Rear-End Collision Injuries Explained: Biomechanics of Whiplash, Delayed Symptoms, and Low-Impact Crash Damage (California Guide)

Introduction: Why Rear-End Collisions Are Routinely Misunderstood

Few words in personal injury law carry more reflexive dismissal than ‘fender bender.’ When two vehicles collide at relatively low speed in a parking lot or at a traffic signal, the scene often looks unremarkable—a crumpled bumper, perhaps a cracked tail light, and two drivers exchanging insurance information on the sidewalk. The property damage appears minor. The occupants seem fine. And yet, within hours or days, one of those drivers may begin experiencing debilitating neck pain, headaches, cognitive fog, or radiating arm discomfort that upends their daily life for months—or permanently.

The scientific and medical literature is unambiguous on this point: the severity of vehicle damage is a poor predictor of occupant injury severity. Rear-end collisions are the most frequently occurring type of motor vehicle crash and account for a disproportionate share of serious soft tissue and neurological injuries. Understanding why requires a working knowledge of the biomechanics of the crash event itself—physics that most insurance adjusters prefer to ignore.

This guide is designed to explain, with scientific precision and legal clarity, exactly what happens to the human body during a rear-end collision, why those mechanisms produce serious and lasting injury, and why the ‘minor impact’ argument so frequently deployed by insurance defense teams is fundamentally at odds with peer-reviewed research.

What Happens to the Body in a Rear-End Collision: The Biomechanics

To understand rear-end collision injury, you must first understand what happens in the fraction of a second after impact. The sequence of events is counterintuitive, which is why these injuries are so frequently underestimated.

Phase 1: Vehicle Acceleration

When a vehicle is struck from behind, it undergoes rapid forward acceleration. This acceleration is transferred through the vehicle frame to the seat. The seat, in turn, pushes the torso of the occupant forward. This all occurs within the first 75 to 100 milliseconds of impact.

Phase 2: The Head-Lag Phenomenon

Here is the critical biomechanical insight: while the torso is being accelerated forward by the seat, the head—resting on top of the cervical spine—does not move immediately. It lags behind due to inertia. According to Newton’s First Law, the head resists the change in motion and effectively stays in place while the torso beneath it is propelled forward. This lag creates a differential velocity between the head and the torso that loads the cervical spine with forces it was not designed to absorb.

Phase 3: Hyperextension (The Extension Phase)

As the torso continues forward and the head continues to lag, the neck is forced into rapid and excessive extension—bending backward beyond its normal range of motion. The cervical spine bows into an unnatural S-shape (as described above), with the lower cervical vertebrae being forced into extension while the upper vertebrae initially remain in flexion. During this phase, the anterior (front) structures of the neck—including the anterior longitudinal ligament, intervertebral discs, and muscle attachments—are placed under tensile (stretching) stress. The facet joint capsules in the posterior (rear) cervical spine undergo compression and shear forces simultaneously.

Phase 4: Hyperflexion (The Rebound Phase)

After the head has reached maximum rearward extension, it rebounds forward in a rapid flexion movement—the forward ‘snap’ that most people associate with whiplash. During this phase, the posterior cervical structures are placed under tensile stress, while the anterior disc space is compressed. The entire extension-then-flexion cycle may be completed within 200 to 500 milliseconds—faster than the human nervous system can initiate a protective muscular response.

Because the motion occurs faster than the muscles can react, there is no active muscular protection. The entire load is absorbed by the passive restraint structures: ligaments, joint capsules, and intervertebral discs.

Why Whiplash Occurs: The Medical Explanation

Whiplash—formally defined by the Quebec Task Force as a bony or soft tissue injury resulting from an acceleration-deceleration mechanism of energy transfer to the neck—is not a single discrete injury. It is a constellation of tissue damage occurring across multiple anatomical structures as a result of the rapid extension-flexion cycle described above.

At the microscopic level, the excessive forces applied during the crash event cause micro-tearing of ligament fibers. The cervical ligaments are viscoelastic structures: they are strong and capable of absorbing substantial loads under normal conditions, but they are vulnerable to rapid, high-rate loading—exactly the type of loading generated in a rear-end collision. When ligament fibers are micro-torn, they do not heal to their original tensile strength. Instead, they heal with scar tissue that is biomechanically inferior, creating chronic instability and pain.

Whiplash Associated Disorders (WAD) are classified on a severity scale from Grade 0 (no complaint or physical signs) to Grade 4 (fracture or dislocation). The majority of rear-end collision victims fall into the Grade 2 category (musculoskeletal signs including decreased range of motion and point tenderness) or Grade 3 (neurological signs including sensory deficits and decreased deep tendon reflexes).

The Role of the Cervical Spine and Facet Joints

The cervical spine consists of seven vertebrae (labeled C1 through C7) stacked vertically and separated by intervertebral discs. The cervical spine serves multiple critical functions: it supports the weight of the skull (approximately 10–12 pounds), allows the complex movements of the head, and protects the spinal cord passing through it.

Between each pair of adjacent vertebrae are two facet joints—small paired joints at the rear of the spine that guide and limit spinal motion. Each facet joint is enclosed in a capsular ligament, a sleeve of connective tissue that holds the joint together while allowing smooth articulation.

Why Facet Joints Are the Primary Pain Generators

Multiple peer-reviewed studies published in leading pain medicine and spine journals have identified the facet joint capsular ligaments as the primary anatomical source of chronic pain following whiplash injury. Research using controlled medial branch nerve blocks—a diagnostic procedure that selectively anesthetizes the nerves supplying the facet joints—has demonstrated that the cervical facet joints are the source of pain in a significant proportion of patients with chronic neck pain following whiplash.

The facet capsular ligament is particularly vulnerable because it undergoes both tensile strain and shear loading during the S-curve phase of the whiplash motion—forces that are especially damaging to viscoelastic tissue. In vitro studies of human cervical facet capsular ligaments have documented that the strains imposed during simulated rear-end collisions can reach or exceed the tissue’s failure threshold even at relatively low impact speeds.

Delayed Injury Symptoms: Critical for Your Legal Claim

One of the most legally significant—and medically well-documented—features of rear-end collision injury is the delayed onset of symptoms. Many victims leave the crash scene feeling shaken but physically intact. They decline emergency medical attention. They go home, sleep, and wake up the next morning barely able to move their neck. By the time they seek medical care, the defense narrative has already been established: ‘If you were seriously hurt, you would have known immediately.’

This narrative is medically false, and the research demonstrating that fact is extensive.

The Physiological Basis of Symptom Delay

The immediate post-crash period is dominated by a significant neurochemical stress response. Adrenaline (epinephrine) and other stress hormones are released in high concentrations, producing analgesic (pain-masking) effects that can suppress the awareness of injury for hours. Simultaneously, the acute inflammatory response—the biological process by which the body responds to tissue damage—unfolds over a period of hours to days. The prostaglandins, cytokines, and other inflammatory mediators responsible for activating pain receptors accumulate gradually, which is why pain intensity typically increases over 24 to 72 hours after the traumatic event.

Muscle spasm—the body’s reflexive attempt to immobilize and protect injured structures—also develops gradually. It is not present at the moment of impact; it develops as the nervous system processes the injury and initiates protective responses.

The practical legal implication is clear: any gap between the crash and the first medical visit does not mean no injury occurred. It means the physiological sequence of injury manifestation took its natural course. An experienced rear-end collision attorney in Los Angeles understands this physiology and knows how to present it effectively to insurance carriers and juries.

Common Injuries from Rear-End Collisions: A Medical Breakdown

Rear-end collisions produce a predictable pattern of injuries that reflects the biomechanical forces described above. The following represent the most clinically significant injury categories:

1. Whiplash / Cervical Strain-Sprain

The term ‘cervical strain-sprain’ more precisely describes the combined muscular (strain) and ligamentous (sprain) injuries that constitute whiplash. Strains involve overstretching or tearing of muscle fibers or their tendinous attachments; sprains involve damage to ligaments. In rear-end collisions, both occur simultaneously across multiple cervical structures. Symptoms include neck pain, restricted range of motion, headache, dizziness, and referred arm pain.

2. Herniated Intervertebral Discs

The intervertebral discs function as shock absorbers between adjacent vertebrae. Each disc has a tough outer ring (annulus fibrosus) and a gel-like inner core (nucleus pulposus). The compressive and tensile forces generated during a rear-end collision can cause annular tears or frank disc herniation—rupture of the outer ring allowing the inner material to protrude into the spinal canal or neural foramen. Disc herniation at any cervical level can compress nerve roots, producing radiculopathy: radiating pain, numbness, or weakness extending into the shoulder, arm, or hand.

3. Traumatic Brain Injury (Concussion)

Perhaps the most underappreciated injury mechanism in rear-end collisions is mild traumatic brain injury. Brain injury does not require a blow to the head—it can result from rapid acceleration-deceleration forces transmitted to the brain through the skull. During the whiplash event, the brain is subjected to inertial loading as it moves within the cranial vault. This can cause axonal shear injury (damage to nerve fiber connections) and microhemorrhages that produce cognitive symptoms including memory difficulties, concentration problems, light and noise sensitivity, sleep disturbance, and emotional dysregulation.

These symptoms—often labeled ‘post-concussion syndrome’—are frequently dismissed by insurance carriers as psychological or pre-existing. The neuroimaging evidence, including diffusion tensor imaging (DTI) studies, increasingly documents structural brain changes following these events.

4. Cervical Facet Joint Injuries

As detailed in the anatomy section, the cervical facet joints are primary injury targets in rear-end collisions. Facet joint injury produces a characteristic clinical picture: local neck pain that is worse with extension and rotation, referred pain to the head (cervicogenic headache), and tenderness over the affected joints. Diagnosis is confirmed by medial branch nerve block procedures. Treatment ranges from physical therapy and anti-inflammatory medications to radiofrequency neurotomy for severe chronic cases.

5. Soft Tissue Injuries

Beyond the cervical spine, rear-end collisions injure the muscles, tendons, and fasciae of the neck, upper back, and shoulder girdle. The trapezius, levator scapulae, sternocleidomastoid, and deep cervical extensors are particularly vulnerable. Myofascial pain syndrome—a condition involving trigger points (hypersensitive nodules within muscle tissue) that refer pain in characteristic patterns—commonly develops following these injuries and can persist for months or years without appropriate treatment.

Low-Speed Crashes Can Still Cause Serious Injury

The most pervasive—and most scientifically indefensible—argument deployed by insurance carriers in rear-end collision cases is the ‘low property damage’ defense. The argument goes: if there was minimal damage to the vehicle, there could not have been sufficient force to cause significant injury. This argument is contradicted by a substantial body of peer-reviewed engineering and biomechanical research.

The key concept is delta-V—the change in velocity of the vehicle during the collision event. Delta-V is the metric most directly correlated with occupant injury risk. However, the relationship between delta-V and vehicle damage is not linear. Modern vehicle bumper systems and structural components are specifically engineered to absorb and distribute crash energy through controlled deformation. When bumper components absorb crash energy, they reduce the delta-V transmitted to the vehicle interior and occupants. But in low-speed crashes where the bumper components do not deform (because the impact is below the threshold that activates their energy-absorbing properties), a greater proportion of the crash energy may be transmitted directly to the vehicle occupants.

In other words, a crash that leaves a vehicle looking virtually undamaged may actually transmit more force to the occupant than a crash that produces visible bumper damage. This is not speculation—it is a documented phenomenon in the automotive safety engineering literature.

Factors That Increase Injury Severity

Not all rear-end collision occupants sustain the same degree of injury for a given impact magnitude. The following individual and situational factors have been documented in the scientific literature as modifying injury risk and severity:

• Seat position and seatback angle: A seatback angled too far rearward reduces the protective ‘ramping’ effect of the seatback and increases head-relative-to-torso excursion during impact.
• Headrest placement: A headrest that is too low or positioned too far from the occupant’s head fails to limit rearward head travel, significantly increasing cervical spine loading. Research consistently identifies poor headrest geometry as a major modifiable risk factor.
• Awareness of impact: Occupants who are aware of an impending collision can pre-tension neck muscles, providing some protective resistance. Unaware occupants—those who do not see the approaching vehicle—sustain greater injury for the same impact magnitude. This is supported by experimental and observational research.
• Gender: Female occupants are documented in peer-reviewed literature to sustain higher rates of whiplash injury and worse long-term outcomes than male occupants for equivalent crash conditions. Differences in cervical spine musculature, head-to-neck mass ratio, and ligamentous laxity are proposed as contributing mechanisms.
• Body size: Smaller individuals have less inertial resistance to head acceleration, potentially increasing cervical spine loading.
• Angle of impact: Oblique rear impacts—those with a lateral component—produce out-of-plane cervical spine loading that may be more injurious than pure rear impacts for the same total impact energy.
• Pre-existing cervical degenerative changes: Occupants with pre-existing disc degeneration or spondylosis are more vulnerable to acute injury and slower to recover. This does not diminish the legal claim—California’s eggshell plaintiff doctrine holds defendants fully responsible for the aggravation of pre-existing conditions.

How Insurance Companies Minimize These Injuries—And Why They Are Wrong

Insurance companies defending rear-end collision claims have developed a set of predictable arguments designed to minimize or eliminate liability for these well-documented injuries. Understanding these tactics—and their scientific refutation—is essential for any rear-end collision victim.

The ‘Low Property Damage’ Argument

As discussed above, this is the most common and most scientifically unsupported defense tactic. Insurance carriers present photographs of minimal vehicle damage alongside the implicit argument that such a crash could not have caused significant injury. The biomechanical research directly contradicts this. A Los Angeles rear-end accident lawyer with expertise in these cases will retain qualified biomechanical engineers to challenge this argument at deposition and trial.

The ‘Negative Imaging’ Argument

When X-rays and MRIs return without obvious acute findings, insurance carriers argue that ‘there’s nothing there.’ As detailed above, the primary anatomical injuries in rear-end collisions—ligamentous micro-tears, facet capsular injuries—are largely invisible on standard imaging. The absence of imaging findings does not equate to absence of injury. Biomechanical injury exists at a tissue level that standard clinical imaging frequently cannot resolve.

The ‘Delayed Claim’ Argument

When a victim does not seek immediate emergency care, insurance carriers characterize this as evidence that no significant injury occurred. The medical literature on post-crash symptom kinetics entirely refutes this. Symptom delay is the physiological norm, not an anomaly. Medical professionals and biomechanical experts testifying in these cases can explain the documented mechanisms that account for delayed symptom onset.

How Experts Reconstruct Rear-End Collisions

In litigated rear-end collision cases, the parties typically retain expert witnesses in biomechanics, accident reconstruction, and medicine. Understanding how these experts operate can help you understand the strength of your claim.

Accident Reconstruction Engineers

Reconstruction experts analyze the physical evidence of the crash—including vehicle damage patterns, electronic data recorder (EDR) data (sometimes called ‘black box’ data), post-impact vehicle positions, and tire marks—to calculate crash parameters including delta-V (the change in vehicle velocity), the direction of force, and the duration of the impact pulse. These calculations are then translated into occupant biomechanics by biomechanical engineers.

Biomechanical Engineers

Biomechanical experts bridge the gap between crash physics and human anatomy. Given the delta-V, impact direction, and occupant characteristics documented by the accident reconstructionist, they apply peer-reviewed biomechanical models to calculate the forces and accelerations imposed on the cervical spine during the crash. They can testify that, for a given crash event, the forces experienced by the cervical spine were sufficient—or exceeded the threshold—to produce the type of ligamentous, disc, and facet joint injury documented in the medical records.

Terms you may hear in this context include: peak head acceleration (measured in g), seat-back induced torso acceleration, head-to-torso relative velocity, cervical spine compression force, and capsular ligament strain rate. These are not abstractions—they are measurable quantities that experts present with quantified confidence intervals.

Rear-End vs. Side-Impact Injury Dynamics: A Brief Comparison

It is worth understanding how rear-end collision injury mechanics differ from side-impact (lateral) collisions, which are also common in Los Angeles traffic. Side impacts impose primarily lateral force vectors on the cervical spine, producing lateral flexion (bending to the side) rather than the anterior-posterior extension-flexion pattern of whiplash. Side impacts more frequently produce bony injuries—rib fractures, pelvic fractures, and lateral spinal compression fractures—because the vehicle structure on the struck side offers less protective distance between the impacting vehicle and the occupant. Rear-end collisions, by contrast, produce a higher proportion of soft tissue and ligamentous cervical spine injuries because the primary force vector is aligned with the spine’s axis of least resistance.

Legal Implications: Translating Injury Science Into Compensation

The science described in this article has direct and significant legal implications for California rear-end collision claims.

Establishing Causation

California personal injury law requires the plaintiff to establish, by a preponderance of the evidence, that the defendant’s negligence caused the plaintiff’s injuries. In rear-end collision cases, causation is frequently disputed. The biomechanical and medical evidence summarized here provides the evidentiary foundation for establishing that the crash event—not some other cause—produced the documented injuries. This is why working with a knowledgeable rear-end collision attorney in Los Angeles who understands how to marshal and present this evidence is essential.

Damages

Once causation is established, the full range of economic and non-economic damages becomes compensable under California law. Economic damages include past and future medical expenses (including the full cost of treatment for chronic conditions resulting from the injury), lost wages and earning capacity, and out-of-pocket expenses. Non-economic damages include past and future pain and suffering, loss of enjoyment of life, and emotional distress. In cases involving significant ongoing impairment, these damages can be substantial.

The Eggshell Plaintiff Doctrine

California recognizes the eggshell plaintiff doctrine: a defendant is fully responsible for the full extent of injury caused, even if the victim was more vulnerable than an ordinary person due to pre-existing conditions. If the rear-end collision aggravated a pre-existing cervical condition and produced chronic pain that would not have occurred in a person without that pre-existing condition, the defendant is still fully liable for the resulting harm.

This doctrine is especially important in rear-end collision cases, where insurance carriers routinely attempt to attribute chronic symptoms to pre-existing degenerative changes rather than the collision. An experienced Los Angeles rear-end accident lawyer knows how to counter this argument with medical evidence and expert testimony.

Frequently Asked Questions

How does a rear-end collision cause whiplash?

When a vehicle is struck from behind, the torso is rapidly accelerated forward by the seat while the head lags behind due to inertia. This creates a differential motion that forces the cervical spine into rapid hyperextension (backward bending) followed by hyperflexion (forward snapping). The entire cycle occurs within 200 to 500 milliseconds—faster than the muscles can respond—meaning all protective forces must be borne by the passive ligaments, joint capsules, and discs of the cervical spine. The resulting micro-tearing of ligament fibers and compression of facet joint capsules constitutes the injury complex known as whiplash.

Can you be seriously injured in a low-speed rear-end crash?

Yes. Peer-reviewed biomechanical research consistently demonstrates that significant cervical spine injury can occur at delta-V values as low as 5 to 8 miles per hour. The degree of vehicle damage is not a reliable predictor of occupant injury because modern bumper systems may absorb crash energy through deformation without transmitting that protection to the occupants, or conversely, may not deform in minor crashes, transmitting the entire crash impulse directly to the vehicle interior.

Why do rear-end collision symptoms appear days later?

Delayed symptom onset is a well-documented physiological phenomenon. In the immediate post-crash period, elevated adrenaline and other stress hormones suppress pain perception. The acute inflammatory response—the mechanism by which injured tissues signal pain—unfolds over hours to days as prostaglandins and cytokines accumulate in the injured area. Protective muscle spasm also develops gradually rather than instantaneously. Symptom delay does not indicate the absence of injury; it reflects the normal biological timeline of injury manifestation.

What is the most common injury in rear-end accidents?

Cervical strain-sprain (whiplash) is the most common documented injury in rear-end collisions, accounting for the majority of post-crash complaints. The deeper injury components—facet joint capsular ligament damage, intervertebral disc tears, and in some cases mild traumatic brain injury—are less frequently diagnosed but no less real. Up to 85% of all neck injuries from motor vehicle crashes result from rear-end impacts specifically.

Why don’t my injuries show up on X-ray or MRI?

Standard X-rays visualize only bony structures and cannot detect ligament micro-tears or capsular injuries. Conventional MRI has limited resolution for soft tissue injuries at the micro-scale. The absence of abnormal imaging findings does not mean the patient is uninjured—it means the injuries are occurring at a tissue level below the resolution threshold of standard clinical imaging. Biomechanical analysis, functional testing, and clinical examination are often more diagnostically informative than imaging alone in these cases.

How does the ‘eggshell plaintiff’ doctrine apply to rear-end collisions?

Under California’s eggshell plaintiff doctrine, a defendant is fully liable for all harm caused by their negligence, even if the plaintiff had a pre-existing vulnerability—such as prior cervical disc degeneration—that made them more susceptible to injury. If the rear-end collision aggravated a pre-existing condition and produced greater harm than would have occurred in a completely healthy individual, the defendant is still responsible for the full extent of the harm caused.

What role does headrest position play in rear-end collision injury?

Headrest geometry is one of the most significant modifiable factors in rear-end collision injury severity. A properly positioned headrest—at the same height as the center of gravity of the head and as close to the head as possible—limits the rearward excursion of the head during the extension phase, reducing cervical spine loading and injury severity. Conversely, a headrest that is too low, tilted too far rearward, or positioned far from the occupant’s head provides minimal protective value and may actually function as a fulcrum that worsens hyperextension injury.

When should I contact a Los Angeles rear-end collision attorney?

You should consult with a rear-end collision attorney in Los Angeles as soon as possible after any crash that results in injury, even if symptoms are mild or just beginning. Early attorney involvement allows for prompt preservation of evidence (including EDR data, surveillance footage, and vehicle inspection), coordination with medical providers, and protection against the common insurance carrier practice of seeking early recorded statements before you have a full picture of your injuries. There is no cost to consult with an attorney—most personal injury lawyers, including our firm, handle these cases on a contingency fee basis.

Conclusion: Invisible Injuries, Real Consequences

Rear-end collisions are the most common mechanism of serious cervical spine injury in the United States, and they are among the most frequently minimized by the insurance industry. The biomechanical evidence reviewed in this article is not ambiguous: the forces generated even in low-speed rear impacts are sufficient to micro-tear cervical ligaments, damage facet joint capsules, herniate intervertebral discs, and in some cases produce concussive brain injury—all in a fraction of a second, before the victim’s nervous system can even process that an impact has occurred.

The symptoms that follow—neck pain, headaches, arm numbness, cognitive difficulties—are not imaginary, are not exaggerated, and are not caused by the desire for compensation. They are the predictable biological consequences of well-documented tissue damage occurring at the intersection of Newton’s laws and human anatomy.

Insurance companies know this. Their claims that ‘the car wasn’t damaged, so you can’t be hurt’ are not made in good faith—they are tactical positions designed to reduce payouts on legitimate claims. The medical and biomechanical literature provides powerful tools to counter these arguments, and experienced personal injury counsel knows how to deploy them.

If you or a member of your family has been injured in a rear-end collision in Los Angeles or anywhere in Southern California, the legal team at Steven M. Sweat, Personal Injury Lawyers, APC is available to evaluate your case. Our firm has spent over 30 years representing injured victims in Los Angeles County and the surrounding Southern California region. We have recovered millions of dollars for clients whose injuries were dismissed, minimized, or denied by insurance carriers—and we know how to make the science work for you.

References and Further Reading

The following peer-reviewed and government sources inform the medical and biomechanical content of this article. Citations are provided for reference and verification purposes:

• Spitzer WO, et al. Scientific monograph of the Quebec Task Force on Whiplash-Associated Disorders. Spine. 1995;20(8 Suppl):1S-73S.
• Barnsley L, Lord SM, Wallis BJ, Bogduk N. The prevalence of chronic cervical zygapophyseal joint pain after whiplash. Spine. 1995;20(1):20-26.
• Lord SM, Barnsley L, Wallis BJ, Bogduk N. Chronic cervical zygapophysial joint pain after whiplash. A placebo-controlled prevalence study. Spine. 1996;21(15):1737-1745.
• Yoganandan N, Cusick JF, Pintar FA, Rao RD. Whiplash injury determination with conventional spine imaging and cryomicrotomy. Spine. 2001;26(22):2443-2448.
• Siegmund GP, Myers BS, Davis MB, Bohnet HF, Winkelstein BA. Mechanical evidence of cervical facet capsule injury during whiplash: a cadaveric study using combined shear, compression, and extension loading. Spine. 2001;26(19):2095-2101.
• Pearson AM, et al. C5-C6 disc space narrowing as an indicator of cervical sprain in rear-end motor vehicle crashes: prospective radiologic study. Radiology. 2004;230(3):655-661.
• National Highway Traffic Safety Administration (NHTSA). Traffic Safety Facts: Rear-End Crashes. U.S. Department of Transportation. DOT HS 811 622.
• Curatolo M, Bogduk N, Ivancic PC, McLean SA, Siegmund GP, Winkelstein BA. The role of tissue damage in whiplash-associated disorders: discussion paper 1. Spine. 2011;36(25 Suppl):S309-S315.
• Vetti N, et al. Are MRI findings in the acute phase related to neck disability and pain three months after whiplash injury? Eur Radiol. 2010;20(5):1160-1168.
• Hartwig M, Roudsari B, Nathens A, Neff M. The relationship between the severity of vehicular damage and injury among occupants involved in motor vehicle crashes. Injury. 2014.

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