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Spinocerebellar Ataxia 42

OMIM ID:

autosomal dominant

Spinocerebellar Ataxia 42

Alternate Names

SCA42

Defective Genes

CACNA1G

Clinical Characteristics

Ocular Features

 Saccadic eye movements with nystagmus and diplopia have been reported (7 of 10 reported patients).

Systemic Features

Cerebellar signs usually have their onset in midlife or later with slow progression.  Most patients are mildly to moderately disabled.  Dysarthria, dysphagia, and a spastic gait are experienced by the majority of individuals.  Hyperreflexia and a positive Babinski sign are commonly presently.  Mild cognitive impairment and depression have been seen in a minority of patients.

Brain MRIs show cerebellar hemispheric and vermian atrophy.  The cerebral cortex appeared histologically normal in one deceased patient.

Genetics

Inheritance

This disorder is caused by heterozygous mutations in the CACNA1G gene (17q21.33).

Pedigree

Autosomal dominant

Autosomal dominant disorders require only one mutation for the disease to be expressed.  Since an affected parent has two chromosomes, only one of which has the mutant gene, parents can expect that half (50%) of their children will receive that one and inherit the disease.  It is common for individuals that inherit the mutation, however, to not have evidence of the disease (nonpenetrance).

Image
Sample pedigree of autosomal dominant inheritance

Autosomal dominant inheritance leads to a vertical pattern of transmission

Treatment & Management

No treatment has been reported.

Selected Resources

Web Resources

Publications

Displaying 1 - 2 of 2

A mutation in the low voltage-gated calcium channel CACNA1G alters the physiological properties of the channel, causing spinocerebellar ataxia

PubMedID: 26715324

A Recurrent Mutation in CACNA1G Alters Cav3.1 T-Type Calcium-Channel Conduction and Causes Autosomal-Dominant Cerebellar Ataxia

PubMedID: 26456284