Spinal Cord Injuries and Syndromes

Chapter Preview

Chapter Synopsis

Spinal cord injury (SCI) is a serious worldwide health problem, often resulting in significant morbidity and permanent neurologic deficits. The American Spinal Injury Association (ASIA) impairment scale can be used to classify the extent of the injury and can also serve as a predictor of neurologic outcome. Several common discrete clinical syndromes are associated with incomplete SCI and cover a broad range of neurologic dysfunction. This chapter reviews the classification, the common incomplete spinal cord syndromes, and the conus medullaris and cauda equina syndromes.

Important Points

ASIA uses a standardized protocol to assess patients with traumatic SCIs to define a neurologic level.
Spinal shock identifies the period of spinal cord dysfunction after a traumatic injury that results in complete loss of motor, sensory, and reflex function below the level of injury.
The significance of spinal shock lies in that determination of the presence of complete versus incomplete SCI, and therefore ultimate prognosis, is impossible during this period.
Neurogenic shock should not be confused with spinal shock; its occurrence is secondary to disruption of the sympathetic pathway, and it manifests as hypotension with bradycardia.
Central cord syndrome is the most common SCI and manifests with quadriparesis with upper greater than lower extremity involvement.
Brown-Séquard syndrome manifests with ipsilateral hemiplegia, ipsilateral loss of proprioception, and contralateral loss of pain and temperature secondary to spinal cord hemisection.
Anterior spinal cord syndrome manifests with complete motor paralysis and loss of pain and temperature sensation with sparing of proprioception and vibration sense secondary to injury to the anterior spinal cord from direct trauma or vascular injury typically to the anterior spinal artery.
Posterior spinal cord syndromes manifest with preservation of motor and pain and temperature with loss of proprioception and vibration sense below the level of injury.
Conus medullaris and cauda equina syndromes are two complex clinical neurologic disorders that are seen with injury to the terminal elements of the spinal cord.

Classification of Spinal Cord Injury

Spinal cord injury (SCI) can be assessed using the International Standards for Neurological Classification of Spinal Cord Injury (ISCSCI), developed by the American Spinal Injury Association (ASIA). This standardized protocol can be used to assess patients with traumatic SCI and to define a neurologic level of injury. This standardized system can be used not only as a framework for classification of injuries but also as a predictor of neurologic and functional outcomes, as well as long-term prognosis. The ASIA standard is applicable only to traumatic SCI and should not be used for the assessment of nontraumatic SCI.

The ASIA assessment consists of a neurologic evaluation of a sensory point within 28 dermatomes on both the right and left sides of the body and an evaluation of muscle strength within 10 myotomes on both sides of the body. The sensory level refers to the most caudal segment of the spinal cord with intact sensory function on both sides of the body. In a similar fashion, the motor level refers to the most caudal myotome that has motor strength of 3 out of 5 or better, with normal strength 5 out of 5 in the level above. The neurologic level of injury is the most caudal level at which both motor and sensory levels are intact. Patients with no neurologic injury have a score of 100 (grade 5 muscle strength, 10 myotomes, left and right sides).

Using the ASIA impairment scale, SCI is classified into levels A to E, in descending order of severity. Complete SCI (ASIA A) is defined as the absence of sensory and motor function in the most caudal sacral segment of the spinal cord. In comparison, incomplete injury (ASIA B to E) is defined as partial preservation of sensory or motor function below the neurologic level, including the most caudal sacral segment. ASIA B is defined as intact sensory function below the neurologic level extending through the sacral segments without intact motor function. ASIA C is defined as intact motor function below the neurologic level, with strength in most key muscles below the level at less than 3 out of 5. ASIA D is defined as intact motor function below the neurologic level, with strength in most key muscles below the injured level greater than 3 out of 5. A patient with completely intact sensory and motor function would be considered ASIA E.

The testing of the most caudal sacral function at S4 to S5 is critical to assessing the extent of the injury within this assessment protocol. Sacral sensation may be assessed by pinprick or light touch sensation at the anal mucocutaneous junction, as well as deep anal sensation with digital rectal examination. The presence of sacral sensation in the absence of distal motor function (sacral sparing) may indicate an incomplete SCI and therefore prognosticate a better potential for neurologic recovery. Motor function at this level is tested by the presence of voluntary contraction of the external anal sphincter on digital examination. The integrity of the connections between neurons within the spinal cord at this level can be monitored by testing for the polysynaptic bulbocavernosus reflex. In normal individuals, involuntary contraction of the rectal sphincter occurs with pinching of the glans penis or by tugging on an indwelling Foley catheter (normal or present bulbocavernosus reflex). The absence of this reflex indicates disruption of supraspinal inputs to the outflow tracts of the lower spinal cord and suggests spinal shock.

The assessment of complete versus incomplete SCI is confounded by the presence of spinal shock, which is a transient period immediately following an injury. Spinal shock manifests as flaccid paralysis, complete loss of sensation, and complete areflexia below the level of the injury. These initial symptoms are followed by a period of hypertonia and spasticity, as well as a variable return of motor and sensory function. The initial phase of spinal shock usually lasts between 24 and 72 hours and can be monitored by assessing the bulbocavernosus reflex.

The dysfunction seen in the initial phase of spinal shock results from a loss of excitatory input to alpha and gamma motor neurons, interneurons, and preganglionic sympathetic neurons from supraspinal centers, as well as increased spinal inhibition secondary to reduced descending inhibition of spinal inhibitory pathways. The spinal neurons, which are isolated from supraspinal input, retain their synaptic contacts from reflex afferents and interneurons and over time acquire new contacts from sprouting of neurons. This feature accounts for the spasticity and hyperreflexia that develop in the later stages of spinal shock.

The return of the bulbocavernosus reflex usually marks the end of the initial phase of spinal shock. Therefore, the determination of complete versus incomplete SCI cannot be made during spinal shock, and the prognosis for recovery should be delayed until return of bulbocavernosus reflex and the end of spinal shock. In the uncommon event that the bulbocavernosus reflex does not return (conus medullaris injury or direct injury to the S3 and lower reflex arc), then the end of spinal shock can be assumed to be after 72 hours from the time of the initial injury.

Spinal shock should be differentiated from neurogenic shock. Neurogenic shock is caused by disruption of the sympathetic pathways within the brain or spinal cord that results in unopposed vagal tone and increased vascular dilatation, with a consequent decrease in systemic vascular resistance. In this situation, hypotension, bradycardia, and hypothermia result. This autonomic dysfunction is most often observed in spinal injuries above the T6 level.

Central Cord Syndrome

Central cord syndrome (CCS) is the most common type of incomplete SCI. It manifests as symmetric incomplete quadriparesis, which disproportionately affects the upper extremities relative to the lower extremities. Sensory impairment is variable, and urinary retention is common.

CCS commonly occurs as a result of hyperextension injury in the presence of previous underlying cervical spondylosis. Injury occurs from posterior compression of the spinal cord by buckling of the ligamentum flavum or by anterior compression by osteophytes. It may also be associated with fracture and disruption of the structural spinal elements in which anteroposterior compressive forces direct the greatest damage to the central portions of the spinal cord parenchyma ( Fig. 19-1 ).