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The use of ultrasound as a tool for diagnosis of motor disorder severity, treatment planning and assessment of treatment eff ectiveness in children with cerebral palsy. 

Aim and background of project

The project set out to investigate the architectural alterations of skeletal muscle following cerebral palsy. If associated with functional and clinical measures of disability, information on muscle architecture via ultrasound scanning could then be used as an accurate, reproducible and un-invasive tool in both the diagnosis of movement disability and the assessment and evaluation of treatment strategies in movement disabilities such as cerebral palsy.

Cerebal palsy (CP) is the result of a non-progressive insult to the developing brain. It is usually associated with various musculo-skeletal disorders (e.g. spasticity, joint contractures, and joint malposition) that may further contribute to the observed motor disability. The associated disorders can progress and diminish patients’ functional capacity through life.

The management of the CP child has traditionally been challenging. Currently, there are very few valid diagnostic modalities that can estimate muscle disorder severity and none with any predictive value to guide the clinician as to when or what treatment modality (e.g., orthoses, casting, botulinum toxin A (BTX) injections or surgical interventions) should be applied. Current practice relies on complicated tests, such as gait analysis, which is diffi cult to run, requires a whole team of experts, is often unavailable and has many limitations. This is further compounded by the often-reduced psychokinetic development and the frequent lack of co-operation of the aff ected children. As a consequence, decisions are often taken based on limited information, which may result in a non-optimal outcome.

Due to the correlation between muscle function and architecture, muscle architectural parameters (i.e. fascicle length, muscle thickness, and fascicle pennation angles) could relate to the degree of motor disability in CP, and therefore, be used in the assessment of movement disability. Muscle and  joint disability can alter the resting length of a muscle-tendon unit and can, theoretically, alter muscle architecture in CP. Furthermore, measurement of muscle architecture in CP, and its short- and long-term adaptation to treatment might be used to assess the effectiveness of conventional treatments, and form new theoretical frameworks for future interventions.

Recent developments in ultrasound scanning have made it possible to measure in-vivo, accurately, reproducibly and non-invasively the dimensions of human skeletal muscle and tendon separately. These measurements can be performed at rest, and therefore, require minimal co-operation by the child. These characteristics offer the unique opportunity to use ultrasound as a tool for diagnosis and assessment of treatment effectiveness in children with CP. The exploitation of this innovative technology application is going to assist in developing better treatment strategies in an important NHS area, through applied scientific research in collaboration with clinicians.

The objectives of the completed project were to measure muscle fibre and tendon lengths with ultrasound in children with CP and compare these measurements with measurements on healthy children. Secondly, to measure muscle fibre and tendon lengths with ultrasound in CP children before application of the treatment modalities prescribed by the clinicians, during, and after treatment. Thirdly, based on the above measurements and additional established measurements of motor dysfunction severity, to develop the necessary guidelines for assisting clinicians in choosing an effective treatment strategy.

Methods with results discussed

Twenty-eight children with CP and 71 typically developing (healthy) children were recruited. Children with CP were diagnosed by the consultant orthopaedic surgeons who collaborated in the project. The functional level was determined using Gross Motor Function Classification System (GMFCS) scores.

For both children with CP and healthy children, an experimental session included ultrasound scanning of the gastrocnemius (calves) muscles. Both legs of children with CP and the dominant leg in healthy children were scanned. Anthropometric information including measurements of leg length, and knee and ankle joint angles at rest were obtained in each session. Co-operative children with CP who were ambulatory participated in gait (motion) analysis.

The main measurements of interest using the ultrasound scanning technique included muscle fascicle length, muscle thickness, and muscle fascicles pennation angle (jointly called muscle architectural parameters), and muscle and tendon lengths. Gait analysis provided information about lower limb joints pattern of co-ordination and range of motion during walking, and the forces involved in producing the observed movement and posture at different stages in a step cycle.

Children with CP were asked to participate in repeat experimental sessions every six months. Those who underwent medical or surgical treatments were asked to participate in pre- and post-treatment experimental sessions. Healthy children participated only once.

From the study, two papers (1 & 2) were published to discuss the architectural differences between two subgroups of children with CP (i.e hemiplegic and diplegic types) and typically-developing children. Two further papers (3 & 4) investigating the effect of spastic diplegia on gastrocnemius muscle architecture, and the effect of treatment on muscle architecture are currently in preparation for publication.

1. Differences in gastrocnemius muscle architecture between the paretic and non-paretic legs in children with hemiplegic cerebral palsy (published in Clinical Biomechanics 2007).

The first study aimed to test the hypothesis that the gastrocnemius muscle fascicle lengths in the paretic leg of hemiplegic children would be shorter than the non-paretic leg, at least in some muscle sections along the bellies of the two muscle heads. Secondary hypotheses were that the muscles in the paretic leg would have undergone atrophy, and a reduction in pennation angle compared to the nonparetic leg. Participants were eight children with spastic hemiplegic CP. Seven of the participants were ambulatory with equinus gait (except patient no. 7 who was not able to walk) and none of the eight participants had undergone any conventional medical treatment (e.g., Botulinum toxin injection, surgical intervention, or casting) before participation in the study.

The results of this study found that the gastrocnemius muscle of the paretic leg in a sample of children with spastic hemiplegic CP had shorter fascicles, smaller thickness and similar pennation angles compared with the non-paretic leg. The muscle fascicle length and thickness findings confirm the hypothesis that that paretic leg of hemiplegic children is shorter than the non-paretic leg. However, the pennation angle findings do not agree with the hypothesis, showing similarities between the paretic and non-paretic leg.

Fascicle lengths were significantly reduced in the paretic leg, compared to non-paretic leg for both muscles. It should be noted that whereas there were no differences in the level of fascicle length reduction among the three gastrocnemius medalis (GM) muscle sections scanned in the paretic leg, for the gastrocnemius lateralis (GL) muscle, fascilcle length differences were found in the middle and proximal sections only, indicating that there may be differences in the level of disease and/or adaptability of serial number of sarcomeres to the CNS lesion between different sections in a given muscle. These findings length was detected in the lower half of the GM muscle in children with diplegia. One possibility for this disparity could be that calf muscle paresis is more prominent in these hemiplegic patients due to differences in the timing and aetiology of brain injury between hemiplegia and diplegia.

The thickness of the GM muscle was reduced by 10%, and by 20% in the GL muscle in the paretic compared with non-paretic legs. Although thickness in a muscle is only a gross approximation of its actual size, the magnitude of muscle thickness differences between legs indicates the presence of substantial muscle atrophy in the affected leg. This finding is consistent with previous findings. This evidence indicates that muscle fibres may adapt to the motor disability caused by the brain injury by losing sacromeres not only in series but in parallel.

For the GM muscle, pennation angles in the paretic and non-paretic legs were similar to values reported in previous research with normally developing children (~22 deg) and children with diplegia (~20 deg). For the GL muscles, the observed values (~14-15 deg) were slightly larger (up to 4 deg) compared to healthy adults. Due to the high correlation between thickness and pennation angle in a healthy muscle, it was expected that the muscle thickness reductions in the paretic compared with paretic legs would also be accompanied by pennation angle reductions. However, the result did not support this hypothesis, as pennation angles were similar in the two legs, supporting previous research.

It is important to confirm the applicability of these findings to other muscles and investigate whether there is a relationship between muscle architecture and conventional indexes of disability in CP (e.g., spasticity and motor function clinical scores) before and after treatment.

2. In vivo gastrocnemius muscle fascile length in children with and without diplegic cerebral palsy (published in Developmental Medicine and Child Neurology 2007).

The second study aimed to examine the effect of spastic diplegic cerebral palsy on in vivo gastrocnemius muscle fascicle length. An ancillary aim was to examine the validity of a normalisation method (i.e., by dividing fascicle length to a person’s leg length) as a means to reduce variability in fascicle length data due to anthropometrical differences. In vivo fascicle length in the gastrocnemius muscle of a group of children with diplegia (n=18) and typically-developing children (n=50) were measured. Statistical methods (e.g. analysis of covariance and regression techniques) were employed to examine the validity of inherent assumptions for normalisation of fascicle lengths.

The effect of spastic cerebral palsy on in vivo gastrocnemius muscle fascicle length is not clear. Similarity of fascicle lengths in children with diplegia and typically developing children, but shortening of fascicle lengths in the paretic legs of children with hemiplegia compared with the non-paretic legs, are both reported. In the former case, comparisons were made between fascicle lengths normalised to leg length, whereas in the latter case, absolute fascicle lengths were compared. The inherent assumptions when normalising fascicle length (measured via ultrasonography) were not validated, raising the possibility that inappropriate normalisation contributed to the controversy. We used statistical methods to control the potential confounding effect of leg length on fascicle length, and tested the feasibility of the normalisation method.

The study found shorter fascicle lengths in gastrocnemius muscle in the sample of children with diplegia than in typically developing children, irrespective of whether absolute or normalised fascicle lengths were compared. One the basis of this data set it was concluded that normalisation of fascicle lengths was justified. It was suggested that other methodological issues (such as sample characteristics) should be considered to identify the underlying cause of the controversial results in the literature. Further studies are required to confirm the applicability of the present results to other muscle before fascicle length can be used as an index for the diagnosis of the severity of the motor disability and for the selection and evaluation of appropriate treatments.

3. In vivo measurement of muscle, tendon, and fascicle lengths in children with diplegia (in preparation).

A third study (in preparation) aimed to examine in vivo the muscle and tendon length differences in children with spastic diplegia and typically developing children. Musculo-tendinous junction of both heads of the calf muscles and the place of insertion of the Achilles tendon on the heel bone were identified in vivo in our groups of children with spastic diplegia (n=18) and typically-developing children (n=50). Muscle and tendon lengths were measured over the surface of the skin and by following the curvature of the muscle and tendon. After statistically controlling the potential influences of anthropometrical and age differences among the participants, we found that gastrocnemius muscles were shorter but the Achilles tendons were longer in children with diplegia than in typically-developing children. Shortness of the spastic muscles was at least due to the shortening of their fascicle lengths, as no alteration in pennation angle was found. Muscle thickness was also reduced in children with diplegia, which can be regarded as an indirect sign of muscle atrophy.

4. Effect of treatment on muscle architecture (in preparation).

A fourth study aimed to examine alterations in muscle architecture in response to medical intervention in children with CP. Eight children with CP, who did not undergo medical intervention, participated in the study. In these patients, gastrocnemius muscle architecture was examined more than once, with approximately six months between successive measurements. Another group of ten children, who underwent medical intervention (surgery, or injection of Botulinum toxin), were also examined before and after treatment. Gait analysis was performed for two participants in the medically treated group who were capable of walking independently and used no assistive device. Muscle fascicle length did not change over time. The time gap between the first and second measurement varied between six and fifteen months. Group analysis was not possible in children who underwent medical intervention, due to the varied range of applied treatment. Individual reports for the participants in this group, and gait information data for all participants are reported. The combined but opposing effects of growth (potentially increasing fascicle length) and spasticity (potentially reducing fascicle length) can result in no alteration of fascicle length over time, as observed in some children with CP. The relative dominant effect of growth and spasticity might explain the observed inconsistency in the results.

In agreement with pervious work, we found that muscle length decreased in the group who underwent surgery. The opposite effect was observed after treatment with Botox. Discrepancy in muscle length results might be partially attributed to the changes in the relative stiffness of muscle and tendon after surgery or injection of Botox. The relative stiffness of tendon might diminish after surgery and resist less against the pull of a spastic muscle. The outcome can be a shorter muscle but longer tendon. After Botox, the muscle might show less resistance against the stretching force during daily activities and stay at a longer equilibrium length with respect to tendon.

Conclusion

In contrast to previous reports, the findings of the present research project show that CP does affect muscle architecture. More precisely, the results show that spasticity is associated with muscle fascicle shortening and atrophy. The results indicate that, whatever the intervention chosen, surgical or not, direct or secondary involvement of the muscle of the paretic site might be beneficial. If, for example, surgical tendon lengthening is performed, which seems to elongate the tendon but further shorten the affected muscle, secondary therapies against muscle atrophy and fascicle shortening might be helpful. Such therapies might include voluntary or artificially evoked muscle contractions against resistance, but the applicability and effectiveness of this concept should be tested before any firm recommendations can be made. Further studies are also required to help establish ultrasound scanning as a tool with diagnostic power in CP. In this respect, the relationship between alterations in muscle architecture and indexes of muscle spasticity in CP (in addition to indexes of functional disability as in the present study) are required.

This information is not meant to replace the advice of any physician or qualified health professional. The information provided by Cerebra is for information purposes only and is not a substitute for medical advice or treatment for any medical condition. You should promptly seek professional medical assistance if you have concerns regarding any health issue.

Page last updated: 16/12/2011 16:16 
 
 
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