The existence of different conductive patterns in unmyelinated and myelinated axons is uncertain. It seems that considering exclusively physical electrical phenomena may be an oversimplification. A novel interpretation of the mechanism of nerve conduction in myelinated nerves is proposed, to explain how the basic mechanism of nerve conduction has been adapted to myelinated conditions.

The neurilemma would bear the voltage-gated channels and Na⁺/K⁺-ATPase in both unmyelinated and myelinated conditions, the only difference being the sheath wrapping it. The dramatic increase in conduction speed of the myelinated axons would essentially depend on an increment in ATP availability within the internode: myelin would be an aerobic ATP supplier to the axoplasm, through connexons. In fact, neurons rely on aerobic metabolism and on trophic support from oligodendrocytes, that do not normally duplicate after infancy in humans.

Such comprehensive framework of nerve impulse propagation in axons may shed new light on the pathophysiology of nervous system disease in humans, seemingly strictly dependent on the viability of the pre-existing oligodendrocyte.

在无髓鞘和有髓鞘轴突中是否存在不同的导电模式尚不确定。似乎只考虑物理电现象可能过于简单化了。对有髓神经的神经传导机制提出了一种新的解释，以解释神经传导的基本机制如何适应有髓条件。

在无髓鞘和有髓鞘条件下，神经鞘膜将承载电压门控通道和 Na ⁺ /K ⁺ -ATPase，唯一的区别是包裹它的鞘。有髓轴突传导速度的显着增加主要取决于节间内 ATP 可用性的增加：髓鞘将通过连接子为轴质提供有氧 ATP。事实上，神经元依赖于有氧代谢和少突胶质细胞的营养支持，而这些在人类婴儿期后通常不会复制。

轴突中神经冲动传播的这种综合框架可能为人类神经系统疾病的病理生理学提供新的思路，这似乎严格依赖于预先存在的少突胶质细胞的生存能力。