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Spinal Cord Trauma and Related Diseases Clinical Presentation

  • Author: Francisco de Assis Aquino Gondim, MD, MSc, PhD, FAAN; Chief Editor: Stephen A Berman, MD, PhD, MBA  more...
 
Updated: Dec 28, 2015
 

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.

The presence of priapism following the spinal shock phase indicates the presence of complete spinal cord injury and is a marker for the progression to complete cord injury.[3]

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).[4] 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.

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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 a 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.

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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.[5]

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Contributor Information and Disclosures
Author

Francisco de Assis Aquino Gondim, MD, MSc, PhD, FAAN Professor Adjunto of Neurology and Clinical Skills, Department of Internal Medicine, Universidade Federal do Ceará, Brazil

Francisco de Assis Aquino Gondim, MD, MSc, PhD, FAAN is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, International Parkinson and Movement Disorder Society

Disclosure: Received travel grants from for: Aché, Biogen, Genzyme, Ipsen, Novartis.

Coauthor(s)

Florian P Thomas, MD, PhD, Drmed, MA, MS Director, National MS Society Multiple Sclerosis Center; Professor and Director, Clinical Research Unit, Department of Neurology, Adjunct Professor of Physical Therapy, Associate Professor, Institute for Molecular Virology, St Louis University School of Medicine; Editor-in-Chief, Journal of Spinal Cord Medicine

Florian P Thomas, MD, PhD, Drmed, MA, MS is a member of the following medical societies: Academy of Spinal Cord Injury Professionals, American Academy of Neurology, American Neurological Association, Consortium of Multiple Sclerosis Centers, National Multiple Sclerosis Society, Sigma Xi

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Howard S Kirshner, MD Professor of Neurology, Psychiatry and Hearing and Speech Sciences, Vice Chairman, Department of Neurology, Vanderbilt University School of Medicine; Director, Vanderbilt Stroke Center; Program Director, Stroke Service, Vanderbilt Stallworth Rehabilitation Hospital; Consulting Staff, Department of Neurology, Nashville Veterans Affairs Medical Center

Howard S Kirshner, MD is a member of the following medical societies: Alpha Omega Alpha, American Neurological Association, American Society of Neurorehabilitation, American Academy of Neurology, American Heart Association, American Medical Association, National Stroke Association, Phi Beta Kappa, Tennessee Medical Association

Disclosure: Nothing to disclose.

Chief Editor

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.

Additional Contributors

Stephen A Berman, MD, PhD, MBA Professor of Neurology, University of Central Florida College of Medicine

Stephen A Berman, MD, PhD, MBA is a member of the following medical societies: Alpha Omega Alpha, American Academy of Neurology, Phi Beta Kappa

Disclosure: Nothing to disclose.

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A T1-weighted MRI that depicts a lesion with high signal enhancement inside the cervical spinal cord. This type of signal enhancement is consistent with blood and is most commonly observed secondary to cord trauma.
 
 
 
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