Spinal shock
Spinal shock was first explored by Whytt in 1750 as a loss of
reflexes, following a spinal cord injury (SCI) – most often a complete transection. Reflexes in the spinal cord below the level of injury are depressed (hyporeflexia) or absent (areflexia), while those above the level of the injury remain unaffected. The 'shock' in spinal shock does not refer to circulatory collapse, and should not be confused with neurogenic shock, which is life-threatening. 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. Whytt, however, may have discussed the same phenomenon a century earlier, although no descriptive term was assigned.[1]
Phases of spinal shock
| Phase | Time | Physical exam finding | Underlying physiological event |
|---|---|---|---|
| 1 | 0–1d | Areflexia/Hyporeflexia |
Loss of descending facilitation |
| 2 | 1–3d | Initial reflex return | Denervation supersensitivity |
| 3 | 1–4w | Hyperreflexia (initial) | Axon-supported synapse growth |
| 4 | 1–12m | Hyperreflexia, Spasticity | Soma-supported synapse growth |
Ditunno et al. proposed a four-phase model for spinal shock in 2004 as follows:[2]
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
deep tendon reflexes, are not restored until Phase 3. 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.
axons, usually from interneurons – this categorizes Phase 3. Phase 4 on the other hand, is soma-mediated, and will take longer for the soma to transport various growth factors, including proteins, to the end of the axon.[3]
Autonomic effects
In spinal cord injuries above T6,
headaches, and other sympathetic effects.[citation needed
]
References
- doi:10.4065/71.4.384. Retrieved 3 August 2020.
- PMID 15037862.
- ^ B. SCHURCH; P.A. KNAPP; D. JEANMONOD; B. RODIC; A.B. ROSSIER (2010). "Case Study: 10 patients with SCI, traumatic spinal cord injury". The Medical Journal of Urology. Archived from the original on 28 August 2010. Retrieved April 20, 2010.