||Correlation between General Movements and Risk Factors in Infants with High Risk for Developmental Delay
||Department of Physical Therapy
small for gestational age
very low birth weight
chronic lung disease
方法：本研究於成功大學附設醫院共招募了21位足月產的新生兒(控制組)，25沒有發展遲緩高危險因子的早產兒(早產控制組)及46位有發展遲緩高危險的新生兒(高危險組)，高危險群包含胎兒小於妊娠年齡、非常低體重、腦部超音波異常及慢性肺部疾病等四個次族群。本研究分別在三個時期，早產(preterm)、扭動運動(writhing)和不安扭動(fidgety)時期，拍攝各46、81及60個整體動作影片。由三位物理治療師評估，受試者整體動作為正常或異常。而異常的腦部超音波則分成輕微 (包含輕微及原本腦部超音波異常後續為正常者)及較嚴重的(包含中等及嚴重的腦部超音波異常)次組別，進行以下統計分析。第一，使用費雪精準檢定(Fisher’s exact test)分析各發展遲緩高危險因子或多個高危險次族群與整體動作間的相關性，並使用克雷莫V係數(Cramver’s V coefficient)分析正常、輕微及較嚴重的腦部超音波及整體動作間的相關性；第二，使用二元羅吉斯迴歸(Binary logistic regression）檢測及比較各高危險發展因子可能造成異常整體動作的風險。
Background and Purpose: Small for gestational age (SGA), abnormal brain ultrasound (AbUS), very low birth weight (VLBW), or chronic lung disease (CLD) are considered as high risk factors of developmental delay. General movements (GMs) are claimed to be endogenous and the qualities of GMs may reflect the maturation and status of an infant’s nervous system. The purpose of this study was to examine the relationships between GMs and above four high risk factors.
Methods: Twenty-one term infants (control group), 25 preterm infants without other high risk factors (premature group), and 46 infants with at least one of following conditions, High risk group (HRG) had four subgroups including SGA, AbUS, VLBW or CLD. Forty-six, 81 and 60 recordings were collected and rated in preterm, writhing and fidgety periods, respectively. GMs were categorized as normal or abnormal. AbUS were divided into two subdivisions, minor AbUS including mild AbUS or initially AbUS but followed normal ultrasound findings and severe AbUS including moderate or severe AbUS. The relationships between SGA, AbUS, VLBW, CLD or multiple risk factors and GMs were determined by Fisher’s exact test; Cramer’s V test was used to examine the relationships between GMs and non-, minor and severe AbUS. Binary logistic regression was applied to determine the contribution of each risk factor to probability of abnormal GMs.
Results and Discussion: SGA was not related to abnormal GMs, but SGA had high percentage of abnormal GMs in the preterm period. “Brain sparing” which may prevent severe brain injury in uterus, and restored supplies of nutrition after birth may be another possible reason that contribute to high incident of early abnormal GMs in SGA. AbUS was related to abnormal GMs in each period. In further examinations, minor AbUS was related to abnormal GMs in the preterm and writhing periods, while severe AbSU was related to abnormal GMs in the fidgety period. The increased severity of AbUS was correlated to abnormal GMs in each period. The possible reasons may be that early abnormal GMs and minor AbUS were attribute to transient brain dysfunction while severe AbUS and abnormal fidgety GMs may attribute to permanent brain dysfunction; however, further study is needed to confirm this speculation. VLBW was related to abnormal GMs in the preterm and writhing periods. Ten participants with VLBW all had AbUS. CLD was not related to abnormal GMs, but incidents of abnormal GMs were high in the preterm and writhing periods. Only 6 participants with CLD and they all had AbUS and VLBW. Logistic regression indicated that among these risk factors, only AbUS had significantly effect on GMs in each period. Minor AbUS was at higher risk for abnormal GMs in the preterm period, while severe AbUS had 20 times of risk for abnormal GMs in the fidgety period in comparison with non-AbUS. When examining the correlation between multiple risk factors (including two or three risk factors) and GMs, multiple risk factors including SGA were related to abnormal GMs in the preterm and writhing periods, while multiple risk factors including risk factors other than SGA were related to abnormal GMs in each period.
Conclusions: This study revealed that AbUS were consistently related to abnormal GMs, while VLBW were related to abnormal GMs in the preterm or writhing periods. SGA and CLD did not related to abnormal GMs. Increased severity of AbSU was related to GMs in each period. Although HRG including 46 participants, the GMs recordings of every participant was not available for examination in the three periods. Particularly, few participants had CLD, and all of them had VLBW and AbUS. Further study is needed to examine the long-term effect of each high risk factor on neurodevelopment by enlarging the sample size in each risk factor and following up the participants.
Chapter I Background Information 1
1.1 Introduction 1
1.2 Purposes 5
1.3 Definitions 6
1.4 Operational definitions 6
1.5 Limitations 7
1.6 Assumptions 8
1.7 Hypotheses 8
1.8 Research questions: 8
1.9 Rationales for the hypotheses 8
1.9.1 Rationale for the first hypothesis 8
1.9.2 Rationale for the second hypothesis 9
1.9.3 Rationale for the third hypothesis 11
1.9.4 Rationale for the fourth hypothesis 12
1.10 Significance of Research Questions 12
1.10.1 Significance of the first research question 12
1.10.2 Significance of the second research question 13
1.11 Needs for Study 13
Chapter II Literature review 15
2.1 Assessment of GMs 15
2.2 High risk factors 17
2.2.1 SGA 17
2.2.2 AbUS 19
2.2.3 VLBW 20
2.2.4 CLD 21
2.3 Common abnormal neurological outcome 23
2.4 Neural Mechanism and Theories of GMs 24
Chapter III Methods 27
3.1 Participants 27
3.2 Procedure 27
3.2.1 Data collection 27
3.2.2 Qualitative assessment of general movement 29
3.3 Statistical analysis 29
Chapter IV Results 31
4.1 The relationships between GMs and high risk factors 33
4.1.1 The relationships between SGA and GMs 33
4.1.2 The relationships between AbUS and GMs 34
4.1.3 The relationships between VLBW and GMs 36
4.1.4 The relationships between CLD and GMs 37
4.2 Contribution of each risk factor to probability of abnormal GMs 37
4.3 The relationship between GMs and multiple risk factors 38
Chapter V Discussion 40
5.1 The relationships between SGA and GMs 40
5.2 The relationships between AbUS and GMs 42
5.2.1 The relationships between AbUS and GMs in different periods 43
5.2.2 The relationship between severities of AbUS and GMs 44
5.2.3 The relationship between transient AbUS and GMs 45
5.3 The relationships between VLBW and GMs 45
5.4 The relationships between CLD and GMs 47
5.5 Contribution of each risk factor to probability of abnormal GMs 48
5.6 The relationship between GMs and multiple risk factors 49
Chapter VI Conclusion 50
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