The risk to other family members depends on the status of the proband 's parents. If a parent is affected, his or her family members may be at risk. All offspring are obligate heterozygotes carriers for a pathogenic variant.
Carrier testing for at-risk relatives requires prior identification of the pathogenic variants in the family. All the daughters of an affected male are carriers; none of his sons will be affected. The proband 's maternal aunts may be at risk of being carriers and the aunts' offspring, depending on their gender, may be at risk of being carriers or of being affected. Carrier testing for females at risk for an X-linked disorder requires prior identification of the pathogenic variant in the family.
Testing of at-risk asymptomatic adult relatives of individuals with hereditary ataxia is possible after molecular genetic testing has identified the specific disorder and pathogenic variant s in the family. Such testing should be performed in the context of formal genetic counseling. In general, molecular genetic test results are not useful in predicting age of onset, severity, type of symptoms, or rate of progression in asymptomatic individuals.
Molecular genetic testing of asymptomatic individuals younger than age 18 years who are at risk for adult-onset disorders for which no treatment exists is not considered appropriate, primarily because it negates the autonomy of the child with no compelling benefit. Further, concern exists regarding the potential unhealthy adverse effects that such information may have on family dynamics, the risk of discrimination and stigmatization in the future, and the anxiety that such information may cause.
See also the National Society of Genetic Counselors position statement on genetic testing of minors for adult-onset conditions and the American Academy of Pediatrics and American College of Medical Genetics and Genomics policy statement : ethical and policy issues in genetic testing and screening of children. DNA banking. Because it is likely that testing methodology and our understanding of genes, allelic variants, and diseases will improve in the future, consideration should be given to banking DNA from probands in whom a molecular diagnosis has not been confirmed i.
Once the pathogenic variant s have been identified in an affected family member, prenatal testing for a pregnancy at increased risk and preimplantation genetic testing for hereditary ataxia are possible. However, in general, age of onset, severity of disease, specific symptoms, and rate of disease progression are variable and cannot be accurately predicted by the family history or molecular genetic testing.
Differences in perspective may exist among medical professionals and within families regarding the use of prenatal testing. While most centers would consider use of prenatal testing to be a personal decision, discussion of these issues may be helpful.
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Management of ataxias is usually directed at providing assistance for coordination problems through established methods of rehabilitation medicine and occupational and physical therapy. Speech therapy may benefit persons with dysarthria. Computer devices are available to assist persons with severe speech deficits. No further modifications are allowed. For clarity, excerpts of GeneReviews chapters for use in lab reports and clinic notes are a permitted use.
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Summary Clinical characteristics. Genetic counseling. Definition Clinical Manifestations of Hereditary Ataxia Clinical manifestations of hereditary ataxia are poor coordination of movement and a wide-based, uncoordinated, unsteady gait. Hereditary ataxia may result from one or any combination of the following: Dysfunction of the cerebellum and its associated systems. A causative i. A clinical phenotype characteristic of a genetic form of ataxia.
Note: In some individuals with no family history of ataxia it may not be possible to establish a genetic cause if results of all available genetic tests are normal. Differential Diagnosis of Hereditary Ataxia Differential diagnosis of hereditary ataxia includes acquired, non-genetic causes of ataxia, such as alcoholism, vitamin deficiencies, multiple sclerosis, vascular disease, primary or metastatic tumors, or paraneoplastic diseases associated with occult carcinoma of the ovary, breast, or lung.
Prevalence of Hereditary Ataxia Prevalence of the autosomal dominant cerebellar ataxias ADCAs is estimated to be approximately , population [ van de Warrenburg et al , Ruano et al ]. Figure 1. Causes The hereditary ataxias can be subdivided first by mode of inheritance i.
Spinocerebellar ataxia SCA is a historical term first used in the s based on Friedreich ataxia as a model. SCA now refers to autosomal dominant hereditary ataxia, and the numbers are assigned in the order in which the disease was identified initially by linkage analysis and more recently by gene discovery. In some SCAs ataxia is the only phenotypic finding e. Some SCAs have spinal cord involvement, but many do not.
Some of the complicated forms have not been given an SCA number e. SCAR refers to autosomal recessive spinocerebellar ataxias. Autosomal Dominant Cerebellar Ataxias ADCA Synonyms for ADCA used prior to the identification of the molecular genetic basis of these disorders were Marie's ataxia , inherited olivopontocerebellar atrophy , cerebello-olivary atrophy , or the more generic term, spinocerebellar degeneration.
Table 1. References included when there is no GeneReview. Episodic Ataxias The episodic ataxias are characterized by periods i. Table 2. Autosomal Recessive Hereditary Ataxias The autosomal recessive hereditary ataxias are listed in Table 3 : The first part of the table lists those autosomal recessive ataxias that are relatively common i. The second part of the table lists autosomal recessive ataxias that are relatively uncommon i. Pontocerebellar hypoplasia [ Namavar et al , Ahmed et al ].
Peroxisomal biogenesis disorders, Zellweger spectrum disorders. Table 3. Table 4. Spastic Ataxias The combination of spasticity with signs of cerebellar ataxia is relatively common and one or the other finding may predominate [ de Bot et al ] see Table 5.
Table 5. Evaluation Strategy Once a hereditary ataxia is considered in a proband i. Clinical Findings Gait ataxia is the common manifestation of these disorders. Family History A three-generation family history with attention to other relatives with neurologic signs and symptoms should be obtained. Molecular Genetic Testing The ordering of molecular genetic tests and interpretation of results is complex and may require the support of an experienced laboratory, clinical geneticist, clinical geneticist, and genetic counselor.
Hypotheses may be based on one or more of the following: Mode of inheritance. Apparent anticipation for a nucleotide-repeat disorder;. Mode of Inheritance More than one affected family member Autosomal dominant inheritance Table 1 and Table 2. A family history in which male and female individuals in multiple generations are affected suggests autosomal dominant inheritance. These five disorders are caused by trinucleotide repeat expansions; many clinical laboratories include them in a small panel [ Ruano et al ].
Autosomal recessive inheritance Table 3. A family history in which only sibs are affected i. Because of their treatability, vitamin E deficiency , Refsum disease , and cerebrotendinous xanthomatosis should be considered even though they are very rare.
X-linked inheritance Table 4. A family history in which affected individuals are male and are related to each other through females suggests X-linked inheritance. If only one member of a family is known to be affected, possibilities to consider are an acquired non-genetic cause , a de novo pathogenic variant associated with autosomal dominant ataxia, decreased penetrance of a pathogenic variant associated with autosomal dominant ataxia, a single occurrence of an autosomal recessive or X-linked disorder in a family, or alternate paternity.
Distinguishing Clinical Features Distinguishing clinical findings exist for a number of inherited ataxias: Because of extensive clinical overlap between all forms of autosomal dominant hereditary ataxia, it is difficult in any given individual with ataxia and a family history consistent with autosomal dominant inheritance to establish a diagnosis without molecular genetic testing.
Clinical findings such as intellectual disability, seizures, eye abnormalities, or peripheral neuropathy may help distinguish between some of the autosomal recessive ataxias. Distinct brief minutes to hours episodes of ataxia separated by normal function strongly suggests an episodic ataxia.
See Table 2. Prominent spasticity suggests one of the spastic ataxias. See Table 5. Other Ethnicity. Single- gene testing may be considered on the basis of an individual's ethnic background Prevalence.
Genetic Counseling Genetic counseling is the process of providing individuals and families with information on the nature, mode s of inheritance, and implications of genetic disorders to help them make informed medical and personal decisions. Mode of Inheritance This GeneReview includes hereditary ataxias that may be inherited in an autosomal dominant manner, an autosomal recessive manner, or an X-linked recessive manner.
Autosomal Dominant Inheritance — Risk to Family Members Parents of a proband Most individuals diagnosed as having autosomal dominant ataxia have an affected parent, although occasionally the family history is negative.
Family history may appear to be negative because of early death of a parent, failure to recognize autosomal dominant ataxia in family members, late onset in a parent, reduced penetrance of the pathogenic allele in an asymptomatic parent, or de novo mutation.
The risk to sibs depends on the genetic status of the proband 's parents. Autosomal Recessive Inheritance — Risk to Family Members Parents of a proband The parents are obligate heterozygotes and therefore carry a single copy of a pathogenic variant. Carrier Heterozygote Detection Carrier testing for at-risk relatives requires prior identification of the pathogenic variants in the family.
X-Linked Inheritance — Risk to Family Members Parents of a proband The father of an affected male will not have the disease nor will he be a carrier of the pathogenic variant. The risk to sibs depends on the carrier status of the mother. Male sibs who inherit the pathogenic variant will be affected; female sibs who inherit the pathogenic variant will be carriers and will usually not be affected.
If the proband represents a simplex case i. Heterozygote Carrier Detection Carrier testing for females at risk for an X-linked disorder requires prior identification of the pathogenic variant in the family. Related Genetic Counseling Issues Testing of at-risk asymptomatic adult relatives of individuals with hereditary ataxia is possible after molecular genetic testing has identified the specific disorder and pathogenic variant s in the family.
Prenatal Testing and Preimplantation Genetic Testing Once the pathogenic variant s have been identified in an affected family member, prenatal testing for a pregnancy at increased risk and preimplantation genetic testing for hereditary ataxia are possible.
Ataxia UK. Spinocerebellar ataxia. Management Treatment of Manifestations Management of ataxias is usually directed at providing assistance for coordination problems through established methods of rehabilitation medicine and occupational and physical therapy. Canes, walkers, and wheelchairs are useful for gait ataxia. Special devices are available to assist with handwriting, buttoning, and use of eating utensils.
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