Full length articlePostural muscle responses and adaptations to backward platform perturbations in young people with and without intellectual disability
Introduction
Young and old individuals with intellectual disability (ID) have reduced postural balance compared to age-matched individuals without ID [1], [2], [3], [4] and they fall more often than their peers [5]. Researchers have found that people with ID have limited ability to anticipate postural adjustments when they move from the sitting to standing position and when they stand on one leg [6]. In addition, these researchers have found that ID-limited people exhibit general stability problems (Forward Reach Test) [4], [7] and gait stability issues (Timed Up and Go Test) [7], [8], but the reason for these problems is unclear. One reason for the reduced postural balance could be that individuals with ID have slower postural muscle responses compared to individuals without ID.
The postural balance system uses principally four different motor control strategies after external perturbations have been attended: ankle, hip, mixed of ankle/hip or step strategies [9], [10]. Ankle strategy restore the CoM primarily around the ankle joints, hip strategy restore the CoM primarily by motions at the hip joints and step strategy restore the CoM by taking a step to reposition the base of support [11]. If the platform on which the subject is standing moves backwards, the subject's body sways forward. If the duration and velocity of the backwards translation is not too difficult, the subject uses an ankle strategy to control the movement in the ankle and knee joint. The muscle synergy for an ankle strategy begins in the gastrocnemius muscles and then proceeds to the hamstrings and then to the paraspinal muscles [12], [13]. For more challenging perturbations, the other strategies are used.
After a perturbation, the first muscle response is a stretch reflex (latency 40–50 ms), followed by automatic postural responses (latency 70–150 ms), and then voluntary reaction responses (180–250 ms) [14]. Delays in the activation could occur from slowed sensory or motor conduction or decreased central processing and can lead to reduced balance control [15].
Studies have shown that persons with decreased central processing – such as in traumatic brain injury [16], Huntington's disease [17], ageing [15], and in children with Down's syndrome [18] – have delayed muscle onset latencies, but no studies have examined muscle onsets for young people with ID. To this end, this study investigates muscle onset latencies from external perturbations. This study included young people with ID and age-matched peers without ID. The use of aged-matched peers presented several questions: Do young people with ID have delayed muscle onset latencies? Are their times to peak amplitude (EMG) slower? Do they exhibit different muscle synergies and strategies? Do young people with ID have a slower adaptation of their postural muscle responses?
Section snippets
Subjects and recruitment
The participants – 56 young people with ID (females 54%) and 43 young people without ID (females 44%) – were recruited from two high schools in Sweden (Table 1). These volunteer participants were randomly picked from a pool of 500 young people who volunteered for an earlier study. All participants were given verbal and written information about the study and informed consent was obtained from the guardians of all young people with ID younger than 18 years old. All participants in the ID group
Results
A moderate correlation between sex and height could be seen (0.643 < p < 0.001), but no other significant correlations were found. The p-values between the groups in onset latency, time to peak amplitude (EMG), and IEMG for the three muscles did not alter because of sex and/or heights. Therefore, the groups were not further stratified to males and females.
No difference in onset latency between the two groups (ID and non-ID) could be found, and there were no changes in onset latency between the
Discussion
The results showed that there were no differences in onset latency, use of muscle synergies, and strategies between young people with and without ID after backward external perturbations. However, people with ID reduced the time to peak amplitude in all investigated muscles and people without ID only reduced time to peak amplitude in one muscle between first and sixth trial. People with ID also decreased their IEMG activation less than people without ID between the first trial and sixth trial.
Conclusion
The results in this study suggest that most postural muscle responses to backward external perturbations for young people with ID are similar to age-matched controls without ID. However, young people with ID did not reduce their IEMG activities as much as their age-matched controls which may be due to limited processing of somatosensory information. This inability to adapt the muscle response to perturbations should be investigated further.
Conflict of interest statement
The authors in this study declare that they have no conflict of interest related to the submitted manuscript.
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