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Spinal Shock

      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.
      • Hall M
      • Hall M
      Whytt, however, may have discussed the same phenomenon a century earlier, although no descriptive term was assigned.
      • Sherrington CS
      • Guttmann L
      Throughout 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.
      • Wilson RH
      • Whiteside MC
      • Moorehead RJ
      Problems in diagnosis and management of hypovolaemia in spinal injury.
      • Zipnick RI
      • Scalea TM
      • Trooskin SZ
      • Sclafani SJ
      • Emad B
      • Shah A
      • et al.
      Hemodynamic responses to penetrating spinal cord injuries.
      and 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
      • Hall M
      • Hall M
      more than 150 years ago. Initially, it was defined by Bastian
      • Bastian HC
      On the symptomatology of total transverse lesions of the spinal cord, with special reference to the condition of the various reflexes.
      in 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
      • Bastian HC
      On the symptomatology of total transverse lesions of the spinal cord, with special reference to the condition of the various reflexes.
      and Kocher
      • Kocher T
      Die Verletzungen der Wirbelsaule zugleich als Beitrag zur Physiologie des menschlichen Ruckenmarks.
      treated 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
      • Sherrington CS
      began 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.
      • Guttmann L
      • Collier J
      Gunshot wounds and injuries of the spinal cord.
      • Pitt GN
      • Collier JS
      Demonstration of cases.
      • Yashon D
      • Guttmann L
      Rehabilitation after injuries to the spinal cord and cauda equina.
      The 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.
      • Sherrington CS
      • Foerster D
      Resection of the posterior spinal nerve-roots in the treatment of gastric crisis and spastic paralysis.
      Evolutionarily higher species had greater degrees of spinal shock, a suggestion that phylogenically new descending tracts may be responsible,
      • Sherrington CS
      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.
      • Hansebout RR
      The neurosurgical management of cord injuries.
      The standard model of spinal cord injury in the laboratory involves the free-weight drop technique and has been used for decades.
      • Ducker TB
      • Hamit HF
      Experimental treatments of acute spinal cord injury.
      • Hedeman LS
      • Shellenberger MK
      • Gordon JH
      Studies in experimental spinal cord trauma. Part 1. Alterations in catecholamine levels.
      • Ito T
      • Allen N
      • Yashon D
      A mitochondrial lesion in experimental spinal cord trauma.
      • Osterholm JL
      • Mathews GJ
      Altered norepinephrine metabolism following experimental spinal cord injury. Parti. Relationship to hemorrhagic necrosis and post-wounding neurological deficits.
      • Osterholm JL
      • Mathews GJ
      Altered norepinephrine metabolism following experimental spinal cord injury. Part 2. Protection against traumatic spinal cord hemorrhagic necrosis by norepinephrine synthesis blockade with alpha methyl tyrosine.
      • Rawe SE
      • Roth RH
      • Boadle-Biber M
      • Collins WF
      Norepinephrine levels in experimental spinal cord trauma. Part 1. Biochemical study of hemorrhagic necrosis.
      The 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.
      • Ducker TB
      • Hamit HF
      Experimental treatments of acute spinal cord injury.
      In 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.
      • Hansebout RR
      The neurosurgical management of cord injuries.
      • Dohrmann GJ
      • Wagner Jr, FC
      • Bucy PC
      The microvasculature in transitory traumatic paraplegia: an electron microscopic study in the monkey.
      • Goodman JH
      • Bingham Jr, WG
      • Hunt WE
      Ultrastructural blood-brain barrier alterations and edema formation in acute spinal cord trauma.
      • Griffiths IR
      Ultrastructural changes in spinal gray matter microvasculature after impact injury.
      By 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.
      • Hansebout RR
      The neurosurgical management of cord injuries.
      • Griffiths IR
      Ultrastructural changes in spinal gray matter microvasculature after impact injury.
      • Hager H
      • Hirschberger W
      • Scholz W
      Electron microscopic changes in brain tissue of Syrian hamsters following acute hypoxia.
      • Lewin MG
      • Hansebout RR
      • Pappius HM
      Chemical characteristics of traumatic spinal cord edema in cats: effects of steroids on potassium depletion.
      The reason for progressive hemorrhage accumulation is obscure. Localized release of catecholamines
      • Osterholm JL
      • Mathews GJ
      Altered norepinephrine metabolism following experimental spinal cord injury. Parti. Relationship to hemorrhagic necrosis and post-wounding neurological deficits.
      • Osterholm JL
      • Mathews GJ
      Altered norepinephrine metabolism following experimental spinal cord injury. Part 2. Protection against traumatic spinal cord hemorrhagic necrosis by norepinephrine synthesis blockade with alpha methyl tyrosine.
      was suggested, but later studies disputed this theory.
      • Hedeman LS
      • Shellenberger MK
      • Gordon JH
      Studies in experimental spinal cord trauma. Part 1. Alterations in catecholamine levels.
      • Rawe SE
      • Roth RH
      • Boadle-Biber M
      • Collins WF
      Norepinephrine levels in experimental spinal cord trauma. Part 1. Biochemical study of hemorrhagic necrosis.
      • Bingham WG
      • Ruffolo R
      • Friedman SJ
      Catecholamine levels in the injured spinal cord of monkeys.
      Hyperbaric oxygen toxicity has produced similar pathologic findings in the spinal cord, a suggestion of a possible toxic response.
      • Balentine JD
      Central necrosis of the spinal cord induced by hyperbaric oxygen exposure.
      Some 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,
      • Ducker TB
      • Perot Jr, PL
      Spinal cord oxygen and blood flow in trauma.
      • Kelly Jr, DL
      • Lassiter KR
      • Calogero JA
      • Alexander Jr, E
      Effects of local hypothermia and tissue oxygen studies in experimental paraplegia.
      and the posterior columns remain relatively resistant to initial ischemia, unlike the rest of the spinal cord.
      • Kobrine AI
      • Evans DE
      • Rizzoli HV
      The effects of ischemia on long-tract neural conduction in the spinal cord.
      Autoregulation of the spinal cord blood flow at the site of impact is known to be impaired.
      • Holaday JW
      • Faden AI
      Naloxone acts at central opiate receptors to reverse hypotension, hypothermia and hypoventilation in spinal shock.
      • Bingham WG
      • Sirinek L
      • Crutcher K
      • Mohnacky C
      Effect of spinal cord injury on cord blood flow in monkey.
      and 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.
      • Griffiths IR
      Ultrastructural changes in spinal gray matter microvasculature after impact injury.
      Spinal cord blood flow may certainly be diminished but may represent decreased metabolic blood flow requirements of the injured parenchyma.
      • Hansebout RR
      The neurosurgical management of cord injuries.
      • Ito T
      • Allen N
      • Yashon D
      A mitochondrial lesion in experimental spinal cord trauma.
      • Griffiths IR
      Ultrastructural changes in spinal gray matter microvasculature after impact injury.
      • Holaday JW
      • Faden AI
      Naloxone acts at central opiate receptors to reverse hypotension, hypothermia and hypoventilation in spinal shock.
      • Bingham WG
      • Sirinek L
      • Crutcher K
      • Mohnacky C
      Effect of spinal cord injury on cord blood flow in monkey.
      Cellular and mitochondrial injury from impact may initiate an eventual cascade of destructive events.
      • Ito T
      • Allen N
      • Yashon D
      A mitochondrial lesion in experimental spinal cord trauma.
      • Clendenon NR
      • Allen N
      • Gordon WA
      • Bingham Jr, WG
      Inhibition of Na+-K+-activated ATPase activity following experimental spinal cord trauma.
      and 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.
      • Hansebout RR
      The neurosurgical management of cord injuries.
      • Griffiths IR
      Ultrastructural changes in spinal gray matter microvasculature after impact injury.
      • Kao CC
      • Chang LW
      The mechanism of spinal cord cavitation following spinal cord transection. Part 1. A correlated histochemical study.
      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.
      • Christensen PB
      • Wermuth L
      • Hinge HH
      • Bomers K
      Clinical course and long-term prognosis of acute transverse myelopathy.
      As a generalization, the more severe the physiologic or anatomic transection of the spinal cord, the more profound the state of spinal shock.
      • Guttmann L
      • Christensen PB
      • Wermuth L
      • Hinge HH
      • Bomers K
      Clinical course and long-term prognosis of acute transverse myelopathy.
      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.
      • Guttmann L
      • Hansebout RR
      The neurosurgical management of cord injuries.
      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,
      • Hall M
      • Steinberg M
      although 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.
      • Collier J
      Gunshot wounds and injuries of the spinal cord.
      • Guttmann L
      Studies on reflex activity of the isolated cord in the spinal man.
      Research of this phenomenon, however, has been inadequate, and to date spinal shock remains poorly understood. The earliest explanation was proposed by Obersteiner,
      • Obersteiner H
      who advanced a theory of molecular disturbances of neurons. Other explanations include a withdrawal of tonic supraspinal facilitation,
      • Sherrington CS
      • Fulton JF
      • Liddell EGT
      • Rioch DM
      The influence of experimental lesions of the spinal cord upon the knee-jerk: acute lesions.
      • Liddell EGT
      Spinal shock and some features in isolation—alteration of the spinal cord in cats.
      • Taborikova H
      • Sax DS
      Conditioning of the H-reflexes by a preceding subthreshold H-reflex stimulus.
      fusimotor depression leading to diminished muscle spindle discharge,
      • Weaver RA
      • Landau WM
      • Higgins JF
      Fusimotor function. Part II. Evidence of fusimotor depression in human spinal shock.
      or increased segmental inhibition.
      • Fulton JF
      • Liddell EGT
      • Rioch DM
      The influence of experimental lesions of the spinal cord upon the knee-jerk: acute lesions.
      • Ashby P
      • Verrier M
      Neurophysiologic changes in hemi-plegia: possible explanation for the initial disparity between muscle tone and tendon reflexes.
      • Ashby P
      • Verrier M
      • Lightfoot E
      Segmental reflex pathways in spinal shock and spinal spasticity in man.
      • Ashby P
      • White DG
      “Presynaptic” inhibition in spasticity and the effect of P(4-chlorophenyl)GABA.
      • Ballif L
      • Fulton JF
      • Liddell EGT
      Observations on spinal and decerebrate knee-jerks, with special reference to their inhibition by single break-shocks.
      • De Gail P
      • Lance JW
      • Neilson PD
      Differential effects on tonic and phasic reflex mechanisms produced by vibration of muscles in man.
      • Eccles RM
      • Lundberg A
      Supraspinal control of interneurones mediating spinal reflexes.
      Electromyographic 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.
      • Ashby P
      • Verrier M
      • Lightfoot E
      Segmental reflex pathways in spinal shock and spinal spasticity in man.
      • Aisen ML
      • Brown W
      • Rubin M
      Electrophysiologic changes in lumbar spinal cord after cervical cord injury.
      • Barnes CD
      • Joynt RJ
      • Schottelius BA
      Motor neuron resting potentials in spinal shock.
      • Calancie B
      • Broton JG
      • Klose KJ
      • Traad M
      • Difini J
      • Ayyar DR
      Evidence that alterations in presynaptic inhibition contribute to segmental hypo- and hyperexcitability after spinal cord injury in man.
      Excessive accumulation of potassium has been evoked as the early cause of hyperpolarization, but this theory remains unproved.
      • Hansebout RR
      The neurosurgical management of cord injuries.
      • Eidelberg E
      • Sullivan J
      • Brigham A
      Immediate consequences of spinal cord injury: possible role of potassium in axonal conduction block.
      Of 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.
      • Aisen ML
      • Brown W
      • Rubin M
      Electrophysiologic changes in lumbar spinal cord after cervical cord injury.
      • Brandstater ME
      • Dinsdale SM
      Electrophysiological studies in the assessment of spinal cord lesions.
      • Goldkamp O
      Electromyography and nerve conduction studies in 116 patients with hemiplegia.
      • Taylor RG
      • Kewalramani LS
      • Fowler Jr, WM
      Electromyo-graphic findings in lower extremities of patients with high spinal cord injury.
      These 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.
      • Aisen ML
      • Brown W
      • Rubin M
      Electrophysiologic changes in lumbar spinal cord after cervical cord injury.
      • Calancie B
      • Broton JG
      • Klose KJ
      • Traad M
      • Difini J
      • Ayyar DR
      Evidence that alterations in presynaptic inhibition contribute to segmental hypo- and hyperexcitability after spinal cord injury in man.
      • Eidelberg E
      Consequences of spinal cord lesions upon motor function, with special reference to locomotor activity.
      • Little JW
      Serial recording of reflexes after feline spinal cord transection.
      • Munson JB
      • Foehring RC
      • Lofton SA
      • Zengel JE
      • Sypert GW
      Plasticity of medial gastrocnemius motor units following cordotomy in the cat.
      • Taylor S
      • Ashby P
      • Verrier M
      Neurophysiological changes following traumatic spinal lesions in man.
      The 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.
      • Aisen ML
      • Brown W
      • Rubin M
      Electrophysiologic changes in lumbar spinal cord after cervical cord injury.
      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.
      • Guttmann L
      • Sherrington CS
      • Ruch TC
      Evidence of the non-segmental character of spinal reflexes from an analysis of the cephalad effects of spinal transection (Schiff-Sherrington phenomenon).
      • Ruch TC
      Release of extensor rigidity of the fore-limb by separation from lumbo-sacral segments.
      In 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.
      • Guttmann L
      In 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.
      • Ruch TC
      Evidence of the non-segmental character of spinal reflexes from an analysis of the cephalad effects of spinal transection (Schiff-Sherrington phenomenon).
      • Teasdall RD
      • Stavraky GW
      Responses of deafferented spinal neurones to corticospinal impulses.
      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.
      • Guttmann L
      • Ruch TC
      • Watts JW
      Reciprocal changes in reflex activity of fore limbs induced by post-brachial “cold-block” of spinal cord.
      • Ruch TC
      • Watts JW
      The effect of post-brachial spinal cord transection on the flexor and extensor reflexes of the fore-limbs.
      Some 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.
      • Guttmann L
      • Hedeman LS
      • Shellenberger MK
      • Gordon JH
      Studies in experimental spinal cord trauma. Part 1. Alterations in catecholamine levels.
      • Teasdall RD
      • Stavraky GW
      Responses of deafferented spinal neurones to corticospinal impulses.
      • Bach-y-Rita P
      • Illis LS
      Spinal shock: possible role of receptor plasticity and nonsynaptic transmission.
      In fact, sectioning of posterior spinal roots for spasticity, as practiced today, was initially performed by Foerster
      • Foerster D
      Resection of the posterior spinal nerve-roots in the treatment of gastric crisis and spastic paralysis.
      at 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.
      • Guttmann L
      • Yashon D
      • Kuhn RA
      Functional capacity of the isolated human spinal cord.
      • Kuhn RA
      • Macht MB
      Some manifestations of reflex activity in spinal man with particular reference to the occurrence of extensor spasm.

      Clinical Course

      The statement Tarlov and Herz
      • Tarlov IM
      • Herz E
      Spinal cord compressive studies: outlook with complete paralysis in man.
      made 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.
      • Christensen PB
      • Wermuth L
      • Hinge HH
      • Bomers K
      Clinical course and long-term prognosis of acute transverse myelopathy.
      • Levine AM
      Cervical spine and cord: trauma.
      Spinal 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.
      • Christensen PB
      • Wermuth L
      • Hinge HH
      • Bomers K
      Clinical course and long-term prognosis of acute transverse myelopathy.
      The 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.
      • Guttmann L
      • Christensen PB
      • Wermuth L
      • Hinge HH
      • Bomers K
      Clinical course and long-term prognosis of acute transverse myelopathy.
      In 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.
      • Guttmann L
      • Hansebout RR
      The neurosurgical management of cord injuries.
      The term “spinal concussion” has been used for decades and may add an element of confusion.
      • Obersteiner H
      • Marburg O
      Die traumatischen Erkrankungen des Gehirns und Ruckenmarks.
      Spinal 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.
      • Marburg O
      Die traumatischen Erkrankungen des Gehirns und Ruckenmarks.
      Spinal concussion rarely occurs, however, and has never been described in conjunction with spinal shock.
      • Guttmann L
      • Groat RA
      • Rambach Jr, WA
      • Windle WF
      Concussion of the spinal cord: an experimental study and a critique of the use of the term.
      • Torg JS
      • Pavlov H
      • Genuario SE
      • Sennett B
      • Wisneski RJ
      • Robie BH
      • et al.
      Neurapraxia of the cervical spinal cord with transient quadriplegia.
      • Zwimpfer TJ
      • Bernstein M
      Spinal cord concussion.
      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.
      • Wilson RH
      • Whiteside MC
      • Moorehead RJ
      Problems in diagnosis and management of hypovolaemia in spinal injury.
      • Zipnick RI
      • Scalea TM
      • Trooskin SZ
      • Sclafani SJ
      • Emad B
      • Shah A
      • et al.
      Hemodynamic responses to penetrating spinal cord injuries.
      • Landreneau RJ
      • Fry WJ
      The right colon as a target organ of nonocclusive mesenteric ischemia: case report and review of literature.
      • Levi L
      • Wolf A
      • Belzberg H
      Hemodynamic parameters in patients with acute cervical cord trauma: description, intervention, and prediction of outcome.
      • Soderstrom CA
      • Ducker TB
      Increased susceptibility of patients with cervical cord lesions to peptic gastrointestinal complications.
      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.
      • Zipnick RI
      • Scalea TM
      • Trooskin SZ
      • Sclafani SJ
      • Emad B
      • Shah A
      • et al.
      Hemodynamic responses to penetrating spinal cord injuries.
      • Soderstrom CA
      • Ducker TB
      Increased susceptibility of patients with cervical cord lesions to peptic gastrointestinal complications.
      In 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.
      • Levi L
      • Wolf A
      • Belzberg H
      Hemodynamic parameters in patients with acute cervical cord trauma: description, intervention, and prediction of outcome.
      Temperature 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.
      • el Rifaei A
      • Hassouna M
      • Fouda A
      • Latt R
      • Sawan M
      • Duval F
      • et al.
      The effect of early bladder stimulation on spinal shock: a preliminary report.
      • Madersbacher H
      The various types of neurogenic bladder dysfunction: an update of current therapeutic concepts.
      Clinically, the spinal shock phase of severe spinal cord injury is heralded by the return of elicited spinal cord reflex arcs.
      • Guttmann L
      Such 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.
      • Guttmann L
      • Yashon D
      • Hansebout RR
      The neurosurgical management of cord injuries.

      Conclusion

      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.

      Acknowledgment

      We are indebted to Mary M. Soper for her help in preparation of the submitted manuscript.

      References

        • Hall M
        On the Diseases and Derangements of the Nervous System, in Their Primary Forms and in Their Modifications by Age, Sex, Constitution, Hereditary Disposition, Excesses, General Disorder, and Organic Disease. H Bailliere, London1841: 256
        • Hall M
        Synopsis of the Diastaltic Nervous System. J Mallett, London1850
        • Sherrington CS
        The Integrative Action of the Nervous System. C Scribner's Sons, New York1906: 240
        • Guttmann L
        Spinal Cord Injuries: Comprehensive Management and Research. 2nd ed. Blackwell Scientific Publications, Oxford (England)1976
        • Wilson RH
        • Whiteside MC
        • Moorehead RJ
        Problems in diagnosis and management of hypovolaemia in spinal injury.
        Br J Clin Pract. 1993; 47: 224-225
        • Zipnick RI
        • Scalea TM
        • Trooskin SZ
        • Sclafani SJ
        • Emad B
        • Shah A
        • et al.
        Hemodynamic responses to penetrating spinal cord injuries.
        J Trauma. 1993; 35: 578-582
        • Bastian HC
        On the symptomatology of total transverse lesions of the spinal cord, with special reference to the condition of the various reflexes.
        Med Chir Trans Lond. 1890; 73: 151-217
        • Kocher T
        Die Verletzungen der Wirbelsaule zugleich als Beitrag zur Physiologie des menschlichen Ruckenmarks.
        Mitt Grenzgeb Med Chir. 1896; 1: 415-480
        • Sherrington CS
        The Integrative Action of the Nervous System. Yale University Press, New Haven (CT)1947
        • Collier J
        Gunshot wounds and injuries of the spinal cord.
        Lancet. 1916; 1: 711-716
        • Pitt GN
        • Collier JS
        Demonstration of cases.
        Proc R Soc Med. 1917; 10: 35-38 (Section of Neurology)
        • Yashon D
        Spinal Injury. 2nd ed. Appleton-Century-Crofts, Norwalk(CT)1986: 32-38
        • Guttmann L
        Rehabilitation after injuries to the spinal cord and cauda equina.
        Br J Phys Med. 1946; 9: 130-137
        • Foerster D
        Resection of the posterior spinal nerve-roots in the treatment of gastric crisis and spastic paralysis.
        Proc R Soc Med. 1911; 4: 226-246
        • Hansebout RR
        The neurosurgical management of cord injuries.
        in: Bloch RF Basbaum M Management of Spinal Cord Injuries. Williams & Wilkins, Baltimore1986: 1-27
        • Ducker TB
        • Hamit HF
        Experimental treatments of acute spinal cord injury.
        J Neurosurg. 1969; 30: 693-697
        • Hedeman LS
        • Shellenberger MK
        • Gordon JH
        Studies in experimental spinal cord trauma. Part 1. Alterations in catecholamine levels.
        J Neurosurg. 1974; 40: 37-43
        • Ito T
        • Allen N
        • Yashon D
        A mitochondrial lesion in experimental spinal cord trauma.
        J Neurosurg. 1978; 48: 434-442
        • Osterholm JL
        • Mathews GJ
        Altered norepinephrine metabolism following experimental spinal cord injury. Parti. Relationship to hemorrhagic necrosis and post-wounding neurological deficits.
        J Neurosurg. 1972; 36: 386-394
        • Osterholm JL
        • Mathews GJ
        Altered norepinephrine metabolism following experimental spinal cord injury. Part 2. Protection against traumatic spinal cord hemorrhagic necrosis by norepinephrine synthesis blockade with alpha methyl tyrosine.
        J Neurosurg. 1972; 36: 395-401
        • Rawe SE
        • Roth RH
        • Boadle-Biber M
        • Collins WF
        Norepinephrine levels in experimental spinal cord trauma. Part 1. Biochemical study of hemorrhagic necrosis.
        J Neurosurg. 1977; 46: 342-349
        • Dohrmann GJ
        • Wagner Jr, FC
        • Bucy PC
        The microvasculature in transitory traumatic paraplegia: an electron microscopic study in the monkey.
        J Neurosurg. 1971; 35: 263-271
        • Goodman JH
        • Bingham Jr, WG
        • Hunt WE
        Ultrastructural blood-brain barrier alterations and edema formation in acute spinal cord trauma.
        J Neurosurg. 1976; 44: 418-424
        • Griffiths IR
        Ultrastructural changes in spinal gray matter microvasculature after impact injury.
        Adv Neurol. 1978; 20: 415-422
        • Hager H
        • Hirschberger W
        • Scholz W
        Electron microscopic changes in brain tissue of Syrian hamsters following acute hypoxia.
        Aerospace Med. 1960; 31: 379-387
        • Lewin MG
        • Hansebout RR
        • Pappius HM
        Chemical characteristics of traumatic spinal cord edema in cats: effects of steroids on potassium depletion.
        J Neurosurg. 1974; 40: 65-75
        • Bingham WG
        • Ruffolo R
        • Friedman SJ
        Catecholamine levels in the injured spinal cord of monkeys.
        J Neurosurg. 1975; 42: 174-178
        • Balentine JD
        Central necrosis of the spinal cord induced by hyperbaric oxygen exposure.
        J Neurosurg. 1975; 43: 150-155
        • Ducker TB
        • Perot Jr, PL
        Spinal cord oxygen and blood flow in trauma.
        Surg Forum. 1971; 22: 413-415
        • Kelly Jr, DL
        • Lassiter KR
        • Calogero JA
        • Alexander Jr, E
        Effects of local hypothermia and tissue oxygen studies in experimental paraplegia.
        J Neurosurg. 1970; 33: 554-563
        • Kobrine AI
        • Evans DE
        • Rizzoli HV
        The effects of ischemia on long-tract neural conduction in the spinal cord.
        J Neurosurg. 1979; 50: 639-644
        • Holaday JW
        • Faden AI
        Naloxone acts at central opiate receptors to reverse hypotension, hypothermia and hypoventilation in spinal shock.
        Brain Res. 1980; 189: 295-300
        • Bingham WG
        • Sirinek L
        • Crutcher K
        • Mohnacky C
        Effect of spinal cord injury on cord blood flow in monkey.
        Acta Neurol Scand Suppl. 1977; 64: 238-239
        • Clendenon NR
        • Allen N
        • Gordon WA
        • Bingham Jr, WG
        Inhibition of Na+-K+-activated ATPase activity following experimental spinal cord trauma.
        J Neurosurg. 1978; 49: 563-568
        • Kao CC
        • Chang LW
        The mechanism of spinal cord cavitation following spinal cord transection. Part 1. A correlated histochemical study.
        J Neurosurg. 1977; 46: 197-209
        • Christensen PB
        • Wermuth L
        • Hinge HH
        • Bomers K
        Clinical course and long-term prognosis of acute transverse myelopathy.
        Acta Neurol Scand. 1990; 81: 431-435
        • Steinberg M
        Die Sehnenreflexe und ihre Bedeutung fur die Pathologie des Nervensystems. F Deuticke, Leipzig (Germany)1893
        • Guttmann L
        Studies on reflex activity of the isolated cord in the spinal man.
        J Nerv Ment Dis. 1952; 116: 957-972
        • Obersteiner H
        Ueber Erschutterung des Ruckenmarkes. M Salzer, Wien (Austria)1879: 531
        • Fulton JF
        • Liddell EGT
        • Rioch DM
        The influence of experimental lesions of the spinal cord upon the knee-jerk: acute lesions.
        Brain. 1930; 53: 311-326
        • Liddell EGT
        Spinal shock and some features in isolation—alteration of the spinal cord in cats.
        Brain. 1934; 57: 386-400
        • Taborikova H
        • Sax DS
        Conditioning of the H-reflexes by a preceding subthreshold H-reflex stimulus.
        Brain. 1969; 92: 203-212
        • Weaver RA
        • Landau WM
        • Higgins JF
        Fusimotor function. Part II. Evidence of fusimotor depression in human spinal shock.
        ArchNeurol. 1963; 9: 127-132
        • Ashby P
        • Verrier M
        Neurophysiologic changes in hemi-plegia: possible explanation for the initial disparity between muscle tone and tendon reflexes.
        Neurology. 1976; 26: 1145-1151
        • Ashby P
        • Verrier M
        • Lightfoot E
        Segmental reflex pathways in spinal shock and spinal spasticity in man.
        J Neurol Neurosurg Psychiatry. 1974; 37: 1352-1360
        • Ashby P
        • White DG
        “Presynaptic” inhibition in spasticity and the effect of P(4-chlorophenyl)GABA.
        J Neurol Sci. 1973; 20: 329-338
        • Ballif L
        • Fulton JF
        • Liddell EGT
        Observations on spinal and decerebrate knee-jerks, with special reference to their inhibition by single break-shocks.
        Proc R Soc Lond. 1925; 98B: 587-607
        • De Gail P
        • Lance JW
        • Neilson PD
        Differential effects on tonic and phasic reflex mechanisms produced by vibration of muscles in man.
        J Neurol Neurosurg Psychiatry. 1966; 29: 1-11
        • Eccles RM
        • Lundberg A
        Supraspinal control of interneurones mediating spinal reflexes.
        J Physiol (Lond). 1959; 147: 565-584
        • Aisen ML
        • Brown W
        • Rubin M
        Electrophysiologic changes in lumbar spinal cord after cervical cord injury.
        Neurology. 1992; 42: 623-626
        • Barnes CD
        • Joynt RJ
        • Schottelius BA
        Motor neuron resting potentials in spinal shock.
        Am J Physiol. 1962; 203: 1113-1116
        • Calancie B
        • Broton JG
        • Klose KJ
        • Traad M
        • Difini J
        • Ayyar DR
        Evidence that alterations in presynaptic inhibition contribute to segmental hypo- and hyperexcitability after spinal cord injury in man.
        Electroencephalogr Clin Neurophysiol. 1993; 89: 177-186
        • Eidelberg E
        • Sullivan J
        • Brigham A
        Immediate consequences of spinal cord injury: possible role of potassium in axonal conduction block.
        Surg Neurol. 1975; 3: 317-321
        • Brandstater ME
        • Dinsdale SM
        Electrophysiological studies in the assessment of spinal cord lesions.
        Arch Phys Med Rehabil. 1976; 57: 70-74
        • Goldkamp O
        Electromyography and nerve conduction studies in 116 patients with hemiplegia.
        Arch Phys Med Rehabil. 1967; 48: 59-63
        • Taylor RG
        • Kewalramani LS
        • Fowler Jr, WM
        Electromyo-graphic findings in lower extremities of patients with high spinal cord injury.
        Arch Phys Med Rehabil. 1974; 55: 16-23
        • Eidelberg E
        Consequences of spinal cord lesions upon motor function, with special reference to locomotor activity.
        Prog Neurobiol. 1981; 17: 185-202
        • Little JW
        Serial recording of reflexes after feline spinal cord transection.
        Exp Neurol. 1986; 93: 510-521
        • Munson JB
        • Foehring RC
        • Lofton SA
        • Zengel JE
        • Sypert GW
        Plasticity of medial gastrocnemius motor units following cordotomy in the cat.
        J Neurophysiol. 1986; 55: 619-634
        • Taylor S
        • Ashby P
        • Verrier M
        Neurophysiological changes following traumatic spinal lesions in man.
        J Neurol Neurosurg Psychiatry. 1984; 47: 1102-1108
        • Ruch TC
        Evidence of the non-segmental character of spinal reflexes from an analysis of the cephalad effects of spinal transection (Schiff-Sherrington phenomenon).
        Am J Physiol. 1936; 114: 457-467
        • Ruch TC
        Release of extensor rigidity of the fore-limb by separation from lumbo-sacral segments.
        Proc Physiol Soc. 1932; 76: 3p-4p
        • Ruch TC
        • Watts JW
        Reciprocal changes in reflex activity of fore limbs induced by post-brachial “cold-block” of spinal cord.
        Am J Physiol. 1934; 110: 362-375
        • Ruch TC
        • Watts JW
        The effect of post-brachial spinal cord transection on the flexor and extensor reflexes of the fore-limbs.
        Am Physiol Soc. 1933; 105: 86-89
        • Teasdall RD
        • Stavraky GW
        Responses of deafferented spinal neurones to corticospinal impulses.
        J Neurophysiol. 1953; 16: 367-375
        • Bach-y-Rita P
        • Illis LS
        Spinal shock: possible role of receptor plasticity and nonsynaptic transmission.
        Paraplegia. 1993; 31: 82-87
        • Kuhn RA
        Functional capacity of the isolated human spinal cord.
        Brain. 1950; 73: 1-51
        • Kuhn RA
        • Macht MB
        Some manifestations of reflex activity in spinal man with particular reference to the occurrence of extensor spasm.
        Bull Johns Hopkins Hosp. 1949; 84: 43-75
        • Tarlov IM
        • Herz E
        Spinal cord compressive studies: outlook with complete paralysis in man.
        Arch Neurol Psychiatry. 1954; 72: 43-59
        • Levine AM
        Cervical spine and cord: trauma.
        in: Poss R Orthopaedic Knowledge Update 3. American Academy of Orthopaedic Surgeons, Park Ridge (IL)1990: 395
        • Marburg O
        Die traumatischen Erkrankungen des Gehirns und Ruckenmarks.
        in: Bumke O Foerster O Handbuch der Neurologic Vol 11. Julius Springer, Berlin1936: 1-177
        • Groat RA
        • Rambach Jr, WA
        • Windle WF
        Concussion of the spinal cord: an experimental study and a critique of the use of the term.
        Surg Gynecol Obstet. 1945; 81: 63-74
        • Torg JS
        • Pavlov H
        • Genuario SE
        • Sennett B
        • Wisneski RJ
        • Robie BH
        • et al.
        Neurapraxia of the cervical spinal cord with transient quadriplegia.
        J Bone Joint Surg Am. 1986; 68: 1354-1370
        • Zwimpfer TJ
        • Bernstein M
        Spinal cord concussion.
        J Neurosurg. 1990; 72: 894-900
        • Landreneau RJ
        • Fry WJ
        The right colon as a target organ of nonocclusive mesenteric ischemia: case report and review of literature.
        Arch Surg. 1990; 125: 591-594
        • Levi L
        • Wolf A
        • Belzberg H
        Hemodynamic parameters in patients with acute cervical cord trauma: description, intervention, and prediction of outcome.
        Neurosurgery. 1993; 33: 1007-1016
        • Soderstrom CA
        • Ducker TB
        Increased susceptibility of patients with cervical cord lesions to peptic gastrointestinal complications.
        J Trauma. 1985; 25: 1030-1038
        • el Rifaei A
        • Hassouna M
        • Fouda A
        • Latt R
        • Sawan M
        • Duval F
        • et al.
        The effect of early bladder stimulation on spinal shock: a preliminary report.
        J Urol. 1989; 141: 1010-1013
        • Madersbacher H
        The various types of neurogenic bladder dysfunction: an update of current therapeutic concepts.
        Paraplegia. 1990; 28: 217-229