Central nervous system injury progression

Hall and Wolf [217] have proposed a hypothesis, concerning the pathogenesis of post-traumatic central nervous system ischaemia, which integrates an injury-induced rise in intracellular Ca2+, the increased synthesis of vasoactive prostanoids and progressive microvascular lipid peroxidation. The model used anaesthetised cats with a contusion injury to the lumbar spinal cord. Antioxidants, vitamin E and selenium, were compared with various Ca2 + antagonists, cyclo-oxygenase inhibitors, a thromboxane synthetase inhibitor and the stable prostacyclin analogue. The most impressive preservation of post-traumatic spinal cord blood flow was provided by the antioxidants. 

The usual definition of a neuroprotectant is an agent that aims to prevent neuronal death by inhibiting one or more of the pathophysiological steps in the processes that follow injury to the central nervous system (CNS) or ischemia due to occlusion of an artery or hypoxia due to any cause. This definition has now been extended to include protection against neurodegeneration and neurotoxins. The extended definition includes interventions that slows or halts the progression of neuronal degeneration. 

Heydrich s sudden collapse—from apparently only minor injuries to coma and subsequent death—may have baffled the doctors, but in retrospect matches completely the symptomatology of BTX poisoning. After an initial period of calm, lasting perhaps for a day or so, the victim lapses into a progressive paralysis which fails to respond to treatment. As X went to work on Heydrich s central nervous system, the doctors could only stand by helplessly as their famous patient succumbed to the classic symptoms of poisoning by BTX ... 

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