As discussed in Chapter 4, the pathogenesis of ALS is multifactorial and includes the interaction of one, or more likely several, susceptibility genes, undetermined environmental factors and cellular ageing mechanisms (Eisen and Krieger, 1993; Eisen, 1995). There is no clear indication when the disease begins, but the symptomatic disease is preceded by an incubation period of unknown length. Duration of symptoms is also quite variable, although disease starting in younger patients runs a significantly longer course (Eisen et al., 1993c). These variables, which are not well understood, have added to the difficulty in assessing treatment which in the past resulted in a degree of therapeutic nihilism. This view is certainly being replaced by growing optimism as several therapeutic strategies based on known or suspected aetiopathogenic mechanisms are being translated into an abundance of therapeutic trials. Given our present knowledge of the aetiopathogenesis of ALS, it seems doubtful that a single, specific compound will be capable of arresting further neuronal loss and promoting regeneration. It is to be expected that the greatest therapeutic success will derive from a combination of substances that are aimed at different aspects of the disorder. This approach is routinely used in cancer therapy. Polytherapies might include neuroprotective agents, strategies directed to combat the terminal cascade of events in ALS, and symptomatic measures. Some of these approaches are summarized in Table 7.1. There are other treatment strategies detailed in this chapter, which, although based on rational concepts, have been only marginally helpful, of no benefit, or whose role is unknown.