Bouldin T W, Cavanagh J B
Am J Pathol. 1979 Feb;94(2):241-52.
The spatio-temporal spread of axonal degeneration in organophosphorous neuropathy has been studied by means of the teased-fiber technique. Young adult cats were given a single intraperitoneal injection of di-isopropylfluorophosphate (DFP) and were killed 14, 18, 20, 21, and 28 days later by intracardiac perfusion with aldehydes. The cats developed clinical signs of delayed neurotoxicity 16 to 18 days after DFP injection. A histologic survey of the central and peripheral nervous systems revealed that the topographic distribution of axonal degeneration was characteristic of a dying-back neuropathy. In teased-fiber preparations from the left recurrent laryngeal nerve, we found that the axonal degeneration was initially focal and nonterminal but that the axonal degeneration subsequently spread in a somatofugal direction to involve the entire distal axon. Nerve fibre varicosities and paranodal demyelination preceded the axonal degeneration. It is concluded that neurotoxic organophosphates induce a focal, distal but not terminal axonal degeneration. This "chemical transection" of the axon then precipitates wallerian degeneration of the more distal axon. Thus, the traditional hypothesis that dying-back neuropathies evolve from a retrograde axonal degeneration is not valid for organophosphorous neuropathy.
采用 teased-fiber 技术研究了有机磷中毒性神经病中轴突变性的时空扩散情况。给成年幼猫腹腔内单次注射二异丙基氟磷酸酯（DFP），并于注射后 14、18、20、21 和 28 天通过心脏灌注醛类进行处死。这些猫在注射 DFP 后 16 至 18 天出现迟发性神经毒性的临床症状。对中枢和周围神经系统的组织学检查显示，轴突变性的地形分布具有轴突缺失性神经病的特征。在左侧喉返神经的 teased-fiber 标本中，我们发现轴突变性最初是局灶性的且并非终末性的，但随后轴突变性沿躯体离心方向扩散，累及整个远端轴突。神经纤维肿胀和结旁脱髓鞘先于轴突变性出现。结论是，神经毒性有机磷诱导局灶性、远端而非终末性轴突变性。轴突的这种“化学横断”随后促使更远端轴突发生华勒氏变性。因此，轴突缺失性神经病由逆行性轴突变性演变而来的传统假说是不适用于有机磷中毒性神经病的。
