Motor Vehicle Accidents:

Little or No Damage Collisions & Demonstrable Verification of Energy Transferences to Cause Bodily Injury


By: Patrick Sundby, Accident Investigator

Specializing in Low Speed and Catastrophic Crashes



In the last two writings we explored how low speed collisions can have substantial energy transfers with minimal (if any) damage.  Here we will discuss the myth of “no damage = no injury” from a vehicle appearance / design point of view and how it relates to injury during a collision.

In order to get into this topic, we need a little history lesson first.  The automotive industry exploded after World War II, with vehicle style being the topic of focus.  The jet age influenced bumpers, headlights, interior components, taillights, even excess in the design – fins.  Something else happened too, for the first time in the automobiles history vehicles were more than “around town” horse-less buggies; the power of the engines and speeds possible dawned a whole new arena – safety.  In the 1960’s vehicle aesthetics began to compromise with safety.  Automotive designers began to consider topics such as; structural integrity, occupant restraints, and crash worthiness.

The industry faced slow growth and change into the 1980’s, each revision or change did bring with it progress and improvement but not enough at any one time to be a huge leap forward.  The changes which were necessary were too cost prohibitive, too experimental, or simply too market risky.  Then in the mid 1980’s a revolution in industry began to take hold – the computer.  The standard personal computer allowed for design changes to be done with much greater efficiency.  Once plugged in and switched on the days spend calculating variables and double checking work became no more complicated than a few clicks.

The computer made it possible for car manufacturers to reduce years of standard research and design practices into just a few months and at the same time it allowed for much more cost effective experimentation and new process development. 

Now that we have completed history 101 let’s discuss the topic of point – “no damage = no injury”

Vehicle design, as an approach or concept, has undergone a substantial overhaul in recent years.  The change has influenced the standard use of bumper covers.  The long standing tradition in automotive design has been to put the bumper outside or separate from the body and to make them of a robust alloy.  (Think about all those classics in “American Graffiti”).  The bumper was designed to be a visual compliment to the overall appearance of the vehicle.  The safety perspective was non-existent with respect to bumpers as they were no more than a sacrificial lamb to save the body from expensive repair. 

In the early 1970’s federal mandates designed to make vehicles safer forced the manufacturers to engineer larger and more structurally sound designs.  The most noted changes where the moving of bumper away from the body itself to an integral part of the body of the car.  This “afterthought” look borrowed from the truck world was the norm until the late 1980’s.  Three things changed in the 1980’s:  First, bumpers began to move to behind urethane bumper covers in widespread use. This gave vehicles a modern look and concurrently helped with aerodynamics.  Secondly, because aesthetics were no longer part of the equation, bumpers became much stronger and included the use of energy absorbing material between the bumper cover and the bumper structure.  Finally, automotive paints had also advanced, including the superior ability to resist cracking & flaking, and paint had become flexible.

These changes also had another positive side effect; because of the elastic properties of urethane and the paint, minor collisions, even those which damaged the bumper behind them, no longer appeared as serious.  Often times a bumper cover needed little more than some prep and paint, where previous designs necessitated changing the whole bumper.

The biggest change between old design and the new one, is the inherent elasticity of the new bumper covers.  These covers can, and often do, rebound to the original design they were formed in and the use of flexible paint means the paint is very likely to rebound as well.  While signs of impact are obvious the assessment of speed from damage is now deceptively poorer.  Obviously when a steel bumper is distorted it stays that way leaving no room for underestimation.

Notice how we have not discussed how these design changes have benefited energy transfer; and this is no mistake.  There simply aren’t any groundbreaking points to discuss.  Changes in vehicle design will not facilitate violation of laws of physics.  All these design changes have accomplished is make the energy transfer in a low speed crash less obvious and less costly.

However, there are simply demonstrable measures that can be taken to assess the effects of energy transfer in no apparent damage collisions:

  1. Remove the cover of the bumper and inspect the materials below the “skin“ of the bumper for internal damage
  2. Check the angle of the passenger seat. Seats are set by the factory at a prescribed angle and when the occupant is thrown backwards, often the seat angle changes rendering demonstrative evidence of force transfer
  3. Have the chassis examined with a laser device most repair shops utilize to ensure the frame of the car is “plumb.” Often in a rear-end collision, the chassis gets distorted and even a 1-degree variation will be evident and that requires energy transferences.

Patrick Sundby has decades of experience in the automotive industry including several years in law enforcement collision investigation. He has also been a driver training and firearms instructor in law enforcement and a police officer for 9 years before specializing in accident investigations. He has had the privilege of participating in both learning and teaching at Prince William County Criminal Justice Training Academy in Virginia and studied at the Federal Law Enforcement Training Center in Georgia. His specialty is low speed and catastrophic crashes and has testified over 500 times at various level. He can be reached at 571-265-8076 or

Dr. Mark Studin is an adjunct associate professor of chiropractic at the University of Bridgeport College of Chiropractic, an Adjunct Professor of Clinical Sciences at Texas Chiropractic College and a clinical presenter for the State of New York at Buffalo, School of Medicine and Biomedical Sciences for postdoctoral education, teaching MRI spine interpretation and triaging trauma cases. He is also the president of the Academy of Chiropractic, teaching doctors how to interface with the legal community ( He teaches MRI interpretation and triaging trauma cases to doctors of all disciplines nationally, and studies trends in health care on a national scale ( He can be reached at or at 631-786-4253.


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Soft Tissue Injuries

What are they and the Long-Term Impact of Bodily Injury




According to the American Academy of Orthopedic Surgery “The most common soft tissues injured are muscles, tendons, and ligaments. Acute injuries are caused by a sudden trauma, such as a fall, twist, or blow to the body. Examples of an acute injury include sprains, strains, and contusions.”  ( We must also not forget that there are other soft tissues that can get injured and the true definition of soft tissue, which is anything not bone is soft tissue. This includes the brain, lungs, heart and any other organ in the body. However, in medicine soft tissue injuries are commonly known to be limited to the muscles, ligaments and tendons. 

When we look at the type of structures that muscles, tendons and ligament are composed of, we will realize that they are connective tissue. According to the National Institute of Health “Connective tissue is the material inside your body that supports many of its parts. It is the "cellular glue" that gives your tissues their shape and helps keep them strong. It also helps some of your tissues do their work ( Unlike fracture repair where the bone is replaced and usually heals properly if aligned and rested, connective tissue disorders undergo a different type of wound repair that has aberrant tissue replacement as sequella to bodily injury and has subsequent abnormal permanent function.

If we focus on sprains or ligamentous injuries, according to the American Academy of Orthopedic Surgery there are three types of sprains:

Sprains are classified by severity:1

  • Grade 1 sprain (mild): Slight stretching and some damage to the fibers (fibrils) of the ligament.
  • Grade 2 sprain (moderate): Partial tearing of the ligament. There is abnormal looseness (laxity) in the joint when it is moved in certain ways.
  • Grade 3 sprain (severe): Complete tear of the ligament. This causes significant instability and makes the joint nonfunctional.

Regardless of the severity of the sprain, there is tissue damage or bodily injury and the next step is to determine if there is healing or wound repair. According to Woo, Hildebrand, Watanabe, Fenwick, Papageorgiou and Wang (1999) “…as a result the combination of cell therapy with growth factor therapy may offer new avenues to improve the healing of ligament and tendon. Of course, specific recommendations regarding growth factor selection, and timing and method of application cannot be made at this time. Previous attempts at determining optimal doses of growth factors have provided contradictory results. Although growth factor treatment has been shown to improve the properties of healing ligaments and tendons, these properties do not reach the level of the uninjured tissue.” (p. s320)

According to Dozer and Dupree (2005) “No treatment currently exists to restore an injured tendon or ligament to its normal condition.” (pg. 231).

According to Hauser, Dolan, Phillips, Newlin, Moore and Woldin (2013) “injured ligament structure is replaced with tissue that is grossly, histologically, biochemically and biomechanically similar to scar tissue. Fully remodeled scar tissue remains grossly, microscopically and functionally different from normal tissues” (p. 6) “the persisting abnormalities present in the remodeled ligament matrix can have profound implications on joint biomechanics, depending on the functional demands placed on the tissue. Since remodel ligament tissue is morphologically and mechanically inferior to normal ligament tissue, ligament laxity results, causing functional disability of the affected joints and predisposing other soft tissues in and around the joints further damage.” (p.7) “studies of healing ligaments have consistently shown that certain ligaments do not heal independently following rupture, and those that didn’t feel, do so characteristically inferior compositional properties compared with normal tissue. It is not uncommon for more than one ligament undergo injury during a single traumatic event.” (p.8) “osteoarthritis for joint degeneration is one of the most common consequences of ligament laxity. Traditionally, the pathophysiology of osteoarthritis was thought to be due of aging and wear and tear on the joint, but more recent studies have shown that ligaments play a critical role in the development of osteoarthritis. Osteoarthritis begins when one or more of ligaments become unstable or lax, and the bones began to track improperly and put pressure on different areas, resulting in the rubbing the bone on cartilage. This causes breakdown of cartilage and ultimately leads to deterioration, whereby the joint is reduced to bone on bone, a mechanical problem of the joint that leads to abnormality of the joints mechanics. Hypomobility and ligament laxity have become clear risk factors for the prevalence of osteoarthritis.” (p.9)

Looking globally at the research over the last 16 years, in 1999 it was concluded that the most current treatments to repair or heal the injured ligament do not reach the level of the uninjured tissue. In in 2005 it was concluded that no treatment currently exists to restore an injured tendons or ligaments to its normal condition. In addition the current standard of ligament research in 2013 concluded that that ligaments do not feel independently, but damage ligaments are a direct cause of osteoarthritis and biomechanical dysfunction (abnormality of joint mechanics). The latest research has also concluded that ligament damage or sprains is the key element in osteoarthritis and not simply aging or wear and tear on the joint.

As a result it is now clear based upon the scientific evidence that a soft tissue injury is a connective tissue disorder that has permanent negative sequela and is the cause of future arthritis. This is no longer a debatable issue and those in the medical legal forum who are still arguing “transient soft tissue injuries” are simply rendering rhetoric out of ignorance and a possible ulterior motive because the facts clearly delineate the negative sequella based upon decades of multiple scientific conclusions.

The caveat to this argument is that although there is irrefutable bodily injury with clear permanent sequella, does it also cause permanent functional loss in every scenario? Those are two separate issues and as a result of the function of ligaments, which is to connect bones to bones the arbiter for normal vs. abnormal function is ranges of motion of the joint. That can be accomplished by either a two-piece inclinometer for the spine, which according to the American Medical Association Guides to the Evaluation of Permanent Impairment, 5th Edition (p. 400) is the standard (and is still the medical standard as the 6th Edition refers to the 5th for Ranges of motion). The other diagnostic demonstrable evidence to conclude aberrant function is to conclude laxity of ligaments through x-ray digitizing. Both diagnostic tools confirm demonstrably loss of function of the spinal joints.   


  1. Sprains, Strains and Other Soft Tissue Injuries (2015) American Academy of Orthopedic Surgery, Retrieved from:
  2. Connective Tissue Disorders (2015) National Institute of Health, Retrieved from:
  3. Woo S, Hildebrand K., Watanabe N., Fenwick J., Papageorgiou C., Wang J. (1999) Tissue Engineering of Ligament and Tendon Healing, Clinical Orthopedics and Related Research 367S pgs. S312-S323
  4. Tozer S., Duprez D. (2005) Tendon and Ligament: Development, Repair and Disease, Birth Defects Research (part C) 75:226-236
  5. Hauser R., Dolan E., Phillips H., Newlin A., Moore R. and B. Woldin (2013)  Ligament Injury and Healing: A Review of Current Clinical Diagnostics and Therapeutics, The Open Rehabilitation Journal (6) 1-20
  6. Cocchiarella L., Anderson G., (2001) Guides to the Evaluation of Permanent Impairment, 5th Edition, Chicago IL, AMA Press

Note about the author: Dr. Mark Studin teaches at the doctoral level as an Adjunct Assistant Professor of Chiropractic at the University of Bridgeport, College of Chiropractic, and an Adjunct Assistant Professor of Clinical Sciences at Texas Chiropractic College. He also teaches at the graduate medical level as a clinical presenter credentialed by the Accreditation Council for Continuing Medical Education in Joint Sponsorship with the State University of New York at Buffalo, School of Medicine and Biomedical Sciences along with being credentialed nationally for chiropractic post-doctoral education in a broad range of clinical subjects. Dr. Studin’s CV can be accessed by CLICKING HERE

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