What Causes CAS?

What Causes CAS?

What Causes CAS and Is It Preventable?

First, it is important for parents to understand that there is most likely nothing that you did to “cause” your child’s speech disability.   It is not about how much you talked to your child or whether or not you had them in daycare, for example.  Your child does not have apraxia because you separated from your spouse or because you moved to a new city.  So while we know that parents have a strong role in healthy child development, unless there was abuse, neglect, or isolation, you are not responsible for causing your child’s speech problems.

The current knowledge that we have about CAS is this.  Childhood Apraxia of Speech may occur in the following 3 conditions:

  • Neurological impairment caused by infection, illness or injury, before, during or after birth.  This category includes children with positive findings on MRI’s (scans) of the brain, or those with brain injury or trauma, etc.
  • Complex Neurodevelopmental Disorders – We know that CAS can occur as a secondary characteristic of other conditions such as genetic, metabolic, and/or mitochondrial disorders.  In this category would be Childhood Apraxia of Speech that occurs with Autism, Fragile X, Galactosemia, some forms of Epilepsy, and some types of chromosome translocations, duplications and/or deletions (genetic conditions).  There are quite a few disorders in which CAS can arise, but that does not mean that all children with these disorders also have CAS.  For example, many children with Galactosemia have a speech problem, and out of those children, only some of them have CAS.  Only some children with autism also have CAS.  Only some children with epilepsy have CAS and so forth.
  • Idiopathic Speech Disorder (a disorder of “unknown” origin) – with this condition, we currently don’t know “why” the child has apraxia of speech.  Children do not have observable neurological abnormalities or easily detected neurodevelopmental conditions.

Some speculate that CAS and other childhood conditions may be a result, in part, of environmental conditions such as exposure to pollutants and toxins before or after birth.   Others speculate that nutritional deficits or malabsorbtions cause CAS.  While toxins and nutritional deficits do cause some developmental problems, to date these theories, as they relate specifically to CAS, are only speculations with no research evidence to support them.

That said, a child’s positive health will contribute to their ability to benefit from their learning exposures every day and from therapy designed to help them.  A child who is healthy is more fully capable of taking advantage of opportunities to learn.  Children who are sick frequently with ear and sinus infections, enlarged tonsils and adenoids, asthma, allergies or have sleep disturbances, attention and behavioral difficulties are going to find it much more difficult to benefit from the help provided.  Helping your child be healthy and thus more “present” and available to the learning opportunities around them is one important way parents can help.

Most likely in the future we will learn that CAS is caused by multiple factors and conditions, not one.  To the extent that research evidence becomes available that CAS is caused by some factor that can be manipulated to reduce or eliminate it, will determine whether or not it is preventable.  Until then, we do know one very critical thing – that appropriate speech therapy, tailored to the difficulty of speech motor planning and provided frequently, is the single most important opportunity for children with CAS to improve their speech capacity.  Children who are able to maintain optimum health will most likely directly benefit the most from appropriate help.

What do Researchers Know About Genetics and CAS?

By Lawrence Shriberg, Ph.D., CCC-SLP

The primary findings on the genetics of CAS have emerged from studies of a London family (the ‘KE’ family), half of whose members have an orofacial apraxia and a reported apraxia of speech. Reviews of this widely-cited project include technical and more accessible descriptions of the mutation on the FOXP2 gene (located on chromosome 7) that has been linked to family members with CAS. A recent overview by researchers in the London-Oxford group that has studied the KE family for over 15 years provides a useful summary of the genomic and other findings, including a partially annotated bibliography (Vargha-Khadem et al., 2005). In response to the question posed in the present CAS forum, there is space for only brief comment on three aspects of this landmark research.

First, the neural phenotypes (i.e., characteristics) emerging from studies of FOXP2 by researchers in a number of disciplines are consistent with the behavioral phenotypes associated with CAS. FOXP2 is expressed widely in cells distributed throughout the brain, which is consistent with the cognitive, language, speech, prosody and other challenges observed in children with suspected CAS. Moreover, findings indicating that FOXP2 is expressed in both sides of the brain, rather than in just one hemisphere, are consistent with the severity and persistence of CAS during and often beyond the developmental period. Recent studies of several species of songbirds (Teramitsu et al., 2004) indicate that FOXP2 is especially active during the periods in which young birds learn their specific calls, providing an attractive animal model for studying comparable processes in children learning the speech and prosodic patterns of their language and local dialect. A complexity in this research is that the gene products of FOXP2 function primarily as switches that regulate other ‘downstream’ genes. Thus, although a great deal is known about FOXP2, the major challenge ahead is to understand the individual and collective effects of the downstream genes it controls-specifically, growth and development of the neural circuits underlying speech-language acquisition and performance. The London and Oxford research groups have recently received grants to do just that, using powerful techniques in bioinformatics and molecular neuroscience. Findings from these studies, which will be reported over the next few years, are expected to address fundamental questions about the developmental neurobiology of verbal trait disorders, including CAS.

A second promising development is that in the past year, three research groups have described case findings supporting the etiologic role of FOXP2 in CAS. The London-Oxford researchers recently reported that in a study of 43 children identified as having CAS, one child (and his affected sibling and their mother) had the same FOXP2 mutation observed in affected members of the KE family (MacDermot et al., 2004). A research group in the United States has reported CAS, as well as dysarthria, in a mother and daughter with a chromosome translocation in a region affecting FOXP2 (Shriberg et al., 2005). A Canadian group has identified a FOXP2 deficit in a child who reportedly has CAS, as well as a craniofacial dysmorphology (Zeesman et al., 2004).

Finally, although FOXP2 appears to be linked to CAS in these new case reports, it is likely that there are other genetic influences underlying alternative forms of CAS. Note that the FOXP2 mutation was identified in only one of the 43 children in the study cited above, leaving unexplained the origin of the other CAS diagnoses. Also, the FOXP2 mutation was not found in an unpublished study of children with suspected CAS (Barbara Lewis, personal communication). In addition to the idiopathic form of CAS (i.e., CAS occurring without other neurodevelopment involvements), apraxia of speech has been reported symptomatically in disorders such as Fragile X, autism, galactosemia, and some forms of epilepsy. Thus, another research challenge is to determine if there may be subtypes of CAS associated with different genetic backgrounds. On this issue, there appears to be notable recent convergence on the perspective that both typical and atypical communication development are controlled by common ‘generalist’ genes, rather than different ‘specialist’ genes (Plomin & Kovas, 2005.) This fundamental distinction is important for continuing research on the genetic origins of CAS. It suggests that in addition to searching for single genes underlying CAS, emphasis should also be placed on identifying interactions among groups of genes, each contributing to the form and severity of CAS. Information on such neural phenotypes, that may also be common to other verbal trait disorders, should in turn, help researchers better define and treat the behavioral characteristics of CAS.

Citations

MacDermot, K.D., Bonora, E., McKenzie, F., Smith, R.L., Sykes, N., Coupe, A-M., et al. (2004, October). Identification of FOXP2 truncation as a novel cause of nonsyndromic developmental speech disorder. Poster session presented at the annual meeting of The American Society of Human Genetics, Toronto, Canada.

Plomin, R. & Kovas, Y. (in press). Generalist genes and learning disabilities. Psychological Bulletin.
Shriberg, L.D., Ballard, K.J., Tomblin, J.B., Duffy, J.R., & Odell, K.H. (2005). Speech, prosody, and voice characteristics of a mother and daughter with a 7;13 translocation affecting FOXP2. Manuscript submitted for publication.

Teramitsu, I., Kudo, L.C., London, S.E., Geschwind, D.H., & White, S.A. (2004). Parallel FOXP1 and FOXP2 expression in songbird and human brain predicts functional interaction. Journal of Neuroscience, 24, 3152-3163.

Vargha-Khadem, F., Gadian, D.G., Copp, A., & Mishkin, M. (2005). FOXP2 and the neuroanatomy of speech and language. Neuroscience, 6, 131-138.
Zeesman, S., Nowaczyk, M.J.M., Teshima, I., Roberts, W., Oram Cardy, J., Brian, J., et al. (2004, October). Speech and language impairment and oromotor dyspraxia due to deletion of 7q31 which involves FOXP2. Poster session presented at the annual meeting of The American Society of Human Genetics, Toronto, Canada.


[Dr. Lawrence Shriberg is Professor of Communication Disorders at the University of Wisconsin – Madison. Additionally, he is co-director of The Phonology Clinic and principal investigator on the Phonology Project at the Waisman Center. He is the chair of the ASHA Ad Hoc Committee on Apraxia of Speech in Children. Dr. Shriberg’s principal research interests focus on the nature and origin of childhood speech disorders, including studies to identify diagnostic markers for clinical subtypes and studies to develop subtype-specific treatment technologies, one such disorder being childhood apraxia of speech. He is also a member of Apraxia Kids’s Professional Advisory Board.]

© Apraxia-KIDS℠ – A program of The Childhood Apraxia of Speech Association (Apraxia Kids)
www.apraxia-kids.org

The Purpose of Genetic Testing and Its Relevance to Children with Apraxia

Published 2009 | By Heidi Feldman, M.D., Ph.D.

The purpose of genetic testing is to provide a genetic diagnosis and to provide as much information as possible to patients and families. First, the information may explain why a child, in this case, has a disorder. Understanding the cause of a disorder is helpful to many families. Second, if the testing reveals a known condition it may provide information about prognosis. Some conditions are associated with various health conditions or behavioral profiles, or levels of functioning. It allows the team and family to prepare, and when possible prevent an adverse outcome. Third, in some cases, the results provide information on recurrence risk. Families may want to have an estimate of the chances another child could be similarly affected. Finally, as we learn more about what the genes do, specific treatments may become available to normalize the biochemical internal environment, if not the gene itself.

The findings of a genetics evaluation are becoming more and more complex and interesting. A new concept, copy number variant (CNV), has entered the vocabulary. It refers to the phenomenon that individuals may have bits of chromosomes that are missing, duplicated, rearranged, or in other ways different from the usual. The phenomenon was uncovered through the Human Genome Project. We did, in the past, think that this was invariably a serious problem for the individual. However, with the new tools available, it turns out that many apparently normal folks have CNV, as it is abbreviated. It is not at all rare. What is not clear is why some CNVs are associated with specific or general problems and others are not. One hypothesis is the size of the CNV that is important. Another hypothesis is the specific bit of DNA that is duplicated or deleted. Certain areas of the genome are more susceptible to CNV than other areas. We often have clinical conditions associated with these CNVs. So, William syndrome and DiGeorge syndrome are CNVs. However, the correlation between the size of the deletion and the symptoms is not high.

Another complication is that the same CNV may be associated with different clinical conditions. So, for example, duplication of Chromosome 15 q11-13 is associated with cognitive impairment, autism, and schizophrenia. What accounts for variation in the phenotype is also still unclear. Another complication is that a CNV may be detected and yet be irrelevant to the child’s condition. The geneticists may need to run a control sample. The parents may be asked to provide a blood sample too. So, the information revealed by genetics testing may not clarify and may actually confuse parents.

At this point, historically, we do not know the implications of many of the abnormalities now uncovered through new testing methods. Some families may have heightened worries about genetics testing. With so much unknown, it is unclear whether the best course of action is to avoid the testing altogether or to seek professional and parent-to-parent support if an abnormality is detected. I vote for support. It is through the testing that we will eventually learn what we need to know.Final issue: The results of genetic testing do not change the child, only our understanding of the child’s condition. The child’s educational, behavioral, and therapuetic programs rarely change based on the results. More importantly, the need for good parenting and all that it entails –love, education, discipline, support –remain essential, whether the child has a genetic variation or not.


[Heidi Feldman is the Ballinger-Swindells Professor of Developmental and Behavioral Pediatrics at Standford University School of Medicine. She is also the Medical Director of the Development and Behavior Unit at Lucille Packard Children’s Hospital. Dr. Feldman has a long-standing research interest in child speech and language. She has published research on childhood apraxia of speech, typical and atypical child language, the developmental implications of otitis media with effusion, children with neuronal injuries and language learning, and the delivery of health care to children with special health care needs. She is a member of the Professional Advisory Board of the Childhood Apraxia of Speech Association of North America.]

© Apraxia-KIDS℠ – A program of The Childhood Apraxia of Speech Association (Apraxia Kids)
www.apraxia-kids.org

INTERESTED IN LEARNING MORE?

CHECK OUT THIS RELATED WEBINAR!

This webinar provides a case-based introduction to the world of genetics with a special emphasis on childhood apraxia of speech (CAS).

This webinar provides a case-based introduction to the world of genetics with a special emphasis on childhood apraxia of speech (CAS). Using the examples of individuals and families with CAS, basic concepts of genetics are illustrated, including chromosomes, genes, mutations, deletions/duplications, and modes of inheritance. Knowledge of genetics has many practical implications, for instance early identification of infants at risk, watching for early signs of the disorder, and developing early interventions.

What Causes CAS?

What Causes CAS and Is It Preventable?

First, it is important for parents to understand that there is most likely nothing that you did to “cause” your child’s speech disability.   It is not about how much you talked to your child or whether or not you had them in daycare, for example.  Your child does not have apraxia because you separated from your spouse or because you moved to a new city.  So while we know that parents have a strong role in healthy child development, unless there was abuse, neglect, or isolation, you are not responsible for causing your child’s speech problems.

The current knowledge that we have about CAS is this.  Childhood Apraxia of Speech may occur in the following 3 conditions:

  • Neurological impairment caused by infection, illness or injury, before, during or after birth.  This category includes children with positive findings on MRI’s (scans) of the brain, or those with brain injury or trauma, etc.
  • Complex Neurodevelopmental Disorders – We know that CAS can occur as a secondary characteristic of other conditions such as genetic, metabolic, and/or mitochondrial disorders.  In this category would be Childhood Apraxia of Speech that occurs with Autism, Fragile X, Galactosemia, some forms of Epilepsy, and some types of chromosome translocations, duplications and/or deletions (genetic conditions).  There are quite a few disorders in which CAS can arise, but that does not mean that all children with these disorders also have CAS.  For example, many children with Galactosemia have a speech problem, and out of those children, only some of them have CAS.  Only some children with autism also have CAS.  Only some children with epilepsy have CAS and so forth.
  • Idiopathic Speech Disorder (a disorder of “unknown” origin) – with this condition, we currently don’t know “why” the child has apraxia of speech.  Children do not have observable neurological abnormalities or easily detected neurodevelopmental conditions.

Some speculate that CAS and other childhood conditions may be a result, in part, of environmental conditions such as exposure to pollutants and toxins before or after birth.   Others speculate that nutritional deficits or malabsorbtions cause CAS.  While toxins and nutritional deficits do cause some developmental problems, to date these theories, as they relate specifically to CAS, are only speculations with no research evidence to support them.

That said, a child’s positive health will contribute to their ability to benefit from their learning exposures every day and from therapy designed to help them.  A child who is healthy is more fully capable of taking advantage of opportunities to learn.  Children who are sick frequently with ear and sinus infections, enlarged tonsils and adenoids, asthma, allergies or have sleep disturbances, attention and behavioral difficulties are going to find it much more difficult to benefit from the help provided.  Helping your child be healthy and thus more “present” and available to the learning opportunities around them is one important way parents can help.

Most likely in the future we will learn that CAS is caused by multiple factors and conditions, not one.  To the extent that research evidence becomes available that CAS is caused by some factor that can be manipulated to reduce or eliminate it, will determine whether or not it is preventable.  Until then, we do know one very critical thing – that appropriate speech therapy, tailored to the difficulty of speech motor planning and provided frequently, is the single most important opportunity for children with CAS to improve their speech capacity.  Children who are able to maintain optimum health will most likely directly benefit the most from appropriate help.

What do Researchers Know About Genetics and CAS?

By Lawrence Shriberg, Ph.D., CCC-SLP

The primary findings on the genetics of CAS have emerged from studies of a London family (the ‘KE’ family), half of whose members have an orofacial apraxia and a reported apraxia of speech. Reviews of this widely-cited project include technical and more accessible descriptions of the mutation on the FOXP2 gene (located on chromosome 7) that has been linked to family members with CAS. A recent overview by researchers in the London-Oxford group that has studied the KE family for over 15 years provides a useful summary of the genomic and other findings, including a partially annotated bibliography (Vargha-Khadem et al., 2005). In response to the question posed in the present CAS forum, there is space for only brief comment on three aspects of this landmark research.

First, the neural phenotypes (i.e., characteristics) emerging from studies of FOXP2 by researchers in a number of disciplines are consistent with the behavioral phenotypes associated with CAS. FOXP2 is expressed widely in cells distributed throughout the brain, which is consistent with the cognitive, language, speech, prosody and other challenges observed in children with suspected CAS. Moreover, findings indicating that FOXP2 is expressed in both sides of the brain, rather than in just one hemisphere, are consistent with the severity and persistence of CAS during and often beyond the developmental period. Recent studies of several species of songbirds (Teramitsu et al., 2004) indicate that FOXP2 is especially active during the periods in which young birds learn their specific calls, providing an attractive animal model for studying comparable processes in children learning the speech and prosodic patterns of their language and local dialect. A complexity in this research is that the gene products of FOXP2 function primarily as switches that regulate other ‘downstream’ genes. Thus, although a great deal is known about FOXP2, the major challenge ahead is to understand the individual and collective effects of the downstream genes it controls-specifically, growth and development of the neural circuits underlying speech-language acquisition and performance. The London and Oxford research groups have recently received grants to do just that, using powerful techniques in bioinformatics and molecular neuroscience. Findings from these studies, which will be reported over the next few years, are expected to address fundamental questions about the developmental neurobiology of verbal trait disorders, including CAS.

A second promising development is that in the past year, three research groups have described case findings supporting the etiologic role of FOXP2 in CAS. The London-Oxford researchers recently reported that in a study of 43 children identified as having CAS, one child (and his affected sibling and their mother) had the same FOXP2 mutation observed in affected members of the KE family (MacDermot et al., 2004). A research group in the United States has reported CAS, as well as dysarthria, in a mother and daughter with a chromosome translocation in a region affecting FOXP2 (Shriberg et al., 2005). A Canadian group has identified a FOXP2 deficit in a child who reportedly has CAS, as well as a craniofacial dysmorphology (Zeesman et al., 2004).

Finally, although FOXP2 appears to be linked to CAS in these new case reports, it is likely that there are other genetic influences underlying alternative forms of CAS. Note that the FOXP2 mutation was identified in only one of the 43 children in the study cited above, leaving unexplained the origin of the other CAS diagnoses. Also, the FOXP2 mutation was not found in an unpublished study of children with suspected CAS (Barbara Lewis, personal communication). In addition to the idiopathic form of CAS (i.e., CAS occurring without other neurodevelopment involvements), apraxia of speech has been reported symptomatically in disorders such as Fragile X, autism, galactosemia, and some forms of epilepsy. Thus, another research challenge is to determine if there may be subtypes of CAS associated with different genetic backgrounds. On this issue, there appears to be notable recent convergence on the perspective that both typical and atypical communication development are controlled by common ‘generalist’ genes, rather than different ‘specialist’ genes (Plomin & Kovas, 2005.) This fundamental distinction is important for continuing research on the genetic origins of CAS. It suggests that in addition to searching for single genes underlying CAS, emphasis should also be placed on identifying interactions among groups of genes, each contributing to the form and severity of CAS. Information on such neural phenotypes, that may also be common to other verbal trait disorders, should in turn, help researchers better define and treat the behavioral characteristics of CAS.

Citations

MacDermot, K.D., Bonora, E., McKenzie, F., Smith, R.L., Sykes, N., Coupe, A-M., et al. (2004, October). Identification of FOXP2 truncation as a novel cause of nonsyndromic developmental speech disorder. Poster session presented at the annual meeting of The American Society of Human Genetics, Toronto, Canada.

Plomin, R. & Kovas, Y. (in press). Generalist genes and learning disabilities. Psychological Bulletin.
Shriberg, L.D., Ballard, K.J., Tomblin, J.B., Duffy, J.R., & Odell, K.H. (2005). Speech, prosody, and voice characteristics of a mother and daughter with a 7;13 translocation affecting FOXP2. Manuscript submitted for publication.

Teramitsu, I., Kudo, L.C., London, S.E., Geschwind, D.H., & White, S.A. (2004). Parallel FOXP1 and FOXP2 expression in songbird and human brain predicts functional interaction. Journal of Neuroscience, 24, 3152-3163.

Vargha-Khadem, F., Gadian, D.G., Copp, A., & Mishkin, M. (2005). FOXP2 and the neuroanatomy of speech and language. Neuroscience, 6, 131-138.
Zeesman, S., Nowaczyk, M.J.M., Teshima, I., Roberts, W., Oram Cardy, J., Brian, J., et al. (2004, October). Speech and language impairment and oromotor dyspraxia due to deletion of 7q31 which involves FOXP2. Poster session presented at the annual meeting of The American Society of Human Genetics, Toronto, Canada.


[Dr. Lawrence Shriberg is Professor of Communication Disorders at the University of Wisconsin – Madison. Additionally, he is co-director of The Phonology Clinic and principal investigator on the Phonology Project at the Waisman Center. He is the chair of the ASHA Ad Hoc Committee on Apraxia of Speech in Children. Dr. Shriberg’s principal research interests focus on the nature and origin of childhood speech disorders, including studies to identify diagnostic markers for clinical subtypes and studies to develop subtype-specific treatment technologies, one such disorder being childhood apraxia of speech. He is also a member of Apraxia Kids’s Professional Advisory Board.]

© Apraxia-KIDS℠ – A program of The Childhood Apraxia of Speech Association (Apraxia Kids)
www.apraxia-kids.org

The Purpose of Genetic Testing and Its Relevance to Children with Apraxia

Published 2009 | By Heidi Feldman, M.D., Ph.D.

The purpose of genetic testing is to provide a genetic diagnosis and to provide as much information as possible to patients and families. First, the information may explain why a child, in this case, has a disorder. Understanding the cause of a disorder is helpful to many families. Second, if the testing reveals a known condition it may provide information about prognosis. Some conditions are associated with various health conditions or behavioral profiles, or levels of functioning. It allows the team and family to prepare, and when possible prevent an adverse outcome. Third, in some cases, the results provide information on recurrence risk. Families may want to have an estimate of the chances another child could be similarly affected. Finally, as we learn more about what the genes do, specific treatments may become available to normalize the biochemical internal environment, if not the gene itself.

The findings of a genetics evaluation are becoming more and more complex and interesting. A new concept, copy number variant (CNV), has entered the vocabulary. It refers to the phenomenon that individuals may have bits of chromosomes that are missing, duplicated, rearranged, or in other ways different from the usual. The phenomenon was uncovered through the Human Genome Project. We did, in the past, think that this was invariably a serious problem for the individual. However, with the new tools available, it turns out that many apparently normal folks have CNV, as it is abbreviated. It is not at all rare. What is not clear is why some CNVs are associated with specific or general problems and others are not. One hypothesis is the size of the CNV that is important. Another hypothesis is the specific bit of DNA that is duplicated or deleted. Certain areas of the genome are more susceptible to CNV than other areas. We often have clinical conditions associated with these CNVs. So, William syndrome and DiGeorge syndrome are CNVs. However, the correlation between the size of the deletion and the symptoms is not high.

Another complication is that the same CNV may be associated with different clinical conditions. So, for example, duplication of Chromosome 15 q11-13 is associated with cognitive impairment, autism, and schizophrenia. What accounts for variation in the phenotype is also still unclear. Another complication is that a CNV may be detected and yet be irrelevant to the child’s condition. The geneticists may need to run a control sample. The parents may be asked to provide a blood sample too. So, the information revealed by genetics testing may not clarify and may actually confuse parents.

At this point, historically, we do not know the implications of many of the abnormalities now uncovered through new testing methods. Some families may have heightened worries about genetics testing. With so much unknown, it is unclear whether the best course of action is to avoid the testing altogether or to seek professional and parent-to-parent support if an abnormality is detected. I vote for support. It is through the testing that we will eventually learn what we need to know.Final issue: The results of genetic testing do not change the child, only our understanding of the child’s condition. The child’s educational, behavioral, and therapuetic programs rarely change based on the results. More importantly, the need for good parenting and all that it entails –love, education, discipline, support –remain essential, whether the child has a genetic variation or not.


[Heidi Feldman is the Ballinger-Swindells Professor of Developmental and Behavioral Pediatrics at Standford University School of Medicine. She is also the Medical Director of the Development and Behavior Unit at Lucille Packard Children’s Hospital. Dr. Feldman has a long-standing research interest in child speech and language. She has published research on childhood apraxia of speech, typical and atypical child language, the developmental implications of otitis media with effusion, children with neuronal injuries and language learning, and the delivery of health care to children with special health care needs. She is a member of the Professional Advisory Board of the Childhood Apraxia of Speech Association of North America.]

© Apraxia-KIDS℠ – A program of The Childhood Apraxia of Speech Association (Apraxia Kids)
www.apraxia-kids.org

INTERESTED IN LEARNING MORE?

CHECK OUT THIS RELATED WEBINAR!

This webinar provides a case-based introduction to the world of genetics with a special emphasis on childhood apraxia of speech (CAS).

This webinar provides a case-based introduction to the world of genetics with a special emphasis on childhood apraxia of speech (CAS). Using the examples of individuals and families with CAS, basic concepts of genetics are illustrated, including chromosomes, genes, mutations, deletions/duplications, and modes of inheritance. Knowledge of genetics has many practical implications, for instance early identification of infants at risk, watching for early signs of the disorder, and developing early interventions.



Credentials:
Hours of Operation:
Treatment locations:
Address:

,
Phone:
Email:

Overall Treatment Approach:
   

Percent of CAS cases:

Parent Involvement:
   

Community Involvement:
   

Professional consultation/collaboration:

Min Age Treated:

Max Age Treated:

Insurance Accepted: