Re: Ditunno JF, Little JW, Tessler A, Burns AS. Spinal shock revisited: a four-phase model. Spinal Cord 2004; 42: 383–395

The review of ‘spinal shock’ by Ditunno et al¹ and the commentary by Silver² shed new insights into the neurophysiologic basis and clinical presentation of this well-documented phenomenon. Such insights are important for understanding the evolution of ‘spontaneous’ recovery and ‘conversions’, that is, progression from one level of neurologic impairment to another. In their model, Ditunno et al¹ attribute the initial phase of areflexia, flaccid paralysis and loss of autonomic function to (a) loss of excitatory input to alpha and gamma motor neurons, interneurons and preganglionic sympathetic neurons from supraspinal centers, and (b) increased spinal inhibition as a consequence of reduced descending inhibition of spinal inhibitory pathways. They characterize these effects as ‘spinal neuron hyperpolarization’. Elsewhere, Little et al³ acknowledge that resolution of conduction block due to resorption of edema or hematomyelia may contribute to motor recovery following incomplete spinal cord injury.

Advances in understanding immune-central nervous system (CNS) signaling,⁴ and the immunological consequence of cord trauma,⁵ suggest that other factors may be contributing to early onset and reversible neurologic deficits. In particular, proinflammatory cytokines and other immune mediators, such as nitric oxide (NO), that exhibit increased expression in the injured cord, have now been shown to block conduction in long tract axons of the mammalian neuraxis.^{6, 7, 8} The conduction blocking effects are dose-dependent.^{6, 7} As the proinflammatory cytokine levels reduce, so axonal conduction is restored. Several proinflammatory cytokines that are known to be present at elevated concentrations within the CNS following neurotrauma, for example, tumor necrosis factor alpha (TNFα), have the capability to induce complete, but reversible, conduction failure.⁷ The mechanisms of cytokine and NO action appear to involve modulation of axonal ion channel conductances.^{6, 7, 8, 9}

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