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.
