: 48  It is important to note, however, that many disorders that cause ataxia and related symptoms exist, and that management strategies that work for some, such as vitamin E supplements for certain acquired ataxias, will not work for hereditary ataxias like SCA1 and can be dangerous to a persons health. : 52 Small cohort studies have shown that individuals with cerebellar disorders recover coordination and have lower SARA scores regardless of stage or severity of their ataxia before therapy when they are regularly participating in physiotherapy or exergaming over individuals who are not. These studies suggest that multidomain physical therapy, more focused coordinative training, and exergaming routines all produced improvements in SARA scores equivalent to at least one year of normal progression, 2.2 points or more on average, over the course of several weeks. While these results are promising, larger scale studies may be necessary to validate these results. Overall, physical therapy for individuals with ataxia has modest evidence supporting its efficaciousness, but current practice uses custom treatments without a standard decision making procedure between clinics, which limits the ability to reproducibly assess the quality of routines in literature.
Several members of the family actively participated in research and the family consented to post mortem examinations of the brains of several deceased relatives. The disease in the Schut family was found to have an autosomal dominant inheritance pattern, and afflicted the spinocerebellar tract. In 1945, John Schut received free medical school education for his service with the United States Army during the second world war and began his own efforts researching hereditary ataxia. : 90–91  Schut developed ataxia like many of his relatives. In 1957, when Schuts ataxia progressed to a point where he was unable to continue work in regular medical practice, he founded the National Ataxia Foundation with lab space donated by Glenwood Hills Hospital in Minneapolis. : 131 John Schuts nephew, Lawerence Schut, also became an ataxia researcher and contributed to localizing a spinocerebellar ataxia gene to the human leukocyte antigen complex in chromosome 6. The success in linking one of these class of diseases to a locus showed that the classification systems in use were unable to distinguish between diseases with many different causes. Many ataxic disorders which were historically identified as Maries ataxia, olivopontocerebellar atrophy or other names were now reclassified as types of spinocerebellar ataxia, each type numbered in order as a new locus was found. In 1993, the gene and a mutation causing spinocerebellar ataxia type 1 was identified. It was the first genetic defect found known to cause an ataxic disorder.