Spinal shock

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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, and should not be confused with neurogenic shock, which is life-threatening.

Phases of spinal shock[edit]

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

Explanation of phases[edit]

Ditunno et al. proposed a four-phase model for spinal shock in 2004 as follows:[1]

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 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.[2]

Autonomic effects[edit]

In spinal cord injuries above T6, autonomic dysreflexia 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 encounterd in below t6 t7 lesions. 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/bowel control, sweating, headaches, and other sympathetic effects.

References[edit]

  1. ^ 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. doi:10.1038/sj.sc.3101603. PMID 15037862. 
  2. ^ Tufts University, Boston, USA – Case Study: 10 patients with SCI, traumatic spinal cord injury UJUS 2009, Retrieved April 20, 2010