Rear-end car collisions subject the human body to rapid acceleration forces that often exceed the tolerance of soft tissues in the neck and spine. Even a seemingly “minor” fender-bender can impart forces far greater than what the body experiences in everyday activities, explaining why whiplash and other injuries frequently occur despite minimal vehicle damage. This chapter breaks down common rear-end collision scenarios by speed, explains key physics concepts like delta-V and acceleration, and presents biomechanical evidence on injury thresholds for the neck and brain. The goal is to clarify, in an authoritative yet accessible way, how and why the forces in rear impacts can overwhelm human tissue limits – even at low speeds – leading to real injuries.
Not all rear-end crashes are alike. The severity of a collision – and the resulting injuries – can vary widely based on the speed change (delta-V) involved. We can roughly classify rear impacts as low-speed (under ~15 mph), moderate-speed (around 15–40 mph), and high-speed (40+ mph), though any cutoff is approximate. In each case, the physics of the crash dictates how much force is transferred to vehicle occupants, and thus what kinds of injuries are likely.
Low-speed rear-end collisions are common in parking lots and stop-and-go traffic. These crashes often result in little or no visible vehicle damage – for example, a “tap” at a stoplight. However, the absence of crumpled bumpers does not mean an absence of force on the occupants. In fact, modern bumpers can rebound without much damage while still transmitting a sharp jolt to the people inside. Research shows that even very low delta-V impacts can and do cause whiplash-type injuries. One analysis of 105 “minimal damage” crashes (mean delta-V ~6.3 km/h, or only ~4 mph) found the struck vehicles experienced an average acceleration of 1.4 g despite the low speed . In that group, 113 occupants sustained a total of 427 documented injuries (mostly neck/back soft-tissue injuries) within five weeks of the crash . Clearly, even a single-digit delta-V can deliver a significant acceleration to the body.
Volunteer crash tests and real-world data have established a surprisingly low threshold for whiplash injury. In one series of carefully controlled rear-impact tests, healthy adult volunteers (with no prior neck issues) were exposed to very low-speed collisions. The results showed about 29% of volunteers developed neck pain symptoms at a delta-V of only ~2.5 mph, and about 38% at 5 mph . These symptoms were short-lived and minor, but they demonstrate that even single-digit mph changes in velocity can sprain neck tissues. In other studies, symptoms have been observed in 28% of test subjects at 3.0 mph collisions and 63% at 7.5 mph collisions . Notably, these tests used prepared, athletic subjects who knew the impact was coming – real drivers struck by surprise might fare worse. Epidemiological research confirms this: one study documented injuries in 38% of women and 19% of men in actual crashes with an average delta-V of just ~4 mph . Another found that claims of injury were made in 21% of rear crashes that caused <$500 in vehicle damage . All of this disproves the old myth that “you can’t get hurt in a fender-bender.” In reality, low-speed rear impacts frequently cause whiplash (neck sprain/strain), even though such soft-tissue injuries might not be visible on X-rays or MRIs.
Why do these minor collisions cause disproportionate injury? The answer lies in the biomechanics of whiplash. In a typical rear-end impact, the struck vehicle lurches forward, pushing the seat (and the occupant’s torso) forward suddenly under the pelvis and mid-back. The head, however, initially lags behind (because it’s not in contact with the seat back), causing the neck to experience a sharp S-shaped curvature – the lower neck is forced into extension while the upper neck flexes, all within milliseconds . This abnormal motion can stretch the cervical spine beyond its normal range. Studies have shown that during even low-speed rear impacts, the movements between some vertebrae can exceed normal physiological limits, especially during that initial whiplash motion phase . In other words, certain spinal segments undergo more bending or shear than they ever would in normal activity, leading to ligament sprains, facet joint capsule microtears, and other soft-tissue damage. The occupant often has no time to brace, and the head can whip backward and forward within a quarter of a second, which is too fast for voluntary muscle guarding. Thus, even a 5–10 mph bump can deliver a “one-two” acceleration to the neck that overstretches tissues before the reflexes or seatbelts catch up.
It’s important to note that vehicle design factors can make low-speed injuries more likely. For instance, if the car bumpers engage and rebound with little deformation (as they are often engineered to do up to ~5 mph), much of the impact energy is transferred to the occupants instead of being absorbed by crumpling metal. It has been rigorously shown that a “no damage” collision can still impart a delta-V of 10 mph or more to the struck vehicle – well into the range that causes injury . In essence, the car might spring back looking fine, but the people inside feel a sharp acceleration. This is why lack of vehicle damage is a poor indicator of injury risk. Biomechanical engineers Batterman and Batterman put it bluntly: the old assumption that a minimal or zero-damage crash corresponds to a delta-V under 5 mph is simply false . A car can sustain no visible damage and yet subject its occupants to a sudden 10+ mph velocity change, which for a human neck is quite violent.
At moderate speeds (say a 15–30 mph difference in speed between vehicles), rear-end collisions generally result in obvious vehicle damage – crumpled bumpers, broken lights, deployed head restraints, etc. The increase in delta-V means the forces on occupants rise substantially compared to low-speed impacts. Soft tissues will almost certainly be pushed beyond their elastic limits, and injuries like whiplash become more severe. Occupants often experience more intense neck sprains/strains, possible disc injuries, and sometimes mild concussions due to the rapid acceleration and deceleration of the head. Indeed, medical imaging has shown that about 25% of rear-impact whiplash patients later exhibit herniated cervical discs . Such disc injuries can occur when the discs are compressed and sheared during the whiplash motion – the tough outer rings of the disc (the annulus fibrosus) can develop small tears when stretched beyond their normal range . Cadaver and computer model studies indicate that during whiplash, the lower cervical discs can undergo strains exceeding their physiological limits, providing a mechanism for these annular tears and disc derangements .
With moderate delta-V collisions, head acceleration forces also climb – often many times the force of gravity (g). Crash tests using instrumented dummies and human volunteers have measured peak head accelerations well above anything encountered in daily life. For example, one comparative study found that in a ~7 mph rear impact, the linear acceleration of the head was about 3 times higher than the highest acceleration recorded during any everyday activity, and the head’s angular acceleration was roughly 13 times higher . To put that in perspective, the jolt from a moderate rear crash dwarfs the forces from activities like plopping into a chair or jogging – it’s not even in the same league. This is consistent with the fact that people do not suffer torn neck ligaments or concussions from sitting down or hopping, yet those injuries emerge in car crashes. In volunteer impact testing at delta-V around 8–10 mph, the measured peak head accelerations often fall in the range of 5–10 g or more, depending on the exact crash pulse and whether the individual was braced. Such forces can easily stretch and strain cervical tissues. The Neck Injury Criterion (NIC) – an index used to gauge whiplash injury risk based on neck forces and bending – also rises sharply with increasing delta-V. Researchers have documented a clear relationship: the larger the change in speed in a rear impact, the higher the NIC values and the greater the likelihood of injury symptoms after the crash .
Occupants in moderate-speed rear crashes may also sustain mild traumatic brain injuries (TBIs) such as concussions, even without striking their head on anything. The rapid forward-back motion can cause the brain to slosh inside the skull, leading to shear strain in neural tissue. In fact, advanced imaging studies have detected diffuse axonal injury (DAI) in patients with whiplash, using diffusion tensor imaging (DTI) to reveal microscopic white matter damage . Six separate DTI studies reviewed in Frontiers in Neurology reported evidence of traumatic axonal injury in whiplash patients – despite those patients having “normal” CT or standard MRI scans . This means the inertial forces of a rear impact can indeed injure the brain’s wiring by stretching axons, even if there was no direct head impact. Biomechanically, the threshold for axonal injury is believed to be on the order of a few tens of percent strain (i.e. if axons are stretched more than ~10–20% beyond their resting length, they can tear or suffer dysfunction). A moderate rear-end crash can produce rotational accelerations of the head that induce exactly these levels of strain in the brain. Thus, symptoms like confusion, dizziness, or memory problems after a rear crash – often labeled “whiplash associated disorders” – may actually indicate a mild TBI from the whiplash mechanism itself.
In moderate collisions, we also start to see a higher likelihood of other injuries such as facet joint damage and muscle injuries. The facet joints (zygapophyseal joints) in the cervical spine are a known source of chronic post-whiplash neck pain. Each facet joint is encapsulated by ligaments, and these capsules can suffer partial tears or inflammation when stretched violently. Experiments have shown that facet capsule ligaments begin to yield (sustain micro-tears) at relatively modest strains – around 70–80% elongation in animal models – well before outright failure . During a 10–15 mph rear impact, it’s quite possible for certain cervical facet capsules to experience these levels of strain, especially at the C5–C7 levels where abnormal extension is concentrated. In fact, simulations and cadaver studies have demonstrated capsular strains beyond physiologic limits in rear impacts, sometimes leading to partial ruptures of the capsule . Such injuries correlate with pain: straining the facet capsule to roughly 15%–50% beyond normal can produce persistent pain responses and even nerve fiber damage in laboratory models .
Neck muscles likewise are not spared. A rear impact can impose very rapid stretching on muscles like the sternocleidomastoid and the deep neck extensors. One study predicted strains of about 7% in the sternocleidomastoid and 21% in the semispinalis capitis during a 10 mph whiplash scenario . Those strain levels exceed what is needed to cause muscle fiber injury (experiments show muscle begins to tear with strains on the order of 20% or less) . This muscle damage often isn’t apparent immediately, but elevated levels of muscle enzymes (like creatine kinase) have been observed in whiplash patients, indicating muscle fiber strain injuries . The net effect is that after a moderate-speed rear crash, an individual might have a constellation of soft-tissue injuries: strained muscles, sprained ligaments, irritated facet joints, and possibly small disc tears – even though X-rays will typically look “normal” (since bones aren’t broken).
High-speed rear-end collisions – such as being hit from behind on a highway by a vehicle traveling 40–60 mph faster – involve much greater energy transfer and often devastating outcomes. At these impact speeds, vehicles undergo severe deformation and the collision forces can approach or exceed the thresholds of serious and life-threatening injury. A very high delta-V (50+ mph, for instance) delivers a violent acceleration to the occupants that can cause fractures, dislocations, and neurological injuries in addition to severe soft-tissue trauma. For example, once delta-V rises above roughly 12–15 mph, the risk of bony cervical spine injury and even spinal cord injury increases substantially . In catastrophic rear-end crashes (such as a stopped car being hit at highway speed), occupants may suffer fractures of the vertebrae (especially at the C7/T1 junction where the neck meets the thorax), severe disc ruptures with nerve compression, or even spinal cord contusion if the force causes instability. Head injuries are also a major concern – the head might strike the head restraint or other parts of the car with great force, compounding the whiplash with direct trauma. Even if the head doesn’t hit anything, the angular acceleration in a high-speed whiplash can be extreme, potentially causing diffuse axonal injury throughout the brain. It’s well known from concussion research that higher acceleration/deceleration increases the probability of traumatic brain injury. Thus, high-speed rear impacts can produce concussions or moderate TBIs, sometimes with loss of consciousness or lasting cognitive deficits, on top of neck injuries.
From a physics standpoint, the kinetic energy of a moving vehicle increases with the square of speed. So a collision at 60 mph involves nine times the energy of one at 20 mph (since 60² vs 20²). While cars have crumple zones to absorb some of that energy, in a high-speed rear-ender those crumple zones may fully collapse and still not dissipate all the force. The remaining energy is imparted to the struck car and its occupants in a very short time. Crash test dummies in standardized rear-impact tests (like the Insurance Institute for Highway Safety’s 20 mph rear impact sled tests for seat/head restraint ratings) record high accelerations that engineers attempt to limit with better seat design. Newer “anti-whiplash” seats allow the seatback to yield and catch the torso more gently, and head restraints are designed to catch the head earlier, all to reduce peak neck loads. These systems can be effective – some advanced head restraint designs have shown up to a 50–75% reduction in whiplash injury risk in real crashes – but they are not foolproof, especially at very high speeds. In summary, at highway speeds, the forces are so high that even the best engineered seats and restraints may not prevent injury. One can expect not only soft-tissue neck injuries but also more serious damage, and in the worst cases fatalities or permanent disabilities, from upper spinal cord trauma or severe brain injury.
To fully appreciate why rear-end collisions can overwhelm the body, it helps to understand some basic crash physics terminology:
Why do rear-end collision forces frequently exceed what our tissues can handle? The human neck is reasonably strong and flexible for normal life, but it has limits. Here we summarize key tissue tolerance thresholds relevant to whiplash:
The neck’s ligaments (which connect bone to bone) and facet joint capsules provide stability but can only stretch so far before incurring damage. Under normal conditions, these tissues experience small strains during neck movements – well under 10% elongation. Whiplash can impose much larger, rapid strains. The facet joint capsule, for example, has been identified as a prime injury site in rear impacts. In controlled experiments, capsular ligaments in the cervical spine show microscopic tearing (“yield”) at about 70–80% strain, corresponding to sub-failure forces . Gross failure (complete rupture) occurs at around 100% strain (double their resting length) or a few Newtons of force in animal models . In a real car crash, it’s unlikely the capsule outright rips in half; instead, it may reach that yield point where some collagen fibers tear and the capsule becomes lax. That is enough to trigger pain. Studies by Winkelstein et al. demonstrated that stretching the facet capsule beyond a certain threshold (on the order of 15–20% beyond its normal range) can cause persistent pain responses in animals, due to injured nerve endings in the ligament . High-speed imaging of cadaver necks in rear impacts has indeed shown facet capsule strains exceeding physiological limits in the lower cervical spine . Moreover, facet joint surfaces can suffer small fractures or cartilage injuries in severe whiplash, and the synovial joint can bleed – all painful lesions documented in autopsies of crash victims .
Other neck ligaments (like the anterior longitudinal ligament that runs along the front of the spine, and the interspinous ligaments between vertebrae) can also be injured. Rapid hyperextension can tear the anterior longitudinal ligament or the front of the disc. The review by Curatolo et al. noted that tears of the anterior disc and longitudinal ligament have a pathologic basis in whiplash trauma – essentially, when the neck is thrown backwards beyond its limit, the front of the disc and ligament can partially rupture . These injuries may not show up on MRI unless severe, but they can generate chronic pain (discogenic or ligamentous pain). In summary, the tolerance of cervical ligaments is often exceeded in a rear impact when the neck is forced into abnormal shapes. The ligaments might not snap completely, but even partial fiber disruption constitutes a sprain that can cause significant pain and instability.
Cervical discs – the cushions between vertebrae – have a tough outer ring (annulus fibrosus) and a gel-like core. During whiplash, discs are subjected to compression, bending, and shearing. The annulus fibrosus is composed of collagen fibers oriented in layers; it normally allows the spine to flex and rotate a bit while keeping the vertebrae aligned. However, if the disc is compressed and twisted beyond its limit, annular fibers can tear. In vitro experiments have indicated that the annulus can fail under high shear/rotation combined with compression. In fact, one cadaveric study cited in the literature found that lower cervical disc annuli can experience strains above physiological range during rear impacts, supporting the possibility of annular fissures from whiplash . A tear in the annulus (especially in the front from hyperextension) may not cause immediate herniation of the nucleus, but it can lead to pain and, over time, disc degeneration or herniation.
Clinical evidence backs this up: imaging studies several months or years post-injury show a higher incidence of disc herniation in whiplash patients. As noted, about 25% of whiplash victims eventually have herniated cervical discs , and about 20% have herniations with nerve root impingement symptoms (radiculopathy) . One long-term study by Panjabi et al. (2004) found that whiplash patients were twice as likely to require cervical disc fusion surgery down the line compared to a control group . This suggests that the crash forces pushed some patients’ discs past the point of recovery, initiating degenerative changes or protrusions that later needed surgical correction. In terms of thresholds: a healthy cervical disc can withstand normal head movements (~45° of flexion/extension, etc.), but a whiplash might momentarily force a segment beyond that – for instance, a sudden 20° hyperextension at C6–C7 combined with shear. That kind of loading could easily produce annular fiber strains > 15%, enough to disrupt the tissue .
It’s also worth mentioning the dorsal root ganglia (DRG) – nerve clusters near the discs – which research (especially by Yoganandan and Cusick) suggests can be injured by the hydraulic pressure transient in the spinal canal during whiplash. When the neck snaps, cerebrospinal fluid can be forced to and fro, possibly bruising the DRGs and causing radiating pain. While this is a different mechanism (hydrodynamic injury), it underscores that the disc/nerve complex in the cervical spine has multiple vulnerabilities during a crash.
The human brain is a soft organ suspended in cerebrospinal fluid inside the skull. Rapid acceleration or deceleration – especially angular acceleration – can cause the brain to deform (stretching and compressing). There is a known tolerance threshold for diffuse axonal injury: research suggests that when brain tissue experiences strains on the order of 5–10%, neuronal function is disrupted, and above ~15–20% strain, many axons can tear, leading to a concussion or diffuse axonal injury. In a prototypical concussion from a head impact, the head might undergo 50–100 g linear acceleration and/or 4,000–6,000 rad/s² angular acceleration. A pure whiplash (no head impact) typically involves lower linear accelerations but can still have considerable angular acceleration of the head-neck. The exact g-forces in a whiplash depend on the crash severity and head restraint effectiveness, but head resultant accelerations of 10–20 g have been recorded in moderate rear impacts – enough to potentially cause a mild TBI if the head rotates rapidly.
Crucially, advanced imaging and neuropsychological testing have confirmed that concussions can result from whiplash mechanisms alone. As referenced earlier, DTI studies show white matter changes (a sign of axonal injury) in patients who suffered whiplash without direct head strikes . These patients often report classic post-concussive symptoms (memory issues, headaches, difficulty concentrating) in addition to neck pain. The DTI findings – e.g. reduced fractional anisotropy in certain tracts – indicate that the brain’s microstructure was affected. While all six studies in one review were case reports (each documenting a whiplash-induced DAI in an individual patient) , the consistency of findings leaves little doubt that the inertial forces in a rear-end crash can exceed brain tissue tolerance. From a mechanics standpoint, if the head is rapidly whipped back and forth with peak angular velocities of, say, 50–100 rad/s, the rotational strain in the midbrain can reach those critical percentages. Even without loss of consciousness, the person can sustain a mild diffuse brain injury.
In terms of thresholds: one can think of the brain’s tolerance in terms of strain or in terms of angular acceleration duration. Short bursts of very high acceleration can be as damaging as longer exposures to moderate acceleration. Current injury biomechanics models (like the Gennarelli brain injury criterion or newer brain injury metrics) continue to be refined, but practically, if a rear impact makes someone’s head bobble violently enough that they feel dazed or see stars, chances are the brain experienced forces beyond its safe limit. This aligns with the observation that some rear-crash victims develop post-concussive syndromes even though nothing struck their head.
The common theme across all these tissues – ligaments, discs, muscles, brain – is that a rear-end collision can impose loads that outstrip the tissue’s ability to elastically deform without damage. The spine is an amazing structure, but it isn’t designed for instantaneous accelerations of many g’s. Each tissue has a threshold (force or strain) above which microstructural failure begins: collagen fibers tear, muscle fibers rupture, axons stretch and break. Unfortunately, the accelerations in even a low-to-moderate crash easily reach or surpass those thresholds. For perspective, a study in Spineconcluded that many whiplash injuries likely stem from actual lesions in the tissues, not just “benign” motion . They emphasized that the absence of findings on MRI doesn’t mean no injury occurred – rather, it often means the damage is at a microscopic level or in structures not easily imaged (facet capsules, tiny disc tears, etc.) . In essence, the forces have exceeded the threshold for injury, but the injury is in soft tissue (which is invisible on X-ray and hard to see on MRI). This is why whiplash is sometimes called an “invisible injury” – very real to the patient, though hard to document objectively.
One point bears repeating, because it is a frequent source of confusion in legal and insurance settings: the amount of vehicle damage is not a reliable indicator of injury risk or severity. Rear-end crashes often produce little car damage yet significant occupant injury, and conversely, a crash that totals a car can leave occupants relatively unscathed (if energy was absorbed well). The relationship is complex. Vehicles are designed with crumple zones to absorb kinetic energy, but the rigid bumper systems in low-speed collisions may not crumple at all – they rebound like a spring. As mentioned, engineering analyses have shown that a car can sustain essentially no visible damage at impact speeds that give the struck car a delta-V of 10 mph or more . That 10 mph delta-V is squarely in the injury-producing range, even if the bumper looks fine. This was demonstrated by engineers who used crash reconstruction algorithms on undamaged vehicles: the math showed that considerable momentum exchange can occur with zero crush (the energy goes into pushing the car forward, not breaking the bumper) . Thus the old adage “no crash damage, no injury” is a myth .
Real-world data support this: Farmer et al. reported that 1 in 5 drivers (21%) in rear crashes with repair costs under $500 still reported neck injuries . Minimal damage doesn’t equate to minimal acceleration. In fact, an unyielding bumper can make things worse for the occupant by resulting in a shorter, higher acceleration pulse. A lightly damaged or undamaged rear end often means the collision was in the elastic range of the bumper – like a rubber ball that bounces back, transferring energy. Compare that to a moderate collision where the bumper and trunk crumple heavily (absorbing energy over a longer time); the latter might actually subject the occupant to a lower peak acceleration despite the greater car damage.
Another reason vehicle damage can be misleading: small cars vs. large cars, and bumper alignment. If a large SUV hits a small sedan, the sedan might crumple (visible damage) and absorb energy, possibly reducing acceleration. But if two equal cars bump and barely scratch, their occupants might get a sharp jolt. Each scenario is different. This is why investigations of injury causation rely more on delta-V and acceleration data than on eyeballing damage. Modern crash sensors and event data recorders (EDRs) can sometimes provide the delta-V of a crash, which is far more informative for injury analysis than repair bills.
It’s also important to dispel the courtroom tactic where defense biomechanical “experts” try to equate crash forces with everyday forces to argue an injury is implausible. For example, they might say “the acceleration was similar to sitting in a rocking chair” – which is a flawed and invalid comparison . Scientific reviews have invalidated these arguments: A 2021 literature review emphatically concluded that comparing an occupant’s crash acceleration to activities of daily living is not scientifically valid, because it ignores the vastly higher injury risk of crash accelerations . If everyday activities had the same injury risk as a 7 mph rear-end collision, we’d expect people to sprain their necks routinely during daily life – which simply doesn’t happen . The truth is that even low-speed crashes are unique events: the alignment of forces, the multi-directional jolt, and the lack of anticipation all combine to make them far more injurious than any voluntary movement a person makes.
Rear-end collisions, even at seemingly insignificant speeds, involve physics that can readily overpower the human body’s tissue tolerances. We’ve seen that a change in velocity of just a few miles per hour can translate to accelerations that stretch neck ligaments, strain spinal discs, and jar the brain. The delta-V of a crash is a critical factor – higher delta-V means more energy to dissipate – but even modest delta-V impacts have been proven to cause whiplash injuries in a significant percentage of people . Acceleration forces in rear impacts routinely reach levels multiple times greater than those encountered in normal activities, which explains why comparing a crash to a minor jolt in daily life is misleading . Crash tests and biomechanics research confirm a positive correlation between impact severity and neck injury criteria, yet also show no clear “safe” threshold below which injuries never occur – injuries have been documented at delta-Vs as low as 2.5–5 mph in some cases .
From a biomechanical perspective, the forces in a rear-end crash frequently exceed the human neck’s physiological limits. The facet joint capsules, cervical discs, and associated musculature can all be pushed beyond their elastic capacity, leading to microtears and inflammation that manifest as pain and dysfunction. These soft-tissue injuries often cannot be seen on imaging, but their presence is supported by both laboratory studies (showing tissue damage at relevant force levels) and clinical outcomes (persistent pain in a subset of whiplash patients corresponds to probable tissue lesions ). The brain, too, can sustain subtle injury from the sudden acceleration-deceleration of a rear impact, as evidenced by DTI scans showing axonal injury in whiplash patients .
Finally, it is critical to understand that low vehicle damage does not equal low biomechanical force on the occupants. A car’s lack of damage can mask a high-energy transfer to the people inside, because modern cars may not crumple at low speeds even as they rapidly accelerate the occupants. Studies indicate at least a 20% injury chance in minimal-damage crashes , and engineering analyses have refuted the notion that one can judge injury potential by a quick look at the bumper . For chiropractors, attorneys, and patients, this knowledge is empowering: it means that complaints of pain after a minor rear-end collision are not only plausible but expected in a significant number of cases, given the physics involved. The whiplash mechanism can produce real injuries that may require treatment and time to heal, even if the crash seemed minor and the car “looks OK.”
In summary, the physics of rear-end collisions – rapid delta-V changes and high accelerations – often overwhelm the body’s normal tissue tolerances. This results in whiplash-associated disorders ranging from neck sprains and disc injuries to concussions, even at speeds where one might not anticipate serious injury. Understanding this helps one appreciate that rear-end crash injuries are grounded in solid science, not anecdote. The forces are quite real and measurable, and so are the injuries that frequently follow. Armed with this knowledge, healthcare providers can better educate patients, and legal professionals can more effectively argue the reality of these injuries, countering the skepticism that sometimes surrounds “low-speed” crashes. The bottom line: physics doesn’t lie – if the forces exceed what the human neck and brain can handle, injuries will occur, regardless of how pristine the car’s bumper might appear.
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