Spinal shock is not really "shock" in the sense of circulatory collapse but rather a transient or temporary (physiologic rather than anatomical) complete loss of all neurologic function, including reflexes and rectal tone, below a specific level that is associated with autonomic dysfunction.
This phenomenon was first described in 1750 by Whytt.
Spinal shock begins within a few minutes following an acute spinal cord injury (but not chronic spinal cord injury), it make take several hours before the full effects occur
It usually recovers within 24 hours but may last over few days to weeks in less common cases. In some rare cases spinal cord shock can last for several more months.
The first reflexes to reappear are polysynaptic in nature, such as the bulbocavernosus reflex.
Bulbocavernosus reflex can be checked by noting anal sphincter contraction in response to squeezing the glans penis or tugging on the Foley. It involves the S1, S2, S3 nerve roots and is spinal cord mediated reflex. Its presence signals the end of spinal shock.
Monosynaptic reflexes, such as the deep tendon reflexes, are not restored until in a later phase - where even hyperreflexia, or abnormally strong reflexes usually produced with minimal stimulation may occur due to sprouting of the interneurons as the lower motor neurons begin to reestablish synapses.
Why spinal shock occur?
Exact pathophysiology is not known but it is thought to be due to neuronal hyperpolarization with loss of potassium ions in the injured cells of the spinal cord.
This is because spinal motor neurons and interneurons normally receive continuous background excitatory input from supraspinal axons, due in part to the waking state and vigilance. Our voluntary movement is superimposed on this background excitation.
Following SCI, background excitation is lost causing neuronal hyperpolarization and spinal neurons become less excitable.
Reference:
Ditunno, JF; Little, JW; Tessler, A; Burns, AS (2004). "Spinal shock revisited: a four-phase model". Spinal cord : the official journal of the International Medical Society of Paraplegia 42 (7): 383–95. URL: http://www.nature.com/sc/journal/v42/n7/full/3101603a.html
Note:
Differentiate spinal shock from neurogenic shock, which refers to the hemodynamic triad of hypotension, bradycardia, and peripheral vasodilation resulting from severe autonomic dysfunction. Neurogenic shock is due to the interruption of sympathetic nervous system control in acute spinal cord injury particularly at level above T6 because the cardiac sympathetic innervation is given out above level of T6.
This phenomenon was first described in 1750 by Whytt.
Spinal shock begins within a few minutes following an acute spinal cord injury (but not chronic spinal cord injury), it make take several hours before the full effects occur
It usually recovers within 24 hours but may last over few days to weeks in less common cases. In some rare cases spinal cord shock can last for several more months.
The first reflexes to reappear are polysynaptic in nature, such as the bulbocavernosus reflex.
Bulbocavernosus reflex can be checked by noting anal sphincter contraction in response to squeezing the glans penis or tugging on the Foley. It involves the S1, S2, S3 nerve roots and is spinal cord mediated reflex. Its presence signals the end of spinal shock.
Monosynaptic reflexes, such as the deep tendon reflexes, are not restored until in a later phase - where even hyperreflexia, or abnormally strong reflexes usually produced with minimal stimulation may occur due to sprouting of the interneurons as the lower motor neurons begin to reestablish synapses.
Why spinal shock occur?
Exact pathophysiology is not known but it is thought to be due to neuronal hyperpolarization with loss of potassium ions in the injured cells of the spinal cord.
This is because spinal motor neurons and interneurons normally receive continuous background excitatory input from supraspinal axons, due in part to the waking state and vigilance. Our voluntary movement is superimposed on this background excitation.
Following SCI, background excitation is lost causing neuronal hyperpolarization and spinal neurons become less excitable.
Reference:
Ditunno, JF; Little, JW; Tessler, A; Burns, AS (2004). "Spinal shock revisited: a four-phase model". Spinal cord : the official journal of the International Medical Society of Paraplegia 42 (7): 383–95. URL: http://www.nature.com/sc/journal/v42/n7/full/3101603a.html
Note:
Differentiate spinal shock from neurogenic shock, which refers to the hemodynamic triad of hypotension, bradycardia, and peripheral vasodilation resulting from severe autonomic dysfunction. Neurogenic shock is due to the interruption of sympathetic nervous system control in acute spinal cord injury particularly at level above T6 because the cardiac sympathetic innervation is given out above level of T6.
1 comment:
"Spinal shock" applies to all phenomena surrounding physiological or anatomical transection of the spinal cord that results in a temporary loss or depression or spinal reflex any more below the level of injury activity. 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 caused by trauma and occurs immediately, but spinal shock has been described with mechanisms of injury that progress over several hours. Spinal reflex arcs immediately above the level of the lesion may be severely depressed based on the Schiff-Sherrington phenomenon. The end of the phase of spinal shock injuries of the spinal cord is indicated by the return of cutaneospinal elicitable abnormal reflexes or muscle spindle arcs. Arcs autonomic reflexes involving relay secondary ganglion neurons outside the spinal cord may be affected to varying degrees during the spinal shock, and return after spinal shock subsides is variable. Turning the spinal cord reflex arcs below the level of injury are irrevocably changed and are the substrate on which rehabilitation efforts are based.
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