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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 below the level of injury are depressed (hyporeflexia) or absent (areflexia), while those above the level of the injury 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 == Ditunno et al. proposed a four-phase model for spinal shock in 2004 as follows: 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.〔Tufts University, Boston, USA – (Case Study: 10 patients with SCI, traumatic spinal cord injury ) UJUS 2009, Retrieved April 20, 2010〕 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Spinal shock」の詳細全文を読む スポンサード リンク
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