case files neurology
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case files neurology

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of age and males outnumber females by 4:1. Approximately 5% of
all spinal injuries occur between birth and 16 years of age, and these pediatric
patients require special consideration as discussed below. Neonatal (birth-
related) spinal cord injury complicates approximately 1 of every 60,000 births
and carries a 50% mortality rate. In childhood, the most common causes of
spinal cord injury prior to 10 years of age are motor vehicle accidents and falls,
whereas in individuals older than 10 years of age, motor vehicle accidents and
sports-related injuries are the most common. With regards to motor vehicle
accidents, children younger than 13 years of age should be restrained passen-
gers in the backseat only in order to avoid potential injury from airbag deploy-
ment. Younger children can sustain significant and often fatal cervical spinal
cord injuries from passenger side airbags. The rate of nontraumatic spinal cord
injury is at least threefold higher than traumatic cases although the epidemio-
logic data is not as complete in this regard.
Types of Spinal Cord Injuries
Patients can also present with incomplete lesions of the spinal cord. For exam-
ple, hemisection produces the classic Brown-Sequard syndrome with ipsilat-
eral weakness and loss of fine touch and vibration sensation but contralateral
loss of pain and temperature below the level of the lesion. This is a result of
fibers in the dorsal column remaining ipsilateral to the brainstem while fibers
in the spinothalamic tract synapse and cross within one or two spinal levels
then travel contralaterally. Trauma would be the most common cause of the
Brown-Sequard syndrome, which rarely presents as a pure unilateral injury.
Anterior cord syndrome is usually caused by either a traumatic or a vascular
insult to the anterior two-thirds of the spinal cord. This results in a bilateral
loss of spinothalamic tract function (pain and temperature) as well as bilateral
weakness (interruption of corticospinal tract) with preservation of dorsal col-
umn function (fine touch, proprioception, and vibration). Central cord syn-
drome is caused by injury to the structures around the spinal central canal.
Although this can occur acutely with trauma, it more commonly occurs with
chronic processes such as intra-axial neoplasms or dilation of the central canal
(referred to as syringomyelia). Clinically this typically presents with a bilat-
eral loss of pain and temperature sensation in the upper extremities as well as
weakness in the same distribution but with preservation of fine touch.
Anatomically this is because the spinothalamic tract decussates immediately
anterior to the central canal. Also, motor fibers traveling to the legs tend to run
more laterally in the spinal cord and are therefore relatively spared.
Once the patient has been stabilized and an expedited neurologic examina-
tion has been performed, the appropriate imaging modality must be selected.
In blunt trauma of patients older than 9 years of age, no spine imaging is nec-
essary if they are alert, conversant, nonintoxicated, and have a normal neuro-
logic examination without cervical tenderness. If patients are younger than 9
years of age then imaging is recommended and should be interpreted by a radi-
ologist accustomed to reviewing spine studies from young children. Bony
structures can also be well imaged using a helical CT scanner. Visualizing the
spinal cord itself is best accomplished using an MRI scan. Children younger
than 9 years can develop spinal cord injury without radiographic abnormality
(SCIWORA). Given the greater mobility and flexibility of the pediatric spine
relative to that found in adults, bony elements can be displaced into the spinal
cord and then revert to their normal position. When this occurs, the patient will
clinically appear to have a traumatic myelopathy (spinal cord injury) on neu-
rologic examination, but no bony or ligamentous damage is seen with plain
films or CT scans. An MRI, however, can demonstrate damage to the spinal
ligaments, injury to the spinal cord, or both.
Initial Management of Spinal Cord Injuries
Management of acute spinal cord injury is focused on preventing additional
damage. This begins in the field with first responders immobilizing the spine
in a neutral position using rigid collars and backboards. Further injury can
occur because of impingement of bony matter onto the cord, excessive move-
ment of the cord as a result of spinal instability, compression of the cord by
hemorrhage, or cord ischemia caused by hypotension. Given the dispropor-
tionately large head size in children relative to the trunk, it is often necessary
to elevate the torso to achieve a neutral position for the neck. In addition to
appropriate positioning, it is vital that an adequate airway is maintained and
that respiration is not diminished by tape and restraints over the torso.
In the ER, once stabilization of airway, breathing, and circulation has been
achieved, a neurologic examination is performed to assess the clinical level of
injury. In this patient there are several findings pointing to an extensive and
likely complete high cervical spinal cord injury. The complete loss of motor and
sensory function of the upper and lower extremities as well as respiratory diffi-
culties but with preservation of reflexes mediated by cranial nerves would be
consistent with this localization (because the upper extremity is innervated by
spinal nerves from C5 to T1 and the phrenic nerve arises from C3\u2013C5). In addi-
tion to loss of motor and sensory function below the level of the lesion, spinal
cord transaction also results in loss of autonomic function, which can produce
spinal shock. The acute loss of descending sympathetic tone produces
decreased systemic vascular resistance, which can result in hypotension. If vagal
output is intact then its unopposed influence can further lower vascular resist-
ance and also result in a paradoxical bradycardia. In the context of spinal shock,
aggressive fluid resuscitation is necessary to maintain perfusion pressure and
prevent cord ischemia. The complete absence of deep tendon reflexes, superfi-
cial cutaneous reflexes, and rectal tone also suggests the presence of spinal
shock. It is important to remember that, as the inflammatory response to the
injury develops and edema occurs the apparent clinical level of the injury can
rise to higher spinal levels or into the brainstem. Finally, it is vital to remember
to place an indwelling Foley catheter to empty the bladder because the patient
will otherwise develop significant urinary retention and stasis.
The Role of Surgery and Steroids
As mentioned above, the principal goal in managing acute spinal cord injury is
to prevent secondary injury. Although the initial traumatic event can produce
major damage, subsequent inflammation, edema, and ischemia can lead to sig-
nificant worsening of this primary insult. Surgical intervention to stabilize the
spine, remove bony matter, evacuate hemorrhage, and decompress the spinal
canal has been evaluated, particularly in adult patients, and remains controver-
sial with little data available in children. Animal work has supported the use of
early decompression in order to improve outcome, but surgery is performed
sooner after the trauma than may be practical clinically. Significant compromise
of the spinal canal and fixation of a very unstable spine are considered the prin-
cipal indications for early surgery in traumatic spinal cord injury at this point.
Given that inflammation plays a major role in mediating secondary injury,
administration of corticosteroids has been studied in acute spinal cord injury.
Certainly the benefits of steroids in subacute spinal cord injury, such as cord
compression by tumor, are well established. However, clinical trials in acutely
injured adults have shown