The relationship between motor control and phonology

在过去的20年里,研究人员带有发展性阅读障碍的想法，表明了特定的语音表征损伤的结果。根据这个语音理论,在拼写的字母系统规则并不完全一致。语音赤字也体现在许多任务涉及语音。下面的essay代写范文进行详述。

Abstract
The goal of this study was to investigate the automaticity/cerebellar theory of dyslexia. We tested phonological skills and cerebellar function in a group of dyslexic 8-12 year old children and their matched controls. Tests administered included the Phonological Assessment Battery, postural stability, bead threading, finger to thumb and time estimation. Results: Dyslexic children were found to be significantly poorer than the controls at all tasks but time estimation. About 75% of dyslexics were more than one standard deviation below controls in phonological ability, and 50% were similarly impaired in motor skills. However, at least part of the discrepancy in motor skills was due to dyslexic individuals who had additional disorders (ADHD and/or DCD). The absence of evidence for a time estimation deficit also casts doubt on the cerebellar origin of the motor deficiency. About half the dyslexic children didn't have any motor problem, and there was no evidence for a causal relationship between motor skills on the one hand and phonological and reading skills on the other. Conclusion: This study provides partial support for the presence of motor problems in dyslexic children, but does not support the hypothesis that a cerebellar dysfunction is the cause of their phonological and reading impairment. 
Keywords: dyslexia, reading, phonology, cerebellum, automaticity, motor control

Introduction 
Over the last twenty years, researchers have converged on the idea that developmental dyslexia (henceforth, dyslexia) results from a specific impairment of phonological representations (Bradley & Bryant, 1983; Snowling, 1987; Snowling, 2000; Vellutino, 1979). According to this "phonological" theory (see Figure 1), a dysfunction in some peri-sylvian areas of the left hemisphere of dyslexic individuals is the cause of a deficit of phonological representations or processes. In alphabetic systems where orthographic rules are not entirely consistent, this provokes difficulty with the learning of grapheme-phoneme rules, hence with reading. The phonological deficit is also manifested in many tasks involving speech sounds. Figure 1 here However, parallel work has emphasised that dyslexics may have more general deficits in the auditory, visual and motor domains. 

This work gave rise to a temporal auditory processing theory of dyslexia (Tallal, Miller, & Fitch, 1993), a visual/magnocellular theory (Lovegrove, Bwoling, Badcock, & Blackwood, 1980; Stein & Walsh, 1997), and an automaticity/cerebellar theory (Nicolson & Fawcett, 1990), respectively. Those three theories are compatible with the idea that a phonological deficit is a direct cause of dyslexia, but challenge the specificity of such a deficit. More precisely, it is hypothesised that the phonological defect itself results from a more general auditory impairment (Tallal et al., 1993) or from a motor (articulatory) dysfunction (Nicolson, Fawcett, & Dean, 2001); the visual deficit is also proposed as an additional source of reading difficulties (Stein & Walsh, 1997). The present paper will focus on the cerebellar theory of dyslexia, attempting to replicate the finding that dyslexic children are impaired on a range of tasks designed to tap the cerebellum, and to provide more insight on the relationship between cerebellar function, phonology and reading. We begin with a brief review of the cerebellar theory of dyslexia.

The cerebellar theory of dyslexia: review and questions 
The cerebellar theory (Figure 2) is primarily based on the observation that dyslexic children often show a range of motor impairments, mostly manifested in overall clumsiness, poor manual dexterity, balance and coordination (Denckla, 1985; Haslum, 1989; Wolff, Cohen, & Drake, 1984). Nicolson and Fawcett (1990) proposed that such motor impairments might be the result of mild cerebellar dysfunction, and set out to test cerebellar function more comprehensively in dyslexic children. They showed that dyslexics were significantly impaired on a large number of motor tasks of a cerebellar battery. Depending on the task, between 40 and 100% of dyslexic children had a performance more than 1 SD below that of a same-age control group (Fawcett, Nicolson, & Dean, 1996; Nicolson & Fawcett, 1995). One study provided evidence for cerebellar impairment outside the motor domain: dyslexics were shown to be poorer at a time estimation task (Nicolson, Fawcett, & Dean, 1995), assumed to tap the timing functions of the cerebellum (Ivry & Keele, 1989).

Another key concept proposed is that of automaticity, the ability to learn and perform a task automatically, without conscious monitoring (like cycling or driving). The hypothesis is that automaticity crucially depends on the cerebellum, and that its impairment in dyslexic individuals may play a role in the aetiology of reading difficulties, as well as of more general learning problems. Evidence for poor automaticity in dyslexic children was provided using a dual-task paradigm (Nicolson & Fawcett, 1990), as well as various learning tasks (Nicolson & Fawcett, 1994; Nicolson & Fawcett, 2000). 

Brain imaging studies also provide some insight into dyslexics' cerebellum. Anatomical studies found metabolic abnormalities (Rae et al., 1998), decreased grey matter density (Brown et al., 2001; Eliez et al., 2000), and excessive asymmetry (Leonard et al., 2001). Functional imaging showed reduced activation in a motor sequencing task (Nicolson et al., 1999), in a reading task (Brunswick, McCrory, Price, Frith, & Frith, 1999) and in a word and non-word repetition task (McCrory, Frith, Brunswick, & Price, 2000). Of course, all these studies also found differences between controls and dyslexics in many other areas besides the cerebellum. Unfortunately, few research groups have attempted to replicate Nicolson and Fawcett's basic findings. This implies that the support for their theory is highly dependent on the particular cohort of dyslexic children that they have followed over the years in Sheffield. One study reported a partial replication, using a balance/dual task (Yap & van der Leij, 1994). 

But another one reported a failure to replicate using the very same task (Wimmer, Mayringer, & Landerl, 1998), and subsequent attempts at finding motor/automaticity impairments in dyslexic children were unsuccessful (van Daal & van der Leij, 1999; Kronbichler, Hutzler, & Wimmer, in press). Findings of poor time estimation in dyslexics were also found hard to replicate (Stringer & Stanovich, 1998). Finally, a study investigating implicit learning of sequences found that dyslexics showed automatic learning to the same extent as controls (Kelly, Griffiths, & Frith, in press). It is quite clear that more studies are needed in order to objectively assess the reality of a cerebellar impairment in dyslexia. This is the first goal of the present study. Wimmer et al. (1998) suggested that the reason for the inconsistency between studies might have to do with the presence of attention deficit/hyperactivity disorder (ADHD) in some dyslexic children. 

Indeed, there is evidence for motor problems in ADHD, and there is a high degree of co-morbidity between dyslexia and ADHD. One study of a representative epidemiological sample of 409 children took into consideration 42 children scoring below the 10th percentile in reading comprehension: 6 of them (14%) were also classified as ADHD and 12 others (29%) were classified as sub-threshold ADHD (Kadesjö & Gillberg, 2001). In another study of a more clinically defined group of 162 children with learning/attention problems, 71 (44%) had a looselydefined reading disorder, 30 of which (42%) were also classified as ADHD (Kaplan, Wilson, Dewey, & Crawford, 1998). Wimmer et al. (1998) and van Daal and van der Leij (1999) hypothesised that automaticity impairments might be found only in such co-morbid individuals, implying that they were in significant proportion within the samples studied by Nicolson and Fawcett (1990) and Yap and van der Leij (1994), whereas they had been screened out in their own respective studies. This hypothesis was supported by a new study showing balance problems only in dyslexic/ADHD comorbid children, not in pure dyslexics (Wimmer, Mayringer, & Raberger, 1999).

These results echo similar earlier findings on manual dexterity tasks (Denckla, Rudel, Chapman, & Krieger, 1985). In the same line of argument, it should be noted that developmental co-ordination disorder (DCD; see DSM-IV, 1994, p. 56) is also co-morbid with both dyslexia and ADHD. Indeed, Kadesjö and Gillberg (2001) found that 47% of their ADHD children also had DCD, and Kaplan et al. (1998) found that 69% of their ADHD and 63% of their dyslexic children also had DCD. Since the cerebellar tasks used on dyslexic children are in the motor domain, it seems even more likely that co-morbidity of dyslexia with DCD might contribute to group differences in those tasks. 

Therefore, a second goal of this study will be to ask whether poor performance in cerebellar tasks is due to co-morbidity. Finally, assuming that findings of a cerebellar dysfunction in dyslexia are reliable, the question remains of whether such a defect can explain the reading impairment. A recent review of the cerebellar theory offered an explicit causal model of the involvement of the cerebellum in dyslexia (Nicolson et al., 2001). Between the cerebellum and the various manifestations of dyslexia, three distinct causal pathways are hypothesised: 1) a general motor skill impairment would directly affect writing; 2) its manifestation in speech articulation would affect phonological skills, hence reading; 3) an automaticity impairment would make the acquisition of visual word forms more difficult, which would have consequences both in reading and spelling (see Figure 2). The third goal of the present study is to assess these hypothetical causal links in the light of the results obtained.（essay代写)

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