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Documentation:FIB book/Spine limits in axial compressive injuries, and how spinal cord injuries are evaluated

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Overview

1.0 Background on Spinal Dislocations and the Spinal Cord

1.1 Epidemiology

Misalignment observed between C6 (superior) and C7 (inderior) vertebrae on sagittal CT scan
Figure 1. CT scan of Spinal Dislocation between C6 and C7

Vertebral dislocations are a significant subset of spinal injury, accounting for 45% of vertebral column injuries[1]. Axial compression of the spine can cause vertebral dislocation, which can injure the spinal cord. Injuries to the spinal cord are most common in young adults, with individuals under 30 accounting for approximately two-thirds of all acute spinal cord injury (SCI) cases[1]. The most common cause of an SCI is a traffic collision, with motor vehicle, pedestrian, and bicycle collisions accounting for 40-50% of cases. Another common injury mechanism is falls, with an incidence rate of 20%. Most spinal dislocations and resultant SCIs sustained in traffic collisions occurred in high-speed motor vehicle accidents [1].

This review aims to cover the anatomy and mechanisms of spinal dislocations, relevant spinal dislocation tolerances, and SCI classification and physiological effects.

1.2 Overview of Spinal Dislocations

The Sagittal plane differentiates the left and ride side of the body
Sagittal Plane

A vertebral dislocation results from significant relative transverse translation of one vertebra relative to an adjacent vertebra [2][3]. This most commonly occurs in the sagittal plane (displayed in Figure 2) in the anterior direction [2] and less commonly laterally and posteriorly[3]. Spinal dislocations can occur with or without vertebral fracture but are often combined[4].

At the vertebral level, spinal dislocations are classified as unilateral or bilateral. In a unilateral spinal dislocation, the articular surface of only one impacted vertebral facet joint loses contact. In contrast, contact between both vertebral facet joints is lost in a bilateral spinal dislocation, which is associated with a greater degree of vertebral displacement due to the greater instability of the structure. The primary mechanism for unilateral dislocations is a combination of flexion and rotation, while flexion along the spinal axis contributes to bilateral dislocations[5]. Dislocations may occur with soft tissue failure only (referred to as a facet dislocation[2]) or with fractures to one or more parts of the vertebrae, in which case they are classified as fracture-dislocations. The latter is the most common mechanism of spinal injury leading to SCI [2][6].

2.0 Biomechanics of Spinal Dislocations From Axial Loading, Spine and Spinal Cord Injury Tolerances

2.1 Compressive Axial Loading

Compressive axial loading of the spine is the application of a force along the vertical axis of the spine. This compressive force compromises the structural integrity of the spine and can often lead to vertebral fractures or dislocations. This type of force is often seen with head-first impacts, such as those in sports or falls, and high-speed impacts in car crashes.

2.2 Spinal Components Responses to Compressive Axial Loading

Various anatomical structures, such as the vertebral body, intervertebral discs, and ligaments, assist the spine in withstanding axial loading[7]. These structures are impact absorbers, levers, and stabilizers. When impact forces exceed the natural tolerance of these soft and hard tissues, they fail and reduce or entirely eliminate their capacity to protect the spinal cord[2].

Each Functional Spinal Unit (FSU) — consisting of two adjacent vertebrae, their intervertebral disc, facet joints, and supporting ligaments — contributes to spinal stability as part of an interdependent system that also includes muscular control[7].

2.2.1 Osseous Structures

Vertebrae are the primary bony structure of the spinal column. These vertebrae are designed to withstand dynamic forces while maintaining a wide range of motion. The vertebral bodies are primarily composed of cancellous bone encased in cortical bone and form the central load-bearing structure of the spine[7]. The anterior vertebral body (centrum) is the primary structure distributing axial loads[7]. The sizes of the vertebrae in the spine increase from the top (cervical spine) to the bottom (lumbar spine) due to the rising axial loads produced by gravity[7], Similar to the size increase, mechanical properties of strength are demonstrated with the lumbar spine having higher axial failure limits than the cervical spine.


The vertebral arch also plays a role in compressive load distribution. Facet joints, located at the junction of each vertebral body, assist in transferring compressive forces and are integral in controlling the cervical spine's rotational, bending, and extension movements[7].

2.2.2 Intervertebral Discs

Lateral and Superior view of the spinal column

Intervertebral discs are crucial in distributing axial loads and shock absorption[7]. Centrally located within the disc, the nucleus pulposus cushions against compressive forces[7]. The nucleus pulposus is encased within the annulus fibrosus, providing additional resistance to concentric axial loads[7]. When subjected to eccentric axial loads, the annulus fibrosus can bulge, leading to disc herniation[7]. As axial loads increase, a disc’s ability to absorb compressive forces degenerates. If this load exceeds the disc’s tolerance, the disc could rupture or collapse, which could lead to nerve compression or other spinal injuries[7].

2.2.3 Facet Joints

Superior and lateral views of the thoracic (Left), cervical (middle) and lumbar (right) spine. The blue highlights are the facet joints

Like intervertebral discs, Facet joints provide articulation between segmental levels[7]. Their primary purpose is to guide movement and resist shear forces, and they also bear some axial load particularly during extension[7]. The orientation and morphology of the facet joints at different spinal levels can influence injury patterns[3]. For instance, the orientation of the superior articular facets in the cervical spine, that allow for greater mobility may contribute to its higher susceptibility to dislocation compared to the thoracic or lumbar spine [3].

2.2.4 Ligaments and Spinal Musculature

Ligaments of the Spine

An FSU is stabilized by numerous viscoelastic ligaments[7]. These ligaments act as passive stabilizers, providing tension-band and translational support [2]. They contribute to the spine’s resistance towards axial loads by preventing excessive motion and maintaining the integrity of the spinal column[2]. If compressive loading causes instability, the capsular ligaments may rupture indirectly, from shear loading [2].

2.3 Spinal Cord

2.3.1 Basic Anatomy of the Spinal Cord

The spinal cord is a cylindrical structure of nervous cells within the vertebral column that transmits information between the brainstem and body. It includes an inner core of white matter and an outer layer of gray matter. The white and grey matter core is protected by three outer meninge membranes: the dura mater, arachnoid mater, and pia mater. The primary function of the outer gray matter core is to process information, while the white matter core transmits signals to the body[8]. The spinal cord has four main sections: cervical, thoracic, lumbar, and sacral, each controlling the upper limbs, trunk, lower limbs, and pelvic region, respectively. An injury to the spinal cord disrupts the transmission of information between the brain and the section of the spinal cord at and below the point of injury[9].

2.3.2 Mechanisms and Impact on the Spinal Cord

Clinically, compression and/or flexion is described as the cause of spinal dislocation [2]. However, these compressive flexion descriptions do not necessarily describe the forces involved at the vertebral level. The dislocation's most consistently observed failure mechanism at the vertebral level is after a large transverse shear force is applied at the joint[2]. However, the initial conditions, including axial forces or spinal orientation during loading, can influence the likelihood and severity of such shear forces during injury. Dislocations cause narrowing of the spinal canal between the posterior arch of one (typically superior) vertebra and the vertebral body of the adjacent (typically inferior) vertebra [2]. This narrowing can directly compress and shear the spinal cord, causing significant neurological injury [2]. The relative translation between adjacent vertebrae also imparts a shear force to the spinal cord [2]. This shear force can produce a band of injured tissue along the shear plane, potentially extending further laterally compared to the damage seen in contusion injuries from burst fractures[3]. Further, the direction of dislocation is important, as dorsoventral dislocation is more severe than lateral dislocation in animal models[3]. In this same animal model, dislocation resulted in the greatest overall loss of white matter and the greatest nerve cell loss in the gray matter horns, compared to contusion and distraction injuries[3]. In a typical dislocation, the inferior facets of the upper vertebra translate and become locked in front of the superior facet of the lower vertebra. The annular fibres, which are the primary form of resistance to translation in the sagittal plane, are often ruptured or torn from the vertebral end plate [2].

The velocity of injury has also been shown to affect spinal cord damage[2]. A study using a rat model demonstrated that graded severity of spinal cord hemorrhage and axonal injury could be achieved by altering the speed and displacement of the spinal dislocation[3]. In contrast, a later study using the same model found that histological SCI severity depended on displacement but not speed[3].

2.4 Injury Tolerances and Failure Mechanisms

Understanding how much mechanical force the spinal column can withstand before failing is important in predicting and preventing SCIs. While many studies we encountered focused on the spine rather than the spinal cord itself, failure of the bony or ligamentous structures often precedes or directly causes cord damage[10]. As such, spinal injury tolerances—particularly in high-risk regions like the cervical spine—are critical to SCI biomechanics.

2.4.1 Cervical Spine Tolerances

Cervical spine injuries are the most commonly observed type of SCI, occurring in 59% of new SCI cases[7].

A study using 13 unembalmed male cadavers subjected cervical spine columns to controlled axial impact (23–152 cm/s), resulting in a mean failure load of 3.5 kN[11]. These failures typically involved vertebral body fractures, suggesting that high compressive force can compromise spinal integrity leaving the cord susceptible to damage.

Another study investigated how age and injury mechanism affect cervical spine tolerance to injury using post-mortem human surrogates (PMHS)[12]. Data from multiple prior studies were analyzed and grouped based on experimental setups. Group A used an upright intact head (cervical column model), where the inferior end of the specimen was fixed, the head balanced upright using a mechanical system, and natural lordosis was removed. Lordosis is the natural curve present in the lumbar spine. A piston then applied axial loading at the head’s vertex.

Group B included two inverted heads. In Study 1, head-T1 specimens were fixed distally with lordosis preserved (C7-T1 joints oriented anteriorly), and a 16 kg torso effective mass was added. In Study 2, occiput-T2 columns were used with an artificial head, fixed T1-T2, and a horizontal C4-C5 disc posture. Lordosis was preserved, C7-T1 remained unconstrained, and a 15 kg torso mass was added. The injuries observed in Group A, where force was applied cranially to caudally, were mainly vertebral body fractures, consistent with compressive failure mechanisms. In contrast, Group B, which simulated head-first impacts, led primarily to ligamentous and soft tissue injuries associated with hyperextension and distractive extension. These are the mechanisms that often precede dislocation[12]. This suggests that a loss of lordosis in the spinal column potentially increases the risk of spine injury.

Quantitatively[12]:

  • Group A tests showed a 50% injury probability at 4.4 kN (age 45) and 3.3 kN (age 62).
  • Group B Study 1 showed a 50% injury probability at 1.9 kN (age 62).
  • Group B Study 2 showed the same at 1.5 kN (age 74).

A third study used 12 sheep cervical spines and compared responses under natural lordotic posture versus a straightened spine[13]. Although anatomical distances and load capacities exist, sheep spines are biomechanically similar to humans and can be scaled as such. While both postures had similar failure loads[13], straight spines failed significantly faster and with less displacement, suggesting increased vulnerability to injury. Failure patterns also differed; straight spines failed more often in anterior structures (meaning the discs), while lordotic spines failed posteriorly (at facet joints)[13]. This reinforces that loss of lordosis may increase dislocation risk by shifting stress to weaker front structures.

2.4.2 Facet Joint Under Combined Loading

Facet fractures are frequently observed in dislocation-related SCIs, so understanding their strain response under loading helps characterize the failure path leading to cord damage[14]. A 2024 study using C5 to C7 human spinal segments tested how facet joints respond to constrained flexion when superimposed with varying axial loads, ranging from light head weight (approximately 50 N) up to 1000 N of compression[15]. Results showed that higher compressive loads significantly increased facet angular deflection (up to 1.47°) and surface strain (maximum shear up to 375 με), indicating greater engagement of the facet joints under these conditions[15]. In contrast, axial distraction led to minimal facet deflection and lower strains. Although non-destructive, the study suggests that axial compression increases the likelihood of facet joint fracture during flexion, reinforcing its role in dislocation-type spinal injuries[15].

2.4.3 Thoracic Spine Axial Compression

A study investigated the biomechanical response of the thoracolumbar spine (T2-L5) to vertical impact loading using PMHSs[16]. Spinal columns were subjected to controlled drop tower tests from increasing heights, simulating axial compression scenarios. The results identified compression-related fractures in vertebral bodies and posterior elements, with increasing forces leading to more severe injuries. A 50% fracture probability occurred at about 3.4 kN for the thoracic spine and 3.7 kN when lumbar levels were also included[16].

The authors noted that fractures involving both anterior and posterior columns were considered clinically unstable, suggesting potential for secondary cord injury[16]. The study provides useful tolerance data for modeling injury thresholds under axial loading, which contributes to understanding more about mechanisms leading to SCI.

2.4.4 Spinal Cord Strain Patterns Under Injury

Finite element modeling has also been used to examine how different injury mechanisms affect spinal cord strain distributions[10]. A 3D finite element model by Greaves et al. demonstrated that dislocation injuries produce the highest peak strains in the lateral and central regions of the cord compared to contusion and distraction injuries[10]. These results show how dislocations are able to directly strain and damage neural tissue, extending beyond vertebral failure alone[10].

2.4.5 Summary and Research Gaps

As observed throughout this section, although existing studies provide insight into vertebral failure mechanisms and spinal cord strain under various loading conditions, there is limited research directly addressing the relationship between axial loading and SCI through dislocation. Most models isolate structural failure or neural strain but do not fully integrate the biomechanics of axial impact, vertebral translation, and resulting cord damage. This gap highlights the need for more research into dislocation-specific SCI mechanisms under axial loads, an area that currently seems underexplored.

3.0 Spinal Cord Injury Identification and Scale

While research gaps exist in SCI tolerances from spinal dislocation due to axial loading, the methods used to evaluate SCIs are thoroughly researched, reviewed, and continuing to be developed.

3.1 Abbreviated Injury Scale (AIS)

The Abbreviated Injury Scale (AIS) is a scoring system that categorizes the severity of isolated injuries by body region. This score is used in calculating the Injury Severity Score (ISS), which is a summation of squares of three AIS injuries from seperate body regions. Injuries for each region are ranked on a scale from 1 to 6, with 1 being an injury of minor severity, 5 indicating severe injury, and 6 indicating non-survivable injuries and/or death[17]. Typically, a maximum abbreviated injury scale (MAIS) is found to identify a patient's most severe injury[18].

It is important to note that the AIS-assigned scores only represent the patient's' likelihood of death and do not take compounding injuries in the same or other body regions into account. The score does not indicate the likelihood of full recovery or return to previous ability. Additionally, studies have found that this scale is not a proper indicator of severity since it neglects aspects contributing to injury, such as the patient’s psychological state, perceived health status (possibly un-updated medical history), and quality of hospital stay[18]. Since SCIs are very complex injuries and have the potential for secondary mechanisms of injury, this scale is not a great quantification of patients' impairment.

3.2 American Spinal Injury Association (ASIA) Impairment Scale (ASIA-IS)

ASIA SCI classification worksheet

The ASIA Impairment Scale (ASIA-IS) allows for better professional medical communication and uses previously documented AIS to predict future patient outcomes, or help epidemiologic and biomechanical research.

3.2.1 Physical Exams

The ASIA-IS values are obtained from three types of physical exams:

3.2.2.1 Myotomal-Based Motor Exam

A myotome is a group of muscles innervated by a single spinal nerve, thus impaired movement can indicate a location or continued area of injury[19]. Humans have 10 myotomes on each side of the median plane, 5 above the waist and 5 at or below. Evaluation of motor skills localized to a specific myotome is performed for both sides (20 exams total), and results are quantified on a 5 point scale, shown in Table 1

Table 1 - The Myotome Strength Grade System - Adapted from Robert TT et al., 2017.
Myotome scale number Myotome strength grade system
0 Total paralysis
1 Palpable or visible contraction
2 Active movement, full range of motion (ROM) with gravity eliminated
3 Active movement, full ROM against gravity
4 Active movement, full ROM against gravity and moderate resistance in a muscle specific position
5 (Normal) Active movement, full ROM against gravity and full resistance in a functional muscle position expected from an otherwise unimpaired person
5* (Normal) Active movement, full ROM against gravity and sufficient resistance to be considered normal if identified inhibiting factors (ie, pain, disuse) were not present
NT Not testable (ie, attributable to immobilization, severe pain such that the patient cannot be graded, amputation of limb, or contracture greater than 50% of the normal ROM)

3.2.2.2 Dermatomal-Based Sensory Exam

A dermatome is a region of skin supplied by all cutaneous branches (cutaneous meaning relating to the skin) of a single spinal nerve[19]. 28 dermatomes stem from the spinal cord on each side of the median plane. Sensation in all 56 of these regions is evaluated with a soft/dull touch (usually a cotton swab) and a sharp touch (usually a safety pin or needle)[20]. Injury scale value for these regions is either 0 - no sensation, 1 - altered sensation or 2 - normal sensation. Exceptionally, if both sharp and soft can be felt but not differentiated, a value of 0 is assigned[20]. Figure 1 highlights the different dermatome regions on one side of the median plane. The regions are symmetrical over this plane.

3.2.2.3 Anorectal Exam

This final exam establishes how “complete” the SCI is, with completeness stemming from full loss of sensation or motor control, and resolution of spinal shock[20]. Spinal shock is a physiologic response to trauma categorized by depolarization of axonal tissue immediately after injury[21]. During spinal shock, a patient’s reflexes will not react to stimuli (including anal contraction). Upon return of this reflex, the patient can be accurately assessed for level of injury. Generally, reflexes return in a few days, however deep tendon reflexes may take weeks to months to reappear[21]. Patients are usually assessed one day to one week post injury[22]. Two tests are performed; a sensory test to distinguish Deep Anal Pressure (DAP), and ability to voluntarily contract the anal sphincter (VAC)[20]. A binary quantification of 0 - absent ability and 1 - present ability is recorded. However, a DAP test is not required if a patient has intact dermatomes at S4/5 (ie, a score of 2).

3.2.2 Neurological Classification

Once the physical tests are completed, the Neurological Level of Injury (NLI) can be determined. The NLI is the most inferior spinal cord innervation with intact dermatomes (and myotomes, where applicable)[20]. This is the most inferior dermatome with a score of 2, and the most inferior myotome with a 3 or above.

3.2.3 Injury Classification

The AISA-IS scale has 5 levels, from A - Complete to E -Normal. If the injury is complete (dermatome S4/5 = 0, DAP = 0), then the injury is immediately assigned Level A. The injury is immediately assigned level B if any sensory but no motor function is preserved. The last three levels differentiate partial, good, and complete function, detailed in Table 2.

Table 2: Injury Scale Classification Levels - Adapted from Robert TT et al., 2017.
A: Complete No functionality distal to the site of the injury. If S4/5 = 0 or DAP = 0, immediate complete classification
B: Sensory Incomplete Sensory function preserved at any point, including S4/5
C: Motor Incomplete VAC is preserved. Motor function is preserved below the NLI and >=50% of myotomes below the NLI have a grade <=3.
D: Motor Incomplete Status of C achieved with >=50% of myotomes below the NLI having a grade >=3
E: Normal Motor and sensory function are normal

3.2.4 Limitations

Injuries are variable in mechanism, as well as short-term and long-term effects. Injury scales struggle to create classifications for all related factors. The sensory scale assessment only accounts for absence or presence of feeling/altered feeling, but this does not represent potential pain or discomfort associated with the dermatome sensory level. Assigning an altered feeling score of 1 quantitatively is better than no feeling - a score of zero, however, if the patient's altered feeling is agonizing pain, they may not view it as “better”. Additionally, like many other injury evaluations, it does not account for competing or combining injuries (lacerations, amputation, speech impairment) that may put the patient at higher risk. Finally, the complete classification cannot measure injury severity, since classification is normalized to the NLI. Only levels C to E factor motor presence in the scale, meaning someone with an L1 ASIA IS A may have more total functionality than someone with a C3 ASIA IS B or C SCI.

4.0 Neurological Consequences of Spinal Dislocations

4.1 Pathophysiology of Spinal Cord Injuries

The general pathophysiology of SCIs develops in two phases. The primary injury phase is caused by loading forces that lead to mechanical injury and damage to the spinal cord. The mechanical forces cause structural damage to the neuronal and vasculature tissue, which results in cell death and dysfunction[23]. Four primary injury mechanisms can cause SCIs: impact plus persistent compression, impact alone, distraction, and laceration/transection, which occur in a short time window. In terms of spinal dislocations, this is likely to be an impact plus persistent compression injury mechanism. There is a crucial 48-hour time window to perform decompressive surgery to mitigate these early effects and reduce the prognosis of the aftereffects[6].

However, studies indicate that the secondary injury phase heavily impacts the severity. This phase involves a complex cascade of cellular and molecular events that further tissue damage, which can last for hours, days, and even week[6]. As a functional outcome, we will limit the discussion of the secondary injury phase as it is outside the scope of the course.

4.2 Classification of Spinal Cord Injuries

SCIs are primarily classified based on the area of the spinal cord affected and the degree of impairment. The degree of impairment is associated with injury scales, which allow clinicians to diagnose SCI severity consistently and accurately against a worldwide standard. Magnetic resonance imaging (MRI) and molecular classifications are standard procedures to further measure the traumatic disruption of grey matter as the injury progresses[24].

4.3 Neurological Functional Outcomes of SCI

The functional outcomes of an SCI are based on the level of injury and the completeness of the injury, as discussed in Section 3.0. Below, we describe some of the long-term effects.

4.3.1 Motor Paralysis

A primary outcome of SCIs is immobility. The severity of motor paralysis depends on the severity of the damage to the spinal cord (as described on the ASIA-IS scale) and the level of damage. Two varieties of paralysis can occur: tetraplegia and paraplegia. Tetraplegia is an SCI to the cervical spinal cord (C1-C8) that affects the function of all four limbs and the torso. Paraplegia occurs when there is damage to the thoracic (T1-T12), lumbar (L1-L5), or sacral spinal cord (S1-S5) and retains the functionality of the arms; however, the torso and lower limbs are affected[24].

4.3.2 Other Functional Outcomes Due to Motor Paralysis

Other critical outcomes that occur due to immobility are:

  • Autonomic Dysreflexia (AD): The body is unable to regulate the sympathetic overactivity below the injury because of a disruption to the central nervous system (CNS) control, leading to severe hypertension and excessive sweating. Typically occurring at injuries above T6[24].
  • Pressure Injuries: A reduction of blood flow due to the prolonged pressure on bony prominences (e.g., elbows, coccyx), causing tissue damage. If left untreated, these injuries can progress into deep open wounds, reaching muscles and bones and introducing infectious agents into the body[24]. Found at SCI at any level or severity.
  • Venous Thromboembolism (VTE): Blood pooling in the veins because of blood clots formed due to reduced blood flow, often caused by immobility. If a clot dislodges, it can travel through the bloodstream to the lungs, causing a pulmonary embolism or to the brain, leading to a stroke[24].
  • Bone Metabolism Dysfunction: Osteoclasts (cells that break down bone tissue) become more active when a person is immobile and not engaging in weight-bearing activities, leading to bone loss, known as osteoporosis[24].
  • Muscle Atrophy: Without the regular stimulation or use of muscles because of an SCI, muscles weaken and shrink[24].

5.0 Conclusion

Dislocation injuries to the spinal cord are complex medical conditions that can cause severe impairments to neurological function. Understanding the mechanisms of injury and the spines tolerances is key to advancements in injury detection, classification, and treatment strategies.

Biomechanical research in spinal injuries, such as axial loading and vertebral stability, can provide meaningful insights into the mechanisms of injury. Clinical research has defined the effect of injury location on functional outcomes. Injury scales such as AIS and ASIA-IS can provide diagnostic tools to aid in the classification of spinal injuries, including dislocations. However, these injury scales have limitations in capturing the unique injury circumstances, including existing conditions, that may contribute to overall condition.

The cervical spinal region receives the vast majority of spinal trauma and SCIs. This can be attributed to the lower mechanical tolerances compared to the thoracolumbar sections of the spine and the greater mobility and exposure to the possible injuries discussed in this paper. While biomechanical studies have provided valuable insights into the failure mechanisms of cervical spinal dislocations, further research is needed to refine the thresholds which bound these injuries. Additional research is also necessary to better understand the biomechanical responses of the thoracolumbar regions of the spine from axial loads. Unlike fractures, where failure loads can be more clearly defined, dislocations involve complex ligamentous and joint mechanics, making it challenging to establish singular failure thresholds. Advancements in computational modeling may also provide a valuable approach to predict dislocation mechanisms better and quantify soft tissue contributions to injury.

6.0 Acknowledgements

Parts of section 2.0 utilized chatGPT as a tool to catch spelling and grammar mistakes. Small sub-sections were inputted to chatGPT along with the prompt “ please make this section more concise and grammatically correct”. The responses from chatGPT were either ignored or implemented, with the implementation process being the author changing small sentence fragments. No section from chatGPT was entirely copied into the text.

References

  1. ↑ 1.0 1.1 1.2 Sekhon, L. H., & Fehlings, M. G. (2001). Epidemiology, demographics, and pathophysiology of acute spinal cord injury. Spine, 26(24 Suppl), S2-12. https://doi.org/10.1097/00007632-200112151-00002
  2. ↑ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 Mattucci, S., Speidel, J., Liu, J., Kwon, B. K., Tetzlaff, W., & Oxland, T. R. (2019). Basic biomechanics of spinal cord injury—How injuries happen in people and how animal models have informed our understanding. Clinical Biomechanics, 64, 58–68. https://doi.org/10.1016/j.clinbiomech.2018.03.020
  3. ↑ 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 Jones, C. F., & Clarke, E. C. (2019). Engineering approaches to understanding mechanisms of spinal column injury leading to spinal cord injury. Clinical Biomechanics, 64, 69–81. https://doi.org/10.1016/j.clinbiomech.2018.03.019
  4. ↑ Roaf, R. (1960). A STUDY OF THE MECHANICS OF SPINAL INJURIES. The Journal of Bone and Joint Surgery. British Volume, 42-B(4), 810–823. https://doi.org/10.1302/0301-620X.42B4.810
  5. ↑ Aarabi, B. , Walters, B. C. , Dhall, S. S. , Gelb, D. E. , Hurlbert, R. J. , Rozzelle, C. J. , Ryken, T. C. , Theodore, N. & Hadley, M. N. (2013). Subaxial Cervical Spine Injury Classification Systems. Neurosurgery, 72 (suppl_3), 170-186. https://doi.org/10.1227/NEU.0b013e31828341c5
  6. ↑ 6.0 6.1 6.2 Hachem, L. D., & Fehlings, M. G. (2021). Pathophysiology of Spinal Cord Injury. Neurosurgery Clinics of North America, 32(3), 305–313. https://doi.org/10.1016/j.nec.2021.03.002
  7. ↑ 7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 7.11 7.12 7.13 7.14 Miele, V. J., Panjabi, M. M., & Benzel, E. C. (2012). Anatomy and biomechanics of the spinal column and cord. Handbook of Clinical Neurology, 31–43. https://doi.org/10.1016/b978-0-444-52137-8.00002-4
  8. ↑ Henmar, S., Simonsen, E. B., & Berg, R. W. (2020). What are the gray and white matter volumes of the human spinal cord? Journal of Neurophysiology, 124(6), 1792–1797. https://doi.org/10.1152/jn.00413.2020
  9. ↑ Cho, T. A. (2015). Spinal Cord Functional Anatomy. CONTINUUM: Lifelong Learning in Neurology, 21(1), 13–35. https://doi.org/10.1212/01.con.0000461082.25876.4a
  10. ↑ 10.0 10.1 10.2 10.3 Greaves, C. Y., Gadala, M. S., & Oxland, T. R. (2008, January 29). A three-dimensional finite element model of the cervical spine with spinal cord: An investigation of three injury mechanisms - annals of biomedical engineering. SpringerLink. https://link.springer.com/article/10.1007/s10439-008-9440-0
  11. ↑ Maiman, D. J., Sances, A. Jr., Myklebust, J. B., Larson, S. J., Houterman, C., Chilbert, M., & El-Ghatit, A. Z. (1983). Compression injuries of the cervical spine: A biomechanical analysis. Neurosurgery, 13(3), 254–260. https://pubmed.ncbi.nlm.nih.gov/6621839/
  12. ↑ 12.0 12.1 12.2 Yoganandan, N., Chirvi, S., Voo, L., Pintar, F. A., & Banerjee, A. (2017a). Role of age and injury mechanism on cervical spine injury tolerance from head contact loading. Traffic Injury Prevention, 19(2), 165–172. https://doi.org/10.1080/15389588.2017.1355549
  13. ↑ 13.0 13.1 13.2 Öktenoǧlu, T., Özer, A. F., Ferrara, L. A., Andalkar, N., Sarioǧlu, A. Ç., & Benzel, E. C. (2001). Effects of cervical spine posture on axial load bearing ability: A biomechanical study. Journal of Neurosurgery: Spine, 94(1), 108–114. https://doi.org/10.3171/spi.2001.94.1.0108
  14. ↑ Nkurikiyumukiza, L., Buteera, A. M., & El-Sharkawi, M. M. (2024). Delayed presentation of lower cervical facet dislocations: What to learn from past reports?. SICOT-J. https://pmc.ncbi.nlm.nih.gov/articles/PMC10798230/
  15. ↑ 15.0 15.1 15.2 Foroutan, P., Quarrington, R. D., Russo, M. P., Ding, B., Cripton, P. A., Costi, J. J., & Jones, C. F. (2024). Facet deflection and strain are dependent on axial compression and distraction in c5–c7 spinal segments under Constrained Flexion. JOR SPINE, 7(3). https://doi.org/10.1002/jsp2.1360
  16. ↑ 16.0 16.1 16.2 Yoganandan N;Arun MW;Stemper BD;Pintar FA;Maiman DJ; (n.d.). Biomechanics of human thoracolumbar spinal column trauma from vertical impact loading. Annals of advances in automotive medicine. Association for the Advancement of Automotive Medicine. Annual Scientific Conference. https://pubmed.ncbi.nlm.nih.gov/24406955/
  17. ↑ Petridou, E. Th., & Antonopoulos, C. N. (2017). Injury Epidemiology. In International Encyclopedia of Public Health (pp. 258–274). Elsevier. https://doi.org/10.1016/B978-0-12-803678-5.00233-2
  18. ↑ 18.0 18.1 Asscheman, S., Versteeg, M., Panneman, M., & Kemler, E. (2023). Reconsidering injury severity: Looking beyond the maximum abbreviated injury score. Accident Analysis & Prevention, 186, 107045. https://doi.org/10.1016/j.aap.2023.107045
  19. ↑ 19.0 19.1 Stecco, C., Pirri, C., Fede, C., Fan, C., Giordani, F., Stecco, L., Foti, C., & De Caro, R. (2019). Dermatome and fasciatome. Clinical Anatomy, 32(7), 896–902. https://doi.org/10.1002/ca.23408
  20. ↑ 20.0 20.1 20.2 20.3 20.4 Roberts, T. T., Leonard, G. R., & Cepela, D. J. (2017). Classifications In Brief: American Spinal Injury Association (ASIA) Impairment Scale. Clinical Orthopaedics & Related Research, 475(5), 1499–1504. https://doi.org/10.1007/s11999-016-5133-4
  21. ↑ 21.0 21.1 Ditunno, J. F., Little, J. W., Tessler, A., & Burns, A. S. (2004). Spinal shock revisited: A four-phase model. Spinal Cord, 42(7), 383–395. https://doi.org/10.1038/sj.sc.3101603
  22. ↑ Kirshblum, S., Snider, B., Eren, F., & Guest, J. (2021). Characterizing Natural Recovery after Traumatic Spinal Cord Injury. Journal of Neurotrauma, 38(9), 1267–1284. https://doi.org/10.1089/neu.2020.7473
  23. ↑ Sterner, R. C., & Sterner, R. M. (2023). Immune response following traumatic spinal cord injury: Pathophysiology and therapies. Frontiers in Immunology, 13, 1084101. https://doi.org/10.3389/fimmu.2022.1084101
  24. ↑ 24.0 24.1 24.2 24.3 24.4 24.5 24.6 Guest, J., Datta, N., Jimsheleishvili, G., & Gater, D. R. (2022). Pathophysiology, Classification and Comorbidities after Traumatic Spinal Cord Injury. Journal of Personalized Medicine, 12(7), 1126. https://doi.org/10.3390/jpm12071126


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