While SCA1 was not significantly correlated with a unique pattern, other possible SCAs can be linked  and absence of a vertical nystagmus following horizontal head shaking reduces the likelihood of an SCA6 diagnosis, while the absence of a square wave pattern during fixation reduces the likelihood of SCA3.One possible system for the differential diagnosis of SCA types is to record the progression of symptoms and use Bayesian probability to build a predictive model, or a Bayesian classifier, that compares the observed data to trends like those described above to find the likelihood of each diagnosis to be correct. One such Bayesian classifier was shown to accurately predict 78% of SCA cases out of a cohort with known types of SCA. The sensitivity and specificity for SCA1 within this model was 76.9% and 98.2% respectively. Regional variance in prevalence, symptoms and clinical assessment might still limit the use of this system on large scales, though the system may implemented by individual clinics using their own regional data. Management
There is currently no cure for Spinocerebellar ataxia type 1. However, some of its symptoms may be managed with physical, occupational or speech therapies, lifestyle and dietary changes, or with medications. Managing symptoms will not prevent the disease from progressing but can be important for maintaining quality of life.
Both of these techniques are difficult to apply to polyglutamine diseases because targeting the polyglutamine tract may cause normal genes to be downregulated as well. SCA1 has also shown to be difficult to target reliably with single-nucleotide polymorphisms limiting the number of ways RNAi and antisense therapy techniques can be designed to treat SCA1. Reducing toxicity and increasing cell survival
Because of the numerous interactions ataxin-1 has with other proteins, techniques for reducing toxicity of the mutant ataxin-1 protein often change the expression of related proteins. For example, ataxin-1-like has many common domains with ataxin-1 and overexpression of ataxin-1-like compete with ataxin-1 and prevent its integration into other complexes, reducing toxicity. This effect was replicated in mice models using AAVs, and shown to be about as effective as RNAi techniques at slowing the progression of symptoms. Similarly, the drug baclofen, which is used to help reduce spasticity in persons with multiple sclerosis and related diseases, operates as an agonist of γ-aminobutyric acid type B receptors (GABABR). This pathway crosstalks with the mGluR1 pathway, which interacts with the ataxin 1 protein and proteins responsible for localization and degradation of ataxin 1, suggesting that baclofen may be a viable treatment for SCA 1 treatment.Molecular chaperones are introduced proteins that may have interactions with the mutant protein that reduce toxicity by various mechanisms.