Whiplash Associated Disorder (WAD) 

Harold and Crewe were the first to use the term whiplash in 1928. Motor vehicle collisions (MVC) are the greatest cause for whiplash injuries and is a rather large topic within the world of physical therapies. Approximately 50% of individuals will recover following a whiplash injury within the first 3 months post injury whilst a remainder of individuals will experience mild to moderate long-term disability (9).

Whiplash-associated disorders (WAD) was defined by the Quebec task force in 1995 as ‘an acceleration–deceleration mechanism of energy transferred to the neck, it is caused by rapid hyperextension or hyeprflexion of the patient's head from sudden acceleration or deceleration (13). It may result from rear-end or side-impact motor vehicle collisions, but can also occur during driving or other mishaps.' 

Despite Quebec's definition, a whiplash injury can also result from a front-end collision, however, the majority of clinical research for whiplash injuries are based around rear impact MVCs. The impact of a MVC can result in bony or soft- tissue injury (whiplash-injury).  Any damage or abnormal change in soft muscular or connective tissue caused by injury are referred to as soft tissue lesions (10). A WAD is generally considered an acute soft tissue injury of the neck with symptoms such as neck pain and stiffness, shoulder weakness, dizziness, vertigo, headache, memory loss and parasthesia in the upper extremities (10). 

The Classification of Whiplash

The Quebec Task Force on Whiplash Associated Disorders classifies a WAD into four grades and is based upon the severity of a person’s symptoms and signs (7):

• Grade 0: No complaints of neck pain and no physical signs.
• Grade I: Complaints of pain in the neck, stiffness or tenderness only. No physical signs.
• Grade II: Neck complaint and musculoskeletal signs including decreased range of motion and point tenderness.
• Grade III: Neck complaint, musculoskeletal signs and neurological signs including decreased or absent deep tendon reflexes, muscle weakness and sensory deficits.
• Grade IV: Neck complaint and fracture or dislocation.

Incidence

The incidence of a WAD in the UK averages to about nine per one thousand people, the highest in Europe. WADs are usually seen in rear-end, low-impact collisions in 90% of road traffic accident cases at speeds of 14 mph. Injuries occur when the trunk is forced back on the seat with hyperextension of the neck followed by a sudden forward recoil (27).

Surprisingly, after searching around 'the biomechanics of the neck and body during whiplash injury', it appears that the medical research world has predominantly focused their attention on rear impact collisions only, despite the possibility of injury occurring during a side or front-end collision. 

Although we can accept that neck injury is mostly regarded as resulting from rear end collisions, we should remind ourselves that almost one third (or approximately 27%) of all neck injuries occur from frontal impacts (16). It has been noted that there might be research papers on the biomechanics of the neck and body during the two other types of collisions. 

However, none could be found in as much detail with what biomechanically happens during a rear impact collision. The focus here will be based around the biomechanics of the body during a rear impact MVC.

Biomechanics & Neck Movement During A Rear Impact Collision

Here helps support and confirm the existence of WADs, especially for rear impact collisions. The above image demonstrates four different phases that biomechanically happen to the head and neck during such an incident. Kinematics and kinetics have been studied using crash dummies, human cadavers, human volunteers and computer models (5). 

During a typical rear-end MVC, injury is caused by abnormal biomechanics of neck motion. A study by Bogduk and Yoganadan (2001) illustrated the body's response after a rear-end impact collision and showed ten different phases that the body can go through from 0 to 400 milliseconds (ms) (5). The magnitude of the cervical spine dynamics and their timing vary between subjects in different vehicles and between different subjects in the same vehicle (5).

For the sake of simplicity, it is suggested that neck movement during a rear impact collision undergoes four main stages:

I. Normal phase: The cervical spine (neck) is held in a neutral position during seated posture. Kaneoka and Ono (2002) explain how during the time period between 0-40 ms of impact, the seat already begins to press the back of an individual and the spine begins to straighten. 

However, cervical motion at this stage has not yet occurred, nor is there a muscular response within the neck (15).

II. S-Shape phase: This phase occurs almost immediately following rear-impact where the neck initially undergoes a horizontal shear force. Also known as the 'retraction' phase, the neck is 'drawn back' horizontally inward to create a 'S-shaped' curvature (5, 12). 

Here, simultaneous upper cervical spine (UCS) flexion occurs along with lower cervical spine (LCS) extension to force the vertebrae within the neck to create an 'S-shape' (5, 12). Neural structures in the UCS and their capsular ligaments are at risk of injury during this phase from facet joint separation and UCS flexion (5, 12, 20). 

According to Panjabi et al., (2004) the potential for injury is the greatest during the s-shape phase as injurious intervertebral rotations can occur prior to when the head contacts the head rest and before cervical musculature contraction occurs to protect the spinal region (which happens later) (20). Bogduk and Yoganandan (2001) highlight how the 'sigmoid' S-shape deformation of the cervical spine occurs at between 50 to 75 ms from MVC impact. 

An outcome during the S-shape whiplash phase can create changes within the cerebrospinal fluid pressure and cause a spinal ganglia injury which can potentially create pain, increased sensitivity, numbness and muscle weakness (20). 

III. Cervical Spine Extension: During this phase the mandible tends to maintain its position in space whilst the upper jaw (or maxilla) lifts up off an inert mandible to open the mouth (4). The cervical spine may fully extend by approximately 200 milliseconds into a C-shape curvature post impact (5). During the extension phase, the anterior structures of the cervical vertebral column can be strained i.e. the intervertebral discs, anterior longitudinal ligaments, pre vertebral muscles and oesophagus or larynx (4). The sternocleidomastoid muscles elongate during hyperextension and posterior structures of the neck vertebrae are subject to compression such as the zygapophysial joints and the spinous processes (4). 

Bogduk (1986) emphasises how the head is not thrown backwards into extension as such, rather its movement is impacted by the trunk moving forwards during this phase. The torso tends to move in a forward and upward motion upon impact whilst the head lags behind as the result of inertia (20). Thus, the torso is responsible for creating the C-shape extension curvature and not the motion of the cervical spine alone. According to Bogduk (1986), injury of the neck is at its greatest risk during the extension phase as there are no anatomical structures to stop the head from extending beyond the limit of its natural range of movement. 

IV. Cervical Spine Flexion: The head achieves its maximum forward excursion by 400 ms (4). Contact of the chin with the chest limits flexion of neck movement and prevents over flexion. During this phase, the vertebrae move within the natural range of motion (4). 

Their study concluded to provide evidence that tissue injury and inflammation in whiplash injury can be objectively visualised and quantified using PET and CT imaging and suggested that lesions in peripheral tissue are respnosible for the development of persistent pain and disability in whiplash injuries. 

MRI Scans

Although this research study is dated back to 2006, Johansson's (2006) study is extraordinary. If litigation whiplash cases amount to the tune of over three to four billion bucks per annum, one can only ask why there are not more detailed modern research case study articles alike. 

Johansson studied three injured patients post MVC who had been examined and diagnosed with no structural lesions initially. One patient, 'Patient 1', was examined via MRI scan and the second patient was examined via 'radiological examinations'. The third, 'Patient 3', underwent clinical examinations at a university hospital with no further detail provided as to what methods were used during the examination process. Two patents were initially diagnosed with 'psychogenic' or 'psychosomatic' disorders and the other signed off as 'fit to work'. 

What is interesting to note is that all three patients were not diagnosed with severe lesions during their acute phases of injury post MVC after clinical examination, but were diagnosed after two to several years post MVCs. Scar tissue had been discovered in all three case studies and all underwent surgery. 

In 'patient 1', scar tissue was found around the odontoid process of C2 and around C1/C2 vertebrae which affected their rotational range of movement and instability was found at C0/C1 with ligamentous injury. It was also discovered that Patients 2 and 3 had scar tissue around the odontoid process of C2 and rotational movements of their heads made either the dens or scar tissue come into contact with their spinal cord. Diagnoses originally made were reclassed as 'severe' and all patients underwent cervical surgical fixation which eradicated their extreme symptoms. 

Perhaps a warning for healthcare practitioners; should patients' symptoms persist despite having had medical imaging (via MRI) during the early stages post injury of a MVC with negative findings, a request for a review via MRI, PET or CT scanning is necessary.

1. Aarnioa, M., Fredrikson, M., Lampa, E., So ̈rensene, J., Gordha, T., Linnman, C. (2022)Whiplash injuries associated with experienced pain and disability can be visualized with [11C]-D-deprenyl positron emission tomography and computed tomography, Pain, 163; 3: 489-495. 

2. Alicia, T., Kapur, S., Mutagi, H. (2014) Whiplash Injury, Continuing Education in Anaesthesia, Critical Care & Pain, 14; 4: 167-170.