CASE REPORT: Conservative care and axial distraction therapy for the management of cervical and lumbar disc herniations and ligament laxity post motor vehicle collision.
By Josh Johnston, DC
Title: Conservative care and axial distraction therapy for the management of cervical and lumbar disc herniations and ligament laxity post motor vehicle collision.
Abstract: This middle-aged female was injured in a vehicle collision causing her to sustain disc and additional ligament injuries in the cervical and lumbar spine. Diagnostic studies included physical examination, orthopedic and neurological testing, lumbar MRI, multiple cervical MRI’s, CRMA with motion cervical radiographs and EMG studies. Typically, conservative care is initiated prior to interventional procedures, and this case study seeks to explore the usage of passive therapy for mechanical spine pain and noted anatomic disc lesions after failure of interventional procedures. She reported both short term and long term success regarding pain reduction along with improvement in her activities of daily living after initiating conservative care, and continued to report further reductions in pain with periodic pain management using conservative care.
Key Words: neck pain, low back pain, paresthesia, disc herniation, spinal cord indentation, CRMA, axial distraction therapy, DRX9000, spinal manipulative therapy, motor vehicle collision
Key: MRI (magnetic resonance imaging); EMG (electromyography study); CRMA (computerized radiographic mensuration analysis); CT (computerized topography); PTSD (Post-traumatic stress disorder); PRN (as needed); VAS (visual analog scale); HVLA (high velocity low amplitude).
Introduction: The 49-year-old married female (Spanish speaking patient) reported that on March 4th, 2014 she was the seat-belted driver of a truck that was struck by a much larger fuel truck changing lines, hitting her vehicle at the front passenger side (far side, side impact). The force of the impact caused her truck to be lifted up and the right wheel popped off. Her head hit the window after impact and the spinal pain and complaints started approximately 24 hours later. Two days after the crash she went to the emergency department. Occupant pictures were taken describing an out of position occupant injury. She did not report any additional significant trauma after the collision.
Prior to her evaluation at our clinic, she utilized multiple providers for diagnosis and treatment over the course of 11 months. She went to the emergency department, utilized 3 pain management medical doctors, neuropsychologist and a cognitive rehabilitation therapist. Imaging included radiographs and MRI of the right shoulder revealing rotator cuff tear; radiographs of the lumbar and thoracic spine, and left hand; CT of the head and cervical spine were performed; MRI cervical (3) and lumbar spine. Medications prescribed included Fentanyl, Percocet, Naprosyn, Cyclobenzaprine, Norco, Hydrocodone-acetaminophen, Soma, and Carisoprodol. Physical therapy was provided for spinal injuries and she did not respond to treatment. The neurosurgeon recommended epidural steroid injections and facet blocks. Cervical nerve blocks and cervical trigger point injections, cervical and lumbar epidural steroid injections (ESI), lateral epicondyle steroid injections were performed, none of which were palliative. Post-concussion disorder and PTSD with major depressive disorder were diagnosed.
On February 12th, 2015, she presented to our office with neck pain (average 6/10 VAS) that affected her vision, with paresthesia’s in both upper extremities radiating to the hands with numbness. She had low back pain (average 6/10 VAS), and she additionally reported paresthesia at the plantar surface of feet bilaterally. She had left elbow pain, right shoulder pain, knee pain, headaches and “anxiety” along with anterior sternal pain.
Her injuries were causing significant problems with her activities of daily living. Summarily she had increased pain with lifting, increased pain and restricted movement with bending, walking and carrying. She had been unable to perform any significant physical activity from the time of the crash in March 2014 until March 2015. Her right hand was always hurting and her forearms. She was not able to clean windows or do laundry, difficulty using stairs, problems with mopping, ironing and cleaning. She had to limit her walking and jogging primarily due to neck pain and right arm pain. She was not able to sit for long periods of time and sleeping was disrupted due to numbness in her hands. She was only able to walk on a treadmill for 10 minutes before having to stop due to pain, prior to the crash she would exercise for an hour.
Prior History: No significant prior musculoskeletal or contributory medical history was reported.
Clinical Findings (2/12/15): She had a height of 5’2”, measured weight of 127 lbs.
Visual analysis of the cervical spine revealed pain in multiple ranges of motion including flexion, extension, bilateral rotation and bilateral side bending. On extension pain was noted in the upper back, on rotation pain was noted in the posterior neck, and on lateral flexion pain was noted contralaterally.
Visual analysis of the lumbar spine revealed pain in the low back on all active ranges of motion, including flexion, extension and side bending, pain primarily at L5/S1.
Dual inclinometer testing was ordered based on visual active range of motion limitations with pain.
Sensory testing was performed of the extremities, C5-T1 and L4-S1. No neurological deficits other than right sided C5 hypoesthesia.
Foraminal compression test produced pain in the cervical spine. Foraminal distraction test caused an increase in pain in the neck. Jackson’s test on the right produced pain bilaterally in the neck. Straight leg raise bilaterally produced low back pain, double Straight leg raise produce pain at L5/S1 at 30 degrees.
Muscle testing of the upper extremities was tested at a 5/5 with the exception of deltoid bilaterally tested at a 4/5. The patient’s deep tendon reflexes of the upper and lower extremities were tested including Triceps, Biceps, Brachioradialis, Patella, Achilles: all were tested at 2+ bilaterally, equal and reactive. No evidence of clonus of the feet and Hoffman’s test was unremarkable.
C3-C5 right sided segmental dysfunction was noted on palpation. T5-T12 spinous process tenderness on palpation. Low back pain on palpation, particularly L5/S1.
I reviewed the cervical MRI images taken May 2014 with the following conclusions (images attached):
Fig. 1 (A) T2 Axial C5/6, 2 months post injury Fig. 1 (B) Sag T2 C5/6
I reviewed cervical MRI images taken September 17th, 2014 approximately 6-months post injury, and rendered the following conclusions:
I reviewed the cervical MRI dated October 24th, 2015 (images attached):
Fig. 2 (A) 3D Axial C4/5, 19 months post injury Fig. 2 (B) Sag T2 C4/5
IMPRESSIONS: C4/5 herniation noted on 10/24/15 was not noted on prior images. The patient reported no additional injury or symptoms between MRI studies, so it is postulated that initial slices revealed a false negative; or due to the severity of abnormal cervical biomechanics, it is possible that the C4/5 disc herniated between the pre/post MRI’s with no significant increase in symptomatology. There was improvement at C5/6 related to disc abnormality and cord involvement (see below).
Fig. 3 (A) 3D Axial C5/6, 19 months post injury Fig. 3 (B) Sag T2 C5/6, 19 months post injury
Functional Radiographic Analysis (Computerized Radiograph Mensuration Analysis):
The cervical flexion/extension images were digitized February 2016 and interpreted by myself and Robert Peyster MD, CAQ Neuroradiology, revealing a loss of Angular Motion Segment Integrity at intersegment C6/C7 measured at 19.7 degrees (maximum allowed 11 degrees), indicating a 25% whole person impairment according to the AMA Evaluation of Permanent Impairment Guidelines 5th edition1. CRMA provided from Spine Metrics, independent analysis.
Evidence of significant ligament injury causing functional subfailure was measured at C3/4 at 10.4 degrees and at C4/5 measuring 10.9 degrees regarding angular motion. Abnormal paradoxical translation motion measured at C6/7 and C7/T1.
Initial Max 4 months later % Improvement
Cervical Extension 44 42 -5%
Flexion 40 62 55%
Cervical Left 25 41 64%
Lateral flexion Right 12 26 117%
Cervical Left 46 59 28%
Rotation Right 43 73 70%
Conservative treatment rendered: A neurosurgical referral was made for assessment and surgical options. Conservative care was initiated despite failure of other medical procedures since there is “further evidence that chiropractic is an effective treatment for chronic whiplash symptoms”2-3. The patient was placed on an initial care plan of 2-3x/week for 5 months, with a gap in passive care for 1 month.
Prior to being placed at maximum medical improvement she had persistent low back symptoms, continued tingling in the fingertips and occasional neck pain at a 4/10, with her upper extremity paresthesia’s improved 50%. She continued with pain management chiropractic care after MMI, approximately 1 visit every 3-4 weeks with axial distraction to the cervical and lumbar spine, chiropractic adjustments as needed (PRN). 2 years/9 months post collision, and 1 year/9 months after initiating conservative care at our clinic, she reports only slight (1-2/10 VAS) spinal complaints with her primary concern being a torn rotator cuff injury from the crash that still requires surgical intervention. After initiating care at our clinic, no other interventional procedures were performed, although medication usage persisted. Due to improvement in symptoms and functional status, spinal surgery was not considered. She still utilizes Aleve PRN, 1-2 tablets. No significant active spinal rehabilitation was utilized. The patient was given at home active care consisting only of cervical and lumbar stretches, walking, and ice to affected areas.
Competing Interest: There are no competing interests in the writing of this case report.
De-Identification: All of the patient’s data has been removed from this case.
Ligament Pathology as Sequella to Trauma Coupled with Alteration of Motion Segment Integrity (AOMSI) or Ligamentous Laxity
By: Ray Wiegand, D.C.
Mark Studin DC, FASBE(C), DAAPM, DAAMLP
A good read to understanding alteration of motion segment integrity (AOMSI) is the article “Biomechanical Analysis of clinical instability in the cervical spine” White, et al., Clin Ortho Relat Res, 1975;(109):85-96.
AOMSI is a biomechanical analysis. It’s all about numbers that have clinical meaning and significance. Threshold values have been determined that quantify without a doubt the patient has serious injury. It is a test of structural integrity of the ligaments interconnecting the motion segments. In this case, structural integrity has to do with the material properties of ligament tissue. Those properties include strength and flexibility. When a material is both strong and flexible, it’s called a semi-rigid material. Strength is related to the composition of the material. Strength might be thought of as load carrying capacity before failure.
Ligament tissue has previously been bench tested to describe its physical characteristics of stress/strain. That is, given so much load (stress) how much elongation will occur (strain). During normal physiologic loads the ligament remains intact and recoils to its original length when the load is removed. If the load becomes too large the materials (ligaments) begin to yield. They go past their elastic limit. When this happens the (strained) ligament fibers will not return to their original shape. The ligament loses its restraining capacity to hold the joint in normal stabilization and hypermobility occurs.
The ligaments, if sufficiently strained or avulsed results in AOMSI. The following paragraphs illustrates that if AOMSI is found there must be gross destruction or yielding of multiple ligaments. We need to build a BIG motion segment with Velcro ligaments. When you tear them off, they make a really nice ripping noise. That drives home the point.
In the White et al work, they found that the motion segment stayed intact i.e., less than 11 degrees’ rotation (angualr mtion) and less than 3.5 mm translation, until they transected over 50% of the ligaments from an anterior or posterior approach. And when they transected from either approach the loss of stability was not linear but suddenly catastrophic. And they meant that suddenly the two vertebra totally separated in rotation or translation.
Suddenly Separated: pulled apart, head off of body, all neural components compromised, paralysis. Keeping that in mind, what are the injuries of someone just under the threshold? Severe to very severe. They stand the possibility of a serious event with much less force.
If AOMSI is detected, think about more than 50% of ligaments transected. That will start to explain the seriousness of the finding. In a patient/child that demonstrates hypermobility everywhere, then you take a statistical average of all segments, and look at the aberrant statistical finding if it exists. There are clues to injury everywhere when you understand what the numbers mean in reference to stability and function.
To diagnose ligament laxity, it is imperative that imaging be performed and a basic flexion-extension x-ray is all that is required. In today’s medical economy, advanced imaging of MRI or CT Scan, although accurate becomes an unnecessary expenditure and an x-ray renders very accurate demonstrative images to conclude a definitive diagnosis. In determining if there is an impairment, it is necessary to follow the AMA Guides to the Evaluation of Permanent Impairment as the 4th, 5th and 6th editions all render an impairment for AOMSI as sequella to ligament laxity, which is damage to the ligament from trauma.
This document is intended to serve as a simple explanation as to the severity of ligament damage and how to demonstrably diagnose the injury. It is also critical to remember that ligament do “wound repair.” In normal physiology, ligaments grow during puberty from cells within the ligaments called fibroblasts. They produce both collagen (white) and elastin (yellow) tissue, which gives the ligaments both tensile and elastic strength. Upon puberty the cells stop producing tissue and remains dormant. Upon injury, the fibroblast reactivates, but can only produce collage leaving the joint wound repaired in an aberrant juxtaposition (place) with poor movement abilities due to the lack of the requisite elastin. In turn, according to Hauser et. Al (2013) this leads to permanent loss of function of the ligament and arthritis of the joint. This is not a speculative statement; it is based upon Wolff’s that dates back to the late 1800’s and has been a guiding principle in healthcare for more than a century.