| Expressive language disorder | |
|---|---|
| Classification and external resources | |
| 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]
Expressive language disorder is now classified as a specific language impairment or SLI, where a child has failed to acquire normal expressive language even though they have been adequately exposed to language and there is an absence of notable medical or genetic causes.
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 due to the fact that "atypical language development can be a secondary characteristic of other physical and developmental problems that may first manifest as language problems" [4].
Willem Levelt outlined the currently accepted theory of speech production. The different components of production are displayed in the Figure 1. 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.
While there is a large amount of heterogeneity in phenotypes of children with expressive language disorder, in terms of impairment and of severity. We can use language models such as Willem Levelt's to propose that individuals of expressive language order have a block in one or more of the cognitive steps involved in language production. [5]
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]
FOXP2 is the first gene that has been identified that is specifically linked to speech and language production.
FOX gene products are transcription factors, meaning that they bind to specific sequences of DNA, and can regulate the expression of genes. Specifically, they are FOX ([forehead box]) proteins, which are important in embryo development -- affecting genes that control cell growth and differentiation.
FOXP2 genes are mutant alleles of the normal FOXP2 gene. They have been found to the be the cause of severe speech impairments.
In 1990, it was reported that the several generations of the KE family suffered from verbal dyspraxia and orofacial praxis that were inherited in a typical autosomal dominant pattern. [8] Further analysis traced this inheritance pattern back to mutations in the FOXP2 genes. These studies have allowed scientists to begin to investigate how changes to one gene can alter human communication.
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, although we need to note that this is the norm, in some individuals, language is lateralized to the right hand side of the brain [9],[10]
Neuroimaging techniques, such as structural MRI 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 order, 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 [12] 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 [13] Other in-depth imaging studies report finding previously undiagnosed lesions in the brains of children with well-characterized developmental language development. [14] 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 [15] 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.
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.
Students diagnosed with an expressive language disability usually qualify for extra educational supports and assistance in school.
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 give 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]
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