunction, producing, for example, low back pain. In situations where additional loads or complex postures are anticipated, the neural control unit may alter the muscle recruitment strategy, with the temporary goal of enhancing the spine stability beyond the normal requirements.” (8) Panjabi’s laboratory is where the idea of biomechanical compensation was conceptualized and proven.
Panjabi’s evidence summarized in the above work is the basis for the underlying mechanics of spine pain that does NOT correlate well to anatomical findings. Anatomical findings are fracture, tumor or infection and allopathy has labeled anything else inaccurately “non-specific.” This concept and approach to spine care continue to maintain a dogmatic perspective in both clinical decision making, provider reimbursement and all too often, the literature, despite compelling evidence to the contrary.
A recent study by Scheer et al. (2016) reports a biomechanical assessment of the spine as critical to spine care including spine surgery. This concept was originally presented at the 2015 AANS/CNS Joint Section on Disorders of the Spine and Peripheral Nerves. The authors state “The cervical spine plays a pivotal role in influencing adjacent and global spinal alignment as compensatory changes occur to maintain horizontal gaze. Concomitant cervical positive sagittal alignment (loss of cervical lordosis) in adult patients with a thoracolumbar deformity is strongly associated with inferior outcomes and failure to reach minimal clinically important difference at 2-year follow-up compared with patients without cervical deformity.” (9) Here we see additional evidence that spinal biomechanical modeling has an effect even in the presence of severe anatomical pathology requiring surgical intervention. In this case, it was even in an adjacent spinal region to the surgical site!
The scientific literature and certainly the surgical community is showing that thorough biomechanical assessment of the patient is a critical component to spine care, particularly in the complex spine pain patient. Without x-rays, the doctor is simply guessing.
One of the primary caveats stated in the ACA’s Choosing Wisely suggestions to not take spinal x-rays is the patient’s exposure to ionizing radiation. Patients routinely ask us about the radiation effects of x-rays, therefore it is imperative that we look at the facts, not the deceptive rhetoric that is so often quoted. According to a recent article from April 2018 by Harvard Health Publishing at Harvard Medical School titled Radiation Risk from Medical Imaging, they state that the average effective dose of a lumbar x-ray is 1.5 mSv. (10) According to the Radiological Society of North America in an article published April 2009 titled The Linear No-Threshold Relationship Is Inconsistent with Radiation Biologic and Experimental Data, they state “Among humans, there is no evidence of a carcinogenic effect for acute irradiation at doses less than 100 mSv and for protracted irradiation at doses less than 500 mSv.” They go on to state “There are potent defenses against the carcinogenic effects of ionizing radiation. Their efficacy is much higher for low doses and dose rates; this is incompatible with the LNT (linear no-threshold) model but is consistent with current models of carcinogenesis.” (11) As one can clearly see, the ionizing radiation effects of taking a set of lumbar x-rays is well below the minimum dosage to have a carcinogenic effect.
The following is a sampling of responses received by the Academy of Chiropractic, these responses were received from an informal survey of doctors of chiropractic nationwide. The instructions were to send over x-rays demonstrating ONLY ANATOMICAL PATHOLOGY and a brief history taken in their offices, many of which showed significant anatomical pathology in the absence of “red flags.” These responses underscore why the options for doctors of chiropractic should not be limited by politics, but instead should be driven by clinical assessment and scientific data. This myopic vision will create a public health risk and is integral in creating an accurate diagnosis, prognosis and treatment plan for our patients particularly in those patients with spine pain not specific to an anatomical lesion. As responsible doctors of chiropractic, we and the profession urge the American Chiropractic Association not to amend it's policy on Choose Wisely, but to rescind its x-ray “suggestions” in any and all formats. Furthermore, terminate all efforts in recommending anything other than each doctor follow their scope of practice in their respective states regarding the utilization of x-ray in clinical practice and the care of their patients. The chiropractic profession needs a strong political advocate and the American Chiropractic Association has historically been a major component in successfully filiing that need, however we need a powerful voice to unite us and not create further division within our profession or waste our valuable and limited resources.
NOTE: Below the references is visual evidence of why x-ray should not be limited in chiropractic
NOTE: The following does not comment or reflect biomechanical pathology or the negative sequela of having it go undiagnosed. That is a topic for a separate article.
The following is a sampling of responses we received from a survey of doctors nationwide 3 days prior to this publishing of this article. The instructions were to send over x-rays for ONLY ANATOMICAL PATHOLGY and a brief history taken in their office within the last 3 months. These responses underscore why the utilization for chiropractors should not be limited as it will create a public health risk and is integral in creating an accurate diagnosis, prognosis and treatment plan for our patients. As responsible doctors of chiropractic we and the profession urge the American Chiropractic Association to terminate all efforts in recommending anything other than each doctor follow their scope of practice in their respective states regarding the utilization of x-ray in clinical practice.
Abdominal Aortic Aneurysm
17 year old male with chronic mid back pain from high school wrestling. Found a compression fracture.
Burst Fracture - Metastatic Cancer
Patient presented upper lumbar pain, adamant that he was cancer free, no problems whatsoever, had been cleared by PCP and oncologist in past, just "needed an adjustment" and was actually rather angry that I would not perform adjustment or treat the day of his exam.
C2 Dens Fracture
This patient is a 25-year-old female with a history of a roll-over accident 10 years ago and recurrent neck pain. During history she said "I think they said something about a neck fracture".
Lumbar Transverse Process Fracture
This patient was referred by an ENT/Facial Plastic Surgeon for evaluation of TMJ/Neck pain. The patient had the mass surgically removed.
Patient was experiencing lower extremity radicular pain. Saw a PT 6 times and a DC 6 times with no relief. Then came to me. I found the Spondylolisthesis. He is doing great without any symptoms now.
L5 Metastatic Cancer
Onset of low back pain and sciatica. X-ray revealed enlargement of L5 spinous process. Patient was reluctant to get MRI. And then I had to fight with insurance carrier to get it authorized. But the x-rays revealed a problem. MRI confirmed metastatic lesion L5-S1 and posterior elements of L5.
Anterior Cervical Discectomy and Fusion
Patient came in complaining of neck pain. Never once stated a prior neck surgery in either the paperwork or when asking about past surgeries.
Congenital Fused Vertebra
C2 Dens Instability
54 year old male delivery driver, acute on chronic onset of low back pain constant 7/10 and neck pain intermittent 5/10 for years. Seen by numerous chiropractors and medical doctors for 30+ years, taking medication for psoriasis. Patient stated that he did not need x-rays just an adjustment and he would be on his way. After x-rays I told the patient go to Kaiser and see a neurosurgeon, I refused to treat and showed him the instability. He protested and said "you are just a f_ _ _ing chiropractor and I have seen many medical doctors over the years and no one has told me anything like I might need surgery. I called him later that day and he did go to Kaiser hospital and was seen immediately a spine specialist.
Thoracic Compression Fracture
56 year old male lifting heavy coffee table 1 week prior, mid back pain acute. No insurance, did not want to spend the money on x-rays. No significant health history.
Lumbar Anterolisthesis of L3
Spinal Fusion from T1-L3
I was asked by an attorney to review a case of a 16 year old female with persistent headaches and neck pain with bilateral paresthesia in her left and right hands. He said he doesn't think she has much of a case. She was involved in a side collision with a pickup truck with a plow in a 30 mph zone. She was evaluated with CT of head and X-rays of neck and back and released by Children's hospital the same day. She has undergone a year of physical therapy for cervicalgia and neurologist for post traumatic headaches. She has 6 degrees of active extension with pain and 48 degrees of active flexion with pain. So I asked for the hospital records including copies of diagnostic imaging for my review. The cervical spine imaging report stated: "unremarkable cervical radiograph without evidence of acute osseous abnormalities." Well I have attached the lateral view for you, which I must strongly disagree with and contacted the radiologist regarding. He asked me at first why I was reviewing the films. I stole your line and said "real doctor's read their own films, would you want a surgeon doing surgery on you without looking at the films." The reply was "good point." He also agreed to write the addendum. I then advised the attorney of my findings and the text message said, "HOLY S!@#! WOW that makes so much sense."
17 year old female presented with lower back pain after baton twirling practice. No trauma. Spondylolysis of L4 most visible on the right posterior oblique.
Note multiple pathologic compression fractures and lysis of right ischial tuberosity. Turned out to be multiple myeloma, Stage 4. L3 is post vertebroplasty.
68 year old male with severe low back and right leg pain. Radiographs exhibit dextrocurvature, severe degeneration and a grade1-2 spondylolisthesis.
AC Joint Separation
Fractured Styloid and Radius
Low-Speed Damages and Injuries
Patrick Sundby, Accident Investigator
Mark Studin DC, FASBE(C), DAAPM, DAAMLP
We have discussed the fallacy of “no damage = no injury” in depth in other papers, but as a reminder, we are interested in the relationship between injury and force experience, not damage induced. The phrase “no damage, no injury” is no more than “deceptive rhetoric” and draws a false causal relationship because it is based in subjective interpretation, dogmatic beliefs and too often, who is paying for your opinion. The extent of the damage, as viewed by each person, varies based on each person’s perspective. For example, what color is the square on the left?
What color is the square on the right?
The majority of the viewers of this article should say the squares are blue, but is it possible someone else sees the colors differently? What if this article was read in print form in black and white? What if the screen settings on a reader’s computer were out of adjustment? What if a reader has a condition which alters the way they see certain colors?
Taking the last variable, if the person with the condition sees the squares as something other than blue, are they wrong? No. To him/her, they genuinely see something else. This example demonstrates the subjective interpretation of the two colors presented to you in the squares.
So how do you resolve this subjective approach to the colors? You need to use an objective standard to gauge the colors against thus allowing you to determine if the colors presented are indeed blue.
In the electromagnetic spectrum, there is a small window in which visible light is located.
Within this small window, modern science has defined the wavelengths of different colors.
Rather than debating the colors of the two squares we can measure the wavelengths and compare them to the objective standard if both squares measure between 450 and 495 nm (nanometers) then both squares are indeed blue.
In the same sense of objectively defining colors, we need to objectively define the relationship between damage and injury. This relationship is defined, objectively, through force. If we can quantify the forces exerted on the vehicle (and by extension the occupant), then we can objectively compare those forces to known standards for injury. This MUST BE the method for defining the causal relationship between a vehicle collision and occupant injury vs. relying on dogma, rhetoric and financially influenced opinions because it relies on physics and the inherent mathematical facts.
Imagine being in a high-risk category for cancer and when at an appointment the doctor stands back, looks you up and down - while clothed, and says “you don’t look sick therefore you don’t have cancer.” This is the same practice when reconstruction is done via an insurance estimate. Ask yourself, how can you possibly know the extent of the damage to a vehicle when you didn’t even remove the bumper cover? When we consider the recent Allstate’s “QuickFoto Claim” where you take a picture of the accident, and they send you a check is a brilliant business move. The unsuspecting claimant thinks that getting a check quickly is a resolution of the damages to their car without ever inspecting the damages below the “skin of the car.”
When considering transference of forces and potential bodily injury, after a complete vehicle exam is done, we can assign a known value for the vehicles change in acceleration. This process can take place via a few avenues. For the sake of this paper and topic, we are going to use the Coefficient of Restitution (CoR).
If we can determine the post-impact speeds, we can then mathematically work the pre-impact speed for the striking vehicle thus eliminating any unknowns. Finally, we can check the work and ask if the results appear reasonable. (Remember 30 divided by 100 is also .3)
Consider the following case:
In this event, we have a typical lower speed collision. This vehicle was rear-ended while stopped and the occupant suffered injury. Further, there is the ever-present claim that “little/no damage = no injury.”
There is clear damage to the bumper cover and rear liftgate as well as some panel fitment issues at the corners. I’m highly suspect if we examined the structure of the bumper, we would find more evidence of the collision, and this would further support an appropriate CoR. After an examination of the vehicle, we could reasonably assign a high CoR to this event and work backward to the striking vehicle’s impact speed. While this would be of interest and worth exploring, we have complete tasks similar to this in previous discussions. This collision is important as there is a second and more specific point highlight. Consider the interior shot of this vehicle.
Consider what the chunk of missing steering wheel tells us. First, we know your average person doesn’t have the strength to tear the steering wheel. We can conclude the force of the collision did this, but how? The occupant was holding the wheel when the vehicle was struck. The collision accelerated the vehicle forward, and the occupant did not move at the same time. Once the occupant had “stretched out,” (the slack or bent arms at rest was gone) the force of the collision was translated to the steering wheel through the occupant. The question is, how much force?
The forces experienced by the steering wheel would be whatever percentage of body weight the occupant had in the torso times the “g-forces” calculated. In simpler terms, if the upper body of the occupant weighed in at “X” pounds, the steering wheel experienced this weight times the g-force. Take a quick second and consider if you had the steering wheel in your hands, what could you do to break it in a similar nature? Jump in it? Have a friend hold one side and pull? What does it really take to do damage like this? This concept is a bit of a trick question, any answer you provide is subjective – lets objectively try to determine the forces at play. This is where you put aside pre-conceived “beliefs” and allow the mathematics of physics to render answers because there are no beliefs in math equations.
When we examine the nature of a low-speed event, we will have to determine the g-forces the occupant experiences. For this example, we will utilize the following the following equation:
Initially, it appears very high values can be substituted, and the formula would still be correct. However, this doesn’t pass a sanity test. While the striking vehicle is not provided, we are assuming it’s the same or negligibly different from the KIA. We know the collision is not 100% efficient so the post-impact speed of vehicle two being 10 mph is not reasonable. In the same sense, the post-impact speed for vehicle one being zero is also not reasonable. (WHY?) We are going to use eight and two, respectively.
If the KIA was accelerated to 8 mph (11.76 fps), we could determine the g-forces be 3.65 at the lumbar spine. We also know the forces experienced at the cervical spine can be two to three times more than the lumbar, 7.3 to 10.95, respectively. These forces greatly exceed a plethora of known standards for cervical spine injury.
The process we just went through provides an objective conclusion for the forces that acted on the vehicle, and ALL of these values are a reasonable fit for the damage profile.
There is one final consideration, the broken steering wheel. The occupant holding the steering wheel would have forces act on them differently likely resulting in different injuries or increasing the forces acting on the body. A case-by-case evaluation for each collision and each occupant is a necessity to thoroughly and accurately establish the objective relationship between the forces the vehicle experienced and the forces the occupant experienced – Indeed, “no damage = no injury” is a myth.
Deceptive Dogmatic Reporting Despite Successful Chiropractic Outcomes
Revealing the deception of low back pain naturally resolving
…and the dogma of non-specific back pain
Mark Studin, DC
William J. Owens DC
Timothy Weir, DC
Citation:Studin M., Owens W., Weir T. (2018) Deceptive Dogmatic Reporting Despite Successful Chiropractic Outcomes, American Chiropractor, 40 (11) 10, 12-15
A report on the scientific literature
Over the past decade, there has been a growing body of evidence demonstrating the “how and why” of chiropractic evidenced-based results. However, there has also been a historical level of reporting dogmatic issues related to the “the natural history of back pain” and “non-specific back pain” that deceptively enter and intersect the conversation to apparently discredit “pro-chiropractic” evidenced-based research that has persisted in contemporary literature. This review is centered on those issues, and the references for the above comments will ensue in the paragraphs below.
The National Institute of Neurological Disorders and Stroke reports “Most low back pain is acute, or short-term, and lasts a few days to a few weeks. It tends to resolve on its own with self-care, and there is no residual loss of function.”
https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Low-Back-Pain-Fact-Sheet. Kaiser Permanente, a national health system reports, “For most patients with back pain, the condition will improve within a few days or weeks.” https://wa.kaiserpermanente.org/static/pdf/public/guidelines/back-pain.pdf
Kaiser Permanente goes on to report, “The primary goal of treatment is to maximize function and quality of life, rather than to eliminate pain. Some ongoing or recurrent pain is normal and not indicative of a serious problem. Avoid exposing the patient to unhelpful or possibly risky interventions. As a general rule, an intervention in which the patient is an active participant (e.g., physical therapy, walking, stretching, yoga) rather than a passive recipient (e.g., chiropractic, massage, acupuncture) is deemed to have greater potential to promote self-efficacy and self-management skills in the long term.”
Gedin, Edmar, Sundberg, and Burström in 2018 reported “Patients with acute back pain reported statistically significant and MCID (Minimal Clinically Important Difference) improvements in back pain intensity, back disability, HRQoL (Health-Related Quality of Life instrument), and statistically significant improvements in self-rated health, over four weeks following chiropractic care. Patients with chronic back pain reported statistically significant, albeit smaller and non MCID, changes for all PRO except self-rated health.
Interestingly, Gedin et al. have a significant level of statistics of demonstrating percentages of subjects who showed improvement and choose not to report that in the written part of the report, thereby not rendering a statistical interpretation. However, they included a caveat to perhaps minimize the positive results by reiterating the same deceptive dogma as discussed above. Gedin et. al then reported “However, it has been suggested that 90% of patients with acute low back pain recover within six weeks (van Tulder et al., 2006), which may also help explain the current findings of rapid improvements.(pg. 16) This opinion published in 2018 was referenced and supported by a 12-year old study which clearly ignored the contemporary literature.
Tamcan, Mannion, Eisenring, Horisberger (2010) reported on the only population-based study these authors were able to identify and concluded “When the 12-month follow-up period was divided into four equal time periods and, subsequently, clusters, it was seen that the majority of individuals placed in the moderate persistent [pain] cluster on the basis of the first 3 months data remained in this cluster at the following intervals. A reasonable consistency across time was also found for the clusters mild persistent and severe persistent. In contrast, the consistency of membership for the cluster initially identified as fluctuating was low, especially after six months.” (pg. 455-456) This study, which again is the only identified population-based study indicates that pain does not resolve “naturally” as was reported: “fluctuation was low, especially after six months.”
Knecht, Humphyres and Wirth (2017) reported on the recurrence of low back pain and stated, “Only 1 in 3 LBP (low back pain) episodes completely resolve within a year, and the percentage of LBP that goes from acute to chronic varies among studies from 2% to 34%.” Knecht et. Al (2017) also went on to report “Patients presenting with a subacute problem, lasting for more than 14 days at baseline, were at higher odds for a recurrent course, whereas the odds for a chronic course were higher only for patients presenting with a chronic problem (≥3 months) at baseline. Downie et al. reported that pain duration of more than five days was a factor that negatively affects prognosis. Similarly, duration of the current episode emerged as the most consistent factor for prognosis after one year in a study by Bekkering et al. and even predicted disability after five years. These findings suggest on the one hand that it might be prudent to seek professional advice [referenced chiropractic care in the article] early on in the pain episode.” (pg. 431)
These papers a part of the research trend supporting what the chiropractic profession has known all along, the natural progression of low back pain resulting in resolution is based on dogma and not supported by the research evidence. Additionally, the low back pain care path reported previously by Kaiser Permanente appears to be biased towards the denial of care and not consistent with the published literature.
Gedin et. Al (2018) also report, “it has been estimated that the vast majority of back pain cases is of non-specific origin.” (pg. 3) The concept of simply focusing on the treatment of non-specific back pain would render chiropractic no different than physical therapists when focusing on the “non-specific” nature of spine pain as the arbiter for care while the focus must be on the biomechanical compensation and individual motor units of the spine. Previous literature has verified that the supposition that “non-specific” is synonymous with ‘unobjectifiable” is erroneous since it was previously reported that chiropractic treats definite biomechanical changes in the motor units of the spine, therefore resulting in “very specific” biomechanical pathology.
Panjabi in 1992, presented a detailed work explaining how the biomechanical systems within the human spine react to the environment, how it can become dysfunctional and cause pain. He stated “Presented here is the conceptual basis for the assertion that the spinal stabilizing system consists of three subsystems, the vertebrae, discs, and ligaments constitute the passive subsystem, all muscles and tendons surrounding the spinal column that can apply forces to the spinal column constitute the active subsystem and finally, the nerves and central nervous system comprise the neural subsystem, which determines the requirements for spinal stability by monitoring the various transducer signals [of the nervous system] and directs the active subsystem to provide the needed stability.” He goes on to state, “A dysfunction of a component of any one of the subsystems may lead to one or more of the following three possibilities, an immediate response from other subsystems to successfully compensate, a long-term adaptation response of one or more subsystems or an injury to one or more components of any subsystem.”
Panjabi continues, “It is conceptualized that the first response results in normal function, the second results in normal function but with an altered spinal stabilizing system, and the third leads to overall system dysfunction, producing, for example, low back pain. In situations where additional loads or complex postures are anticipated, the neural control unit may alter the muscle recruitment strategy, with the temporary goal of enhancing the spine stability beyond the normal requirements.” (pg. 383) This is where the idea of biomechanical compensation was identified.
Panjabi’s lifelong work summarized in the above work is the basis for the underlying mechanics of spine pain that does NOT correlate well to anatomical findings. Anatomical findings are fracture, tumor or infection and allopathy has labeled anything else “non-specific low back pain” which continues to maintain a dogmatic perspective in both clinical decision making and all too often, the literature, despite compelling evidence to the contrary.
Cramer et al. (2002) further clarified the biomechanics of spinal failure at the motor until level and reported, “One component of spinal dysfunction treated by chiropractors has been described as the development of adhesions in the zygapophysial (Z) joints after hypomobility. This hypomobility may be the result of injury, inactivity, or repetitive asymmetrical movements… one beneficial effect of spinal manipulation may be the “breaking up” of putative fibrous adhesions that develop in hypomobile or ‘fixed’ Z joints. Spinal adjusting of the lumbar region is thought to separate or gap the articular surfaces of the Z joints. Theoretically, gapping breaks up adhesions, thus helping the motion segment reestablish a physiologic range of motion.” (p. 2459)
Evans (2002) reported, “on flexion of the lumbar spine, the inferior articular process of a zygapophyseal joint moves upward, taking a meniscoid with it. On attempted extension, the inferior articular process returns toward its neutral position, but instead of re-entering the joint cavity, the meniscoid impacts against the edge of the articular cartilage and buckles, forming a space-occupying ‘ lesion’ under the capsule: a meniscoid entrapment. A large number of type III and type IV nerve fibers (nociceptors) have been observed within capsules of zygapophyseal joints. Pain occurs as distension of the joint capsule provides a sufficient stimulus for these nociceptors to depolarize. Muscle spasm would then occur to prevent impaction of the meniscoid.” (pg. 252)
Evans (2002) continued, “an HVLA manipulation, involving gapping of the zygapophyseal joint reduces the impaction and opens the joint, so encouraging the meniscoid to return to its normal anatomical position in the joint cavity. This ceases the distension of the joint capsule, thus reducing pain.” (p. 253)
The involvement of nociceptors and nociceptive impulses stimulates the cortical regions of the brain which evokes a cortical response to that noxious stimuli. Haavik et al. (2017) reported the effects of a chiropractic spinal high velocity-low amplitude adjustment by stating “These results are consistent with previous findings that have suggested increases in strength following spinal manipulation were due to descending cortical drive and could not be explained by changes at the level of the spinal cord.” (pg. 1)
The persistent utilization of “non-specific” in reference to specific biomechanical alterations and failure in the human spine is dogmatic and deceptive since it “lumps together” all types of manual treatment, where chiropractic, based upon its unique application differs from other forms of manual therapy performed by physical therapy, acupuncture, and massage therapy. It differs in the ability of chiropractors to diagnosis and manages spinal compensation. In comparison to each other, each discipline is disparate in goals, application, and science and when not considered as such, lends itself to continue deceptive dogmatic arguments ignoring the evidenced-based truths of chiropractic.
CASE REPORT: SEVERE DISC HERNIATION WITHOUT RADICULAR SYMPTOMATOLOGY
Richard A. Laviano DC
The patient was a very pleasant 43-year-old male presenting to the clinic with acute onset of low back pain that started 7 days ago after performing some heavy lifting at work. The pain was in the lumbosacral region and right sacral leg joint region and surrounding musculature that radiated into the posterior aspect of the right leg. No numbness or tingling was present. No loss of bowel or bladder control. Any type of movement that involves bending and twisting greatly exacerbates the pain. The pain is constant and especially worse in the mornings. The patient presented with inability to fully weight-bear on the right leg and thus presented with a right limp.
The patient indicated that he had not experienced prior symptoms similar to his current complaints and was symptom-free at the time of the incident above. The patient’s medical, surgical, and family history was unremarkable. He is a healthy Hispanic male.
His superficial appearance did not indicate any apparent distress. Further, observation showed minor’s sign to be present. This sign is present when the patient, in arising from a chair, leans forward, jackknifing the thighs and the dorso-lumbar spine so that the head is over the feet. Using the hands on the thighs or the arms of the chair, the patient pushes the body to an upright position, thus sparing lower limb effort. The presence of this sign is usually indicative of sciatica. There was no apparent spine tilt with him standing upright.
The patient was 5 feet 8 inches at 156 pounds, well-developed with a body temperature of 99.2°F. His blood pressure was slightly elevated at 149/81 mm Hg and a heart rate at 72 beats per minute. On examination, the eyes, ears, and throat appeared normal.
Gait analysis reveals complete loss of normal gait pattern greatly favoring his left leg.
The patient’s range of motion was decreased in all ranges with pain and spasm in the erector spinae muscles including the iliocostalis lumborum and iliocostalis thoracics muscles bilaterally. Muscles of the lower extremity were 5 out of 5 for all muscles in the left leg. A 3 out of 5 test was noted in right anterior tibialis muscle and right extensor hallucis longus muscle. No atrophy was noted. The patient’s deep tendon reflexes of the upper and lower extremities were noted to be a 2+ rating bilaterally for patellar and Achilles. Cranial nerve testing also showed to be normal. The patient had normal sensation symmetrically and bilaterally.
Orthopedic testing showed positive straight leg raise test both in the supine and seated position (slumps) with reproduction of patient shooting pain along the posterior aspect of the right leg with a patient audible response due to the severity of pain. Bechterew’s test also showed positive on the right side.
Palpation of the lumbar spine showed tenderness along L3-L5 facet joints and surrounding musculature. Spasming noted in during palpation of the erector spinae muscles bilaterally. Edema is noted in this region as well.
A full spine weight bearing radiographic study was taken (utilizing views: APOM, AP cervical, AP Thoracic, AP lumbopelvic, lateral cervical, lateral thoracic, and lateral lumbar). An MRI of the lumbar spine was also ordered immediately before beginning treatment. See figures below.
The radiographic study showed loss of normal lumbar lordosis consistent with an acute injury. No degenerative changes are present. Neural foramina appear patent. No evidence of fracture or dislocation. A moderate left list of the lumbar spine is noted consistent with a disc injury. Acetabular joints appear normal. The adjacent soft tissue appears normal.
Image 1 – loss of lumbar lordosis with left list, Antalgia, seen on radiograph.
Magnetic Resonance Imaging:
MRI Study was reviewed, and findings included: Marrow edema was normal with no signs of fracture. The vertebral alignment showed loss of normal lumbar lordosis and caddy lever appearance of L3 on L4. Hemangiomas noted at L1 and L5 in trabecular bone vertebral bodies. Conus medullaris and cauda equina appear normal. There is a T2 hyperintense signal cystic structure noted at the posterior aspect of the conus medullaris at T12-L1. This is incompletely evaluated in this study. L1-L2 appears normal with no stenosis of the neural foramina or central canal. L2-L3 shows posterior central annular fissure. The high signal in this fissure indicates it is acute. No central canal or neural foraminal stenosis. L3-L4 showed mild disc bulging with a superimposed right paracentral disc extrusion1 at L3-L4 with migration inferior-ward displacing the thecal sac and the fourth lumbar nerve root before it reaches the L4-L5 neural canal on the right. L4-L5 shows moderate disc bulging with a superimposed posterior left paracentral disc protrusion type herniation with an annular fissure. Due to the high signal in this fissure, it is most likely acute. L5-S1 appears normal with no central canal or neural foraminal stenosis. Recommendations included a thoracic spine study to assess cystic lesion as noted above. Immediate neurosurgical consultation is also recommended. See Images 2 through 5 below.
Image 2 – extrusion herniation with inferior migration.
Image 3 – displacement of thecal sac posteriorly on the right side.
Image 4 – compression occurring just before neural canal but displacing L4 nerve.
Image 5 – Neural Canals are patent.
After MRI results were reviewed patient was immediately referred for a neurosurgical consult. Neurosurgical consultation recommended that the patient is removed from his repetitive occupation for 2 weeks and begin oral steroid treatment. After a few weeks, the patient reported that he had significantly improved and is now able to perform all activities of daily living including work with no discomfort. Based upon the neurosurgeon’s recommendation, collaborative care with chiropractic treatment will commence ensuring biomechanical stability.
NOTE ON STEROID USE WITH MECHANICAL SPINE ISSUES: Goldberg et al. (2015) reported: Despite conflicting evidence, epidural steroid injections are frequently offered under the assumption that radicular symptoms are caused by inflammation of the affected lumbar nerve root. Epidural steroid injections are invasive, generally, require a pre-procedure magnetic resonance imaging (MRI) study and expose patients to fluoroscopic radiation. Also, the US Food and Drug Administration recently warned of rare, but serious neurologic sequella from [epidural steroid injections]. Oral administration of steroid medication may provide similar anti-inflammatory activity, does not require an MRI or radiation exposure, can be delivered quickly by primary care physicians, carries less risk, and would be much less expensive than an [epidural steroid injection]. Oral steroids are used by many community physicians, have been included in some clinical guidelines, and are noted as a treatment option by some authors. However, no appropriately powered clinical trials of oral steroids for radiculopathy have been conducted to date. To address this issue, we performed a parallel-group, double-blind, randomized clinical trial of a 15-day tapering course of oral prednisone vs. placebo for patients with acute lumbar radiculopathy associated with a herniated lumbar disk... (p. 1916).
Results showed that “participants in both blinded treatment groups showed an improvement in symptoms over the initial 6 weeks, with more gradual reductions until the 24-week visit, after which changes were more variable. Baseline ODI [Oswestry Disability Index] scores were 51.2 and 51.1 in the prednisone and placebo groups, respectively; corresponding ODI scores at 3 weeks were 32.2 and 37.5” (Goldberg, 2015, p. 1919-1920). This indicates that both at 3 and 6 weeks there was no difference in the placebo vs. oral steroid groups. “Among patients with acute radiculopathy due to a herniated lumbar disk, a short course of oral steroids, compared with placebo, resulted in modest improvement in function and no significant improvement in pain” (Goldberg, 2015, p.1922)
Although the patient presented with some classical signs of disc injury, some signs of disc injury were not present: Antalgia, numbness or tingling in the lower extremity or loss of bowel or bladder control. The outstanding feature of this case was the motor deficit noted in the right anterior tibialis and right extensor hallux longus muscle both having their roots in L4 and L5. It is important to note, however, that positive orthopedic testing with production radicular pain without motor or sensory loss is still an indication for advanced imaging particularly with straight leg raise (SLR) and slumps test3. One study showed that adding hyperextension test and Bell test to the straight leg raise test have shown to be more sensitive and specific than the SLR test alone4. The patient had not been evaluated by any other physician before being evaluated by us. This is a clear example although the patient did not have all the signs indicating acute disc injury, severe disc injury indeed occurred. The patient’s inability to axial load during a range of motion testing is also demonstrated by the two acute annular fissures as noted above. Chiropractic manipulation is contraindicated in this case due to the severe extruded disc at L3-L4 with migration. Advanced imaging, particularly Magnetic resonance imaging, in this patient’s case significantly improved our ability to give an accurate diagnosis and prognosis of their condition.
CASE REPORT: Chiropractic High Velocity-Low Amplitude Adjustments in the Presence of a Herniated Disc without Compromise of the Cauda Equina
By: Steve Lininger, DC, CICE
TITLE: Chiropractic High Velocity-Low Amplitude Adjustments in the Presence of Herniated disc without Compromise of the Cauda Equina
Abstract: The objective was to demonstrate where an MRI was initially utilized to diagnose a lumbar herniated disc with no evidence of compromise of the cauda equina, and the patient was then subsequently safely and effectively treated with chiropractic high velocity-low amplitude adjustments.
Background: (1) High-Velocity Low Amplitude (HVLA) thrust techniques are among the most commonly used manipulative treatment techniques. (2) Most patients do not experience significant adverse effects following the use of these techniques. (3, 4) There is currently no strong evidence to suggest that HVLA thrust techniques should not continue to be used, where applicable, by appropriately trained and competent practitioners. (5) In a major study, Eighty Percent (80%) of the patients studied had a good clinical outcome with post-care visual analog scores accompanied with resolution of abnormal clinical examination findings (following chiropractic care). Anatomically, after repeat MRI scans, Sixty-Three percent (63%) of the patients studied revealed a reduced size or completely resorbed disc herniation (following chiropractic care) (5).
Key Words: Chiropractic, Spinal Adjustment, MRI, Herniation
Introduction: A 39-year-old male patient presented to our clinic on 05/30/17 with; lower back pain, weakness, burning in his left leg, and pains that radiate from his lower back into his left leg. The patient reported that he had lower back and left leg symptoms for approximately the past two months. The patient reported that he had previously been treated by two practitioners before arriving at our clinic with little to no changes in pain levels or function. The patient stated that he had also been having symptoms of irregular balance and painful and limited sexual relations due to pain.
The patient initially reported 5 out of 10 lower back pain on the verbal analog scale, as well as radiating left leg pains.
History: The patient states that he did not have any back or left leg pains prior to the initial episode of two months. There were no reported injuries or traumas.
Objective Findings: An examination was performed and revealed the following:
Vitals: 157/112 Blood Pressure. Pulse is 76 beats per minute. Temperature is 99.5F.
Range of Motion:
Lumbar Motion Studies:
Flexion: Normal = 90 Exam- No pain present.
Extension: Normal = 25 Exam- No pain present.
Left Lateral Bending: Normal = 25 Exam- Pain present at above 10 degrees and spasms.
Right Lateral Bending: Normal = 25 Exam- Pain present at above 10 degrees and spasms.
The Orthopedic testing revealed the following positive orthopedic tests in the lumbar spine: Lasegue’s Straight Leg Raise Test with pain located at the L5/S1 level, Straight Leg Raise Test with pain located at the L5/S1 level, Valsalva’s Test indicating the presence of a space-occupying lesion at the Lower lumbar region.
The Neurological examination revealed normal 5/5 = Full range of Motion / Maximum Strength in the; Quadriceps, Hamstrings, Calfs, and Extensor Hallicus Longus muscle regions. Hammer reflex testing revealed 2+ = Normal reflex findings in the; Patella and Achilles reflexes. Pinwheel dermatome testing revealed abnormal Left-Sided Hypoesthesia in the following levels; L1, L2, L3, L4, L5, and S1. The patient was unable to perform the Heel Walk over a three-foot range.
Because of the patient’s symptoms of; radiating and burning left leg pains, which clinically correlated with the patient’s objective findings of; Left-sided Hypoesthesia upon at L1, L2, L3, L4, L5, and S1 demonstrated upon pinwheel dermatome testing, a Lumbar MRI was ordered on 05/30/17 to diagnose lumbar disc pathology.
The MRI images were personally reviewed. The lumbar MRI revealed a lateral protrusion-type herniation at the level of L5/S1 with impingement on the left S1 nerve root. Additionally, there is a left lateral disc protrusion-type herniation with a torn annulus at L4/5 with no nerve root impingement. There is disc bulging at the; L3/4, L4/5, and L5/S1 levels.
Lumbar MRI Studies
After reviewing the history, examination, and MRI’s, it was determined that chiropractic adjustments were clinically indicated with modalities including; intersegmental traction, electric muscle stimulation, wobble chair exercises, and standing on a vibration platform. Diversified technique adjustments combined with “Pettibon” Rehab equipment and protocols were used to adjust the subluxation diagnosed levels of; C4, C5, T4, and T5, L4, L5. Although there were herniated and bulging discs present in the lumbar spine there was no compromise of the cauda equina. Therefore; there was no contradiction to performing a spinal adjustment because there is no stenosing of the cauda equina present on the MRI or root involvement in the central canal. As long as there is enough space between the cauda equina and the herniation or bulge then performing chiropractic adjustments are a reasonable treatment protocol.
Lumbar Motion Post-Treatment Physical Examination:
Flexion: Normal=90 Exam- 90 with no pain
Extension: Normal=50 Exam- 25 with no pain
Left Lateral Bending: Normal=25 Exam- 25 with no pain
Right Lateral Bending: Normal=25 Exam- 25 with no pain
The patient responded favorably to the spinal adjustments and therapies over the course of three months of care. During the treatment plan, the patient was seen three times weekly, and a reevaluation was performed approximately every thirty days. At the end of the third month, the patient demonstrated subjective and objective improvement. The patient demonstrated; decreased spasms and tender points, decreased pain scores, an increase in the ability to perform ADL’s with a normal sleeping schedule. The patient states that he no longer had the same difficulties with sexual performance and daily work and home activities. His Oswestry Disability Questionnaire score which was initially a 68%, reduced to 0%. His verbal analog scale which was initially a 5 out of 10, reduced to a zero out of ten. His pinwheel test dermatomal findings demonstrated normal findings at the end of his care plan. The patient is now able to Heel Walk over a three-foot range.
The patient presented two months post the onset of symptoms. The symptoms were constant and idiopathic. The pain was located in the lower back and the left leg. The history and examination indicated the presence of a space-occupying lesion in the lumbar region. Lumbar MRI was ordered, and two lumbar protrusions were detected at the L4/5 and L5/S1 levels as well as disc bulges at; L3/4, L4/5, and L5/S1 levels. Because the herniations and bulges were not compromising the cauda equina, it was safe to adjust the lumbar spine (6). The patient after chiropractic care went from a 5 out of 10 on the verbal analog scale to a 0 out of 10 and regained full ranges of motion in the lumbar spine with no residual pain upon movement.
Competing Interests: There are no competing interests in the writing of the case report.
De-Identification: All of the patient’s data has been removed from this case.
Efficacy of Chiropractic Treatment for Post-Surgical Continued Low Back and Radicular Pain
81% of chiropractic post-surgical patients showed greater than 50% reduction in pain.
Mark Studin DC
William J. Owens DC
A report on the scientific literature
Park et. Al (2016) reported that low back pain radiating into the lower extremities have greater impact on disability and time off work that any other medical condition. Vleggeert-Lankamp, Arts and Jacobs (2013) reported “The term ‘failed back surgery syndrome’ (FBSS) is used to describe a clinical condition defined by persistent or recurrent complaints of leg pain and/or back pain regardless of one or more surgical procedures of the lumbar spine. The definition of FBSS (failed back surgery syndrome) is modified by some authors by adding that at least one surgical intervention was to be performed and that pain should persist after the last surgical intervention, for at least one year.1 The term implies that the surgery plays a role in the cause of the pain, although in most cases the surgical intervention was technically successful. It is known that nearly 20% of patients undergoing spine surgery will require secondary surgery for persistent pain or surgery-related complications during the subsequent years.” (pg. 48) El-Badawy and El Mikkawy (2016) reported that failed back surgery syndrome occurs with lateral disc surgery upwards of 17%, spinal stenosis 29% and instability 14.8%.
Perhaps the reason for failed back surgery syndrome is what the surgeons have considered their “gold standard, fusion and the ensuing loss of mobility of the spinal motor unit. Mulholland (2008) reported “Spinal fusion became what has been termed the “gold standard” for the treatment of mechanical low back pain, yet there was no scientific basis for this.” (pg. 619) The history of spinal fusion is both fascinating and disturbing and reveals why chiropractic both helps post-surgical cases and should always be considered first, prior to surgery as an option.
Mulholland (2008) continued:
In 1962 Harmon presented a review paper at the western orthopaedic association meeting in San Francisco, in which the term “Instability” appears.
However, Harmon’s description of what he meant by instability (unfortunately in a footnote) is revealing “Spinal instability refers to a low back-gluteal-thigh clinical triad of symptoms that may be accompanied (overt cases) by incapacitating regional weakness and pain. This is the effect of disk degeneration with or without disc hernia. Some may be asymptomatic or slightly symptomatic when instability is compensated by muscle or ligament control. It does not refer to spinous process or laminal hypermobility which some surgeons like to demonstrate at the operating table nor does this clinical concept parallel the common spinal hypermobility, which is the product of intervertebral disc degeneration, demonstrable in flexion-extension filming of the region, since the anatomic hypermobility is not always productive of symptoms”
Sadly this description of instability appears to have been ignored, and the concept of mechanical instability as a cause of back pain was progressively accepted. Harmon’s view of the effect of fusion was that it cured pain by reducing the irritation of the neural contents produced by movement. His paper was influential as he emphasized the importance of appropriate investigations prior to fusion and the segmental nature of back pain but unfortunately his use of the term instability was interpreted as supporting the view that segmental abnormal movement was the cause of the pain.
In 1965 Newman in an editorial concerning lumbo-sacral arthrodesis (surgical immobilization) refers to the need to stabilize the lumbar spine in patients with back pain after discectomy for a lumbar root entrapment.
At the beginning of the seventies the perception was that disc degeneration led to abnormal translational movement, and this was painful.
McNab in 1971 who had done much work on the disturbance of movement in the degenerate disc described what he termed the “traction spur,” a particular type of anterior osteophytes which he said was related to an abnormal pattern of translational movement. This view again supported the concept of instability. He added the important caveat that it “was impossible to establish the clinical significance of the traction spur as a statistically valid investigation the traction spur was revisited in the late eighties and was shown to be no different to claw osteophytes, and often both would be present in the same patient. It was not related to abnormal movement.”
Although McNab used the term instability, he used it in the sense that the spine was vulnerable to acute episodes of pain, because the degenerate disc rendered it more easily injured. He did not view it as a cause of chronic back pain.
Kirkaldy Willis set out his views on instability in 1982. In “Instability of the Lumbar Spine” he described the process of disc degeneration as passing through a stage of dysfunction, (intermittent pain), instability which caused more persistent pain but then with time stabilizing to a painless state. This was his explanation for the observed fact that many very degenerate discs were painless. However, he at that stage was somewhat unhappy with an entirely mechanistic view for pain. Hence, he writes “Instability can be defined as the clinical status of the patient with a back problem who with the least provocation steps from the mildly symptomatic to a severe episode”. Further he writes “Detectable increased motion does not always solicit a clinical response, and that abnormal motion may be abnormal increase or abnormal decrease”. He further writes “It is insufficient to detect the abnormal increased motion, but the mechanism by which it precipitates the symptomatic episode must also be identified”. Indeed in the seven cases he reported only one patient had backache alone, the others were all radicular problems. His paper shows that identifying abnormal movement establishes the fact that the segment is disordered, but he does not in that paper indicate that movement itself is the cause of pain.
Subsequently in his very influential book “Managing Back Pain” in 259 pages just one page is devoted to the rationale of lumbar fusion. The only reason for fusion appeared to be that, other treatments had failed, that it was reasonable from the psychological viewpoint, and that instability was present. Instability is defined elsewhere in the book as increased abnormal movement, and this is illustrated by x-rays purporting to show abnormal rotations and various types of abnormal tilt. He accepts that such appearances may be entirely painless, but in the patient with back pain they identify the causative level, and fusion is justified.
However, in a joint paper with Depuis in 1985 entitled “Radiological Diagnosis of Degenerative Lumbar instability” they write “A lumbar motion segment is considered unstable when it exhibits abnormal movements. The movement is abnormal in quality (abnormal coupling patterns) or in quality (abnormal increase of movement...) Pain is a signal of impending or actual tissue damage-and when present it indicates that a mechanical threshold has been reached or transgressed. Repeated transgressions will damage the stabilizing structures beyond physiological repair, thus putting abnormal demands on secondary restraints”.
Hence from being a method of identifying an abnormal degenerate disc, abnormal motion itself became the injurious agent.
In 1985 Pope and Panjabi in a paper entitled “Biomechanical definition of spinal instability” wrote “Instability is a mechanical entity and an unstable spine is one that is not in an optimal state of equilibrium. (...In the spine stability is affected by restraining structures that if damaged or lax will lead to altered equilibrium and thus instability. Instability is defined as a loss of stiffness”. Panjabi’s views were generally accepted by basic scientists interested in this field.
Subsequently Panjabi concluded that increased movement was not necessarily a feature of what he termed instability, but reduction in the neutral zone was. However, in a more recent paper he has abandoned the concept of instability altogether and ascribes chronic back pain as being caused by ligament sub-failure injuries leading to muscle control dysfunction.
However, throughout the period from the fifties to the nineties, the Panjabi view held sway, and the term instability evolved from being a useful term to denote a segment that was abnormal due to a degenerate disc, to a term denoting a diagnosis of an abnormal, (usually increased) pattern of movement with a translational component. The abnormal movement was thought to be the cause of the pain and clearly fusion or stopping movement was a logical treatment.
However, the inability to show that abnormal or increased movement was a feature peculiar to the painful degenerate disc, combined with the fact that despite more rigid fusions using pedicle fixation, the clinical results of fusion had not improved, was increasingly casting doubt on the concept of instability. The paper by Murata combining MRI examination with flexion and extension films in patients with back pain, showed that increased angular and translational movement was a feature of the normal or mildly degenerate disc, not of the markedly degenerate disc, where movements were reduced. In 1998 Kaigle et al. demonstrated that comparing patients with normal subjects there was always less movement present in the degenerate spine. It was therefore generally accepted that the effect of disc degeneration was to reduce movement not to increase it, as the term “instability” would imply. It may be argued that, unfortunately, this reduction of movement is associated with abnormal patterns of movement, and this is the meaning of “instability”. However despite considerable efforts over many years, using flexion/extension films, no clear relationship has been established between pain and such abnormal movements. In other words, patients with degenerative disc disease may exhibit abnormal patterns of movement yet have no pain.
By the mid-nineties, instability was still the term used to describe the disorder that we treated by fusion, but the failure to improve results by the introduction of pedicle fixation, caused many surgeons to question the concept of instability, but surgeons were all aware that fusion although unpredictable in terms of clinical result, was the best surgical treatment for chronic low back pain. It was well recognized that clinical success was unrelated to the success of the fusion, pseudarthrosis was as common amongst successful patients as in those who had failed. Was there anything else that a fusion did to the intervertebral disc unrelated to the fact that it stopped movement? (pgs. 619-623)
Mulholland (2008) concluded with a powerful statement that perhaps sums up why chiropractic realizes significant result when treating post-surgical cases.
Abnormal movement of a degenerated segment may be associated with back pain but is not causative. The concept of instability as a cause of back pain is a myth. The clinical results of any procedure that allows abnormal disc loading to continue are unpredictable. (pg. 624)
To underscore the point of fusion being a failed surgical paradigm in many patients, Gudavalli, Olding, Joachim, & Cox (2016) reported,
Surgical decompression of the lumbar spine in older patients had a 24% reoperation rate, and a 20-fold increase in lumbar surgical fusion rates among Medicare enrollees is reported. Lumbar cage fusion rates increased from 3.6% in 1996 to 58% in 2001, and the result was increased complication risk without improved disability or reoperation rates. Adjacent segment degenerative changes and instability at the level immediately above single-segment fusion with clinical deterioration are shown in up to 90% of the cases. The incidence of radiographic adjacent segment disease following fusion has been reported to be as high as 50% in the cervical spine and 70% in the lumbar spine at 10 years. However, the incidence of clinically relevant symptomatic adjacent segment disease is quite lower, estimated at 25% in the cervical spine and 36% in the lumbar spine at 10 years.
Comparing surgery with nonsurgical treatment for back and radicular pain shows that intensive rehabilitation is more effective than fusion surgery, and nonsurgical treatment of low back and radicular pain patients is reported to reduce lumbar disk surgery by approximately two-thirds. Chronic low back pain in 349 patients aged 18-55 years found no evidence that surgery was any more beneficial than intensive rehabilitation. A study of 600 single-operated low back patients showed that 71% did not return to work 4 years after surgery, and 400 multiple-operated backs showed that 95% did not return to work 4 years later. (pg. 124)
Gudavalli, Olding, Joachim, & Cox (2016) went on to report what has been found clinically effective in both pre and post-operative cases, "Treating lumbar disk herniation and spinal stenosis patients successfully with conservative care is documented. Chiropractic manipulation prior to spine surgery is appropriate. Previous reports of the biomechanical changes in the spine when CTFD (Cox technique, flexion-traction) spinal manipulation is applied include decreased intradiscal pressure; intervertebral disk foraminal area increase; increased intervertebral disk space height; and physiological range of motion of the facet joint." (pg. 124)
Regarding post-surgical care, Gudavalli, Olding, Joachim, & Cox (2016) concluded,
81% of the (post-surgical chiropractic) patients showed greater than 50% reduction in pain levels at the end of the last treatment. At 24-month follow-up, 78.6% had continued pain relief of greater than 50%. (pg. 121)
Although one of the goals of chiropractic care is pain relief, there are still the underlying biomechanical pathologies to consider that are concurrently treated while under chiropractic care. The more pressing issue in the post-surgical cases are “could these surgeries been avoided” in the first place with correcting the underlying biomechanical pathologies prior to surgery This underscores the overwhelming need for chiropractic as Primary Spine Care providers being the first treatment option. It goes back to the adage “drugless first, drugs seconds and surgery last.” It’s just common sense and chiropractic has been verified in numerous outcome studies proven to be the most effective 1st treatment option for spine.
High Speed, HIGH ENERGY can = Serious Bodily Injury
Low Speed, HIGH ENERGY can = Serious Bodily Injury
The Injury Arbiter: Energy
Patrick Sundby, Accident Engineer
Mark Studin DC, FASBE(C), DAAMLP, DAAPM
The modern age, say the last 100 years, has done more to advance mankind than at any other time in our history. Great strides have been made in technology, health, and transportation. The advancements in transportation have made even the farthest corners of the earth accessible in only a few hours. As a point of reference: From Los Angeles to Washington D.C., the SR 71 Blackbird made the trip in under 70 (yes, seven – zero) minutes… almost 30 years ago.
While this fast-paced pattern of “make, then break” records has become the new norm, there are some ideologies in each industry which persist in urban myths, dogma or just plain falsehoods and must be tirelessly worked to dispel them. With regards to transportation, one of the most egregious misnomers is the slower you go, the less likely you are to be injured and this falsehood is easy to dispel because physics and inherent math verifies the truth.
Before we explore this myth, let's discuss the physics of injury. Why can we go so fast, (2,200 miles per hour in the case of the Blackbird’s trip) and not be injured yet we fall a few feet and break a bone? The answer is “time”. The time it takes to speed up or slowdown coming to a complete stop is what causes injury (death if severe enough). “It's not the fall, it's the sudden stop at the end.”
Consider the advancements in vehicle safety and design. There was a time when vehicles did not have any safety equipment. These vehicles would crash and stop; under Newton’s laws, the occupant would keep going at the same speed the vehicle was traveling at and collide with the interior of the vehicle. In this collision, there was the sudden stop for the car, but not the occupant; the result… Injury.
The safety advancement: Lap belts. You no longer hit the inside of the vehicle in a crash, the seat belt did its job to keep you from the sudden stop but the lap belt put extreme, sometimes paralyzing strain on the occupant’s body. The lumbar spine is not designed to keep the top half of you in place during a crash and there is the space that normally resides between the occupant and the seatbelt at some point. Again, in a very short amount of time, the occupant is forcibly colliding with the seat belt, even if it is an inch. However, different parts of the spine are not designed to support adjacent regions with these forces and the adjacent spinal regions have to attempt to stabilize forces it was not intended to stabilize.
The safety advancement: Shoulder belts. These were designed to restrain your upper body and not stress your lumbar spine and again you couldn’t hit the inside of the vehicle in a crash. The shoulder belt did its job to keep you from the sudden stop and hitting the interior of the car, but this design has some flaws too. First, it can distribute the forces unevenly across your body. Secondly, now that your upper body is restrained, your cervical spine has to keep your head in place during a crash – a job it's not designed to do. In addition, the sudden stop of your body means your organs can crash into your skeleton and each other.
The safety advancements: Airbags & designed failure of the seatbelt. Most vehicles on the road today have a big bag of air waiting to deploy in the event of a collision and for front-end collisions, the sensors are located in the front, while the side airbags have side sensors, and both will only deploy if those respective sensors are activated through significant force and resultant deformity of the vehicle. This bag is coupled with seatbelts which will stretch at a predetermined point, and the goal of both is for you to not be stopped so suddenly, in other words, to attempt to give you more time to come to a complete stop.
The safety advancement: Crumple Zones. Manufacturers discovered they could make a vehicle fail in a way that was predictable. This expected behavior meant the vehicle could take extra time to crush (usually in milliseconds) and further extend the time it takes an occupant to slow down.
Safety Advancement Conclusion: These advancements in safety do nothing if the nature of the collision renders them useless or the collision is not violent enough to “need” them (low speed). Seatbelts and Airbags do nothing for an occupant of a vehicle which is rear-ended. If a vehicle has a collision which is not severe enough to deploy the airbag and stretch the seatbelt then both these features are useless for safety. If the vehicle cannot crumple or does so minimally, then the occupant doesn't get the benefit of the energy absorbing design. The safety advancements in modern vehicles are designed to increase the time it takes for you to slow down, but if they are not available to you (as is the case in low-speed crashes), then you are no better off than being in a vehicle with no safety features at all.
The next logical question, "How fast can you go and still have the collision be low-speed AND suffer an injury?" is a complex one. There are dozens of variables which dictate the outcomes of a crash, and as such, each item is a subject onto itself, however, to list a few vehicle types, vehicle mechanical condition, speed, the angle of collision, etc. The answer will come from the math of the forces involved, along with the vehicle and occupant “known information;” the weight of the car and the occupant, the speed of the vehicle, the braking distance, etc. and then apply it to a sample to illustrate how to understand Low speed can equal high energy.
We are going to focus on the forces transferred from one vehicle to another. Understanding how a vehicle behaves in a low-speed event and how the forces are transferred is the key to the debunking the myth of “low speed = no injury” because it is not about the speed, it is about the energy the occupant is exposed to as a result of the crash.
Let’s make the vehicle simpler, a cart with a seat…
(Credit: GM Owners Manuals)
For the moment, let us assume the collision doesn't use the crumple zones or any built-in, predictable, deformation to the advantage of the occupant. We will also assume there are two carts and striking cart weighs twice what the victim cart weighs (including any occupants) and the striking vehicle has a post-impact speed of 4 miles per hour.
Some basic calculations result in us knowing the change in speed for the red cart to be 12 miles per hour. Further, if the change happened in .1 seconds the red cart occupant would experience 5.5 gs at the lumbar spine.
To fully understand how that is derived, and the injury potential, we need to calculate the “G-Forces” the occupant’s body is exposed to in this “low-speed” model. It’s all in the math (physics) that is often confusing, but the final numbers bear significant injury potential.
Now, in the real world, the vehicle will always absorb some of the energy, the transfer is never 100% efficient. Let's change the scenario a little bit. What happens if both carts absorb 10% each, totaling 20% of the speed lost to crumple zones?
Again, if the change happened in .1 seconds the red cart occupant would experience just over 5 g’s at the lumbar spine.
The math here is greatly simplified for a demonstration of concept, (energy absorbed) is a complex process detailed in other programs. The above is not a proven method for actual collision reconstruction.
In both examples 10 miles per hour is a very striking low speed in the grand scheme; it’s a common collision speed among parking lot and heavy traffic collisions. The g-forces experienced at the cervical spine are two-three times that of the lumbar spine. In both examples, the cervical spine would experience at least 10 g's to 15 g’s of force, which is well above the injury threshold at either end of the spectrum.
Let’s add some real-world context to this concept. Below are photographs from the NHTSA database. The listed change in velocity for this vehicle is 12 miles per hour.
This vehicle was also rear-ended, the listed change in velocity is 8 miles per hour.
In both cases, the database reports (See the links to the NHTSA below) at least a cervical spine injury, but as you can see, there is little damage to the vehicles. While several factors must be considered to determine if the injury is a result of a car collision, at the same time, the lack of damage or appearance of speed doesn't negate the possibility.
Injury can, and often does, occur in what seems to be the most miniscule collisions. There is no validity to “low speed = no injury” as that is nothing more than an “urban myth” or dogma.