Motor disorder and anxious and depressive symptomatology: A monozygotic co-twin control approach

Research in Developmental Disabilities 32 (2011) 1245–1252

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Research in Developmental Disabilities

Motor disorder and anxious and depressive symptomatology: A monozygotic co-twin control approach Jillian G. Pearsall-Jones a,b,*, Jan P. Piek a, Daniela Rigoli a, Neilson C. Martin a, Florence Levy c a

School of Psychology and Speech Pathology, Curtin Health Innovation Research Institute, Curtin University, Perth, Western Australia 6845, Australia The Center for Cerebral Palsy, Perth, Western Australia 6929, Australia c School of Psychiatry, University of New South Wales, Sydney, New South Wales 2006, Australia b

A R T I C L E I N F O

A B S T R A C T

Article history: Received 15 April 2010 Received in revised form 12 January 2011 Accepted 20 January 2011 Available online 23 February 2011

The aim of this study was to investigate the relationship between poor motor ability and anxious and depressive symptomatology in child and adolescent monozygotic twins. The cotwin control design was used to explore these mental health issues in MZ twins concordant and discordant for a motor disorder, and controls. This methodology offers the unique opportunity to control for genetic effects and shared environmental influences, and permits the investigation of non-shared environmental influences. The Developmental Coordination Disorder Questionnaire was used to identify 23 sets of twins discordant for a motor disorder, 23 sets concordant for a motor disorder, and 773 sets of twins with no motor disorder from a total sample of 2122 Australian sets of twins. The Strengths and Weaknesses of ADHD Symptoms and Normal Behaviour questionnaire was used to exclude participants with high Attention Deficit Hyperactivity Disorder symptomatology. Anxious and depressive symptomatology were assessed using Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, Text Revision (DSM-IV-TR) based questionnaires on Generalised Anxiety Disorder and Sad Affect. Results indicated significantly higher levels of anxious and depressive symptomatology in twins with a motor disorder in discordant pairs compared to their co-twins without a motor disorder, and controls. There were significantly higher levels of anxious symptomatology in twins with a motor disorder in discordant sets than in sets of twins concordant for a motor disorder. There were significantly higher levels of anxious symptomatology in concordant twins than in controls. Implications of these findings are discussed with emphasis on understanding and recognising the relationship between a motor disorder and anxious and depressive symptomatology in clinical practice for children and adolescents with these disorders. ß 2011 Elsevier Ltd. All rights reserved.

Keywords: Zygosity Discordant Concordant Anxiety Depression Motor disorder ADHD Aetiology

1. Introduction Developmental Coordination Disorder (DCD) is the most common motor disorder of childhood, affecting approximately 6% of children aged 5–11 years (American Psychiatric Association, 2000). The DSM-IV-TR defines DCD as a significant impairment in the development of motor coordination that is diagnosed when motor coordination is markedly poorer than expected for the child’s age and intellectual ability. Movement difficulties must significantly interfere with the individual’s daily life or academic achievement, and must not be due to physical or neurological defects, such as cerebral palsy or hemiplegia. * Corresponding author at: School of Psychology, Curtin University of Technology, GPO Box U1987, Perth 6845, Western Australia, Australia. Tel.: +61 8 9443 0249; fax: +61 8 9266 2464. E-mail address: [email protected] (J.G. Pearsall-Jones). 0891-4222/$ – see front matter ß 2011 Elsevier Ltd. All rights reserved. doi:10.1016/j.ridd.2011.01.042

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DCD has been associated with poorer psychosocial wellbeing than found in typically developing children and adolescents. For instance, in children aged 8–10 years and adolescents aged 12–14 years, Skinner and Piek (2001) found that children with DCD perceived themselves as having poorer social support and being more anxious than children without DCD. Anxiety was found to be higher in adolescents than in 8–10 year olds. In their study on questionnaire data of children with DCD, and semistructured interviews of 12 mothers of these children, Stephenson and Chesson (2008) found that children with DCD experienced emotional problems that mothers reported as anger, frustration, unhappiness, distress, depression, low self esteem, shyness and embarrassment. These mothers also reported that the impact of these difficulties in their children affected the entire family, and at times also the extended family. Using the Children’s Depression Inventory (Kovacs, 1992), Francis and Piek (2003) found that young school age children with DCD reported significantly higher levels of depressive symptomatology in comparison to children without poor coordination. Piek, Barrett, Smith, Rigoli, and Gasson (2010) explored the relationship between anxious and depressive symptomatology in children aged 6–12 years and motor performance as assessed by their parents 11 times between the age of 4 months and 4 years. They found that stability of gross motor scores over this time predicted degree of anxious and depressive symptomatology at school age. Anxiety and depression are recognised as significant mental health problems during childhood and adolescence (Compas, Connor-Smith, & Jaser, 2004; Roberts, 1999), although their relationship to developmental disorders is unclear, just as causal pathways for motor disorders are numerous and unclear (Pearsall-Jones, Piek, & Levy, 2010). In particular, it is unclear whether emotional problems share the underlying aetiology of developmental disorders such as DCD, or are a result of the environmental influences on the child with DCD. Child and adolescent depression has been associated with numerous risk factors, including genetic effects (Rice, Harold, & Thaper, 2002; Thapar & McGuffin, 1994). Studies have shown the importance of both genetic and environmental influences on depression, particularly non-shared intra- and extra-familial environmental experiences (Birmaher et al., 1996; Cytryn & McKnew, 1996). Birmaher and colleagues reviewed the literature on major depression and dysthymic disorder over 10 years prior to 1996. The authors pointed out the importance of exploring the combined effects of the variety of bio-psycho-social correlates that have been identified with the onset and course of early onset depression, including genetic, cognitive and familial factors. Many studies that examine genetic and environmental influences have used twin designs to investigate aetiology. Traditionally, twin studies have focussed on comparisons between dizygotic (DZ) twins, who share approximately 50% of their genes, and monozygotic (MZ) twins, who share up to 100% of their genes. However, developments in science have highlighted epigenetic and other factors that can lead to changes in the phenotype without altering DNA. Eaves, Silberg, and Erkanli (2003), in a study of female twins, highlighted the importance of taking into account epigenetic factors in causal pathways of depression and anxiety. They used a Markov Chain Monte Carlo approach (Gilks, Richardson, & Spielgelhalter, 1996) to explore the relationship between anxiety and depression. They found that genetic influences on pre-pubertal anxiety affected vulnerability to post-pubertal depression. They also found that twins at high genetic risk for anxiety experienced greater levels of adverse environmental factors. Thirdly, they found that those twins with higher risk genetically, and greater liability for the combination of anxiety and depression, were more vulnerable and sensitive to the negative aspects of their environment. In addition, there were genetic vulnerabilities to depression in these twins that increased sensitivity to environmental stress. Other factors that may lead to differences between MZ twins include prenatal exposure or response to infections and toxins (Iwayama, Hosono, Yamamoto, Oshiro, & Ueda, 2007), or at birth, that may affect one twin but not the other (Dulie`ge, Amos, Felton, Biggar, & Goedert, 1995; Forrester, Lees, & Watson, 1966). Discordant outcome may also result from order at birth (Hartley & Hitti, 2005; Smith, Fleming, & White, 2007), or birth presentation and complications (Bjelic-Radisic et al., 2007). A number of studies have concluded that at delivery the second born twin is at higher risk of poor outcome than the first—such as needing intubation or resuscitation, suffering respiratory distress syndrome, and having a lower 5 min Apgar score (Hartley & Hitti, 2005). Hartly and Hitti found a sixfold increase in fetal distress in second compared to first born twins. They attributed this disadvantage to a deterioration in the intrauterine environment following the birth of the first twin. Pearsall-Jones et al. (2008) used the same sample of MZ twins discordant and concordant for a motor disorder as described in the present study, and twins discordant and concordant for ADHD and comorbid motor disorder and ADHD. Second born twins in sets in which neither met criteria for motor disorder nor ADHD were at greater risk for oxygen perfusion difficulties than first born twins. In another study based on a subset of twins from the present study, it was found that twice as many second as first born twins met criteria for a motor disorder. Second born twins attained significantly lower scores on 1 min Apgar, gross motor scores and bimanual dexterity scores (Pearsall-Jones, Piek, Rigoli, Martin, & Levy, 2009). It was argued that oxygen perfusion difficulties before or at birth may be an aetiological factor for some children with a motor disorder. There is little literature on our understanding of motor disorders in relation to the aetiology of common childhood and adolescent mental health disorders such as anxiety and depression. In their study of MZ twins discordant for DCD, Piek et al. (2007) used a MZ twin-differences design (Martin, Boomsma, & Machin, 1997), and found that children and adolescents with DCD had higher levels of depressive symptomatology than did their co-twins without DCD. This co-twin control design, with its focus on MZ twins discordant for physiological and biobehavioural disorders, provides a unique means by which to control for potentially confounding factors such as genotype, gender, age, socioeconomic status, and shared family environment (Vitaro, Brendgen, & Arseneault, 2009). This approach provides the unique opportunity to investigate nonshared environmental influences in these disorders, adding to our understanding of the aetiology of both physiological and biobehavioural disorders.

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The aim of the present study was to use the MZ co-twin control design to determine whether anxious and depressive symptomatology were significantly higher in twins with a motor disorder compared to their co-twin without a motor disorder. Given that, according to Barkley (1990) and others, children with a diagnosis of a motor disorder have a 50% chance of having Attention Deficit Hyperactivity Disorder (ADHD), children and adolescents with high levels of ADHD symptomatology were excluded from the study. It was hypothesised that there would be higher levels of both anxious and depressive symptomatology in twins with a motor disorder compared to their co-twin without a motor disorder. It was also hypothesised that there would be higher levels of emotional symptoms in second born than first born twins because more second than first born twins in discordant sets had a motor disorder. It should be noted that higher levels of depressive symptomatology have been identified for participants with a motor disorder in a similar discordant sample of twins used in the current study (Piek et al., 2007). However, the current study also explores depressive symptomatology in twins concordant for a motor disorder and in control twins without a motor disorder. Importantly, anxious symptomatology has not previously been explored in MZ twins discordant and concordant for a motor disorder in comparison to twins without a motor disorder. 2. Materials and methods 2.1. Participants This study was part of the Australian Twin and Attention Project (Bennett et al., 2006; Levy & Hay, 2001). Participants were recruited from 3180 families of twins aged 6–18 years registered on the voluntary Australian Twin Registry. A total of 2122 Twin and Sibling Questionnaires were returned (66.73%) by major caregivers, primarily mothers. Of these, 47 families were excluded as their twins were outside the study’s age range when parents completed the questionnaire. The total eligible sample of 2075 twin pairs was separated into two groups, MZ and DZ, based on parent report of prior DNA testing or on a zygosity questionnaire. As a result, 922 sets of MZ twins were identified. Using the Developmental Coordination Disorder Questionnaire (DCD-Q – Wilson, Kaplan, Crawford, Campbell, & Dewey, 2000) and the Strengths and Weaknesses of ADHD Symptoms and Normal Behaviour (SWAN – Swanson et al., 2001), which formed part of the Twin and Sibling Questionnaire, twins who met the questionnaire criteria for a motor disorder and ADHD were identified. All twins with insufficient data to establish status for motor ability or ADHD were excluded, as were all twins who met criteria for both a motor disorder and ADHD or ADHD only. The sets of twins who remained formed the sample for the current study: 23 sets discordant for a motor disorder and 23 sets concordant for a motor disorder. From the 773 sets from the larger sample who did not meet the criteria for a motor disorder or ADHD, 23 pairs were selected as the control group, matched for age and sex with the sets of twins discordant for a motor disorder. There were no significant differences between the three groups in gestational age at birth or birth weight. Mean age, range, sex, gestational age and birth weight for each group can be found in Table 1. In order to compare discordant and concordant twins, 23 twins from the concordant group and the control group were matched for birth order (10 first born, 13 second born) with the discordant twins with a motor disorder. DCD-Q scores for these groups can be found in Table 2. DNA zygosity was confirmed for 13 of the 23 twins in the motor disorder discordant group, for six of the 23 twins in the motor disorder concordant group, and seven of the 23 twins in the control group. Given that parent report was the only means for identification of motor disorder in this study, due to the large size of the study sample, it should be noted that individual testing to determine criterion A of the DSM-IV (1994) (American Psychiatric Association, 1994) for DCD could not be examined. Hence the term motor disorder is used rather than DCD. 2.2. Measures 2.2.1. Zygosity assignment The process for designating zygosity was as follows. Parents were asked whether the zygosity of their twins had been confirmed by a test. If they answered ‘Yes’, they were asked to provide information on how this had been ascertained. If they answered ‘No’, or they were unsure, they were asked to complete a twin similarity questionnaire, on which validity has been demonstrated (Cohen, Dibble, Grawe, & Pollin, 1975; Nichols & Bilbro, 1966). This questionnaire had six questions on similarity between the twins (height, weight, facial appearance, hair colour, eye colour, and complexion), for which response choices were ‘Not at all’, ‘Somewhat’, and ‘Exactly’; and six on confusion by others (mother, father, other people in the family,

Table 1 Age, gender, gestational age at birth (GA) and birth weight for motor disorder discordant and concordant twins and controls. Group

Motor disorder discordant (n = 23)

Motor disorder concordant (n = 23)

Control (n = 23)

Mean age in years (SD) Age range in years Males/females (%male/%female) Mean GA at birth in weeks (SD) Mean birth weight in grams (SD)

11.9 (3.7) 6.5–16.7 10/13 (43.5%/56.5%) 36.2 (2.2) 2466 (404)

12.9 (3.3) 6.5–18.0 11/12 (47.8%/52.2%) 35.16 (3) 2363 (609)

12.2 (3.6) 6.4–16.7 10/13 (43.5%/56.5%) 36.35 (2.2) 2449 (472)

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J.G. Pearsall-Jones et al. / Research in Developmental Disabilities 32 (2011) 1245–1252 Table 2 DCD-Q scores of 23 twins with a motor disorder in the discordant group, 23 twins in the motor disorder concordant group and 23 control twins. n = 23 twins

Mean (SD)

Range

Discordant affected Concordant Controls

60.30 (3.04) 57.83 (3.93) 79 (5.61)

53–63 49–63 66–85

strangers; ‘Are they as alike as two peas in pod?’; ‘Do they have very similar personalities?’), for which response choices were ‘Yes’ or ‘No’. They were also asked ‘Did they have one placenta?’ and ‘Do they have the same blood group?’ Discriminant Function Analysis was used to combine these to assess similarity between the twins in terms of personality, appearance, and biology. Zygosity determination from such questionnaires has been shown to have high agreement with zygosity determination using blood tests or genetic markers (McGuffin, Owen, O’Donovan, Thapar, & Gottesman, 1994). All opposite sex twins were assigned as DZ. In cases in which zygosity could not be determined by test or questionnaire, or in which parents assigned zygosity based on unreliable methods only (e.g. ‘shared placenta’ or ‘same blood group’), data were assigned as missing. 2.2.2. Developmental Coordination Disorder Questionnaire (DCD-Q) The DCD-Q (Wilson et al., 2000) parent rated questionnaire features 17 items on a 5 point scale ranging from 1 ‘Not at all like this child’ to 5 ‘Extremely like this child’. The final seven questions are reverse scored. The DCD-Q includes four subtypes: general coordination; control during movement; gross motor/planning; and fine motor/handwriting. Parents are asked to complete the questionnaire by comparing their child to children of the same age. The total score is 85. Because the Twin and Sibling Questionnaire, in which the DCD-Q was embedded, has a four point scale, to make it easier for parents completing the combined questionnaire, the 3 was omitted to make a 4 point scale of 1, 2, 4, 5. For inter-item reliability Cronbach’s alpha was .88 for the full scale and from .86 to .88 for each item if deleted (Martin, Piek, & Hay, 2006). Rather than using a fixed score to assign individuals as affected or unaffected, for this measure the cut-off score was calculated using the formula:

Cut-off score ¼ Mean  ð1:65  Standard Deviation ½SDÞ On this scale a low score assigns the participant to the ‘affected’ group, a high score to the ‘unaffected’ control group (Martin et al., 2006; Pearsall-Jones et al., 2008; Piek et al., 2007). Concurrent validity has been established by Wilson et al. (2000), by correlating the DCD-Q with the Movement Assessment Battery for Children (M-ABC) (Henderson & Sugden, 1992) (r = .59, p < .0001) and the Bruininks–Oseretsky Test of Motor Performance (Bruininks, 1978) (r = .46 to .54, p < .0001). Wilson and colleagues demonstrated the construct validity by finding significant differences in scores between a group without DCD, a group of suspected DCD, and a group with DCD. Schoemaker et al. (2006) and Civetta and Hillier (2008) evaluated the validity and reliability of the DCD-Q using the M-ABC. Both groups concluded that the DCD-Q demonstrated high validity and reliability. Using the McCarron Assessment of Neuromuscular Development (MAND – McCarron, 1997), as the criterion measure, Loh, Piek, and Barrett (2009) found the DCD-Q excellent in identifying children with severe motor deficits. 2.2.3. Strengths and Weaknesses of ADHD Symptoms and Normal Behaviour Symptoms for ADHD were assessed using the parent-rated Strengths and Weaknesses of ADHD Symptoms and Normal Behaviour (SWAN) scale (Swanson et al., 2001), which is based on the 18 ADHD symptoms listed in the DSM-IV (1994). Observations are based on the child’s behaviour over the previous month compared to other children of the same age. Scores range from ‘Far below average’ (scored as +3) to ‘Far above average’ (scored as 3), reflecting both strengths and weaknesses. The scores are summed then divided by nine for the inattention and hyperactivity/impulsivity subscales, and by 18 for the combined subscale to obtain a mean score for each subtype. The SWAN cut-off points between children and adolescents with and without inattention and hyperactivity/impulsivity are calculated from the distribution of scores using the formula:

Cut-off score ¼ Mean þ ð1:65  SDÞ A high score indicates status as ‘affected’, a low score indicates ‘unaffected’. Importantly, this scale is one of few that measures strengths as well as weaknesses. In their study, Martin et al. (2006) reported that Cronbach’s alpha was .95 for both the inattention and hyperactive/impulsive scales, which indicated good internal reliability. 2.2.4. Generalised Anxiety Disorder The Twin and Sibling Questionnaire incorporated the Australian Twin Behaviour Rating Scale (ATBRS), developed specifically for use in the Australian Twin ADHD Project (Levy, Hay, McLaghlin, Wood, & Waldman, 1996). The ATBRS included DSM-IV (1994) based questions to assess for disorders of childhood and adolescence, including ADHD, Conduct

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Disorder, Generalised Anxiety Disorder and Separation Anxiety. There were nine questions for assessment of anxious symptomatology, for example: ‘Shows excessive anxiety and worry about events and activities (e.g., school or work performance)’; ‘This child’s excessive worry is associated with the following complaints: restlessness, feeling ‘keyed up’ or ‘on edge’; easily fatigued; difficulty concentrating or mind ‘going blank’; irritability; muscle tension; sleep disturbance. Symptoms were coded in the same manner as motor disorder and ADHD symptoms. The internal reliability of this scale has shown a high coefficient alpha of .911 (Levy, Hay, Bennett, & McStephen, 2005). This questionnaire does not provide a diagnosis of anxiety, but rather is a reflection of anxious symptomatology, which is the terminology used throughout this paper. 2.2.5. Depressive symptomatology (‘Sad Affect’) Included in the Twin and Sibling Questionnaire were 12 questions for assessment of depressive symptomatology, or Sad Affect, based on DSM-IV (1994) criteria for depression (Hartman et al., 2001). Questions included: ‘Tendency to cry without any reason’; ‘Has a sad facial expression’; ‘Feels worthless’. These items were sourced from a more comprehensive questionnaire that included the ‘Sad Affect’ construct among other childhood internalising and externalising problems (Hartman et al.). Responses for the 12 items are rated on a 4-point scale, and are summed to produce a ‘Sad Affect’ score with a possible total score of 36. Higher scores indicate a greater number of depressive symptoms. An internal reliability of .72 Cronbach’s alpha was found in a twin sample from research involving an earlier wave of the Australian Twin ADHD Project. It also reported a Chronbach’s alpha ranging from .68 to .72 for each item if deleted (Levy, Bennett, Hartman, Hay, & Sergeant, 2006) for the 12-item ‘Sad Affect’ scale. This demonstrates an acceptable internal reliability for the ‘Sad Affect’ scale. This questionnaire does not provide a diagnosis of depression, but rather a reflection of depressive symptomatology, which is the terminology used throughout this paper. 2.3. Procedure The project was approved by the Curtin University Human Research Ethics Committee and by the Australian Twin Registry. The Twin and Sibling Questionnaire was completed by the mother of the twins, or if that was not possible, by a carer who knew all of the children in the family well. Questionnaires were mailed to families. 3. Results 3.1. Paired twin comparisons Means for anxious and depressive symptoms and t-tests for the first born (Twin 1) and second born (Twin 2) for all three groups of 23 sets of twins each can be found in Table 3. Paired-sample two-tailed t-tests showed that there were no significant differences between Twin 1 and Twin 2 for anxious and depressive symptoms in any of the three groups. In the discordant group, there were significantly higher levels of anxious symptomatology (t(20) = 3.589, p = .002) and depressive symptomatology (t(21) = 3.332, p = .003) in twins with a motor disorder. 3.2. Group comparisons Marginal means and standard deviations for anxious and depressive symptoms for the three groups can be found in Table 4. Univariate Analysis of Covariance (with age and sex as covariates) indicated significant group differences for depressive symptoms (F(2,62) = 6.177, p = .004, partial h2 = .166). There were significant group differences for depressive symptoms between motor disorder concordant twins and controls (5.073 vs. 1.821; p = .007), and between affected discordant twins Table 3 Means (SD) and paired samples t-tests for anxious and depressive symptoms in first born (Twin 1) and second born (Twin 2) twins for the sets concordant and discordant for motor disorder and for controls. Motor disorder concordant (n = 23 sets)

Motor disorder discordant (n = 23 sets)

Control (n = 23 sets)

T1

T2

T1

T2

T1

T2

Anxious symptoms

3.00 (3.69) (n = 21) t(20) = .267, p = .792

3.14 (4.29) (n = 21)

4.24 (3.63) (n = 21) t(20) = 2.46, p = .808

4.48 (5.65) (n = 21)

1.50 (2.58) (n = 22) t(21) = .721, p = .479

1.83 (3.16) (n = 23)

Depressive symptoms

5.09 (4.67) (n = 23) t(22) = .000, p = 1.000

5.09 (4.77) (n = 23)

4.59 (4.14) (n = 22) t(21) = .701, p = .491

5.0 (4.27) (n = 22)

1.77 (2.82) (n = 22) t(21) = 1.298, p = .208

2.41 (3.43) (n = 22)

Note: Data on some twins were missing.

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Table 4 Means (SD) for anxious and depressive symptom scores for the motor disorder concordant, motor disorder discordant and control groups. Motor disorder concordant (n = 23 twins)

Anxious symptoms Depressive symptoms

Motor disorder affected discordant (n = 23 twins)

Control (n = 23 twins)

Mean

SD

Mean

SD

Mean

SD

3.286* (n = 21) 5.13*** (n = 23)

4.279 4.779

5.636*,** (n = 22) 5.59y (n = 22)

5.314 4.436

1.318** (n = 22) 1.818***,y (n = 22)

2.495 1.967

Note: Data on some twins were missing. * p = .043. ** p = .001. *** p = .007. y p = .002.

and their co-twins without a motor disorder and controls (5.648 vs. 1.821; p = .002), but not between twins with a motor disorder in discordant sets and twins in concordant sets. Univariate Analysis of Covariance indicated significant group differences for anxious symptoms (F(2,60) = 6.102, p = .004, partial h2 = .169). There was also a significant effect for age (F(1,60) = 4.275, p = .043, partial h2 = .067), with older twins in the discordant group having more anxious symptomology than younger twins. However, using the Bonferroni correction, this was no longer significant at the .01 level. For anxious symptoms, there were statistically significant differences between scores of motor disorder discordant twins and concordant twins (5.636 vs. 3.286; p = .043), and between affected discordant twins and controls (5.636 vs. 1.318; p = .001). 4. Discussion The co-twin control design permitted the investigation of non-shared environmental influences in anxious and depressive symptomatology, which are reflective of disorders that have been associated with motor disorders in childhood and adolescence (Skinner & Piek, 2001). This methodology was used to explore these mental health disorders in MZ twins concordant and discordant for a motor disorder. Firstly, although second born twins have been found to be at higher risk than first born twins for a motor disorder (Pearsall-Jones et al., 2008; Pearsall-Jones et al., 2009), in the current study there were no significant birth order differences for anxious and depressive symptoms. This suggested that symptoms of anxiety and depression were not related to disadvantages to the second born twin in the event of intrauterine compromise following the birth of the first twin, as found by Hartley and Hitti (2005). Skinner and Piek (2001) found that non-twin children and adolescents with a motor disorder reported poorer psychosocial wellbeing, and higher levels of anxious symptomatology, than did children and adolescents without a motor disorder. Francis and Piek (2003) also found higher reported levels of depressive symptomatology in young children with poor coordination in comparison to their peers without poor motor coordination. In the current study, the significantly greater levels of anxious and depressive symptoms in twins with a motor disorder in the discordant group, compared to their co-twin controls (reported by parents), is consistent with the findings by Stephenson and Chesson (2008). They reported that mothers perceived their children with a motor disorder as being angry, distressed and depressed. In the current study, cotwins without a motor disorder in discordant sets were reported by parents as having lower levels of anxious and depressive symptomatology than their co-twins with a motor disorder. This suggested that the aetiology of anxious and depressive symptomatology in these twins was due to non-shared environmental effects (having or not having a motor disorder) rather than to genetic or shared environmental effects. An interesting extension of this study would be to have child and adolescent twins discordant and concordant for motor difficulties self report on their perception of anxious and depressive symptomatology. The significantly higher levels of anxious symptomatology in twins with a motor disorder in discordant sets than found in twins concordant for a motor disorder added support to a role for environmental effects for anxiety, as in concordant sets it is possible that a shared environmental experience of having a motor disorder set the twins less apart from each other than was the case in discordant sets. The twin relationship has been recognised as being closer than relationships between non-twin siblings (Rende, Slomkowski, Lloyd-Richardson, & Niaura, 2005; Smith, 2007). Therefore sharing a disorder such as a motor disorder may result in fewer psychosocial consequences in twins given their close relationship. Given the findings of Eaves et al. (2003) on the complex relationship between genetic and environmental effects, the interactions between these two, and the correlation between genes and the environment, the added sensitivity found in twins at high risk genetically for anxiety might make twins with a motor disorder more vulnerable and at risk for depression. In the current study, concordant twins had lower movement scores, indicating increased impairment, on the DCD-Q than did twins with a motor disorder in discordant sets. This adds strength to the argument that in these children and adolescents, anxious symptomatology and motor disorder are not of the same aetiology. Although the motor disorder was significantly worse in concordant twins than in twins with a motor disorder in discordant twins, anxious symptomatology was significantly less in concordant twins than in twins with a motor disorder in discordant sets. The significantly lower DCD-Q

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scores obtained by twins without a motor disorder in discordant sets compared to control sets in which neither twin had a motor disorder warrants further investigation, but is outside the scope of this study. Given that there were no significant differences between groups in gestational age at birth or birth weight, the differences could not be attributable to these factors. It is possible that factors that were associated with aetiology of the motor disorder in twins with a motor disorder in discordant twins might have affected both twins, but one to a lesser extent than the other. Future research on MZ twins discordant for a motor disorder might explore this further. Limitations in this study are that movement ability and attention were assessed using parent-rated questionnaire. Questionnaire data do not provide a psychiatric DSM-IV-TR (2000) clinical diagnosis of DCD or ADHD. However, the screening measures used, the DCD-Q and SWAN, have produced comparable prevalence rates to those reported in the DSMIV-TR. Questionnaire items used to measure anxious and depressive symptomatology similarly do not provide a formal psychiatric diagnosis of anxiety or depression, as impairment criteria were not included. However, these constructs were assessed as continuous dependent variables (McDougall, Hay, & Bennett, 2006). 5. Conclusion The co-twin control design was used to clarify the relationship between motor ability and anxious and depressive symptomatology in monozygotic twin children and adolescents. This methodology offered the unique opportunity to control for genetic effects and shared environmental influences, and thus enabled the investigation of non-shared environmental influences, to explore mental health disorders such as anxious and depressive symptomatology in MZ twins concordant and discordant for a motor disorder. The findings that twins with a motor disorder in sets discordant for a motor disorder experienced higher levels of anxious and depressive symptomatology than did twins in sets concordant for a motor disorder and twins without a motor disorder highlight the need to screen children and adolescents with a motor disorder for mood disorders, such as anxiety and depression. This has important implications for clinical practice, treatment, policy development and research. In particular, the study draws attention to the possibility and/or likelihood of increased anxiety in children with a motor disorder. The findings by Piek et al. (2010) of the relationship between stability of gross motor scores in young children aged 4 months to 4 years, and the degree of anxious and depressive symptomatology at school age, in conjunction with findings in the current study, have important implications for detecting motor disorders at the earliest possible stage, and for the implementation of therapies such as occupational and physiotherapy, as well as counselling and psychotherapy as appropriate. Acknowledgements This research was funded in part by the National Health and Medical Research Council of Australia. The authors would like to thank Grant Baynam for his assistance with data collection and entry, the Australian Twin Registry, and the many families who kindly gave their time to be involved in this study. This research was facilitated through the Australian Twin Registry which is supported by an Enabling Grant from the National Health and Medical Research Council administered by The University of Melbourne. 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