These health risks increase with the severity of the disease, especially if an affected person does not receive or comply with adequate treatment. Persons with a delusional disorder have a significantly high risk of developing psychiatric comorbidities such as depression and anxiety. This may be attributable to a genetic pattern shared by 55% of SDD patients.Shared delusional disorder can have a profoundly negative impact on a persons quality of life. Persons diagnosed with a mental health disorder commonly experience social isolation, which is detrimental to psychological health. This is especially problematic with SDD, as social isolation contributes to the onset of the disorder; in particular, relapse is likely if returning to an isolated living situation, in which shared delusions can be reinstated. Causes
While the exact causes of SDD are unknown, the main two contributors are stress and social isolation.People who are socially isolated together tend to become dependent on those they are with, leading to an inducers influence on those around them. Additionally, people developing shared delusional disorder do not have others reminding them that their delusions are either impossible or unlikely. As a result, treatment for shared delusional disorder includes those affected be removed from the inducer.Stress is also a factor, as it is a common factor in mental illness developing or worsening. The majority of people that develop shared delusional disorder are genetically predisposed to mental illness, but this predisposition is not enough to develop a mental disorder. However, stress can increase the risk of this disorder.
Diagnosis
Classification
A few SCAs remain unspecified and can not be precisely diagnosed, but in the last decade genetic testing has allowed precise identification of dozens of different SCAs  and more tests are being added each year. In 2008, a genetic ataxia blood test developed to test for 12 types of SCA, Friedreichs ataxia, and several others. However, since not every SCA has been genetically identified some SCAs are still diagnosed  by neurological examination, which  may include a physical exam, family history, MRI scanning of the brain and spine, and spinal tap.Many SCAs below fall under the category of polyglutamine diseases, which are caused when a disease-associated protein (i.e., ataxin-1, ataxin-3, etc.) contains a large number of repeats of glutamine residues, termed a polyQ sequence or a "CAG trinucleotide repeat" disease for either the one-letter designation or codon for glutamine respectively. The threshold for symptoms in most forms of SCA is around 35, though for SCA3 it extends beyond 50. Most polyglutamine diseases are dominant due to the interactions of resulting polyQ tail.The first ataxia gene was identified in 1993 and called "Spinocerebellar ataxia type 1" (SCA1); later genes were called SCA2, SCA3, etc. Usually, the "type" number of "SCA" refers to the order in which the gene was found. At this time, there are at least 29 different gene mutations that have been found.The following is a list of some of the many types of Spinocerebellar ataxia. Others include SCA18, SCA20, SCA21, SCA23, SCA26, SCA28, and SCA29.