The term “spinal shock” applies to all phenomena surrounding physiologic or anatomic transection of the spinal cord that results in temporary loss or depression of all or most spinal reflex activity below the level of the injury. Hypotension due to loss of sympathetic tone is a possible complication, depending on the level of the lesion. The mechanism of injury that causes spinal shock is usually traumatic in origin and occurs immediately, but spinal shock has been described with mechanisms of injury that progress over several hours. Spinal cord reflex arcs immediately above the level of injury may also be severely depressed on the basis of the Schiff-Sherrington phenomenon. The end of the spinal shock phase of spinal cord injury is signaled by the return of elicitable abnormal cutaneospinal or muscle spindle reflex arcs. Autonomic reflex arcs involving relay to secondary ganglionic neurons outside the spinal cord may be variably affected during spinal shock, and their return after spinal shock abates is variable. The returning spinal cord reflex arcs below the level of injury are irrevocably altered and are the substrate on which rehabilitation efforts are based.
The term “spinal shock” was introduced more than 150 years ago in an attempt to distinguish arterial hypotension due to a hemorrhagic source from arterial hypotension due to loss of sympathetic tone resulting from spinal cord injury.
2Whytt, however, may have discussed the same phenomenon a century earlier, although no descriptive term was assigned.
4Throughout the years, confusion has developed, surrounding the supposed original intent of spinal shock and a concept that evolved relative to the “shock” inflicted on the isolated lower spinal cord segment after severe spinal cord injury and the resultant induced absence of reflex function. Combining terminology is commonplace even today.
6and any coherent discussion necessitates redefinition.
In this review, spinal shock applies to all phenomena surrounding physiologic or anatomic transection of the spinal cord that results in temporary loss or depression of all or most spinal reflex activity below the level of the lesion. As subsequently discussed, arterial hypotension may or may not be a part of this process.
Historical Background And Current Concepts
Spinal shock was first described by Hall
2more than 150 years ago. Initially, it was defined by Bastian
7in 1890 as complete severance of the spinal cord that results in total loss of motor and sensory function below the level of the lesion, as well as permanent extinction of tendon reflexes and muscular tone despite the reflex arc remaining intact. Bastian
8treated many patients with spinal cord injuries, but death was ubiquitous soon after injury—hence, Bastian's use of the term “permanent” in his definition. Sherrington
9began important spinal cord injury studies before the turn of the 20th century that have continued for decades. Research in combination with improved patient care and survival of patients with spinal cord injuries throughout the years, as well as two world wars, replaced Bastian's use of the term “permanent” with temporary extinction of the reflex arc below the level of the lesion.
13The Sherrington school of thought led to the modern mechanistic concept of spinal shock. This theory hypothesized that reflex depression or abolition of the lower transected cord is the consequence of sudden withdrawal of a predominantly facilitatory influence of descending supraspinal tracts, a phenomenon that results in a disruption of transmission at the synapse and renders the process of interneuronal conduction difficult or impossible. Several laboratory findings led to Sherrington's theory. Immediate transection of the spinal cord by any means, physiologic or anatomic, led to spinal shock. Immediate sectioning of posterior columns, the phylogenically new ascending sensation pathways, had little or no effect. Immediate sectioning of the posterior roots resulted in minimal or no spinal shock; however, it substantially affected spinal spasticity.
14Evolutionarily higher species had greater degrees of spinal shock, a suggestion that phylogenically new descending tracts may be responsible,
To date, no unifying anatomic or physiologic reason explains spinal shock despite more than a century of pathologic and physiologic studies involving acute spinal cord injury in laboratory and clinical series. Understanding of these events has improved, however, and directly correlates with enhanced ability to manage such patients clinically.
Pathologic Features Of Spinal Cord Injury
Spinal shock occurs only with physiologic or anatomic transection or near transection of the spinal cord; however, in clinical and laboratory series, the spinal cord is rarely anatomically transected.
15The standard model of spinal cord injury in the laboratory involves the free-weight drop technique and has been used for decades.
21The response varies, depending on the species. With beagles, a 375-g-cm force will produce complete and prolonged paraplegia in 50&x0025; of the animals, and serious neurologic deficits remain in the other half. A 400-g-cm force causes paraplegia in almost 100&x0025; of the animals, and forces greater than 450- to 500-g-cm produce profound mechanical damage and maceration of the spinal cord.
16In the model of severe spinal cord injury, the cord may appear grossly normal for several minutes, although it is rendered physiologically nonfunctional. Ultrastructurally, however, the most obvious changes are hemorrhage and protein extravasation in the central gray matter virtually immediately after impact; by 4 hours, central hemorrhagic necrosis is noted in the entire central gray matter within the impacted area and the adjacent white matter.
24By 24 hours, the central gray matter and most of the adjacent white matter are necrotic, and only a thin rim of white matter remains. Spinal cord edema maximizes by 3 to 6 days and may persist for 12 to 15 days, but the structural damage has occurred long before this time.
26The reason for progressive hemorrhage accumulation is obscure. Localized release of catecholamines
20was suggested, but later studies disputed this theory.
27Hyperbaric oxygen toxicity has produced similar pathologic findings in the spinal cord, a suggestion of a possible toxic response.
28Some researchers suggest that vascular damage and ischemia are the main culprits, but spinal cord blood flow and tissue oxygenation have been found to be variable at the site of the injury,
30and the posterior columns remain relatively resistant to initial ischemia, unlike the rest of the spinal cord.
31Autoregulation of the spinal cord blood flow at the site of impact is known to be impaired.
33and 20 to 30 minutes after injury, vascular occlusions in arterioles and venules are common. Endothelial disruption in these vessels, however, is rare. As with other types of spinal cord injury such as irradiation or ischemia, the blood vessels are resistant to the surrounding neuropil destruction in that they can still be visualized in areas of total necrosis.
24Spinal cord blood flow may certainly be diminished but may represent decreased metabolic blood flow requirements of the injured parenchyma.
33Cellular and mitochondrial injury from impact may initiate an eventual cascade of destructive events.
34and this cascade of destruction remains a primary focus of treatment today.
By 2 months after injury, only a small shell of outer rim of white matter remains. By 1 to 2 years, cavitary healing often occurs, which is unique to the central nervous system. Resorption and phagocytosis of the necrotic debris are the usual causes of cavitation, but autolysis due to lysozomal accumulation at the site of the injury has also been proposed.
The pathophysiologic aspects of spinal cord injury are still being debated. Nevertheless, the consensus is that the surrounding white matter may not be initially destroyed in less severe injuries, but preservation of the long tracts in the white matter necessitates that some type of treatment must be initiated within the first few hours. This potential therapeutic window is the target of current spinal cord preservation studies in the laboratory and clinical settings.
Pathophysiologic Thophysiologic Characteristics Of Spinal Shock
Investigators know that spinal shock occurring in laboratory animals with immediate compression of the spinal cord differs from that occurring with gradual compression. Even species behave differently, and the most substantial degrees of spinal shock are induced in the higher primates and witnessed most profoundly in humans. Clinical studies of transverse myelitis suggest that spinal shock may be induced up to several hours after the onset of injury.
36As a generalization, the more severe the physiologic or anatomic transection of the spinal cord, the more profound the state of spinal shock.
The isolated spinal cord closest to the disruption is the most severely affected-loss of reflex function occurs. The spinal cord segment most distal to the transection may be depressed later; in fact, the farther it is from the site of injury, the more likely it will retain some reflex capabilities. In clinical series, patients with high-level cervical spinal cord injuries are likely to retain distal sacral reflexes such as bulbocavernosus and anal wink despite loss of all other reflexes. The lower the spinal cord injury, the more likely that all distal reflexes will be absent. With a partial spinal cord injury, sacral sparing exists, and sensation remains in the sacral regions. This entity has a distinctly different prognosis from that of a complete spinal cord injury. Retention of sacral reflex arcs such as bulbocavernosus and anal wink during spinal shock that results from high-level cervical spinal cord injuries should not be confused with sacral sparing of sensation. If distal sacral reflex arcs are elicitable with spinal shock associated with high-level cervical spinal cord injury, they may remain depressed or intact indefinitely, or they may become areflexic within hours to days after injury. Reflex arcs at the level of spinal cord injury may remain permanently absent if portions or all of the arc components are permanently injured.
The course of depression that spreads from proximal isolated spinal cord to distal isolated spinal cord within minutes suggests a physiologic process. A well-known fact is that persons undergoing decapitation will retain their knee jerks for a few minutes,
37although such reflexes are rendered immediately and profoundly depressed. Of interest, in cases of completely developed spinal shock, absent knee jerks can be restored during the first 5 to 10 days after injury by applying faradic current to the quadriceps.
38Research of this phenomenon, however, has been inadequate, and to date spinal shock remains poorly understood. The earliest explanation was proposed by Obersteiner,
39who advanced a theory of molecular disturbances of neurons. Other explanations include a withdrawal of tonic supraspinal facilitation,
42fusimotor depression leading to diminished muscle spindle discharge,
43or increased segmental inhibition.
49Electromyographic studies suggest that presynaptic inhibition occurs during spinal shock due to hyperpolarization of neurons, which effectively blocks monosynaptic and polysynaptic reflex arcs through the spinal cord.
52Excessive accumulation of potassium has been evoked as the early cause of hyperpolarization, but this theory remains unproved.
53Of note, in cervical spinal cord injury, as with the upper motor neuron injury associated with cerebral stroke, lower motor neuron death and subsequent collateral reinnervation by remaining neurons below the level of the lesion have been identified on electromyographic studies.
56These findings are also demonstrated clinically by noting that atrophy is more profound with high-level spinal cord injury in the lower extremities, even with well developed spasticity, than would be expected from disuse atrophy alone.
60The reason for this is obscure, but some lower motor neurons possibly receive substantial neuronal trophic support from suprasegmental regions. When deprived of this support, these select neurons may undergo degeneration and then die.
Although the distal severed spinal cord has received the most attention, investigators have known for almost a century that the proximal spinal cord also undergoes changes, and these cephalad effects are known as the Schiff-Sherrington phenomenon.
62In clinical series, an upward spread of reflex depression is common. Transient loss of upper extremity reflexes with upper thoracic spinal cord lesions has been previously noted, and this reflex depression usually abates after a few hours or days.
4In early clinical series, such loss was presumed to be an extension of “concussion” to the area of injury, but subsequent laboratory experiments suggest otherwise. In a series of articles, Ruch and Watts 61-64 confirmed Sherrington's earlier work by describing augmentation of extensor reflexes and depression of flexor reflexes induced by postbrachial spinal cord enlargement transection either anatomically or physiologically with novacaine or “cold block.” Transection of the spinal cord as low as the third lumbar segment affects the excitability of the forelimbs. Subsequent work has suggested that the lumbosacral spinal cord segments are somehow involved in the reflex activity of the forelimbs. Sectioning of all the lumbosacral posterior roots at the lumbosacral enlargement before severance of the spinal cord below the cervical region does not change the reflex depression above the level of transection. This finding suggests that the mechanism is through intrinsic spinal cord parhways.
Clinically, spinal shock in humans can persist for days to weeks, but it may be prolonged because of toxic or septic conditions such as urinary tract infections or pressure sores. Muscle spindle reflexes always return except at vertical spinal cord injury levels, and they generally return in a caudal to cephalad direction. The result is always spasticity or hyperactive reflexes with abnormal spread to adjacent isolated spinal cord segments. Because autonomic function involves second-order neurons located in ganglia outside the spinal cord, the return of vasomotor tone, ejaculation, and sweating can be variable and can add considerably to long-term morbidity. Return of muscle spindle reflex activity and progression to spasticity are not indicators of the spinal shock “wearing off” but are hypothesized to be an active reorganization of receptors involving mechanisms of upregulation, enhanced sensitivity, increased number of receptors, or any combination of these.
64Some evidence, both anatomically and electrophysiologically, shows that posterior root fibers in the isolated spinal cord sprout new collaterals and produce diffuse and multiple new synaptic connections with motor neurons and intemeurons. In the absence of supraspinal inhibition, this diffuse collateral reinnervation of spinal cord neurons by posterior root axons has been suggested as the foundation for the subsequent hyperactive or spastic reflexes of spinal cord injury.
66In fact, sectioning of posterior spinal roots for spasticity, as practiced today, was initially performed by Foerster
14at the turn of the century, and survivors had good results. Spasticity development in flexion or extension was initially thought to be complete spinal cord severance in the former and partial severance in the latter; however, experience with the multiple spinal cord injuries that occurred during World War II and the improved imaging studies that have evolved leave little doubt that early positioning of the limbs, which facilitates sensory and proprioceptive input to the isolated spinal cord through the dorsal roots, considerably affects whether spastic flexion or extension synergy is produced. This clinical finding also supports posterior root influence in the development of spasticity and the specific patterns that may be affected.
The statement Tarlov and Herz
69made in 1954 is true today—there is no well-documented case of complete recovery of function in any patient with immediate and complete severance of spinal cord function regardless of treatment, although substantial improvement may occur. Numerous cases have described useful recovery after complete loss of spinal cord function when the injury process is gradual; however, even in the setting of gradual spinal cord injury, the occurrence of spinal shock may worsen the prognosis.
70Spinal shock is demonstrated only in the setting of severe spinal cord injury that occurs during a relatively brief period. Such shock is most commonly witnessed with immediate spinal cord injury related to trauma, but it can occur up to hours after progressive injury due to other mechanisms.
36The presence of spinal shock seems to be prognostic only as it applies to the temporal profile for the mechanism of injury. Spinal cord injury with concomitant spinal shock usually has a worse associated prognosis than does the same degree of spinal cord injury without spinal shock because the injury is inflicted during a shorter period.
36In addition, patients with equivalent degrees of spinal cord injury and spinal shock may do somewhat better if they have early resumption of reflex spinal cord function.
The term “spinal concussion” has been used for decades and may add an element of confusion.
71Spinal concussion, a poorly understood phenomenon, is defined as partial spinal cord sensory or motor deficits (or both) that rapidly and completely resolve within 24 to 72 hours and that are never associated with permanent spinal cord injury.
71Spinal concussion rarely occurs, however, and has never been described in conjunction with spinal shock.
A typical case of spinal shock manifests with acute or subacute spinal cord injury and the absence of motor and sensory function below the level of the lesion. Reflex arcs below and closest to the level of the lesion are absent, but even in cases of verified transection, distal reflexes such as the bulbocavernosus or anal wink may never be absent. The higher the transection, such as high-level cervical spinal cord injury, the more likely that the most distal sacral reflex arcs may remain intact although depressed. Reflexes immediately above the level of the lesion may also be depressed because of loss of ascending distal cord influence or the Schiff-Sherrington phenomenon. Autonomic reflexes are variably affected, depending on the level of the lesion. Despite diffuse spread of sympathetic tone through the paravertebral ganglia, the blood pressure will be decreased to some degree because of the following: loss of lower extremities sympathetic tone and pooling of venous blood with low thoracic lesions, pooling of venous blood in the lower extremities and abdominal viscera with upper thoracic lesions, and absence of cardiovascular intrinsic sympathetic tone with loss of thoracolumbar vascular tone in cervical lesions.
Investigators have known for more than a century that hypotension occurs with spinal cord injury. Nevertheless, recent studies of documented complete cervical spinal cord injuries suggest that the prevalence of severe hypotension that necessitates treatment is perhaps 20 to 30&x0025; in a select series.
77In fact, distinguishing complete from incomplete spinal cord injury or determining prognosis by the presence or absence of sympathetic tone in a large series of patients has not been shown to be statistically significant.
76Temperature control will be affected concomitant with the amount of sympathetic loss. Sacral parasympathetic reflex arcs are also affected, and distal colonic and bladder reflexes are depressed or absent. Small bowel ileus is common for various reasons but is usually transient.
Clinically, the spinal shock phase of severe spinal cord injury is heralded by the return of elicited spinal cord reflex arcs.
4Such return is usually from the caudal to cranial levels of the spinal cord and may be demonstrated by abnormal cutaneospinal reflexes, such as Babinski's sign, or exaggerated muscle spindle reflex arcs. The resultant spinal reflexes are irrevocably changed from their preinjury state and are the substrate on which rehabilitation efforts are directed.
Clinically, spinal shock comprises all the spinal cord function changes that encompass physiologic or anatomic transection of the spinal cord, with resultant temporary loss or depression of all or most spinal reflex activity below the level of the injury. Spinal shock usually occurs with immediate spinal cord injuries of trauma but has also occurred with mechanisms of injury inflicted over several hours. The presence of spinal shock seems to be prognostic only as it applies to a temporal profile—that is, for the same degree of spinal cord injury, the presence of spinal shock implies a more rapid evolution of injury and a worse prognosis. Distal spinal cord segment sacral reflex arcs such as the bulbocavernosus or anal wink may remain variably present with high-level cervical spinal cord injuries. Reflex arcs immediately proximal to the level of injury may be depressed on the basis of the Schiff-Sherrington phenomenon. Autonomic reflexes are variably affected during the spinal shock phase of spinal cord injury because they involve secondary neurons in ganglia outside the spinal cord. The spinal shock phase of spinal cord injury ends when the elicitable reflexes such as cutaneospinal or muscle spindle reflex arcs return. Resumption of reflex function is usually from caudal to rostral spinal cord levels and is always abnormal. Reflexes may never return at areas of the spinal cord permanently damaged by the injury. The returning spinal cord reflex arcs and their ultimate level of function are the focus of rehabilitation.
We are indebted to Mary M. Soper for her help in preparation of the submitted manuscript.
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