Calming the excitement in ALS

The concept of excitotoxicity, first established by the pioneering work of John Olney,¹ traditionally has been applied to lesions of the CNS, focusing mostly on glutamate as a neurotoxic excitatory amino acid neurotransmitter. Indeed, glutamate excitotoxicity remains one of the best-supported theories for motor neuron death in amyotrophic lateral sclerosis (ALS),² and was the pharmacologic inspiration for riluzole, which remains the only drug proven to slow the course of ALS.³ The excitotoxic model of disease can be appropriately extended to the peripheral nervous system (PNS), where overactivity of peripheral axons leads to symptoms of fasciculations and cramping. However, the increased firing of peripheral axons could also result in antidromic stimulation of parent motor and sensory neurons, resulting in increased excitatory activity and possibly excitotoxic injury. In this model, therapeutic interventions are directed at reducing axonal firing, which can be accomplished by blocking sodium channels.

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