Rethinking Acute Traumatic Central Cord Syndrome
CASE
The patient in this case is a 64-year-old male with a history of hypertension, chronic obstructive pulmonary disease, rheumatic heart disease, and a previous C3-C6 laminectomy and fusion who presented to the Emergency Department (ED) with a chief complaint of new-onset, bilateral upper extremity weakness and paresthesia following an unwitnessed fall. The patient reported that he syncopized and struck his forehead on a stovetop before regaining consciousness on his kitchen floor. He additionally endorsed mild headache and neck pain.
On arrival to the ED, the patient was hypertensive to 180/80, but his vital signs were otherwise within normal limits. He was awake, alert, and able to actively participate in his evaluation. His physical exam was notable for midline cervical tenderness and severely diminished motor strength in his bilateral upper extremities, as well as mildly diminished strength in his bilateral lower extremities. Sensation to light touch and temperature was intact, though patient reported subjective numbness and paresthesias in his upper extremities, which he described as a “sandpaper-like” feeling. While in the ED, the patient had an episode of urinary incontinence, which was unusual for him.
Computed tomography imaging revealed adjacent segment disease – degenerative changes commonly seen following spinal fusion – in the patient’s cervical spine but was otherwise negative for acute processes. Magnetic resonance imaging (MRI) was significant for increased T2 signal in the cervical cord at C4-5 and C5-6.
DIAGNOSIS
The patient was diagnosed with acute traumatic central cord syndrome (ATCCS).
DISCUSSION
ATCCS is the most common form of incomplete spinal cord injury. It typically presents as bilateral upper extremity weakness, though symptoms including less-severe lower extremity weakness, sensory deficits below the level of injury, and bladder dysfunction can also occur [[i]]. First described in 1951 by Taylor et al, ATCCS results when a hyperextension injury of the cervical spine leads to spinal cord impingement by “inward bulging” of the posterior ligamentum flavum [[ii]]. Several theories to explain how this impingement leads to the deficits seen in ATCCS have been proposed, though there is little consensus among researchers. For decades, it was accepted that the central portions of the corticospinal tracts preferentially contain motor neurons that innervate the upper extremities, while those portions of the tract that lie more peripherally innervate the sacrum and lower extremities [[iii]]. Axonal injury to the central cord, therefore, would result in motor weakness more pronounced in the upper extremities. However, recent studies have failed to demonstrate evidence of such segregated somatotropic organization of the corticospinal tracts [[iv],[v]]. Levi, et al recently postulated that the corticospinal tracts, in their entirety, preferentially serve motor function to the upper extremities, while the lower extremities are innervated by other descending tracts [[vi]].
Patients with a narrowed cervical spinal canal are predisposed to ATCCS, as even minimal anterior displacement of the ligamentum flavum could result in spinal cord impingement. Consequently, the condition often occurs in older adults with known degenerative changes of their cervical spine following relatively low-velocity mechanisms of injury, such as ground-level falls. When ATCCS occurs in young, otherwise healthy patients who are not predisposed to the condition, it is most often the result of high-velocity mechanisms of injury, such as a motor vehicle accident [[vii]].
ATCCS is largely a clinical diagnosis, but it can be confirmed by the presence of T2 hyperintensity on MRI at the level of the involved region of the spinal cord. Extent of spinal cord compression, hemorrhage and swelling may be visualized, and are all associated with a poorer prognosis for neurologic recovery [[viii]]. Early surgical intervention has been increasingly preferred to conservative management for patients with moderate to severe impairment, and a systematic review suggests that surgical intervention may lead to improved neurologic outcomes [[ix]]. Surgery typically consists of anterior or posterior decompression and, in some cases, fusion. ED treatment of ATCCS consists of supportive measures and, when necessary, management of neurogenic shock. These measures may include cervical spine immobilization, volume resuscitation, and vasopressor support to improve spinal cord perfusion by maintaining mean arterial pressure (MAP) above 85 mmHg. These medical interventions have been shown to optimize potential for neurologic recovery [[x]].
CASE RESOLUTION
The patient received supportive measures while in the ED. He was admitted to the surgical spine service and underwent non-emergent C3 laminectomy and decompression, and C2-T2 posterolateral fusion. His symptoms were mildly improved at discharge. Notably, the patient had improved strength in his lower extremities, and he was no longer experiencing episodes of urinary incontinence. His symptoms of upper extremity weakness and paresthesias were largely unchanged.
TAKE-AWAYS
· ATCCS classically presents as bilateral upper extremity weakness, though lower extremity weakness, sensory deficits, and bladder dysfunction can also occur.
· ATCCS may result when hyperextension injury causes axonal damage in the corticospinal tracts.
· MRI is the imaging modality of choice to confirm ATCCS.
· ED management of ATCCS includes cervical spine immobilization and improving spinal cord perfusion to optimize neurologic recovery.
· Decompression and fusion are the definitive management in moderate to severe ATCCS.
Author: Dr. Taylor Marquis is a second-year emergency medicine resident at Brown Emergency Medicine
Faculty Reviewer: Dr. Michelle Myles is an attending physician and clinician educator at Brown Emergency Medicine
REFERENCES
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