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This article has been subjected

to double blind peer review

The incidence of spinal cord injury worldwide stands at about 20 new

cases per million of population a year (Glass 1999), but is double this figure in the US (DeVivo 2002).

In the western world, the greatest causes of spinal and spinal cord injuries are related to risk taking incidents, such as drink driving and non-adherence to safety procedures (DeVivo 2002, Grundy et al 2001, Healy et al 2004). As such, these may be preventable through educative strategies and by enforcing road safety and health and safety measures.

Spinal cord trauma can lead to different degrees of motor and sensory loss. This article will examine the effects of injury events on the spinal cord by relating the biomechanics of injury to the anatomy of the vertebral column.

It will also consider the neurological sequellae of injury and describe some of the presentations classified under the Inter-national Standards for Neurological Class-ification of Spinal Cord Injury (American Spinal Injury Association 2002).

THE VERTEBRAL COLUMNThere are three points along the vertebral column that are particularly susceptible to injury: the junctions of C7 and T1 and that of T12 and L1, and vertebra T7. To understand why these areas are susceptible, it is important to be familiar with the anatomy of the vertebral column.

The vertebral column comprises 33 vert-ebrae that are held firmly together by ligaments forming a ‘fortress’ around the spinal cord.

Most of the vertebrae conform to the standard model, with a large vertebral body, spinous and transverse processes, laminae and pedicles.

Those of the upper cervical spine however, namely the atlas and the axis, and those in the sacrococcygeal region, are unusual.

The upper cervical spine is the only region where significant rotation is needed. This is facilitated by the odontoid, or peg, process that protrudes upwards from the body of the axis and articulates with a facet on the posterior surface of the anterior ring of the atlas, acting as a pivot for the latter.

The vertebrae in the sacrococcygeal region, meanwhile, are fused into a solid mass, but with intervertebral foramina persisting between the sacral vertebrae.

The spinal column is comprised of more than bone. Each vertebra must articulate with other vertebrae and bones, and there needs to be some flexibility and mobility in the intervertebral joints. This is provided by the intervertebral discs between the junction of C1 and C2 and that of L5 and S1, which also help to absorb shock.

There are eight types of spinal ligaments, which connect vertebrae throughout the column, either to other vertebrae or to other bone such as the ribs, and help to keep the column stable (Table 1).

SPINAL CORD INJURY: CAUSATION AND PATHOPHYSIOLOGYIn the second of three articles on spinal cord injury, FINTAN SHEERIN describes some of the causes and effects of spinal cord trauma

Fintan Sheerin BNS, PgDipEd, RMHN, RGN, RNT is a lecturer practitioner in spinal cord injury, National Spinal Injuries Unit, Mater Misericordiae University Hospital, Dublin, and school of nursing and midwifery, University College Dublin

Table 1. Types of spinal ligament

> Ligamentum flavum: between laminae

> Supraspinous ligament: between the tips of spinous processes

> Interspinous ligament: between spinous processes

> Anterior longitudinal ligament: on the anterior surface connecting the body of one vertebra to that of another

> Posterior longitudinal ligament: on the posterior surface connecting body to body

> Intertransverse ligament: between transverse processes

> Ligamentum nuchae: between cervical spinous processes

> Radiate ligaments: connecting vertebrae to ribs.

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Cervical regionOf the five regions, the cervical is most flex-ible and mobile. The vertebrae here are small with superior articular facets facing posterio-medially and upwards (Barker 2001).

The nearly horizontal direction of the spinous processes in this region allows for greater extension, with the exception of C1 and C2, which articulate differently and which have only rudimentary spinous processes.

Force applied to the cervical spine does not always result in localised vertebral damage, however, because the flexibility of the region, and the ability of the neck to move in anteriorposteriolateral directions, can help transfer the force downwards to the thoracic spine where there is little or no flexibility.

Thoracic regionThe thoracic spine has larger vertebrae and thinner interverterbal discs than the cervical region, and has inferiorly directed spinous processes (Tortora and Grabowski 1996). The superioposteriolateral orient-ation of superior articular facets and the articulation with the ribs create a relatively rigid and immobile structure (Chiles and Cooper 1996).

The junction between C7 and T1 represent the border between the flexible cervical spine and the rigid thoracic spine, and is the most susceptible to vertebral column damage. This is because, when force is applied to the cervical spine, it is directed downwards because of the latter’s flexibility, and is focused on the cervical-thoracic junction. The region must be examined on X-ray therefore before it is given the all-clear (Prendergast and Sullivan 2000, Walker 1998, Young and Shea 1998).

A similarly important junction exists between T12 and L1, which is between the rigid thoracic and more mobile lumbar regions. This is the second most common site of spinal injury (Chiles and Cooper 1996).

Another significant injury site is T7, the apex of the largest primary curve of the vertebral column. Primary curves are remnants of the spinal curve present at birth (Sheerin 2004).

This vertebra is at risk of injury because it provides a ‘buckling’ point if compressive forces are applied directly along the axial skeleton.

The vertebral column can be described therefore as a stable structure that supports the upper appendicular skeleton and head, while protecting the delicate neurological tissues of the spinal cord.

It can be divided into five principle regions: cervical, thoracic, lumbar, sacral and coccygeal. Each has specific structural variations and properties (Fig. 1).

The cervical and thoracic regions are the most common sites of spinal injury.

Fig. 1. Vertebral column divisions and characteristics

Cervical

> flexible

> allows movement

> seven verterbrae

> small bones

Thoracic

> inflexible and rigid

> allows little movement

> 12 verterbrae

> larger bones

Lumbar

> slightly flexible

> allows some movement

> five verterbrae

Sacral

> inflexible: fused

> no movement

> five verterbrae

PETE

R G

ARDE

NER

Coccygeal

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CAUSATION OF SPINAL CORD INJURYThe main causes of spinal cord injury fall into the following categories: > Traumatic: motor vehicle accidents

(MVAs), falls, sports injuries, objects falling onto the head, assault

> Non-traumatic: degenerative, infective or oncogenic spinal lesions.

Of the principal mechanisms of injury, however, MVAs (Guin 2001) and falls (DeVivo 2002) account for the vast majority.

Motor vehicle accidentsMotor vehicle accidents account for around 39 per cent of spinal cord injuries in the UK (Harrison 2004).

The mechanism of injury in MVAs can be simple or can involve a complex combination of forces focused on the vertebral column. These forces are limited by safety devices such as side impact bars, airbags and head rests.

When a vehicle is travelling at, say, 70mph, everything in the vehicle, including the driver, is travelling at the same speed. The impact of the vehicle with another vehicle or object leads to a sudden deceleration to 0mph. Because it is secured to the vehicle by the seatbelt, the driver’s body achieves this sudden velocity change, but the head does not.

Instead, the head continues to travel forward until the vertebral structure prevents it from any further displacement. It then travels downwards causing severe distraction – or pulling apart – of the posterior vertebral column, and damage to the ligamentous complex between, and covering, the spinous processes: a hyperflexion injury.

At the same time, there is severe compression along the anterior vertebral column with the potential for vertebral body damage (Fig. 2). The force of the forward moving vehicle creates an equal and opposite force when it suddenly stops. This violently ‘whips’ the driver’s head and neck in the opposite direction.

If the headrest is absent or ineffective, the driver’s head moves back over the upper edge of the seat and then downwards leading to severe anterior distraction with anterior longitudinal ligamentous damage, and posterior compression with fractures of the spinous processes: a hyperextension injury.

These two events allow the vertebrae to ‘ride over’ those below them, resulting in spinal cord contusion or transection caused by the loss of vertebral alignment. These injuries usually involve the low cervical region, namely C5 to C7 (Hickey 2003).

It is important to remember that during an MVA there may be other forces at play that can cause different injuries. If the vehicle turns over for example, the driver’s head can rotate leading to displacement of facet joints.

The forces involved in MVAs can cause such severe damage to vertebrae C1 and C2 that the cord is affected, so that the person involved cannot self-ventilate. In such circumstances, death is the most common outcome (Schoen 2000).

Fig. 2. Mechanism of injury in motor vehicle accidents

HAR

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FallsFalls account for about 46 per cent of spinal cord injuries in the UK (Harrison 2004).

There are many types of fall, including those from a height, at ground level, from the ground into a hole, on a flat surface, or up stairs or steps.

Each of these types of fall involves a force being imposed onto the vertebral column, each from a different angle.

Typically, falls from a height are from second or third storey levels (National Spinal Injuries Unit 2005). They might be suicide attempts, or be caused by a loss of balance from a window, ladder, roof or scaffold (Fig. 3).

The forces involved in falling from a height are similar to those involved in

MVAs. The individual falls and the fall is broken by contact with a solid barrier causing a sudden change in the velocity of the body to 0mph.

On impact, an equal and opposite force is created and meets the impacting individual.

If the person falls on the feet, the two forces travel longitudinally along the vertebral column, which causes ‘axial loading’, and meet at a point where the forces are concentrated.

This can compress vertebrae and the spinal cord, cause burst fractures, and force bone fragments to enter the spinal canal. There may also be fractures to the lower extremities.

If the person falls on the buttocks, a hyperflexion injury to the lumbar area may result, again with compression fractures.

Similar injuries are also found in diving, which is one of the sports most associated with spinal cord injury.

In this scenario, however, it is the person’s head that hits a solid surface, potentially leading to a mid-thoracic injury and possible hyperextension or hyperflexion in the cervical region, depending on the position of the head.

Falls up stairs are commonly associated with hyperextension injuries to the neck. Hyperextension occurs when a person climbing stairs unbalances and falls onto them face first (Fig. 4).

Typically, the person hits their chin on a stair, which forces the neck into hyperextension. This is also found in bathroom falls when a person steps out of a bath or shower onto a tiled surface and falls face first.

These injuries are often seen in older people (Hickey 2003) and, while the events themselves may not lead to spinal cord injuries, they can cause rupture in anterior longitudinal ligaments resulting in anterior vertebral column weakness.

Decisions regarding the clearance of the cervical spine in such patients should not be made without magnetic resonance imaging (Young and Shea 1998), because patients are at high risk of further injuries due to bone movement and displacement.

Sports related injuriesTen per cent of spinal cord injuries in the UK are sports related (Harrison 2004).

Fig. 3. Injury following fall from height

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They result from the same mechanisms as MVAs and falls: compression, distraction, hyperf lexion, hyperextension and rotation.

PATHOPHYSIOLOGYWhen the spine is subjected to the sort of events described above, it undergoes an exaggerated range of normal movements, including forced flexion, extension and rotation.

Flexion involves movement towards the midline, with the chin coming down onto the chest, while extension involves movement away from the midline, with the occiput being forced onto the back.

Both flexion and extension involve compression and distraction to specific parts of vertebrae, but vertebrae may also experience severe generalised compression and distraction due to some of the injury events outlined above.

If spinal cord injury occurs, the resulting presentation is produced by both the primary event and a ‘cascade of secondary pathophysiological mechanisms’ (Young and Shea 1998).

Table 2 shows that primary injury is caused essentially by trauma and results in haemorrhagic changes that lead to ischaemia and necrosis (Hickey 2003). Secondary injury though results from various chemical and vascular changes.

Fig. 4. Hyperextension injury due to a fall on stairs

Sapru (2002)

Time after injury Pathophysiology Observed change

PrimaryImmediately Traumatic structural damage Disruption of spinal cord and surrounding vascular components with

resulting compromise of vascular supply, leading to ischaemia

SecondaryFew minutes to few hours

Release of vasoactive agents, and cellular enzymes

Infiltration of site by neutrophils and macrophages

Changes to microvessels in the central grey matter

Multifocal haemorrhages

Postcapillary venule distension

Increase in intracellular calcium levels Damage to vascular endothelium

Leakage of erythrocytes into perivascular spaces

Increase in extracellular potassium levels and resulting depolarisation of cells

Conduction block

By between four and eight hours

Hypoxia induced catecholamine release

Elevated calcium remains

Further haemorrhage and necrosis

Appearance of aneurysms and vessel rupture in lateral columns of the spinal cord

By 24 hours Thrombi formation in capillaries

Table 2. Primary and secondary spinal cord injuries

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Spinal and neurogenic shockThe first article in this series (Sheerin 2004) explains that the spinal cord is the reflex centre for the body. For example, the classic tendon reflex occurs when the spinal cord interpretes sensory input signifying a risk to the body’s integrity, and initiates a protective motor response.

But not only somatic reflexes pass through the spinal cord. The cord is associated intimately with the autonomic nervous system and is the integrating centre for autonomic reflexes.

The autonomic nervous system acts continuously, through its sympathetic and parasympathetic divisions, to maintain an equilibrium in the functioning of the smooth muscle, cardiac muscle and the glands. The scope of this control can be seen in Fig 5.

The effects of each division on specific organs and vessels is described in Table 3.

The sympathetic division has a particular relationship with the cord because they are linked by the communicating branches of the spinal nerves in the thoracolumbar region (Fig. 5). These links are described as the ‘thoracolumbar outflow’.

The parasympathetic outflow is, how-ever, only partly related to the spinal cord because it has its greatest outflow from the brainstem, via the cranial nerves, with a smaller part located in the sacral region of the cord. This part of the parasympathetic outflow is therefore described as the ‘craniosacral outflow’. Up to 80 per cent of the parasympathetic outflow emanates through cranial nerve X, the vagus nerve.

When the spinal cord is injured, there is a sudden loss of conduction due to the migration of potassium ions from inside the cells into the extracellular spaces.

This is associated with a transient loss of somatic and autonomic reflex activity below the level of neurological damage. This is termed ‘spinal shock’.

Most spinal cord injuries affect the cervical and high thoracic region (DeVivo 2002) so there is often relative loss of sympathetic outflow with continued unopposed parasympathetic, namely vagal, activity.

The signs of this imbalance are:> Hypotension: due to passive dilation

of abdominal blood vessels, caused by loss of sympathetic tone, and decreased cardiac output

Table 3. Autonomic effects on specific organs

Organ and Action Parasympathetic effect Sympathetic effect

Respiratory System

Bronchioles Constricted Dilated

Rate of ventilation Decreased Increased

Secretions Increased No direct effect

Cardiovascular System

Rate and force of heartbeat Decreased Increased

Coronary vessels Constricted Dilated

Skeletal vessels No direct effect Dilated

Visceral and dermal vessels No direct effect Constricted

Blood pressure Decreased Increased

Digestive System

Peristalsis Increased Decreased

Muscular sphincters Relaxed Contracted

Salivary glands Thin, watery saliva Viscid saliva

Gastrointestinal secretions Increased No direct effect

Glycolysis and gluconeogenesis No direct effect Increased

Urinary System

Bladder muscle Contracted Relaxed

Sphincters Relaxed Contracted

Skin

Secretion of sweat No direct effect Increased

Erector pili muscles No direct effect Contracted

Hickey (2003)

Table 4. Physiology of neurogenic shock

Spinal cord injury above T6

Sympathetic outflow to systemic

vascular system

Sympathetic outflow with unopposed parasympathetic stimulation to heart

Passive dilation of systemic vascular

system

Reduced preload

Reduced stroke volume

Reduced afterload

Reduced heart rate

Reduced cardiac output

Neurogenic shock: hypotension, bradycardia, altered thermoregulation

Spinal shock

Zed

jlik

(199

2)

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> Bradycardia: due to unopposed vagal stimulation of the heart

> Loss of thermoregulation, poikilo-thermia: due to passive dilation of dermal blood vessels and consequent inability to maintain body heat, and to loss of sweat gland activity in neurologic-ally impaired skin.

This autonomic initiated cardiovascular condition is termed ‘neurogenic shock’ and is typically seen between four and six hours after injury in patients with cord lesions above T6 (Table 4).

Spinal and neurogenic shock are transient conditions that can last between 48 hours and six weeks post-injury.

Fig. 5. Autonomic nervous system

Sympathetic division Parasympathetic division

Eye

Salivary glands

Trachea

BronchiPostganglionic fibres

Postganglionic fibres

HeartPreganglionic fibres

Preganglionic fibres

Liver

Gallbladder

Adrenal gland

Stomach

Kidney

Alimentary tract

Urinary bladder

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Assessment of resolved spinal shock is based on the return of the sacral reflexes, in particular the bulbocavernosus and anocutaneous reflexes (Hickey 2003). These are somatic reflexes, the earliest to return after spinal shock has passed.

CLINICAL SYNDROMESThe absence of spinal activity that characterises the period of spinal shock makes it impossible for clinicians to assess actual neurological status.

This only becomes clear after resolution of spinal shock, when a diagnosis of complete or incomplete spinal cord injury can be made.

According to the American Spinal Injury Association (ASIA), complete spinal cord injuries are defined as those involving the most sacral segments of the cord, S4 and S5 (ASIA 2002).

Incomplete injuries do not involve these two sacral segments and can lead to a diagnosis of one of the four classic cord syndromes, or a diagnosis that comprises elements of several (American Spinal Injuries Association 2002).

The classic cord syndromes, as described by Bing (1921), are: anterior cord syndrome, posterior cord syndrome, central cord syndrome, and Brown-Séquard’s syndrome.

Anterior cord syndromeAnterior cord syndrome typically results from damage to the anterior two thirds of the spinal cord, but can also be due to damage to the anterior spinal artery.

The resulting ischaemia leads to variable loss of motor function and of pin prick and temperature sensation below the level of the lesion (Hayes et al 2000). Sensibility to light touch, deep pressure, vibration and proprioception are preserved (Hickey 2003) (Fig. 6).

Anterior cord syndrome has a 10 to 20 per cent potential of motor recovery (Kirschblum and Donovan 2002).

Posterior cord syndromeThis rare presentation is, in a sense, complementary to anterior cord syndrome, because it involves the posterior third of the spinal cord, known as the dorsal column.

This region is sensory in nature, and provides pathways for transmitting impulses relating to light touch, deep pressure, vibration and proprioception and kinaesthetic awareness. These senses are lost, while motor function and sense of pain and temperature are preserved (Fig. 7).

The preservation of motor function, however, can be countered by loss of positional senses, leading Kirschblum and Donovan (2002) to conclude that the potential for ambulation is poor.

Fig. 7. Posterior cord syndrome

Loss of impulses relating to light touch, deep pressure, vibration and proprioception and kinaesthetic awareness

Area of cord damage

Fig. 6. Anterior cord syndrome

Variable loss of motor function and of pin prick and temperature sensation below the level of the lesion

Area of cord damage

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Central cord syndromeThis is a syndrome usually involving the cervical region of the spinal cord, and is one that tends to affect older people with cervical spondylosis who have experienced hyperextension injuries (Chiles and Cooper 1996, Kirschblum and Donovan 2002, Nelson et al 2001).

It is suggested that spondylosis and hyperextension injuries cause anterior-posterior compression of the cord with inward bulging of the ligamentum flavum, which places pressure on the cells of the anterior horn. This will predispose the person to developing oedema in the central cord region (Hickey 2003).

To understand this more fully, a basic review of the anatomy of the lateral corticospinal tract may be useful. This tract, which controls voluntary movements in the contralateral limbs, is organised so that the cervical fibres are located medially to the thoracic, lumbar and sacral fibres.

Because of this positioning, in people with spondylosis and hyperextension injuries, central pressure is exerted on cervical as well as thoracic fibres, leading to greater motor loss in the upper limbs than the lower limbs, and variable bowel and bladder dysfunction (Fig. 8).

The involvement of the lower motor neurones, which supply the upper limbs, explains the characteristically flaccid arms of the person with central cord syndrome, while damage to upper motor neurones, which supply the lower limbs, can cause spasticity there. There may also be variable sensory loss below the level of the injury. Cervical cord syndrome has good potential for recovery, especially in younger patients (Kirschblum and Donovan 2002).

Brown-Séquard’s syndromeThe classic description of this syndrome involves a hemisection of the spinal cord due to a penetrating injury, for example from a knife or gun.

This is a rare condition, and most patients present with Brown-Séquard plus syndrome, characterised by relative ipsilateral hemiplegia, which is loss of motor function on the same side of the body, with relative contralateral hemianalgesia, which is sensory loss to the opposite side of the body (Hayes et al 2000, Roth et al 1991).

This asymmetrical presentation is due to the levels at which the ascending and descending pathways cross over.

In ascending pathways, which are con-cerned with pain and temperature, first order neurones enter the cord via the posterior nerve root and synapse with second order neurone in the posterior grey horn.

The second order neurones then cross over at this level before ascending in the lateral spinothalamic tract.

Loss of voluntary motor control on same side as cord damage Loss of pain and temperature sense on opposite side

Area of cord damage

Fig. 9. Brown-Séquard syndrome

Fig. 8. Central cord syndrome

Loss of of motor function and of pin prick and temperature sensation below the level of the lesion

Incomplete loss of the above

Area of cord damage

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DeVivo M (2002) Epidemiology of traumatic spinal cord injury. In Kirshblum S et al (eds) Spinal Cord Medicine. Philadelphia PA, Lippincott Williams and Wilkins.

Glass C (1999) Spinal Cord Injury: Impact and coping. Leicester, BPS Books.,

Grundy D et al (1991) Diving into the unknown. British Medical Journal. 302, 6778, 670-671.

Guin P (2001) Advances in spinal cord injury care. Critical Care Nursing Clinics of North America. 13, 3, 399-409.

Harrison P (2004) Spinal cord injury incidence update: UK database summary 2001. Spinal Cord Injury Link. 3, 2, 4.

Hayes K et al (2000) Classifying incomplete spinal cord injury syndromes: algorithms based on the international standards for neurological and functional classification of spinal cord injury patients. Archives of Physical Medicine and Rehabilitation. 81, 5, 644-652.

Healy D et al (2004) Speed and spinal injuries. Injury. 35, 9, 908-912.

Hickey J (2003) The Clinical Practice of Neurological and Neurosurgical Nursing. Fifth edition. Philadelphia PA, Lippincott Williams and Wilkins.

Kirschblum S, Donovan W (2002) Neurologic assessment and classification of traumatic spinal cord injury. In Kirshblum S et al (eds) Spinal Cord Medicine. Philadelphia PA, Lippincott Williams and Wilkins.

National Spinal Injuries Unit (2005) NSIU Database. Dublin, Mater Misericordiae University Hospital.

Nelson A et al (2001) Nursing Practice Related to Spinal Cord Injury and Disorders: A core curriculum. New York NY, Eastern Paralyzed Veterans Association.

Prendergast V, Sullivan C (2000) Acute spinal cord injury. Critical Care Nursing Clinics of North America. 12, 4, 499-508.

Roth E et al (1991) Traumatic cervical Brown-Séquard and Brown-Séquard-plus syndromes: the spectrum of presentations and outcomes. Paraplegia. 29, 9, 582-589.

Sapru H (2002) Spinal cord: anatomy, physiology, and pathophysiology. In Kirshblum S et al (2001) Spinal Cord Medicine. Philadelphia PA, Lippincott Williams and Wilkins.

Schneck C (2002) Anatomy, mechanics, and imaging of spinal injury. In Kirshblum S et al (eds) Spinal Cord Medicine. Philadelphia PA, Lippincott Williams and Wilkins.

Schoen D (2000) Adult Orthopaedic Nursing. Philadelphia PA, Lippincott.

Sheerin F (2004) Spinal cord injury: anatomy and physiology of the spinal cord. Emergency Nurse. 12, 8, 30-36.

Tortora G, Grabowski S (1996) Principles of Anatomy and Physiology. Eighth edition. New York NY, Harper-Collins College Publishers.

Walker M (1998) Protection of the cervical spine in the unconscious patient. Care of the Critically Ill. 14, 1, 4-7.

Young W, Shea M (1998) Acute management of spine and spinal cord injury. Trauma Quaterly. 14, 1, 21-42.

Zejdlik C (1992) Management of Spinal Cord Injury. Second edition. Boston MA, Jones and Bartlett.

Damage to this pathway, therefore, results in contralateral hemianalgesia below the level of the injury.

Ninety per cent of the fibres in the descending pathway, which concerns voluntary movement, cross over at the level of the medulla oblongata, and travel in the lateral corticospinal tract.

Because the crossing over occurs at a level above the spinal cord, any damage to the pathway below this results in ipsilateral hemiplegia below the level of the injury (Fig. 9).

Similarly, fibres of the dorsal white columns of the cord, which concern touch, deep pressure, vibration and proprioception, remain uncrossed until they reach the medulla. Loss of these sensations will, therefore, be ipsilateral.

Recovery from Brown-Séquard’s syndrome is very likely, with between 75 and 90 per cent of patients being able to walk independently after rehabilitation (Roth et al 1991).

CONCLUSIONThere are diverse manifestations of spinal cord injury and it is helpful to relate mechanism of injury to the likely or potential pathophysiology.

Although presentation varies, there are principles underpinning the nursing management of patients with this type of trauma.

The third and final article on spinal cord injury applies these principles to the care of patients immediately after the injury period but before admission to specialised spinal cord injury units.

References

American Spinal Injury Association (2002) International Standards for Neurological Classification of Spinal Cord Injury. Revised edition. Chicago, ASIA.

Barker E (2001) Anatomy and physiology of the spine and spinal cord. In Nelson A et al (eds) Nursing Practice Related to Spinal Cord Injury and Disorders: A core curriculum. New York NY, Eastern Paralyzed Veterans Association.

Bing R (1921) Compendium of Regional Diagnosis in Affection of the Brain and Spinal Cord. Second edition. New York NY, Rebman.

Chiles B, Cooper P (1996) Acute spinal injury. The New England Journal of Medicine. 334, 8, 514-520.

Dawodu S (2001) Spinal Cord Injury: Definition, epidemiology, pathophysiology. emedicine. www.emedicine.com/pmr/topic182.htm (Last accessed December 9 2004)