A disc bulge

The insured’s vehicle struck the claimant’s vehicle. The claimant filed for permanent disability due to lower back pain.   GEI was retained to review and comment on the claimant’s MRI, which was submitted in support of the permanent disability claim.

From Wikipedia, “The Intervertebral disc is the structure between the vertebrae (bones of the spine), which act as both a spacer and a shock absorber.   The disc is composed of two parts: a soft gel-like middle (nucleus pulposus) surrounded by a tougher fibrous wall (annulus fibrosus).”

The failed intervertebral disc has been studied with respect to mechanical degeneration and physiopathology since at least the 1940’s.  Historically, studies involved the post-mortem examination of specimens representing a broad age range that were presumed not to have suffered from disc disease.   The assumption in such studies was that the observed changes in the intervertebral discs represented normal changes due to aging and the common mechanical stresses of daily activities.   More recently, with the proliferation of MRI technology, in vivo studies have made it possible to identify the prevalence of pathological discs in the asymptomatic (people without pain or other complaints) population and to contrast the prevalence between the asymptomatic and symptomatic populations.

Coventry et al. (1945) documented severe degenerative changes in intervertebral discs leading them to hypothesize that poor blood supply and exposure to micro-trauma doomed the discs to early degenerative changes.   Ekert and Decker (1947) noted that intervertebral discs demonstrated changes in physical characteristics, shape, and structure with increasing age.   Kieffer et al. (1969) reported findings consistent with Ekert and Decker, but also found annular tears in 35% of the discs in individuals over 40 years of age.   Keiffer et al. also noted that disc rupture occurred frequently without symptoms of nerve root compression.   More recently, Bates and Ruggieri (1991) found that radial tears in the annulus fibrosus were likely due simply to the aging process.   The confusion regarding traumatic verses normal change persists today.  Sether et al. (1990) stated that traumatic disc pathology could be differentiated from the pathology seen in normal aging while Modic and Herfkens (1990) and Czervione (1993) argued that such a distinction was not possible.

Paajanen et al. (1989) examined 20-year-old military recruits and found degenerated discs in 57% of individuals who claimed to experience lower back pain and 35% of individuals who were asymptomatic.   Parkkola et al. (1993) found degenerative lumbar discs in 60% of symptomatic patients examined and in 43% of an age-matched asymptomatic control group.

Disc pathology, therefore, is common even in the asymptomatic population.   More importantly, the finding that a disc is pathological after a traumatic event does not mean that it can be attributed to the event.

Intervertebral discs throughout the spine are subjected to both axial and bending loads.   The lumbar discs are subjected to much higher compressive loads than the cervical spine because of the large weight-bearing requirements and muscular attachments to the lumbar segments.  In acute single-event rapid loading of the spine, vertebral bodies fail (ie. the bone breaks) rather than intervertebral discs.   Vertebral bodies and their joints represent the weak links when loading is significant and rapid in the lumbar spine.   The experimental evidence is clear in this regard.   King (2002) stated:

“With regard to the relationship between disc rupture and impact loading on the spine, it can be safely said that disc ruptures do not occur as the result of a single loading event, unless there are associated massive bony injuries to the spine.”

Small repetitive loads, however, can result in intervertebral disc bulging and failure in the  spine.   When the torso is bent forward, backwards, or sideways stress is applied to the  intervertebral discs, and when weight is added, loads increase dramatically (Nordin and Frankel, 2001).   More disc investigation has been done on the lumbar disc than the cervical disc although the basic biomechanics apply to both. Nachemson (1966 and 1970) and Wilke (1999) measured in-vivo loads on the lumbar discs in various body positions, and verified the high level of disc loading during forward bending; lifting with straight knees further increased lumbar spinal loading.   In addition, they found that moderate loads imposed on the lumbar spine on a daily basis could potentially result in bulges, protrusions, and/or ruptures of intervertebral discs.   Yang et al. (1988) were able to produce human cadaver lumbar disc herniations with the application of repetitive combined loads of torsion, compression, and flexion.   Failure occurred in the cadaver specimens after approximately 20,000 loading cycles.   Gordon et al. (1991) were able to produce disc failures at an average of 36,750 loading cycles when cadaver motion units were subjected to axial loads combined with flexion and rotation.

It is clear that the moderate loads imposed on the lumbar or cervical spine on a daily basis can result in a bulge, protrusion, and subsequent rupture of intervertebral discs.   The intervertebral disc is known to degenerate and weaken over time.   Acute high-velocity trauma, however, results in fracture of the bony elements before, or coincident with, disc failure.

Finally, it is clear that disc pathology is much more common in the general population than previously believed and disc bulges, protrusions, and even frank herniations are often present in patients that have not been injured.

In this specific case, the claimant’s low back pain was consistent with the degenerative changes present at all levels in his lumbosacral spine.   The pathology present was consistent with his age and work history.    His disc bulges were consistently posterior and his spondylosis was consistently anterior, supporting the fact that the changes were due to repetitive forward bending/lifting.

All of the structural changes in the lumbosacral spine noted by the MRI were the result of long-term degenerative change.   None were the result of single event trauma.

The $2 million auto rear ender

The case involves a two car traffic collision. The insured’s vehicle rear-ended the plaintiff’s vehicle. After the accident, the plaintiff was unable to work and eventually had  spinal surgery, which she claimed was the result of a 50 mph collision.  Her lawsuit for more than $2 million was for medical costs, and lost future earnings.  The process of evaluating her claims required two disciplines.

First, an accident reconstructionist calculated the impact speed of the insured into the claimant vehicle and the g-forces experienced.  He reviewed photographs, police reports, vehicle specifications, and the repair work orders for the two cars.  He then calculated the speeds and g-forces of the collision.  His conclusion was that the striking speed was about 10 mph.  The speed change, or Delta V to the claimant vehicle was about 7 mph. The Delta G, or force as applied to the rear of the claimant vehicle was about 11.5 G’s.

Secondly, a biomechanist used these numbers to evaluate the probability of injury from the accident.

The first step was to carefully examine the details of the accident.  In summary, the plaintiff was stopped at a red traffic light and did not see the insured until she was hit.  The insured had been slowing as he approached the red light but overestimated his stopping power and struck her car.  The plaintiff’s car did not strike the car ahead of her.  Both vehicles were driven away from the scene of the accident.  The mechanics of the accident, including the path that the plaintiff traveled within her car, were carefully analyzed and documented.

Next, the medical history of the plaintiff was examined.  She was a middle aged woman who had worked as a nurse prior to the accident.  She had no prior accidents or surgeries.  The responding officer stated in his report that at the scene of the collision she complained of soreness, but refused any medical aid.   She told him that she was okay and did not need an ambulance or medical assistance.  Later in the day her husband took her to a Community Hospital for complaints of general muscular pain.  She was examined and her back was x-rayed.  The x-rays showed no acute fractures, but revealed chronic degenerative disc disease.  She was discharged with prescriptions for muscle relaxants, pain killers, and an anti-inflammatory.

She then sought follow-up treatment from her chiropractor, Dr. 1 for continued complaints of pain.  In addition to his treatments, he referred her to Dr. 2 for an orthopedic evaluation.  Dr. 2 felt that she had sustained soft tissue injuries from the accident, and started her on physical therapy, which she continued for several months.

He then referred her for MRI examinations of her spine.  The MRI examinations confirmed the degenerative changes noted in the earlier x-rays. Dr. 2 referred her for neurological examinations to Dr. 3.  He found her neurological functions to be completely intact.  He found degenerative disc disease in both the cervical and lumbar spine.
A few months later Dr. 4, an orthopedic surgeon  examined her.  He felt that she suffered from a cervical strain and sciatica.  Following additional physical therapy, Dr. 4 prescribed cervical spine epidural injections.  Dr. 5 then examined her for pain management.  Dr. 5 also discussed possible surgical options with her.

Dr. 6 (a neurosurgeon) then examined her.  At the time of the examination, she had neck pain that radiated to her right upper extremity and lower back pain that radiated to her right lower extremity.  Dr. 6 performed a posterior lumbar interbody fusion on the plaintiff (L4-L5), which reduced her pain to pre-accident levels.

The biomechanist’s next phase was analysis: occupant motion (i.e. occupant kinematics) and the injury biomechanics of low-speed, rear-impact collisions are well documented and well understood because of numerous human volunteer studies.  In rear-impact collisions the apparent motion of the head and torso is toward the rear of the vehicle.  As her vehicle accelerated forward from the rear-end impact, the seatback and headrest moved into her.

The seatback and headrest acted to maintain the postural relationship of the driver’s spinal elements by limiting extension of the cervical and lumbar spine and by preventing differential motion between spinal segments.  In her rear-impact collision with the given delta velocity there was no potential for injury during the initial rearward movement of the occupant.

The seatback and headrest also absorbed energy, thereby limiting the forward bounce-back acceleration of the driver and the energy available to produce differential motion in cervical and lumbar spinal segments, this time in flexion.  In a rear-impact collision, the head moves into the headrest and may then rebound.  Although the peak acceleration of the head occurs as the head moves backward (in relation to the vehicle) and produces maximum deformation of the headrest, the potential for injury comes during the rebound phase.  Numerous studies demonstrate that at the speeds involved in this crash there was no potential for injury during the rebound phase.  Other injury mechanisms were evaluated and then ruled out as being inconsistent with the facts of this particular accident.

His conclusion was that she experienced delayed onset muscle soreness following the accident.  Such muscle strain, however, would have resolved without treatment.  Acute cervical or lumbar spinal trauma, or aggravation of previous spinal pathology, was absolutely inconsistent with the maximum loading that she experienced during the accident.  Her degenerative disc disease would have ended her nursing career regardless of the accident. His report referenced thirty studies that supported his opinion.

The jury agreed, and awarded the plaintiff $60,000.