In diagnosing<unk>  the individuals clinical history or their past health examinations, a current physical examination to check for any physical abnormalities, and a genetic screening of the patients genes and the genealogy of the family are done. The large category of cerebellar ataxia is caused by a deterioration of neurons in the cerebellum, therefore magnetic resonance imaging (MRI) is used to detect any structural abnormality such as lesions which are the primary cause of the ataxia. Computed tomography (CT) scans can also be used to view neuronal deterioration, but the MRI provides a more accurate and detailed picture.<unk>  types Currently there are 27 subtypes have been identified: SCA1-SCA4, SCA8, SCA10, SCA12- SCA14, SCA15/SCA16, SCA17- SCA23, SCA25, SCA27, SCA28, SCA32, SCA34- SCA37,<unk>  and dentatorubral pallidoluysian atrophy . Type 1 Type I<unk>  is characterized by different symptoms of ataxia as well as other conditions that are dependent on the subtype. Type 1<unk>  is divided into 3 subclasses based on pathogenesis of the subtypes each contain. L-Glutamin * Subtype 1 -subtypes in the first subclass are caused by CAG nucleotide repeats in the DNA, which code for the amino acid glutamine. This glutamine is toxic to the cell on the level of proteins and has degenerative effects. Within the first subclass of Type 1 are SCA1, SCA2, SCA3, SCA17, and DRPLA. This first subclass is the most common of Type 1<unk> s with SCA3 being the most common subtype of all of Type 1. SCA3, Machado-Joseph disease, is the most common because the mutation repeats more than 56 times while the regular length is around 13 to 31. * Subtype 2 -the second subclass of Type 1<unk>  is also caused by the same nucleotide repeats but instead in RNA and in a region that does not code for proteins. Gene expression is affected instead of proteins in subtype two SCAs because of this. Subtype 2 contains SCA8, SCA10, and SCA12. * Subtype 3 -the third subclass of Type 1<unk>  is caused by different mutations and deletions in genes. It comprises SCA13, SCA14, SCA15, SCA16, SCA27, and SCA28. Type 2/3 Type II<unk>  is composed of SCA7 and syndromes associated with pigmentary maculopathies. SCA7 is a disease that specifically displays retinal degeneration, along with the common degeneration of the cerebellum. Moving further into SCA7's pathology, a similar genetic process is described, while the function of ATXN7 (an ataxin gene) is much like a component of the SAGA complex. The SAGA complex uses two histone-modifying techniques to regulate transcription. These activities are the Gcn5 histone acetyltransferase and the Usp22 deubiquitinase. Mutant ATXN7 in HAT activity causes an increase in activity, which was reported from an in-vivo analysis in the retina. There are also studies that show a loss in activity when human ATXN7 in yeast was used. The SCA7 autosomal-dominant inheritance pattern is similar to a mutant ATXN5-induced gain in Gcn5 HAT. Spinocerebellar ataxia type 15 has been classified as an<unk>  Type III as it has been noted to have postural and action tremor in addition to cerebellar ataxia. Additionally, spinocerebellar ataxia type 20 (SCA20) is organized in<unk>  III that often exhibits disease-like symptoms at an earlier age, sometime starting at fourteen years old.
Autosomal dominant cerebellar ataxia
Autosomal recessive cerebellar ataxia
Non-progressive congenital ataxia
Benign hereditary chorea
Spinal muscular atrophy with lower extremity predominance 1
Autosomal recessive cerebellar ataxia type 1
Tropical ataxic neuropathy
Spinocerebellar ataxia