Rehabilitation. Spinal Cord and Fixation Devices Research Paper

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Introduction

The spinal cord is a major component of the central nervous system (CNS) that provides mobility, reflexes and facilitates other human activities and actions. Though this cord is protected by the vertebral column, it is never hundred percent safe from injury. Even an injury to the vertebrae may end up inflicting injury to the cord. Spinal cord injury (SCI) is a major cause of mobility and mortality worldwide (Badoe et al., 2000).

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As per the fact sheet released by the Spinal Cord Injury Information Network in January 2008, there are 40 cases each million US populations develop spinal cord injury (excluding cases that die at the scene), with 12000 new cases every year. It is estimated that there are more than ¼ of a million US populations are living with spinal cord injury with an average age of 39.5 years. Males make up 77.8 % of cases; most of them are Caucasians, followed by African-Americans, Hispanic and only 2.4% are of other ethnic groups.

About 42 % of cases occur because of motor vehicles accidents. More than 34% showed tetraplegia (paralysis of three limbs), 23% had complete paraplegia (complete paralysis of the lower limbs), and less than 1 % showed total neurological recovery. The average life expectancy of these patients increases (still less than for other populations), however, the quality of life is impaired (decreased motor function and ventilator dependency) (Spinal cord information Network, 2008).

The spinal cord extends from the brain base through the foramen magnum to pass through the vertebral canal (guarded by the vertebral column) until the first lumbar vertebra level. Nerve roots leave the spinal cord taking exit through the foramina of the vertebral bodies. The number of nerve roots matches the number of vertebrae. There are eight cervical roots (an extra root between the seventh cervical vertebra and first thoracic), 12 pairs of thoracic roots, five pairs of lumbar roots, and five pairs of sacral roots.

The spinal cord is shorter than the spinal canal; therefore, the course of the roots is angled downwards to exit from the spinal canal. After taking the exit, these roots become a part of the peripheral nervous system carrying motor orders from the brain and sensory information from the body. This occurs through nerve fibers bundles (spinal tracts). The lower part of the spinal cord (conus medullaris) regulates other body functions (bladder, bowel, and normal sexual functions). As the bone of the vertebral column protects the spinal cord, injury to the vertebrae or ligaments has to precede injury to the cord. A simple trauma may injure the spinal cord.

Even a simple bruise might cause swelling of the cord. An important prognostic feature is to notice whether the injury is complete (loss of voluntary and involuntary reflexes) or partial. This occurs at the injury level and below. Below the first lumbar vertebra level, injury to the vertebral column will not affect the cord; instead, it affects the cauda equina (Milton S. Hershey center). Spinal cord injuries can be acute (traumatic) or chronic (nontraumatic).

Acute traumatic cord injuries may result from a car or sports accidents, gunshots, wounds, or falls (all caused by external forces). Chronic nontraumatic injuries to the cord result from diseases, secondary lesions of primary tumors, or other pathological conditions as spondylolisthesis. Spinal cord injuries may be classified according to the type of injury into complete (injury to the entire thickness of the cord at a certain level) or incomplete (only a part of the cord is injured at a certain level). According to their level, cord injuries are classified into cervical (result in paraplegia), thoracic, lumbar, and sacral. Neurological signs differ according to the injury level.

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Thus, spinal (vertebral) fixation is two or more vertebrae with artificial material to provide stability and prevent further damage to the cord. Although it is difficult to predict the extent of healing (recovery) at the time of diagnosis yet, there are cases of partial or near-complete recovery months or even years after the time of diagnosis. Therefore, fixation is an essential step of management (Sean MCNamee, 1998, p.1).

Complications of spinal cord injuries are governed by the mode of onset (acute or chronic), injury level, and patient mobility after settling down. Spinal shock is characterized by hypotension and depression of reflexes below the injury level; it occurs in high (cervical) injuries. Acute respiratory distress syndrome also occurs in high injuries as well as autonomic dysreflexia. Thrombo-embolic disease and fluid and nutrition deficiencies and imbalance are commonly encountered.

Bladder and bowel complications depend on the injury level. Therefore, treatments of spinal cord injuries are multifaceted, with the following principles: 1- Achieve spinal stability. 2- In incomplete injuries, decompression of the cord or roots is involved. 3- Incomplete injuries, surgical intervention has to be weighed carefully and better kept for purposes of stabilization (Nicholas and others, pp. 91-94).

Proceeding with this background information, this study has been conceived with the main aim of taking stock of the various spinal cord fixation devices. This study reviews the major causes of spinal cord injury (SCI), classification of SCI and classifies spinal cord injury (SCI) characteristics, biomechanics of the spine and spinal injuries, mechanics of spinal fixation, and stabilization. Finally, the study assesses different spinal fixation techniques, materials, and suitable injury prevention and management options.

Spinal Cord & Spinal Cord Injury (SCI)

The spinal cord is the continuation of the neuronal tissue of the brain, which forms the most important component of the central nervous system (CNS). It spreads from the upper two-thirds of the spinal canal, finally terminating below the first lumbar vertebra, which then broadens to form the conus medullaris. With an average length of 43-45 cm, the spinal cord consists of 8 cervical nerves (C1-C8), 12 thoracic nerves (Th1-Th12), five lumbar nerves (L1-L5), and sacral nerves (S1-S5).

Signals to the back of the head, neck, shoulders, arms & hands, and the diaphragm are all controlled by the cervical nerves C1 to C8, whereas signals to the chest muscles, some back muscles, parts of the abdominal and the lumbar spinal nerves are controlled by the thoracic nerves Th1 to Th12. The L1-L5 control signals to the lower parts of the abdomen and the back, the buttocks, and parts of the leg. The signals to the thighs, lower parts of the leg, feet, and the external genital organs are controlled by the spinal nerves S1 to S5.

A cord injury is accompanied by an alteration of respiratory muscles whose importance is a function of the level and the incomplete or complete status of the neurological impairment. Cardio-vascular problems due to loss of compensatory mechanisms may be at the forefront and have to be preventively taken into account by a well-driven resuscitation (Jacquot F. et al., 2007). Upon injury, the spinal cord blood flow loses the power for autoregulation, and this happens close to the level and to the proximity of injuries (See, Guha, Tator & Rochon, 1989).

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This leads to a decline of the spinal cord blood flow, following the decline of the systemic arterial blood pressure closely. This always occurs in cases of tetraplegia or high paraplegia, secondary to the loss of the sympathetic system, and it thus causes hypoxemia to the level of the injured zones. Experimental studies clearly show the role of the “secondary injury” in the constitution of the neurological deficit.

ASIA Score: The standard form.
Fig-1: ASIA Score: The standard form.

If some cellular bodies and axonal continuations in the traumatized area are immediately destroyed (primary lesion), others are victims of vascular, biochemical and electrolytic modifications that lead to their destruction in minutes or hours. Even in cases of complete cord section, the metameric levels adjacent to the destroyed area may suffer and be lost irremediably due to the evolution of the secondary injury. If no combined injury threatening the vital prognosis is present, the problem is that of the cord injury.

The examination of motricity and sensitivity defines the level of injury. It has been codified by the American Spinal Injury Association, and a motor and sensory score known as “ASIA score” have been established (Fig-1). The motor score is based on the examination of 10 key-muscles on each side (Table-1). For each movement, force is measured and assigned a coefficient from 0 (absence of muscle contraction) to 5 when contraction creates a movement in all the joint amplitude against a complete resistance. The maximal total score is so 100 (50 on the Right and 50 on the Left).

10 key-movements of the ASIA score and corresponding mesmeric level.
Table-1: 10 key-movements of the ASIA score and corresponding mesmeric level.

The sensory score is established after studying tact and prick sensitivity on a key point in each of 28 dermatomes on each side. Absence of sensitivity is quoted: 0, the hypo or the hyperesthesia : 1 and normal sensitivity : 2. It is preferable to begin the examination by testing the light touch and the lower part of the body. The superior level of the neurological injury is defined in France as the first abnormal metameric level ; in the English-speaking world, it is defined as the last normal metameric level. Thus a T10 paraplegia is T9 in the US. There is a recent tendency to use the US way for result comparisons ( since our C7 quads have no triceps while the American C7 have…)

Finally, the examination seeks to specify the incomplete or complete status of the cord injury. The deficit may be complete or partial, on the sensory or motor side. The persistence of any sensitivity, even in a very limited area, or any muscle activity, below the level of injury, especially in the sacral metameric area (sensitivity of the anal margin, deep anal sensation, voluntary contraction of the external sphincter) signs by definition the incomplete status of the neurological injury.

Often there is a dissociation between the sensory and motor level, especially, in complete injuries, the sensory level is usually lower than the motor level. The precise study of the sensitivity, the motricity, reflexes under the injury level, as well as of sphincters, is mandatory. One can then classify the neurological injury according to the modified Frankel scale which is shown in table II.

  1. Complete neurological injury. No sensory or motor function is preserved below the level of injury, especially in S4-S5 segments.
  2. Incomplete neurological injury. Only the sensory function is preserved below the neurological level, sometimes in S4-S5 segments.
  3. Incomplete neurological injury. Some motor function is preserved under the level of injury and the majority of key muscles short of this level have a score inferior to 3.
  4. Incomplete neurological injury. Motor function preserved under the level of injury and the majority of key muscles have a score equal or superior to 3.
  5. Motor and sensory functions normal.

Table II: The modified Frankel scale.

The predictive value on the functional prognosis of the complete or incomplete status of the neurological injury is considerable. The injury is sometimes associated in the first hours that follow the trauma to an initial phase of “spinal shock” that characterizes by an abolition of all reflexes below the cord lesion. This state is transitory and disappears with the installation of cord automatism. One can assert with certainty the complete status of the injury only after resolution of the spinal shock, usually after several days.

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The incomplete status of the cord injury allows to classify it among one of the different incomplete clinical syndromes, that gives a first idea of the functional recovery potential. These clinical syndromes are by definition:

  • Central cord syndrome: occurs almost exclusively in the cervical region, produces a sacral sensory sparing and typically more important a motor impairment in the upper limb than the lower limb.
  • Syndrome of Brown-Séquard : a unilateral lesion that produces a motor and proprioceptive impairment on the same side as the injury, and a loss of thermal and pain sensitivity on the contralateral side.
  • Anterior cord syndrome: an injury that produces a variable motor, thermal and pain impairment, but preserves the proprioception.
  • Conus medullaris syndrome : injury to the cone and lumbar roots, that produce areflexia to the bladder and lower limbs. The sacral reflexes may be preserved (bulbocavernosus reflex, miction)
  • Cauda equina syndrome : lumbosacral nerve root injury, with areflexia of the bladder and lower limbs.

The examination is difficult in the context of an ambulance setting ; however, a prospective multicenter pre-hospital trial has shown the feasibility and reliability of the pre-hospital examination.

Biomechanics of the spine and spinal injuries

The vertebral column has two essential functions, protection of the spinal cord, and structural support (as an axial skeletal support). From a biomechanical viewpoint, the spine is a semirigid (rigid vertebral units connected by ligaments, and intervening disks) link related to motion (kinetic). There are intrinsic and extrinsic forces that affect its actions. The intrinsic forces are those produced by muscles attached to it (specially the paravertebral and abdominal muscles).

Intrinsic forces are essential to movement and have a protective role in reducing stress by delivering it along the spine length. Extrinsic forces result from impact of effects outside the body as walking, sitting preserving the erect position, minor trauma into a door or a chair, or momentum following a car stop. Therefore, these forces are random in direction and extent and can be shear (cut off), torsion (twisting), or bending types of forces.

The vector of forces acting on the spine may lead, in cases of trauma, to failure at a weak point whose location depends on many factors. Failures at the ligaments of the spine lead to sublaxation with or without fracture of the vertebra, with or without intervertebral disk herniation. The vertebral structure is another biomechanical factor that affects the location of the weak point. Vertebral fractures are classified into posterior fractures involving posterior structural components (neural arch, vertebral processes, and ligaments), anterior fractures involving the vertebral bodies and intervertebral disks, and fractures involving both anterior and posterior components.

Because of the vertebra structure, the design of the posterior apparatus makes it apt to diffuse tensile forces but less resistant to compression. The design of the anterior apparatus, on the other hand, makes it more apt to uphold compressive forces. The spine structure as a unit permits movements in planes other than anterior and posterior, the rotation and lateral bending movements, although limited, result in greater loading modes. Therefore, force extent, direction, type and frequency play an important role in fracture and dislocation of the spine (Smith & Walter).

Biomechanics of Injury

In the early literature of CSI, researchers focused on the movement of the head during injury and ascribed the primary mechanism of suspected injury in the cervical spine to that specific movement.28–30 However, further study has shown that the observed motion at the head during injury is not a reliable indicator of spine movement responsible for creating the injury.24,25,31–33 The biomechanics in the spine and extent of injury to the spine depend on the impact location on the head and the orientation of the cervical spine at the time of impact.24–27 The initial, and often the more critical, injury occurs as soon as 2 to 30 milliseconds after impact, well before observed motion in the cervical spine and head occurs.24–26

References

Badoe E. A. A, Jaja M. O. A, Archampong E. Q (eds). Principles and practice of surgery, including pathology in the tropics. University of Ghana, Accra. 2000.

Guha A, Tator CH, Rochon J Spinal cord blood flow and systemic blood pressure after experimental spinal cord injury in rats. Stroke. 1989;20(3):372-7.

Milton S. Hershey Medical Center. Dept. home page. Penn State Hershey University. 2008. Web.

Spinal Cord Injury: Facts and Figures at a Glance. Dept. home page. The Spinal Cord Injury Information Network. 2008. Web.

Sean McNamee, PT. “Spinal Cord Injuries.” Theranotes 1998: 1. Ed. Therapy Skill Builders. San Antonio: a division of The Psychological Corporation. Art. 0761670696.

Jacquot F., Loubert G., et. Al., ‘Initial management of acute traumatic spinal cord injuries’, Hospital Raymond Poincaré, 2007.

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IvyPanda. 2021. "Rehabilitation. Spinal Cord and Fixation Devices." October 11, 2021. https://ivypanda.com/essays/rehabilitation-spinal-cord-and-fixation-devices/.

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IvyPanda. "Rehabilitation. Spinal Cord and Fixation Devices." October 11, 2021. https://ivypanda.com/essays/rehabilitation-spinal-cord-and-fixation-devices/.

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