by Chloe E Robbins, The University of Arizona
The human central auditory nervous system (CANS) is responsible for processing and maintaining the integrity of sound stimuli, both simple and complex, from the peripheral auditory system for interpretation at the cortical level. When pathologies arise in this system, abilities such as understanding speech, localization, lateralization, and discrimination of signals can become significantly impaired. If the anatomy of the CANS is compromised, the proper functioning of the system cannot be maintained. The etiological basis of central auditory processing disorder (CAPD) can be divided into three categories: neurological disorders (traumatic brain injury, seizure disorders, cerebrovascular accidents, etc.), myelin maturational delay, and neuromorphological abnormalities such as polymicrogyria, ectopic areas, and migrational problems (Chermak & Musiek, 2011).
Neuromorphological abnormalities have been noted in numerous individuals who present with learning problems, with one of these problems being developmental dyslexia. These anatomic abnormalities are often found in the perisylvian region of the left hemisphere, which is primarily an auditory area. Demonet, Taylor, & Chaix (2004) define developmental dyslexia as “an unexpected, specific, and persistent failure to acquire efficient reading skills despite conventional instruction, adequate intelligence, and sociocultural opportunity” (p. 1451). Diaz, Hintz, Kiebel, & von Kriegstein (2012) cite developmental dyslexia as the most common learning disability with a prevalence of 5% to 10% in children (p. 13841). Drake (1968) was one of the first to report on postmortem anatomical findings in an individual with a developmental learning disability. Upon examination, several ectopic areas were found in the white matter of the brain (Drake, 1968, p. 19). The cause of these neuromorphological abnormalities has been cited as congenital. Chermak & Musiek (2011) discuss ectopic areas as “small nests of normal cells [in an abnormal place]” and polymicrogyria as “underdeveloped gyri in greater number than seen in normal brains” (p. 241). In 2005, Barkovich, Kuzniecky, Jackson, Guerrini, & Dobyns classified perisylvian polymicrogyria as a condition caused by abnormal cortical organization (including late neuronal migration). If these ectopic areas and polymicrogyria are sufficient enough in size and number, auditory processing ability will be negatively affected.
Following Drake, Galaburda began publishing findings of the same nature. In 1985, Galaburda, Sherman, Rosen, Aboitiz, & Geschwind studied four brains of individuals with known developmental dyslexia. Upon examination, it was found that all four brains contained cortical developmental abnormalities in the frontal and superior temporal gyri. The majority of these anomalies were present in the left hemisphere and two of the brains showed polymicrogyria as part of these irregularities in structure.
Galaburda et al. (1985) state, “The lesions seen in these brains are developmental anomalies acquired some time before birth, probably during the middle of gestation, a time that coincides with peak rates of neuronal migration from the germinal zones to the cerebral cortex” (p. 229). It was also reported that a majority of the lesions were located in the perisylvian regions of the left hemisphere and had an effect on the frontal and superior temporal gyri. These findings illustrate that the anatomical variations found in these brains were affecting auditory structures and subsequently, their cortical connections to cognitive areas of the brain. In addition to abnormalities in the cortex, the authors found cortical symmetry in the planum temporale in all four brains. Galaburda et al. discuss that most brains from individuals who do not have neurological problems show an asymmetry of the planum temporale with the larger structure being found in the left hemisphere, which was shown by Geschwind & Levitsky in 1968. The asymmetry of the planum temporale in normal subjects and the symmetry that exists in those with developmental dyslexia has been confirmed in numerous studies including Hynd, Semrud-Clikeman, Lorys, Novey & Eliopulos (1990), Larsen (1990), Beaton (1997), Morgan & Hynd (1998), Hugdahl, Heiervang, Ersland, Lundervold, Steinmetz & Smievoll (2003), and Bloom, Garcia-Barrera, Miller, Miller & Hynd (2013). An illustration of a typical brain with asymmetry of the planum temporale can be seen in Figure 1.
Following Galaburda’s work in 1985, Galaburda, Menard & Rosen published a paper in 1994 in which they measured the cross-sectional neuronal area of the medial geniculate nuclei (MGN) in five dyslexic and seven control brains. They decided to undergo this examination due to the report of abnormal auditory processing noted in dyslexics. Upon examination, it was found that the dyslexic group showed a right-left asymmetry of MGN neuron size while the controls had symmetry in this area. The dyslexics also had significantly smaller MGN neurons on the left side. More small neurons and fewer large neurons were seen overall in the dyslexic brains compared to the control group, as well as in the left MGN specifically. It is from this study that Galaburda et al. determine that the problems that characterize developmental dyslexia may be a result from auditory processing deficits and not deficits localized solely in the language areas of the brain.
In 2004, Ramus examined the neurobiology of dyslexia and discussed the two theories regarding its pathophysiology. These two views can be categorized into the phonological theory and the magnocellular theory. Ramus summarizes the phonological theory as “a specific deficit in the representation and processing of speech sounds…thought to cause difficulty in learning and handling the relationship between letters and speech sounds (grapheme-phoneme correspondences)” (Ramus et al., 2004, p. 720). Alternatively, the magnocellular theory regards sensorimotor deficits, such as auditory processing problems, as having a causal relationship with the phonological deficits as opposed to simply existing with them. Ramus argues that the magnocellular theory cannot stand alone in explaining the cause of developmental dyslexia due to the low prevalence of these symptoms within the dyslexic population as a whole.
In 2012, Diaz, Hintz, Kiebel, & von Kriegstein published a study examining the physiology of the same structures in both dyslexics and controls and attempted to combine aspects of the phonological theory and the magnocellular theory to explain the physiology of developmental dyslexia. In the study, functional magnetic resonance imaging (fMRI) was used to study MGB responses to fast changing speech by measuring changes in blood oxygen level. The experiment consisted of both a phonological task and a speaker task. It was found that the dyslexic individuals performed worse compared to controls for both tasks and that abnormal left MGN activity was noted in the dyslexics for the phonological task when compared to controls. From their findings, Diaz et al. (2012) postulate that the deficits in reading associated with dyslexia are caused in part by abnormalities in the sensory thalami. This information leads to the assumption that if the MGN are not functioning properly, then tasks such as speech perception in noise, phonological processing, speech discrimination, and the ability to process fast stimuli sequences will be compromised. The authors emphasize the role of the MGN in cortical feedback and speech processing, and theorize that by changing the previously held view of the function of the MGN, key components from both the phonological and magnocellular theories become essential in understanding the physiology of developmental dyslexia.
In more recent years, the anatomical deviations and subsequent auditory processing disorders present in those with learning impairments have been studied and reaffirmed by Boscariol. In 2009, Boscariol et al. reported on the auditory processing deficits of 14 year-old twins with perisylvian polymicrogyria who both were diagnosed with specific language impairment (SLI) in childhood. For central auditory processing, testing revealed that one or both twins had an abnormal performance on the dichotic digits—binaural integration task, the right attention condition of the nonverbal dichotic test, as well as the left attention condition for the same task. One of the twins had an abnormal performance on random gap detection testing as well. Apart from these deficits, one or both twins showed impairment in syntax and phonology. In addition, both twins performed low for the following tasks: phonological awareness, school performance test (SPT) written/reading, SPT arithmetic, non-word written/reading, oral speed reading, and text understanding.
The results of the auditory processing tests reaffirm that abnormalities in the perisylvian region negatively affect auditory processing. The children also demonstrated a difference in verbal and performance intelligence, often seen in those with learning disabilities of this nature. Boscariol et al. state that auditory processing deficits can lead to language impairment due to the association between the two areas of the brain.
In 2010, temporal auditory processing in those with developmental dyslexia and cortical malformation was studied by Boscariol, Guimaraes, Hage, Cendes, & Guerreiro. In their study, a group of children with developmental dyslexia and a control group underwent Random Gap Detection Tests. From testing, it was found that the dyslexic group performed significantly poorer than the control group in temporal processing. In addition to the auditory tests, magnetic resonance imaging (MRI) revealed bilateral perisylvian polymicrogyria in seven out of the eleven children in the dyslexic group. There was also less activity in the left perisylvian area of the brain in the dyslexic group as measured by positron emission tomography (PET) and fMRI.
In regards to the results of the temporal auditory processing tests, Boscariol et al. (2010a) states, “Changes in temporal auditory processing make it more difficult to perceive subtle cues in speech resulting in difficulties in phonological processing” (p. 542). The authors also point out that lesions can have effects on distal areas of the brain and affect various functions. The interdependency of phonological processing and auditory processing previously examined by Diaz et al. (2012) is discussed as well, which is key to understanding why auditory processing deficits are found in those with dyslexia.
Boscariol et al. (2010b) published another study examining auditory processing disorders in those with perisylvian syndrome. Two groups comprised their study, with Group I consisting of children with bilateral perisylvian polymicrogyria and Group II consisting of control children. Behavioral auditory tests revealed a statistically significant difference between the two groups in results from dichotic digit tests, non-verbal dichotic tests, and random gap detection tests. Boscariol et al. discuss that there are key central auditory structures on the Sylvian fissure, responsible for sound detection, nonverbal auditory processing, temporal and phonological processing, and visual-auditory integration. Every individual in Group I showed polymicrogyria along the left Sylvian fissure which compromised their central auditory processing abilities. The results from the temporal processing tasks showed a correlation between auditory processing disorders and SLI. These anatomical abnormalities and subsequent performance on temporal central auditory tests offer an explanation for the difficulties that individuals with dyslexia experience in areas of reading, writing, and speech perception.
In 2011, Boscariol et al. examined auditory processing disorders in children with language-learning impairments including SLI and developmental dyslexia. The relationship between the severity of the impairments and the severity of cortical malformations was studied. For this study the children were divided into three groups: children with language-learning impairment and bilateral perisylvian polymicrogyria (Group I), children with language-learning impairment and normal MRI (Group II), and normal children (Group III).
Children in all three groups underwent a neurological examination, MRI, IQ assessment, language evaluation, learning evaluation, and a hearing evaluation consisting of peripheral tests and central auditory processing tests. Boscariol et al. (2011) found that “patients with malformation of cortical development present with a worse performance in areas of language, learning and some tasks of auditory processing than patients with no cortical malformation” (p. 829). Their findings are consistent with the previous data that show that brain anomalies in the perisylvian region can result in decreased performance in auditory, language, and learning abilities. A summary of Boscariol’s functional findings from three of the research articles discussed in this paper is included in Figure 2 below.
As seen through the various research studies that have examined the polymicrogyria and ectopic areas in those with developmental dyslexia and learning disabilities, the areas affected are primarily auditory structures. Although the causal relationship between phonological and sensory deficits remains controversial, the fact remains that the region in which these anatomical abnormalities are located is primarily in the perisylvian region. The perisylvian region comprises the area immediately surrounding the Sylvian fissure and is made up of chiefly auditory areas. Anatomic structures essential for auditory processing such as the insula, Heschl’s gyrus, and the planum temporale are located in this part of the brain.
The anatomical and functional findings from this area of research are essential to understanding the pathology of these learning disabilities and help to show the complex interaction of these auditory structures with other parts of the brain that are essential for reading, writing, and speech perception. These findings show that the ability to perform these oral and written tasks cannot be done without proper central auditory nervous system function, and a breakdown in these functions are often seen alongside developmental dyslexia or other learning disabilities. With the knowledge that auditory structures are most often affected by these abnormalities, further research can be done to determine the best intervention for these individuals in order to improve their auditory processing and subsequent learning deficits.
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Grant numbers P50 AG05681, P01 AG03991, R01 AG021910, P20 MH071616, U24 RR021382 (OASIS data).