Expressive language disorder

Expressive language disorder
Classification and external resources
Specialty psychiatry
ICD-10 F80.1

Expressive language disorder is a communication disorder in which there are difficulties with verbal and written expression.[1] It is a specific language impairment characterized by an ability to use expressive spoken language that is markedly below the appropriate level for the mental age, but with a language comprehension that is within normal limits.[2] There can be problems with vocabulary, producing complex sentences, and remembering words,[3] and there may or may not be abnormalities in articulation.[2]

As well as present speech production, very often, someone will have difficulty remembering things. This memory problem is only disturbing for speech; non-verbal or non-linguistically based memory will be unimpaired. An example of a child with expressive language disorder can be seen here.

Expressive language disorder affects work and schooling in many ways. It is usually treated by specific speech therapy, and usually cannot be expected to go away on its own.

Expressive language disorder can be further classified into two groups: developmental expressive language disorder and acquired expressive language disorder. Developmental expressive language disorder currently has no known cause, is first observed when a child is learning to talk, is more common in boys than girls, and is much more common than the acquired form of the disorder. Acquired expressive language disorder is caused by specific damage to the brain by a stroke, traumatic brain injury, or seizures.

Care must be taken to distinguish expressive language disorder from other communication disorders, sensory-motor disturbances, intellectual disability and/or environmental deprivation (see DSM-IV-TR criterion D). These factors affect a person's speech and writing to certain predictable extents, and with certain differences.

Careful diagnosis is also important because "atypical language development can be a secondary characteristic of other physical and developmental problems that may first manifest as language problems".[4]

Models of language production

Willem Levelt outlined the currently accepted theory of speech production. Words are produced after the concept waiting to be produced is conceptualized, related words are selected, encoded and the sound waves of speech are produced.[5]

Association with language networks

There is also a lot of debate about whether specific language impairments, such as expressive language disorder, are caused by deficits in grammar or by a deficit in processing language information.[6] However, an alternative hypothesis to the cause of SLIs has been posited, called the Procedural Deficit Hypothesis. The Procedural Deficit Hypothesis opines that we can explain language impairments due to abnormal development of brain structures that are involved in procedural memory, our memories that remember how to perform different cognitive and motor tasks. The procedural memory system is associated with basal-ganglia circuits in the frontal lobe and further investigation of this particular hypothesis could aid in the development of a clinical neurological picture of what the underlying causes of SLI are.[7]

Scientific studies of speech and language

Some of the earliest neuroscientific discoveries were related to the discovery that damage to certain areas of the brain related to impairments in language, such as the discovery of Wernicke's area and Broca's area. Lesions in these parts of the brain impair language comprehension and language production, respectively. Paul Broca was the first to note that the left hemisphere of the brain appeared to be localized for language function, particularly for right handed patients. Modern neuroscientific research has verified this, though language may be lateralizaed to the right hemisphere in some right-handed individuals.[8][9]

Developmental verbal dyspraxia

In 1990, it was reported that the several generations of the KE family suffered from developmental verbal dyspraxia and orofacial praxis that were inherited in a typical autosomal dominant pattern.[10] Further analysis traced this inheritance pattern back to mutations in the FOXP2 genes.[11][12] These studies have allowed scientists to begin to investigate how changes to one gene can alter human communication.

FOXP2 is the first gene that has been identified that is specifically linked to speech and language production. Mutant alleles of the normal FOXP2 gene have been found to be the cause of severe speech impairments.[11]

Specific language impairment

Neuroimaging techniques, such as structural and functional MRI, found no significant differences between individuals with SLI and normal controls. However, more subtle and sophisticated techniques, such as voxel-based morphometry studies have allowed researchers to identify bilateral abnormalities in neural volume in areas of the brain associated with motor functions, such as the caudate nucleus, in the affected members of the KE family when compared to the unaffected family members. This volume reduction showed a high correlation between reduced volume and tests of oral praxis, supporting the idea that odd development of the caudate nucleus is related to the problems in motor control observed in the KE family.[11]

Due to the vague nature of the diagnosis of expressive language disorder, there is little specific scientific research that we can currently locate. A larger body of research exists around neuroscientific studies with children diagnosed with a specific language impairment (SLI). fMRI studies have shown that children with SLI have a significantly smaller left hemispheric pars triangularis (Broca's area) and asymmetry of dominance of language structures, as opposed to the more typical left hemisphere dominance.[13] Scientists are beginning to elucidate differences in activation patterns in children with SLIs using neuroimaging techniques to capture brain activity while performing different cognitive tasks. A major observation is lack of left hemisphere lateralization in major language structures such as the inferior frontal gyrus-opercularis, inferior frontal gyrus-triangularis, supramarginal gyrus and superior temporal gyrus. The same study reported hypoactivation and hyper activation of other brain regions - the supramarginal junction and anterior insula, respectively.[14] Other in-depth imaging studies report finding previously undiagnosed lesions in the brains of children with well-characterized developmental language development.[15] Together, these findings strongly suggest that language impairments are the result of an underlying neurological defect in an area of the brain related to language.

Studies looking at long-term outcomes for individuals with specific language impairments such as expressive language disorder track these individuals from childhood to adulthood. As Whitehouse and his colleagues [16] suggest, "When childhood language problems persist into adulthood, they can have far reaching consequences in terms of academic, social and vocational outcomes." These researchers found that children diagnosed with an SLI would have persistent problems with language and are more likely to pursue vocational training rather than university, thereby avoiding professions requiring high levels of literacy. A lower socioeconomic status was also noted by adults who were diagnosed with an SLI as a child. Whitehouse [16] also reported that these adults had more difficulties in establishing friendships, most likely due to a decreased ability to express themselves socially.

Current educational interventions for students with an SLI

Specific language impairments are often secondary characteristics of other disorders such as autism spectrum disorder and attention deficit hyperactivity disorder. In these cases, issues with speech and language are often not treated specifically, but rather attention is given to the primary complaint. Due to the high correlation of an SLI with other disorders, it is difficult to tell the difference between "pure SLI" or language impairments due to the presence of another disorder.[17]

The focus and attention on the need for effective literacy instruction in the current educational climate is large. It is widely recognized that literacy needs to be taught across all curricula and verbal fluency correlates positively academic achievement. Literacy strategies are now being taught in an inclusive manner, rather than the traditional pull-out system, it is assumed that successful teaching strategies for high needs students are good for all students. Basic principles for interventions for students with a specific language impairment follow - the necessity to set specific goals, to manipulate the classroom environment and curricula so that there are many opportunities to use grammar effectively, the importance of consistently modelling high quality speech, the use of a wide variety of text and literature, and to value comprehension as the most important goal for students to achieve.[18] There is no current cure-all intervention for students with SLIs, however, this is an ever expanding field of research.

Special education coding

Students diagnosed with an expressive language disability usually qualify for extra educational supports and assistance in school.

In Alberta schools

An expressive language disability or delay in kindergarten age children is classified as a Communication Disability/Delay under a Code 30. If there is no marked improvement in the child's ability to express themselves verbally once the student enters Grade 1, a child can be given a Code 57 for a Communication Disability. This diagnosis must be given from a Speech-Language Pathologist in order for the child to receive continued special education funding.[19]

See also

References

  1. ↑ "Expressive language disorder". The Better Health Channel (BHC).
  2. 1 2 "F80.1 Expressive language disorder". ICD-10 Version:2010.
  3. ↑ "Expressive language disorder - developmental". MedlinePlus Medical Encyclopedia.
  4. ↑ McLaughlin MR (May 2011). "Speech and language delay in children". Am Fam Physician. 83 (10): 1183–8. PMID 21568252.
  5. ↑ Levelt WJ (November 2001). "Spoken word production: a theory of lexical access". Proc. Natl. Acad. Sci. U.S.A. 98 (23): 13464–71. PMC 60894 Freely accessible. PMID 11698690. doi:10.1073/pnas.231459498.
  6. ↑ Joanisse MF, Seidenberg MS (July 1998). "Specific language impairment: a deficit in grammar or processing?". Trends Cogn. Sci. (Regul. Ed.). 2 (7): 240–7. PMID 21244922. doi:10.1016/S1364-6613(98)01186-3.
  7. ↑ Ullman MT, Pierpont EI (June 2005). "Specific language impairment is not specific to language: the procedural deficit hypothesis". Cortex. 41 (3): 399–433. PMID 15871604. doi:10.1016/s0010-9452(08)70276-4.
  8. ↑ Knecht S, Deppe M, Dräger B, et al. (January 2000). "Language lateralization in healthy right-handers". Brain. 123 (1): 74–81. PMID 10611122. doi:10.1093/brain/123.1.74.
  9. ↑ Pujol J, Deus J, Losilla JM, Capdevila A (March 1999). "Cerebral lateralization of language in normal left-handed people studied by functional MRI". Neurology. 52 (5): 1038–43. PMID 10102425. doi:10.1212/WNL.52.5.1038.
  10. ↑ Hurst JA, Baraitser M, Auger E, Graham F, Norell S (April 1990). "An extended family with a dominantly inherited speech disorder". Dev Med Child Neurol. 32 (4): 352–5. PMID 2332125. doi:10.1111/j.1469-8749.1990.tb16948.x.
  11. 1 2 3 Vargha-Khadem F, Gadian DG, Copp A, Mishkin M (February 2005). "FOXP2 and the neuroanatomy of speech and language" (PDF). Nat. Rev. Neurosci. 6 (2): 131–8. PMID 15685218. doi:10.1038/nrn1605.
  12. ↑ Liégeois F, Baldeweg T, Connelly A, Gadian DG, Mishkin M, Vargha-Khadem F (November 2003). "Language fMRI abnormalities associated with FOXP2 gene mutation". Nat. Neurosci. 6 (11): 1230–7. PMID 14555953. doi:10.1038/nn1138.
  13. ↑ Gauger LM, Lombardino LJ, Leonard CM (December 1997). "Brain morphology in children with specific language impairment". J. Speech Lang. Hear. Res. 40 (6): 1272–84. PMID 9430748. doi:10.1044/jslhr.4006.1272.
  14. ↑ de Guibert C, Maumet C, Jannin P, et al. (October 2011). "Abnormal functional lateralization and activity of language brain areas in typical specific language impairment (developmental dysphasia)". Brain. 134 (Pt 10): 3044–58. PMID 21719430. doi:10.1093/brain/awr141.
  15. ↑ Webster RI, Erdos C, Evans K, et al. (August 2008). "Neurological and magnetic resonance imaging findings in children with developmental language impairment". J. Child Neurol. 23 (8): 870–7. PMID 18660471. doi:10.1177/0883073808315620.
  16. 1 2 Whitehouse AJ, Watt HJ, Line EA, Bishop DV (2009). "Adult psychosocial outcomes of children with specific language impairment, pragmatic language impairment and autism". Int J Lang Commun Disord. 44 (4): 511–28. PMC 2835860 Freely accessible. PMID 19340628. doi:10.1080/13682820802708098.
  17. ↑ Hans Van Balkom; Verhoeven, Ludo Th (2004). Classification of developmental language disorders: theoretical issues and clinical implications. Hillsdale, N.J: Lawrence Erlbaum Associates. ISBN 0-8058-4122-9. OCLC 803128031.
  18. ↑ Fey ME, Long SH, Finestack LH (February 2003). "Ten principles of grammar facilitation for children with specific language impairments". Am J Speech Lang Pathol. 12 (1): 3–15. PMID 12680809. doi:10.1044/1058-0360(2003/048).
  19. ↑ Alberta Education Special Education Coding Criteria 2011/2012.

Further reading

This article is issued from Wikipedia. The text is licensed under Creative Commons - Attribution - Sharealike. Additional terms may apply for the media files.