Long non‐coding RNAs (lncRNAs) are RNAs that exceed 200 nucleotides in length and that are not translated into proteins. Thousands of lncRNAs have been identified with functions in processes such as transcription and translation regulation, RNA processing, and RNA and protein sponging. LncRNAs show prominent expression in the nervous system and have been implicated in neural development, function and disease. Recent work has begun to report on the expression and roles of lncRNAs in motor neurons (MNs). The cell bodies of MNs are located in cortex, brainstem or spinal cord and their axons project into the brainstem, spinal cord or towards peripheral muscles, thereby controlling important functions such as movement, breathing and swallowing. Degeneration of MNs is a pathological hallmark of diseases such as amyotrophic lateral sclerosis and spinal muscular atrophy. LncRNAs influence several aspects of MN development and disruptions in these lncRNA‐mediated effects are proposed to contribute to the pathogenic mechanisms underlying MN diseases (MNDs). Accumulating evidence suggests that lncRNAs may comprise valuable therapeutic targets for different MNDs. In this review, we discuss the role of lncRNAs (including circular RNAs circRNAs) in the development of MNs, discuss how lncRNAs may contribute to MNDs and provide directions for future research. During development, distinct classes of long non‐coding RNAs (lncRNAs) display specific spatiotemporal patterns to drive motor neuron (MN) differentiation and maturation leading to the generation of functional subsets of MNs. MN diseases such as ALS are characterized by changes in the expression of specific classes of lncRNAs and mutant antisense (AS) RNAs, resulting in disease phenotypes. These include the formation of aberrant RNA accumulations (foci) that sequester and interfere with RNA‐binding protein (RBP) function and the production of toxic peptides (DPRs). These changes ultimately lead to MN degeneration and muscle atrophy.