A disc bulge

Some readers gave us feedback from last month’s Garagram.   Thank you, for this helps us to know what is effective and what is not.

In particular, for some readers, we missed the mark in explaining what really happened.   Accordingly, I’ll try again, from a different direction.

To start out, let me review the scientific method.  As the judge said to Perry Mason, “Where are you going with this?”   I’m laying a foundation for later discussion.   The scientific method starts with a hypothesis, an unproven theory.   The scientist then proposes an experiment to validate the hypothesis. If the theory is correct, then the experiment will have the predicted outcome.

When the scientist conducts his experiment and the results support the hypothesis, he publishes those results.   Other scientists are invited to repeat the experiment to prove the point.   When a large group of scientists have achieved the same result, they generally accept the hypothesis as fact.  It is no longer just a theory, now you have a consensus.

Now if someone later conducts the same experiment and gets a different result, then that disproves the hypothesis.   Note that this scientific method can never absolutely verify a theory, but it can falsify a theory.   As Albert Einstein said, “No amount of experimentation can ever prove me right; a single experiment can prove me wrong.”

In forensic investigations we deal with historical events that cannot be scientifically repeated in exactly the same way they originally occurred.  Historical events have dozens of known variables  (most non-repeatable) and thousands of unknown variables.   Having said that, we have a problem as the insurance and legal industries require an answer as to the mechanism of causation.   Ascribing causation must therefore be made by individuals with training and experience in that field of the particular loss.   This is why we hire experts.

When an expert expresses an opinion about causation, it is based upon his observations of the particular failure and how the characteristics of this particular failure match those of other failures that he has seen in his professional career.  He does not say “This, with absolute certainty, was the mechanism of the failure”.    He does say, “My expert opinion of the failure was …”   He is correct in his opinion, if he was given all the data and he acted in a diligent, unbiased, and truthful manner.

Now let us return to last month’s case.  In this situation, 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.

Our PhD biomechanist produced a seven page report to the client, which was heavily edited to become the page and a half of the Garagram.

At no point did we say that the claimant was not in pain.   We did not say that he was not permanently disabled.   We did not, in any way, say that he was faking.

What we did say, was that the injuries that were exhibited were not caused by this single auto accident.   So what was that based upon?

This opinion was based upon the review of the MRI, the training and experience of the expert, and a review of applicable studies done by dozens of researchers on disk bulge causation.

Hundreds of theories have been proposed and scientifically tested to answer the question, “How do discs fail?” The scientific literature is rich with studies on this topic.

The consensus is that when you put enough force on a disc, in a single event, to cause it to rupture, you will also discover that the surrounding bones will break before the disc ruptures.  Several of the studies that support this consensus were referenced in the paper.

So what does cause a disc to rupture?   Many scientific studies demonstrate that repetitive overloading will rupture discs, (hence, the many bad backs of people who spent 20 years carrying heavy loads).   We also know that a large percentage of the population have disc bulges with no clear causation mechanism.  Many of them are asymptomatic, which is to say, that even though they have disc bulges, they are pain free and have a full range of motion.

Returning to the case at hand, the biomechanist opinion was that the observed injuries (the disc bulges shown in the MRI) were not the result of the single auto accident.

Did the accident make him feel worse?   Most likely, but that was not the question we were asked. We were asked, “Did this specific auto accident cause the disc bulges?”

The answer was no.

A broken leg

This month’s Garagram examines the question-could an injury have been prevented by seatbelt use?

The injury accident occurred when a small car was struck at the left front by a van. The driver was listed on the police report as unbelted.

The driver suffered a number of injuries from the impact, most of which were minor in nature.   The single significant injury to the driver was a split fracture of the lateral aspect of the right tibial plateau (a broken leg).

The question was, “Would the injury have had a significantly lower probability of occurrence if the seat belt had been used?” To answer the question, our biomechanical expert examined three areas:

1. The driver’s whole body motion due to the impact (kinematics).
2. The loading mechanism that produces the specific injury suffered (lateral fracture of the tibial plateau).
3. The experimental and epidemiological evidence related to restraint used and knee injuries.
1. Kinematics: At impact the driver would move toward the point of impact. In this case, that was forward and to the left.   This motion would result in left side head contact with the B-pillar or left front window, left lateral knee/thigh contact with the left front door panel, and right knee impact with the steering column.

The described kinematic motion would be modified to some extent by reflexive bracing. Because the sequence of events leading to impact happened in front of the driver, the driver would have reflexively braced.  Bracing the right foot on the brake (or against the floor pan) would force the pelvis rearward stabilizing and fixing the right lower extremity between the floor pan and the seat back.

2. The loading mechanism (lateral fracture of the tibial plateau): Fractures of the tibial plateau occur as a result of strong varus (inward) or valgus (outward) forces combined with axial loading (such as pressing hard on the brake pedal).   When varus or valgus forces are combined with axial loading, the respective condyle (the knuckle of the joint, the round projection or rounded articular area) exerts both a shearing and compressive force on the underlying condyle.   The applied forces produce either a failure fracture or ligament injury, but rarely both.   It is generally believed that intact collateral ligaments are the determining factors with respect to whether fracture or ligament damage occurs (in other words, an already loose joint will tear the ligaments, a strong/tight joint will transfer the impact forces to the bone).   Accordingly, intact collateral ligaments on one side of the knee are necessary to create a fracture of the contralateral plateau.   The medial collateral ligament acts to limit medial opening of the joint and increases the valgus force as it drives the lateral femoral condyle into the lateral aspect of the tibial plateau, causing a fracture. The result can be a split fracture, a depressed fracture, or both.   The magnitude of the forces applied determines both the degree of fracture comminution (the process of grinding or crushing a solid into fine particles) and the degree of fracture depression.

The frontal collision with pre-impact bracing of the right lower extremity, right knee fixed by the steering column, and leftward motion of the torso, describes exactly this well established mechanism for producing lateral split fracture of the right tibial plateau.

3. The experimental and epidemiological evidence:  Studies by Pattimore et al. (1991), Thomas et al. (1995), Kuppa and Fessahaie (2003), Morgan et al. (1991), McGovern et al. (2000), and Rastogi et al. (1986) were examined in detail and found to be applicable to this particular accident.  The conclusion drawn from the review of the scientific literature was that the incidence of femoral fracture was not significantly different for restrained or unrestrained occupants.

Based on his review of the evidence and applicable literature, as well as his education, training, and experience, our expert noted that the driver’s kinematics created the precise mix of loading conditions recognized as producing lateral tibial plateau fracture.  Therefore, he concluded that if the driver had been wearing the seat belt the probability of a broken leg from this accident would have been the same.

Auto collision injury biomechanical analysis

GEI was assigned to perform a biomechanical analysis of the injury potential from an auto collision when the claimant’s Camaro was rear-ended by the insured’s pickup truck.   Based upon the vehicle damage, the accident reconstruction consultant calculated the impact speed to be in the range of 6 to 7 mph.

This caused a change in velocity (Delta V) of the Camaro in the range of 3 to 4 mph resulting in acceleration in the range of 1.3 to 1.8 g’s.   This minor, low-velocity impact was consistent with the cost of repairs done on the Camaro (parts $124, paint $230, and labor  $1,117).

Per deposition statements, the claimant was wearing a three-point seat belt and consequently was well restrained.   Her deposition statement claimed that her body moved “forward and back,” due to the impact. This was inconsistent with the laws of physics.

On impact, her head and thorax would tend to move backwards and her thorax would be pushed against the seat back.

There was no evidence that due to impact, any of her body segments struck any interior parts of the car.   She claimed that she “held the steering wheel tightly.”   In view of this, it was clear that she did not suffer injury due to direct-impact of body segments.

The g levels experienced by the claimant were in the range of 1.3 to 1.8 g’s.  These g levels fall well within the range of g levels experienced by people during the course of their daily lives.   It is noteworthy to compare the g levels experienced by the claimant to those measured by Szabo et al. (SAE 940532) in a study which subjected human volunteers (both male and female, ages 27 to 58 years old) with various degrees of cervical and lumbar spine degeneration, to impulsive loads. During the study, g levels in the range of 10 g’s at the head, between 5 and 7 g’s at the cervical spine and 3 to 5 g’s at the lumbar spine were experienced by these volunteers.  The impacts caused no injury to any of the volunteers and caused no objective changes in the condition of their cervical or lumbar spines, which already displayed various degrees of degeneration, as documented by pre- and post-test MRI scans.

A subsequent MRI of the claimant’s cervical spine found a spur in the anterior aspect of C-4 vertebral body and hypertrophy of the uncinate process of the vertebra.   In addition, despite a 1 mm bulge of the disc, no central canal stenosis was found.   The spur and hypertrophy (enlargement/growth) were manifestations of degenerative processes and were not attributable to the accident, both on account of the small magnitude of g forces, and the short duration of time between the accident and MRI date.

The claimant later complained of right hand numbness and a “hand swelling like a balloon.” The cause may have been arterial blockage, vein blockage, or nerve compression.
Blockages were ruled out, which left a mechanical compression of the nerve.

A neurosurgeon, consulted some nine months later, diagnosed a compressive neuropathy and opined that the condition was due to fibrosis of scaleneous muscle, which causes a squeezing effect on the brachial plexus.

Formation of fibrous tissue on scaleneous muscle requires a cause and requires time for the effect (fibrous tissue formation) to develop. The cause and effect could not be attributed to the accident since her hands were maintained steady on the steering wheel and did not impact any object on the interior of the car during the subject accident.

It was noted by later physical therapists that the claimant might be aggravating her symptoms by moderate to heavy household work at her home, and in the care of her young daughter, and her disabled parents.   Despite rehabilitation education to “pace herself,” there was evidence of increased arm use in unsupported positions, and prolonged forward head posture with increased cervical pain/sprain.

The claimant’s condition of heightened pain and discomfort was reasonable given her medical condition of steadily evolving degenerative joint disease, coupled with her history of prior motor vehicle accidents.  The subject rear-end accident, however, did not cause her symptoms or condition.

Rear-ended: a biomechanical analysis

GEI was assigned to perform a biomechanical analysis of the injury potential from an auto collision when the claimant’s Camaro was rear-ended by the insured’s pickup truck.  Based upon the vehicle damage, the accident reconstruction consultant calculated the impact speed to be in the range of 6 to 7 mph.

This caused a change in velocity (Delta V) of the Camaro in the range of 3 to 4 mph resulting in acceleration in the range of 1.3 to 1.8 g’s.   This minor, low-velocity impact was consistent with the cost of repairs done on the Camaro (parts $124, paint $230, and labor  $1,117).

Per deposition statements, the claimant was wearing a three-point seat belt and consequently was well restrained.   Her deposition statement claimed that her body moved “forward and back,” due to the impact. This was inconsistent with the laws of physics.

On impact, her head and thorax would tend to move backwards and her thorax would be pushed against the seat back.

There was no evidence that due to impact, any of her body segments struck any interior parts of the car.   She claimed that she “held the steering wheel tightly.”   In view of this, it was clear that she did not suffer injury due to direct-impact of body segments.

The g levels experienced by the claimant were in the range of 1.3 to 1.8 g’s.  These g levels fall well within the range of g levels experienced by people during the course of their daily lives.   It is noteworthy to compare the g levels experienced by the claimant to those measured by Szabo et al. (SAE 940532) in a study which subjected human volunteers (both male and female, ages 27 to 58 years old) with various degrees of cervical and lumbar spine degeneration, to impulsive loads. During the study, g levels in the range of 10 g’s at the head, between 5 and 7 g’s at the cervical spine and 3 to 5 g’s at the lumbar spine were experienced by these volunteers.  The impacts caused no injury to any of the volunteers and caused no objective changes in the condition of their cervical or lumbar spines, which already displayed various degrees of degeneration, as documented by pre- and post-test MRI scans.

A subsequent MRI of the claimant’s cervical spine found a spur in the anterior aspect of C-4 vertebral body and hypertrophy of the uncinate process of the vertebra.   In addition, despite a 1 mm bulge of the disc, no central canal stenosis was found.   The spur and hypertrophy (enlargement/growth) were manifestations of degenerative processes and were not attributable to the accident, both on account of the small magnitude of g forces, and the short duration of time between the accident and MRI date.

The claimant later complained of right hand numbness and a “hand swelling like a balloon.” The cause may have been arterial blockage, vein blockage, or nerve compression.
Blockages were ruled out, which left a mechanical compression of the nerve.

A neurosurgeon, consulted some nine months later, diagnosed a compressive neuropathy and opined that the condition was due to fibrosis of scaleneous muscle, which causes a squeezing effect on the brachial plexus.

Formation of fibrous tissue on scaleneous muscle requires a cause and requires time for the effect (fibrous tissue formation) to develop. The cause and effect could not be attributed to the accident since her hands were maintained steady on the steering wheel and did not impact any object on the interior of the car during the subject accident.

It was noted by later physical therapists that the claimant might be aggravating her symptoms by moderate to heavy household work at her home, and in the care of her young daughter, and her disabled parents.   Despite rehabilitation education to “pace herself,” there was evidence of increased arm use in unsupported positions, and prolonged forward head posture with increased cervical pain/sprain.

The claimant’s condition of heightened pain and discomfort was reasonable given her medical condition of steadily evolving degenerative joint disease, coupled with her history of prior motor vehicle accidents.  The subject rear-end accident, however, did not cause her symptoms or condition.

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.