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Spinal shock was first defined by Whytt in 1750 as a loss of sensation accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) -- most often a complete transection. Reflexes in the spinal cord caudal to the SCI are depressed (hyporeflexia) or absent (areflexia), while those rostral to the SCI remain unaffected. Note that the 'shock' in spinal shock does not refer to circulatory collapse.

Phases of Spinal Shock

Explanation of Phases

Ditunno et al. proposed a four-phase model for spinal shock in 2004.

Phase 1 is characterized by a complete loss -- or weakening -- of all reflexes below the SCI. This phase lasts for a day. The neurons involved in various reflex arcs normally receive a basal level of excitatory stimulation from the brain. After an SCI, these cells lose this input, and the neurons involved become hyperpolarized and therefore less responsive to stimuli.

Phase 2 occurs over the next two days, and is characterized by the return of some, but not all, reflexes below the SCI. The first reflexes to reappear are polysynaptic in nature, such as the bulbocavernosus reflex. Monosynaptic reflexes, such as the deep tendon reflexes, are not restored until Phase 3. Note that restoration of reflexes is not rostral to caudal as previously (and commonly) believed, but instead proceeds from polysynaptic to monosynaptic. The reason reflexes return is the hypersensitivity of reflex muscles following denervation -- more receptors for neurotransmitters are expressed and are therefore easier to stimulate.

Phases 3 and 4 are characterized by hyperreflexia, or abnormally strong reflexes usually produced with minimal stimulation. Interneurons and lower motor neurons below the SCI begin sprouting, attempting to re-establish synapses. The first synapses to form are from shorter axons, usually from interneurons; this is Phase 3. Phase 4, on the other hand, is soma-mediated, and as it takes longer for axonal transport to push growth factors and proteins from soma to the end of the axon, it takes longer.

Autonomic Effects

In spinal cord injuries above T6, autonomic dysreflexia may occur, from the loss of autonomic innervation from the brain. Sacral parasympathetics (S2-S4) are lost, as are many sympathetic levels, depending on the level of the SCI. Cervical lesions cause total loss of sympathetic innervation and lead to vasovagal hypotension and bradyarrythmias -- which resolve in 3-6 weeks. Autonomic dysreflexia is permanent, and occurs from Phase 4 onwards. It is characterized by unchecked sympathetic stimulation below the SCI (from a loss of cranial regulation), leading to often extreme hypertension, loss of bladder/bowel control, sweating, headaches, and other sympathetic effects.

References

1. Ditunno JF, Little JW, Tessler A, Burns AS. Spinal shock revisited: a four-phase model. Spinal Cord. 2004 Jul;42(7):383-95.

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