Spinal shock was first defined by Whytt in 1750 as loss of sensation with motor paralysis with early loss but gradual reflex recovery, after spinal cord injury (SCI) - most often a complete transection. Reflexes in the spinal cord below the level of injury are depressed (hiporefleksia) or absent (areflexia), while those above the injury rate remain unaffected. 'Shock' in spinal shock does not refer to circulatory collapse, and should not be confused with life-threatening, neurogenic shock.
Video Spinal shock
Phase 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 the reflexes under SCI. This phase lasts for one day. The neurons involved in various reflex arcs usually receive an inflammatory stimulation rate from the brain. After SCI, these cells lose this input, and the involved neurons 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 under SCI. The first reflex that reappears is polysinaps in nature, such as bulbocavernosus reflexes. Monosynaptic reflexes, such as deep tendon reflexes, are not restored until Phase 3. Reflex recovery is not rostral to the caudal as before (and generally) believes, but otherwise results from polysynaptic to monosynaptic. The reason reflexes return is the hypersensitivity of reflex muscles after denervation - more receptors for neurotransmitters are expressed and therefore easier to stimulate.
Phases 3 and 4 are characterized by hyperreflexia, or abnormal reflexes that are usually produced with minimal stimulation. Interneurons and lower motor neurons under SCI begin to grow, trying to rebuild synapses. The first synapses formed are from shorter axons, usually from interneurons - this categorizes Phase 3. Phase 4 on the other hand, is soma-mediation, and will take longer for soma to transport various growth factors, including proteins, to the end. of axons.
Maps Spinal shock
Autonomous effects
In a spinal cord injury above T6, neurogenic shock may occur, from loss of autonomic innervation of the brain. Parasympathetic is preserved but synergy between sympathetic and parasympathetic systems is lost to high thoracic and cervical SCI lesions. Sacral parasympathetic damage can be found in lesions below T6 or T7. Cervical lesions cause loss of sympathetic innervation and lead to vasovagal hypotension and bradyarrhythmias - which heal within 3-6 weeks. Autonomic dyslexesis is permanent, and occurs from Stage 4 and beyond. It is characterized by uncontrolled sympathetic stimulation under SCI (from loss of cranial regulation), which causes frequent hypertension, loss of bladder or bowel control, sweating, headache, and other sympathetic effects.
References
Source of the article : Wikipedia
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