eMedicine Specialties > Neurology > Introductory Topics

Spinal Cord Trauma and Related Diseases

Author: Francisco de Assis Aquino Gondim, MD, MSc, PhD, Professor Adjunto II, Departments of Physiology and Pharmacology, Neurology Residency Program Director, Faculdade de Medicina, Universidade Federal do Ceará, Brazil
Coauthor(s): Florian P Thomas, MD, MA, PhD, Drmed, Director, Spinal Cord Injury Unit, St Louis Veterans Affairs Medical Center; Associate Program Director, Associate Professor, Departments of Neurology, Molecular Virology, and Molecular Microbiology and Immunology, St Louis University School of Medicine
Contributor Information and Disclosures

Updated: Jan 24, 2008

Introduction

Background

Spinal cord disease can result from diverse pathologic processes including trauma. Irrespective of the pathogenesis, it can lead to significant impairment of motor, sensory, or autonomic function.

This review focuses on the clinical description of common patterns of spinal cord involvement. Considerable differences exist in terms of clinical complications after traumatic and nontraumatic spinal cord injury (SCI). In this article, the general principles of management of traumatic SCI are emphasized. For specific nontraumatic neurologic diseases that affect the spinal cord, see Multiple Sclerosis, Amyotrophic Lateral Sclerosis, and other articles listed in Differentials).

Pathophysiology

Trauma to the spinal cord typically leads to a combination of symptoms and signs resulting from immediate and delayed injury.

The initial mechanical trauma is secondary to traction and compression forces. Direct compression of neural elements by bone fragments, disc material, and ligaments damages both the central and peripheral nervous systems. Blood vessel damage also leads to ischemia. Rupture of axons and neural cell membranes also occurs. Microhemorrhages occur within minutes in the central gray matter and progress over the next few hours. Massive cord swelling happens within minutes. The cord fills the whole spinal canal at the injury level and leads to further secondary ischemia. Loss of autoregulation and spinal shock cause systemic hypotension and exacerbate ischemia.

Ischemia, toxic metabolic compounds, and electrolyte changes cause a secondary injury cascade. Hypoperfusion of gray matter extends to the surrounding white matter and alters the propagation of action potentials along the axons, contributing to spinal shock. Glutamate is a key element in the excitotoxicity. Massive release of glutamate leads to overstimulation of neighbor neurons and production of free radicals, which kill healthy neurons. Excitotoxic mechanisms kill neurons and oligodendrocytes, leading to demyelination. AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid) glutamate receptors play a major role in oligodendrocyte damage. Additionally, recent evidence has shown that a wave of apoptosis further affects the oligodendrocytes up to 4 segments from the trauma site days and weeks after the initial trauma. Syringomyelia may develop as one outcome of this cascade.

Frequency

United States

Traumatic SCI accounts for an estimated annual incidence of approximately 40 cases per million population, or approximately 11,000 new cases each year, in the United States (published figures range from 28-55 cases per million people). This number excludes those who died at the scene of an accident. Currently, 183,000-230,000 patients with SCI (721-906 people per million population) are alive in the United States.

International

SCI incidence is estimated at 15-40 cases per million population. In Australia, recent statistics report an age-adjusted rate of 14.5 cases per million population.

Mortality/Morbidity

In 1927, Harvey Cushing described an 80% mortality rate for World War I soldiers with SCI in the first few weeks because of infections from bedsores and catheterization, with survival restricted to partial lesions. Today, in well-organized spinal cord centers, 94% of patients survive the initial hospitalization.

• Recent statistics show the cost of the care of patients with C1-4 tetraplegia at approximately $572,178 in the first year and approximately $102,491 for each subsequent year. Estimated lifetime costs for high tetraplegia are $2,185,667 for 25-year-old individuals and $1,286,714 for 50-year-old individuals. This amount does not include indirect costs such as loss of productivity, which vary with the educational background. Overall, lifetime costs range from $500,000 to $2 million, depending on the extent of injury and the location. Total direct costs for patients with SCI in the United States exceed $7 billion per year.
• Life expectancy is greatly decreased, although major advances of medical management have markedly prolonged survival. In the past, renal failure was the leading cause of death after SCI. Currently, pneumonia, pulmonary emboli, and septicemia surpass renal failure. For further details of the epidemiology, please see information provided by the National Spinal Cord Injury Association.

Race

Recent statistics show higher rising incidence of SCI in black people in the United States. According to the National Center for the Dissemination of Disability Research, from 1973-1978, 77.5% of the persons in the database were white people, 13.5% were black people, 5.7 % were Hispanic people, and 0.8% were Asian people. However, since 1990, only 59.1% were white people, while 27.6% were black people, 7.7% were Hispanic people, 0.4% were American Indian people, and 2.1% were Asian people.

Sex

Traumatic SCI is more common in young adult males, who are usually at a higher risk for motor vehicle accidents, violence, falls, and injury from recreational activities such as diving. The male-to-female ratio in the United States is 4:1.

Age

The average age of injury in the United States is 31.7 years, with the greatest frequency occurring in people aged 15-25 years. The age span is similar throughout other countries.

Clinical

History

The rapid onset of symptoms after trauma usually makes the diagnosis obvious. With any trauma, especially to the head or neck and with whiplash injury, spinal injury should be immediately suspected. Patients with cervical stenosis may be especially prone to SCI, and the diagnosis may be challenging in patients after high cervical lesions, when unresponsiveness may follow hypotension and respiratory failure. C2 injuries, especially odontoid fractures, must be ruled out in older patients with neck pain after even a minor injury. SCI may be overlooked in patients with concomitant trauma to the head or to multiple body parts, especially if patients are confused or only have limited SCI. Therefore, SCI must be considered after any major traumatic event, and the patient's neck should be stabilized until SCI is ruled out.

SCI in elderly patients is also challenging. When patients with underlying cervical stenosis are found unresponsive after a fall at home or in a nursing home, diagnosis may be difficult because of concomitant multiple medical problems. In addition, respiratory distress or hypotension due to spinal shock may lead to a confusional state that may deviate attention to a brain lesion, prevent immediate diagnosis, and further contribute to worsening of the spinal lesion.

A high degree of suspicion is also warranted for patients who are at high risk for SCI because of concomitant medical problems such rheumatoid arthritis, Down syndrome, neck dystonia or torticollis, and congenital neck abnormalities.

Leg claudication may indicate lumbar spinal stenosis, especially if accompanied by weakness or numbness. Patients with cervical spinal stenosis can present with arm wasting and/or atrophy (ie, lower motor neuron changes) from anterior horn cell or root involvement and leg stiffness and/or spasticity (ie, upper motor neuron changes).

Acute SCI must be suspected whenever someone presents with a combination of autonomic (ie, urinary retention, constipation, ileus, hypothermia, hypotension, bradycardia), motor (ie, hemiplegia and/or hemiparesis sparing the face, paraplegia and/or paraparesis, tetraplegia and/or tetraparesis), and sensory (ie, lack of sensation at a certain level, hemisensory loss) symptoms. They vary according to the phase of SCI, ie, acute, subacute, or chronic.

In the acute phase, physicians must be vigilant in cases of sudden onset of quadriparesis (with or without respiratory distress); paraparesis; loss of sensation or bowel or bladder control; sexual dysfunction; or symptoms of neurogenic shock such as lightheadedness, diaphoresis, and bradycardia. The classic syndromes of incomplete SCI are described below.

In the subacute phase, patients may report pain, which can be progressive depending on pathology and rapidity of the process.

Complete spinal cord transection syndrome

In the acute phase, the classic syndrome of complete spinal cord transection at the high cervical level consists of respiratory insufficiency; quadriplegia with upper and lower extremity areflexia; anesthesia below the affected level; neurogenic shock (ie, hypothermia and hypotension without compensatory tachycardia); loss of rectal and bladder sphincter tone; and urinary and bowel retention leading to abdominal distention, ileus, and delayed gastric emptying. This constellation of symptoms is called spinal shock. Horner syndrome (ie, ipsilateral ptosis, miosis, anhydrosis) is also present with higher lesions because of interruption of the descending sympathetic pathways originating from the hypothalamus.

Lower cervical level injury spares the respiratory muscles. High thoracic lesions lead to paraparesis instead of quadriparesis, but autonomic symptoms are still marked. In lower thoracic and lumbar/sacral cord lesions, hypotension is not present but urinary and bowel retention are.

Anterior cord syndrome

The anterior cord syndrome is typically observed with anterior spinal artery infarction and results in paralysis with loss of pain and temperature sensation below the level of the lesion and relative sparing of touch, vibration, and proprioception (because the posterior columns receive their primary blood supply from the posterior spinal arteries).

Central cord syndrome

Central cord syndrome is typically observed in syringomyelia, central canal ependymoma, and trauma. It is associated with more significant arm weakness than leg weakness and variable sensory deficits; often, the most affected sensory modalities are pain and temperature because the lateral spinothalamic tract fibers cross just ventral to the central canal. This is sometimes referred to as dissociated sensory loss and is often present in a capelike distribution.

Acute traumatic central cord syndrome is typically considered to be caused by a hemorrhage that affects the central part of the spinal cord, destroying the axons of the inner part of the corticospinal tract devoted to the motor control of the hands. However, others have proposed that destruction of the motor neurons supplying the muscles of the hand was the most likely cause. A recent MRI study corroborates the first hypothesis (corticospinal tract rather than motor neuron destruction).¹ The traumatic injury is usually caused by severe neck hyperextension and is characterized by initial quadriplegia replaced over minutes by leg recovery. In addition to the distal more than proximal arm weakness (man-in-a-barrel syndrome), bladder dysfunction, patch sensory loss below the level of the lesion, and considerable recovery occur.

Brown-Séquard syndrome

Brown-Séquard syndrome is essentially equivalent to a hemicordectomy. Ipsilaterally, paralysis, loss of vibration and position sense below the level of the lesion, hyperreflexia, and an extensor toe sign are present. In addition, ipsilateral segmental anesthesia occurs at the level of the lesion. Contralaterally, loss of pain and temperature sensation occurs below the level of the lesion (beginning perhaps 2-3 segments below). Brown-Séquard syndrome is more common after trauma. However, the full spectrum of this syndrome is rarely observed in clinical settings.

Cauda equina and conus medullaris syndromes

Patients with lesions affecting only the cauda equina can present with a polyradiculopathy with pain, radicular sensory changes, asymmetric lower motor neuron–type leg weakness, and sphincter disturbances. This can be difficult to distinguish from involvement of the lumbosacral plexus or multiple nerves. Lesions affecting only the conus medullaris cause early disturbance of bowel/bladder function.

Physical

Motor weakness (especially paraparesis or quadriparesis) can be flaccid in the acute phase or when the anterior horn is involved. Identification of affected muscle and the sensory level helps with injury localization.

Reflexes are lost immediately after SCI. Superficial abdominal reflexes are elicited by running a semisharp stimulus in any abdominal quadrant (upper quadrants are best) toward the umbilicus. Then, umbilical movement toward the stimulus (ie, abdominal muscle contraction in that quadrant) is observed.

The cremasteric reflex is elicited by running a semisharp stimulus down the upper inner thigh. As this is elicited, look for contraction of the cremasteric muscle (ie, scrotal elevation).

An anal wink is contraction of the anal sphincter on irritation, elicited by a light stroke with a semisharp stimulus to the perianal area. As this is elicited, look for a characteristic puckering of the anus.

The bulbocavernosus reflex is elicited by lightly tapping the dorsum of the penis or gently moving a urinary catheter, if in place. The intact reflex results in contraction of much of the pelvic floor musculature.

To check for a sensory level, separate testing of pinprick, light touch, and vibration senses is helpful in order to discriminate conditions such as Brown-Séquard syndrome. The stimulus should be applied and moved rostrally until a change is noted in the quality or intensity of the stimulus. This may be confirmed by moving caudally as well. Usually, some physiological overlap occurs at the sensory level when the examiner first moves rostrally then caudally. This examination may be performed anteriorly or posteriorly. Sensation over occiput should be checked when high cervical lesions are suspected because this area is supplied by upper cervical dorsal roots.

With the resolution of the spinal shock phase, areflexia and hyporeflexia are replaced by hyperreflexia with increased tone and extensor great toe sign (Babinski sign) develops. In humans, the spinal shock phase lasts for few weeks, and it can be prolonged when the patient develops complications such as bedsores and urinary tract infections.

Withdrawal reflexes may be exaggerated to the point of flexor spasms and may be accompanied by sweating, piloerection, and automatic emptying of the bladder or rectum (also called the mass reflex).

The Beevor sign is elicited by having the patient flex the neck to look at the umbilicus; if the umbilicus moves upward, it implies intact abdominal motor control down to approximately the T10 level and loss of motor function below.

The Lhermitte sign or symptom results from neck flexion, which stretches and irritates damaged fibers in the dorsal columns of the cervical spine. It results in an electroshock sensation going down the arm or down the back, indicating probable meningeal or dorsal column pathology. It is a poor localizer within the cord.

Causes

Such injuries result from motor vehicle and workplace accidents, community violence, and recreational activities. In the United States, motor vehicle accidents account for 36-48%, violence for 5-29%, falls for 17-21%, and recreational activities for 7-16% of events.

The spinal cord is located inside the vertebral canal, which is formed by the foramina of 7 cervical, 12 thoracic, 5 lumbar, and 5 sacral vertebrae. Cervical and lumbar spondylosis are particularly common in elderly patients, making them prone to SCI. Cervical SCI is common with relatively minor trauma in patients older than 65 years. Return of functional motor recovery in this group is delayed.

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