Spinal shock

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Spinal shock
Cervical Spine MRI (T2W).jpg
Cervical spine MRI showing a C4 fracture and dislocation resulting in spinal cord compression
SymptomsTemporary loss or decrease of reflexes[1]
ComplicationsNeurogenic shock[2]
Duration4 to 12 weeks[3]
CausesSpinal cord injury[1]
Risk factorsSubstance misuse[4]
TreatmentSupportive care[4]

Spinal shock is the temporary loss or decrease of reflexes below the level of a spinal cord injury (SCI).[1] There is also generally no motor or sensory function below the injury.[2] Onset is usually sudden.[1] Low blood pressure may or may not be present.[1] It can be complicated by neurogenic shock, which is low blood pressure due to loss of sympathetic tone as a result of a spinal cord injury.[2]

It most commonly occurs from injury, such as a motor vehicle collision, fall, sports accident, or self-harm.[1][4] Other causes may include low blood pressure or as a complication of angiography.[4] The underlying mechanism involve near or complete disruption through a level of the spinal cord.[1] Spinal shock is deemed to have resolved as reflexes return, despite the reflexes never returning to normal.[1] It generally lasts 4 to 12 weeks, after which spasticity occurs.[3]

There is no specific treatment once the injury has occurred.[4] Efforts generally include preventing low blood pressure and low oxygen levels.[4] Long term care is generally required.[4] Males are affected four times more often than females.[4] The condition may have been described as early as 1750 by Whytt, though the term itself was first used in 1841 by Hall.[1]

Phases

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:[5]

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. 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 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.[6]

Autonomic effects

In spinal cord injuries above T6, neurogenic shock may occur, from the loss of autonomic innervation from the brain. Parasympathetic is preserved but the synergy between sympathetic and parasympathetic system is lost in cervical and high thoracic SCI lesions. Sacral parasympathetic loss may be encountered in lesions below T6 or T7. Cervical lesions cause total loss of sympathetic innervation and lead to vasovagal hypotension and bradyarrhythmias – 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 or bowel control, sweating, headaches, and other sympathetic effects.

References

  1. 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Atkinson, Patty Pate; Atkinson, John L.D. (April 1996). "Spinal Shock". Mayo Clinic Proceedings v. 71(4): 384-389. doi:10.4065/71.4.384. PMID 8637263. Retrieved 3 August 2020.
  2. 2.0 2.1 2.2 Dave, S; Cho, JJ (January 2020). "Neurogenic Shock". PMID 29083597. Cite journal requires |journal= (help)
  3. 3.0 3.1 Ko, Hyun-Yoon (2019). Management and Rehabilitation of Spinal Cord Injuries. Springer. p. 124. ISBN 978-981-10-7033-4.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 4.6 4.7 Ziu, E; Mesfin, FB (January 2020). "Spinal Shock". PMID 28846241. Cite journal requires |journal= (help)
  5. Ditunno, JF; Little, JW; Tessler, A; Burns, AS (2004). "Spinal shock revisited: a four-phase model". Spinal Cord. 42 (7): 383–95. doi:10.1038/sj.sc.3101603. PMID 15037862.
  6. Tufts University, Boston, USA – Case Study: 10 patients with SCI, traumatic spinal cord injury UJUS 2009, Retrieved April 20, 2010