After more than a century of scientific study and philosophical debate, the neurobiology of psychiatric disorders is still unclear. However, an emerging hypothesis contends that psychiatric and related functional symptoms are rooted in an inherent hyperexcitability of the neurological system. Particularly under the influence of stress, too many neurons fire for too long, resulting in circuit-specific psychiatric symptoms such as anxiety, depression, irritability, insomnia, inattention, and obsessional thinking as well as various physical symptoms that have no identifiable organic cause, such as migraine headache, fibromyalgia, irritable bowel, and chronic pain. Based on this hypothesis, anticonvulsant drugs, which could more aptly be called “Neuroregulators” because of their proposed mechanism of action, should have emerged as the drugs of choice for most of these disorders. Yet the use of anticonvulsants, at least for psychiatric disorders, dwindles in comparison to antidepressants, antipsychotics, psychostimulants, and sedative hypnotics. This article addresses the dearth of anticonvulsant drug use and the hypothetical reasons that several other classes of drugs continue to be used ahead of anticonvulsants despite the expanding base of evidence in support of the neuronal hyperexcitability hypothesis. The article will also propose new ways that anticonvulsants could be used to optimize their effectiveness for the wide range of disorders they should be able to treat, and it will discuss the means by which anticonvulsants could, in theory, be used prophylactically to prevent the development of an equally wide range of general medical conditions, including diabetes, high blood pressure, cardiovascular disease, autoimmune disease, dementia, and cancer.