Review

The effectiveness of passive stretching in children with cerebral palsy

Tamis Pin* MSc, Probationary PhD Candidate, University of Melbourne, Victoria; Paula Dyke MSc, Manager, School-aged Programme; Michael Chan MSc, Senior Physiotherapist, Cerebral Palsy Association of WA, Western Australia, Australia. *Correspondence to first author at PO Box 143, North Melbourne, VIC 3051 Australia. E-mail: tamispin@hotmail.com

Passive stretching is widely used for individuals with spasticity in a belief that tightness or contracture of soft tissues can be corrected and lengthened. Evidence for the efficacy of passive stretching on individuals with spasticity is limited. The aim of this review was to evaluate the evidence on the effectiveness of passive stretching in children with spastic cerebral palsy. Seven studies were selected according to the selection criteria and scored against the Physiotherapy Evidence Database scale. Effect size and 95% confidence intervals were calculated for comparison. There was limited evidence that manual stretching can increase range of movements, reduce spasticity, or improve walking efficiency in children with spasticity. It appeared that sustained stretching of longer duration was preferable to improve range of movements and to reduce spasticity of muscles around the targeted joints. Methods of passive stretching were varied. Further research is required given the present lack of knowledge about treatment outcomes and the wide use of this treatment modality.

Cerebral palsy (CP) is an umbrella term covering a group of non-progressive, but often changing, motor impairment syndromes secondary to lesions or anomalies of the brain arising in the early stages of its development.1 This neurological disorder can cause secondary changes in the musculoskeletal system such as decreased muscle strength, tightness or contractures around joints, and abnormalities in both bony structures and gait.2 Passive stretching is a common treatment to combat this soft tissue tightness.3,4 The stretching can be done manually by the therapist or the patient or by other external devices such as splints, casts, or tilt-table.5 Despite the widespread use of passive stretching, there is a lack of research evidence demonstrating its effectiveness and the rationale behind the stretch-based techniques in spastic human muscles.5,6 Clinicians seek the best evidence available from existing research studies to support their intervention procedures.7 This review aims to investigate the current research evidence on the effectiveness of passive stretching in children with spastic CP by using the World Health Organizations International Classification of Impairment, Disability and Handicap (ICIDH-2) to classify the outcomes described by different studies as recommended by the American Academy of Cerebral Palsy and Developmental Medicine (AACPDM).7 Method
SEARCH STRATEGY

The clinical question of this review was: Does passive stretching improve passive joint range of movements and reduce spasticity more effectively in children with CP than no passive stretching? The inclusion criteria of this review were: (1) studies on children under 18 years of age with spasticity due to CP; (2) studies demonstrating the effects of passive stretching programmes with reported findings for analysis of its effectiveness; (3) studies with all research designs except expert opinions; and (4) fully published studies in peerreviewed journals. Studies that compared passive stretching programmes with the effects of medications, surgery, or serial

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Table I: Methodology assessment of studies according to the Physiotherapy Evidence Database (PEDro) scale
Study Specified Random eligibility allocation of criteriaa participants Concealed allocation Similar Blinded prognosis participant at baseline Blinded therapists Blinded assessors More than 85% FU for at least one key outcome Yes Yes Yes Yes Yes

Fragala et al. (2003)20 Lespargot et al. (1994)19 McPherson et al. (1984)21 Miedaner and Renander (1987)16 ODwyer et al. (1994)14

Yes Yes Yes Yes Yes

No No No Yes Yes

No No No No No

Yes Yes Yes Yes Yes

No No No No Yes

No No No No No

Richards et al. (1991)17 Tremblay et al. (1990)18

Yes Yes

Yes Yes

No No

Yes Yes

No No

No No No Yes Yes to half of participants No No No No

Yes Yes

aThis criteria is not counted for the total PEDro score; FU, follow-up.

casting were excluded as the area of interest was mainly on passive stretching without assistance from surgery and antispasticity medications. Electronic databases (Medline, CINAHL, PsycINFO, Embase, full Cochrane Library, and Physiotherapy Evidence Database [PEDro]) were searched from the earliest date until April 2006. The keywords used for the search were cerebral palsy, muscle spasticity, stretching, physical therapy, and range of movement. Subject headings, truncations, and thesaurus were used wherever possible. Reference lists in relevant studies and review articles were examined. The titles and abstracts of articles identified in the initial search were initially

screened by the first author (TP) against the inclusion and exclusion criteria. When the title and abstract did not indicate clearly if an article should be included, the complete article would be read to determine its suitability.
QUALITY ASSESSMENT OF METHODOLOGY

All the included studies were scored on their methodological rigour with the PEDro scale.8 The PEDro scale examines 11 aspects of the quality of methodology: (1) specification of eligibility of participants; (2) randomization of participants; (3) allocation concealment of participants; (4) comparability of subject groups at baseline; (5) blinding of participants; (6)

Table II: Summary of study characteristics

Study Research design Level of evidence Participant characteristics Nr of participants Treatment Control group group 7 7a Age range

Fragala et al. (2003)20 Lespargot et al. (1994)19 McPherson et al. (1984)21

Multiple single-subject ABAB design Before-and-after design Multiple single-subject design

II

Children with spasticity in lower limbs with classification of Levels IV and V by GMFCS Children with spastic CP with spasticity in hip adductors Children with severe spastic quadriplegic CP with knee contracture Children with severe physical and cognitive impairment and decrease in joint ranges of lower limbs Children with spastic CP with spastic triceps surae Children with spastic diplegia or hemiplegia Children with spastic CP (diplegia, hemiplegia, and quadriplegia)

418

10

20

III

4a

913 (median 10y 3mo) 1018

Miedaner and Renander Multiple single-subject (1987)16 with randomized cross-over design ODwyer et al. (1994)14 Richards et al. (1991)17 Tremblay et al. (1990)18 Randomized controlled trial Randomized controlled trial Randomized controlled trial

13

13a

620 (mean 10y 6mo)

I I I

8 8 11

7 11

619

313 (mean 7y [SD 3]) 10 314 Experimental group (mean 7y [SD 2y 7mo]) Control group (mean 5y 11mo [SD 2y 5mo])

aParticipants acting as their own contols. GMFCS, Gross Motor Function Classification System; CP cerebral palsy. ,

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Table I: continued
Intention to treat analysis Between group statistical analysis for at least one key outcome Yes No Yes Yes Yes Point estimates of variability for at least one key outcome No No No Yes Yes PEDro score

of participants in the study). The averages of the standard deviations of the group means and the numbers of participants would be used if there were participant and control groups.11 This formula for calculating the effect size with 95% CI was chosen as it has been deliberately simplified for clinicians who are not experienced in complicated statistical calculations.11 Results An electronic search on various databases and reference lists identified 615 articles, among which 10 studies met the inclusion criteria. The full articles of these 10 studies were reviewed and three studies were further excluded because of the following reasons. One study was a systematic review12 that evaluated studies on passive stretching of participants in vegetative and minimally conscious states. As the participants had heterogeneous diagnoses and included both adults and children, it was excluded from this report. Two papers13,14 reported the data of the same study,14 and hence they were treated as a single entity.14 One study15 did not have any intervention but investigated the time that the soleus muscle was stretched during daily activities in a 24-hour period in children with CP so as to deduce how long the muscle needed to be stretched to prevent contracture.15 Therefore, this report analyzed the results from seven research studies on the effects of passive stretching in children with CP . The scoring of each study with the PEDro scale is listed in Table I. The median score of the seven studies was 6 (interquartile range is 46.5). According to the AACPDM evidence table of internal validity, four studies are level I randomized controlled trials (Table II).14, 1618 There was no available information from these four studies to determine if the allocation was concealed (criterion 3). The participants, therapists, and assessors in most of the studies were not blinded (criteria 57). Most of the studies were able to follow up all the participants and all except one study19 used statistical comparison of at least one key outcome measure between the study and control groups (criteria 811). Hence, although more than half of the studies are of level I or II evidence, their methodological quality is average. Table II summarizes the characteristics of the research participants in these seven studies. The participants were aged from 3 to 20 years of age. As there was no raw data available in two studies including participants more than 18 years of age,14,16 it was impossible to exclude the data relating to those participants more than 18 years of age. These two studies were still included in this review of the effects of passive stretching in children with CP . Table III summarizes the outcomes of interest of these seven studies and codes the outcomes of interest according to the different dimensions of disablement. All the outcomes of interest in these studies were at the level of impairment.7
CHANGE IN RANGE OF MOVEMENTS

Yes Yes Yes Yes Yes

4/10 3/10 4/10 7/10 8/10

Yes Yes

Yes Yes

Yes Yes

6/10 6/10

blinding of therapists; (7) blinding of assessors; (8) more than 85% follow-up of participants in at least one of key outcomes; (9) intention to treat analysis; (10) between group statistical analysis of at least one of the key outcomes; and (11) point estimate of at least one of the key outcomes. According to the PEDro guidelines, a positive answer to each of the criteria 2 to 11 will yield one point, obtaining a PEDro score between 0 to 10.8 The details of the scoring criteria can be found in their weblink (http://www.pedro.fhs.usyd. edu.au/criteria.html). The PEDro scale has been shown to have moderate interrater reliability (intraclass coefficient for the total score is 0.56, 95% confidence interval [CI] 0.470.65).9 The AACPDM evidence table of internal validity was used to grade the levels of evidence of each selected study.7 This classification of levels of evidence is a modification of Sacketts hierarchy of levels of evidence,10 but it includes and grades single subject research design, which is increasingly common in research in the developmental disability domain.7 This grading procedure was done independently by the first (TP) and second (PD) authors. Any disagreements were resolved with discussion.
DATA EXTRACTION

Data from all the included studies were summarized in the format as suggested by the AACPDM.7 The format includes: participants characteristics (number in each group, target population, diagnosis, numbers in each diagnostic subgroup, and ages), intervention used, control used, research design and level of evidence for the study, and outcomes of interest.
DATA ANALYSIS

Effect sizes with 95% CIs were calculated if raw data were available in the studies.11 The effect sizes give easy understanding of how big the treatment effect is and the clinical significance of these statistically significant treatment effects can also be justified. The effect size was the difference between the means of outcome measures of the participant and control groups. If there was no control group, the difference of the pre- and posttreatment means would be used as the participants were acting as their own controls. The 95% CI was approximated by the following formula: 3 x SD/N (SD, standard deviation; N, number

There are five studies investigating the effect of passive stretching in improving the range of movement of identified joints.14, 16, 1921 Two studies showed an increase in range of movement poststretching (of level III21 and level I16 evidence). The study by McPherson et al.21 of level III evidence showed that there was a significant reduction in knee flexion contracture in three out of four treatment periods and a significant increase in knee flexion contracture in three out of four non-treatment periods. The difference in means between treatment and

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Table III: Summary of study results

Study Intervention Outcome of interest Measures Dimension of disablement I

Fragala et al. (2003)20

Manual stretch with hold for 4060s, 3 times for each movement, 1 or 2 times per week and routine positioning regime in classrooms Manual stretch for 1520min in physiotherapy session and wedge-sitting 57h daily

Passive range of hip flexion, hip extension, hip abduction, popliteal angle, knee flexion, and knee extension Passive hip abduction angle

Goniometer

Lespargot et al. (1994)19

Specially designed apparatusa

McPherson et al. (1984)21

First year: manual stretch with hold for 60s, 5 repetitions for each joint, 3 times a day and 5 days a week Second year: 30min on prone-stander per day, 30min on supine positioning device per day, 5 days a week Manual stretch with 5 repetitions for each joint, hold for 2060s. One group having 5 days a week and one group having 2 days a week. After 5 weeks, the groups were switched for another 5 weeks

Range of knee flexor contractures

Goniometer

Hypertonicity

Specially designed apparatusb Goniometer

Miedaner and Renander (1987)16

Passive range of movement of hips, knees, ankles, and forefeet

ODwyer et al. (1994)14

Sinusoidal stretch by specifically designed apparatus using stretch reflex as biofeedback, 30min per session, 3 times per week for average 42 days Standing in tilt-table with various ankle positions for 30min each time

Spasticity of triceps surae Contracture of triceps surae

Tonic stretch reflex Ankle joint passive torque EMG Video recording Spastic Locomotion Disorder Index Kin-Com dynamometer and surface electrodes (in terms of torque, ankle angle, and EMG)

I I

Richards et al. (1991)17

Muscle activation of tibialis anterior and triceps surae Gait analysis EMG during walking

I I I

Tremblay et al. (1990)18

Standing in tilt-table with ankles in dorsiflexion for 30min

Quality of passive movement of ankles

Quality of voluntary contraction of triceps surae

Kin-Com dynamometer and surface electrodes (in terms of torque and EMG)

aThe reliability and validity of the apparatus not mentioned in the text; bInter- and intrareliability of this apparatus were reported in the text on measuring tone over wrists; cfavours stretches. ND, no difference before and after stretches; I, impairment; PROM, passive range of movements; CI, confidence interval; NS, non-significant results; NA, not applicable; EMG, surface electromyography; PF, plantarflexion; DF, dorsiflexion; TS, triceps surae; TA, tibialis anterior.

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Table III: continued

Results Statistics Effect size (95% CI)

Statistically decrease in PROM after the first non-stretch phasec

Wilcoxon signed-rank test. Z-statistic=1.999, p=0.046

No raw data provided for calculation. Authors defined changes >8 as real differences

No comparison of outcome of interest before and after stretchesc

Not specified in text. Raw data provided for 4 participants. Calculation of effect size shown no significant difference found before and after stretching Wilcoxon Match-paired, signed-rank test p<0.05 and p<0.02 respectively Wilcoxon Match-paired, signed-rank test p<0.05

Hip abduction with knee flexion, 6.13 (6.31 to 18.57) and 1.38 (5.02 to 2.26). Hip abduction with knee extension, 0.63 (8.76 to 10.02) and 2 (11.06 to 7.06) Unable to calculate (see text under section Change in range of movements for explanation) 1.56 (3.1 to 0.02)

3 out of 4 treatment periodsc 3 out of 4 non-treatment periodsc 1 out of 4 treatment periodsc

In right hip flexion and right straight-leg raising i.e. 2 out of 7 joints after 5 days per week stretch.c No significant difference between the 2 regimes of manual stretching except in right straight-leg raising i.e. 1 out of 7 joints Significant decrease in spasticity of triceps suraec ND

Hip flexion: F=10.21, p< 0.01 Straight leg raising: F=5.71, p< 0.01

Right hip flexion 12 (1.52 to 22.48) Right straight leg raising 8.2 (0.19 to 16.21)

F(1, 12) >6.83, p<0.025 and F(1, 12) >5.61, p< 0.05 NS

No raw data provided for calculation NA

Significant reduction in pre/post-ratio of tibialis anterior in initial gait cyclec ND ND

p<0.01 NS NS

No raw data provided for calculation NA NA

Decreased resistance to passive movements of ankles immediately and up to 35min after stretchc decreased EMG response during passive movements of ankle immediately and up to 35min after stretchc

p<0.05

At 30=0.28 (0.56 to 0) At 60=0.56 (0.89 to 0.23) At 60 after 25min=0.67 (1.26 to 0.19) At 60 after 35min=0.65 (1.24 to 0.06) TS EMG 30DF=0.23 (0.39 to 0.07) 30PF=0.2 (0.37 to 0.03) 60PF=0.41 (0.71 to 0.11) 120PF=0.26 (0.47 to 0.05) 60PF after 25min=0.42 (0.73 to 0.11) 60PF after 35min=0.33 (0.65 to 0.01) TA EMG 30DF=0.33 (0.59 to 0.07) 60DF=0.48 (0.85 to 0.11) 120DF=0.35 (0.61 to 0.07) 30PF=0.44 (0.73 to 0.15) 60PF=0.46 (0.86 to 0.06) 0.71 (0.28 to 1.14)

Increased torque during PFc

p< 0.05

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non-treatment phases were <10 in general. The effect size and 95% CI in this study were unable to be calculated due to the small sample size (four participants) and the violation of assumption of normal distribution of data. The study by Miedaner and Renander of level I evidence16 showed a statistically significant increase in two out of 14 joint measurements after stretching five times a week for 5 weeks. The effect sizes of these two measurements were 8.2 and 12 respectively. One study of level II evidence showed loss in range of movements in 28 motions after the cessation of passive stretching in one out of four phases of study periods.20 No raw data was provided for the calculation of the effect sizes but the authors defined that changes greater than 8 were considered not due to measurement errors. Thus, it is believed that the difference in these 28 motions should be greater than 8. One level I evidence study, however, showed no difference in the range of movement of triceps surae poststretching.14 Although the level V study by Lespargot19 did not use statistical comparison in range of movements before and after stretching, raw data of the four participants were available for the calculation of the effect size and the 95% CI. No statistical difference in the range of hip abduction was demonstrated after passive stretching (Table III).
CHANGE IN SPASTICITY

available end range of movement by mechanical means such as standing table or position equipment.14,17,18 The other category is manual stretching, i.e. by holding the joint to the available end range of movement manually for a set amount of time and then releasing it.16, 1921 The latter, therefore describes a short time limit for stretching (expressed as seconds), when compared with the first category (expressed as minutes, or up to 57h in some studies). Three studies combined sustained and manual stretching as their intervention procedures.1921 It is of interest to compare the effects of manual and sustained stretching. The study using manual stretching of shorter duration by Miedaner and Renander16 (level I evidence) showed some significant increases in range of movements but only in a small portion of total measurements taken. The effect sizes were small (Table III). In studies using sustained stretching, the studies by ODwyer et al.14 (level I evidence) and Tremblay et al.18 (level I evidence) demonstrated a statistically significant decease in spasticity after stretching. The study by Richards et al.17 (level I evidence) concluded there was no clinical significance in their statistically significant findings in the reduction of spasticity following sustained stretching. Discussion
CHANGE IN RANGE OF MOVEMENTS

In terms of changes in spasticity poststretching, there are four studies (level III,21 level I,14 level I,17 and level I18 evidence) all showing a reduction in spasticity posttreatment. McPherson et al.21 reported that there was a statistically significant reduction in hypertonus over the knee joints in one out of four treatment periods (effect size was 1.56 units in the torque of passive knee flexion; Table III). ODwyer et al.14 found a decrease in spasticity in the triceps surae after the stretching but no raw data provided for calculation of the effect sizes. Richards et al.17 demonstrated a significant reduction in the electromyography (EMG) pre/post-ratio for the tibialis anterior muscles only at the initial gait cycle after 30 minutes of stretching on a tilt-table. The difference between the treatment and control groups was 0.25 (no 95% CI calculated). The authors considered this reduction to be clinically non-significant17 as the reduction was not demonstrated in the other outcome measure used in the study (Spastic Locomotion Disorder Index). Tremblay et al.18 reported a significant reduction in resistance during passive plantar flexion of the ankles after stretching and the effect lasted up to 35 minutes poststretching on a tilt-table (effect sizes ranging from 0.28 to 0.67). In addition, there was a significant reduction in the surface EMG post/pre-ratio during passive shortening in the ankle muscles (effect sizes ranging from 0.20 to 0.42 for triceps surae and 0.33 to 0.48 for tibialis anterior muscles; Table III).18
CHANGE IN GAIT

There is conflicting evidence on whether passive stretching can increase the range of movement in a joint. One study14 of high level of evidence and good methodological quality showed no difference poststretching but three studies16,20,21 of moderately poor to good methodological quality showed improvements in the range of movement. For those studies showing improvements in the range of movements, the effect sizes were fairly small (in general less than 10). One may argue that some increase in range of movements can assist in positioning of these children. An increase in range of hand and hip movements is also important in hand and perineal hygiene respectively. However, these arguments can only be verified with more rigorous studies. As most of the authors in these studies did not declare their acceptable cut-off points for clinical significance, it is difficult to judge if those improvements in range of movements were clinically relevant.11 Hence, there appears to be no conclusive evidence to definitely state that passive stretching can increase the range of movement in a joint, although there is some evidence favouring passive stretching in an increasing range of movements in children with CP .
CHANGE IN SPASTICITY

Richards et al.17 (level I evidence) also examined the effects of passive stretching on childrens gait pattern. They did not find any significant changes in gait patterns as measured by video recording after 30 minutes of stretching on a tilt-table.
COMPARISON OF MANUAL AND SUSTAINED STRETCHING

There is some evidence to suggest that passive stretching can reduce spasticity in children with CP as those studies showing favourable outcomes after passive stretching were mainly of higher levels of evidence and had more rigorous methodology. Similar to the range of movements, the effect sizes were fairly small and it was difficult to judge if the decrease was clinically significant. In addition, the reduction in spasticity was unable to be carried over to more functional activity such as walking.
COMPARISON OF MANUAL AND SUSTAINED STRETCHING

The nature of the stretching intervention used in the studies varied in method and dosage. The stretching regimes can be roughly divided into two categories.5 The first category involves sustained stretches by holding the targeted joint to the

From the reported studies, there appears to be some evidence to indicate sustained stretching is preferable to improve range of movements and to reduce spasticity of targeted joints in children with spasticity. More studies of higher levels of evidence

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and better methodological quality showed improvements in the range of movements and spasticity by means of sustained stretching, although the effect sizes were small. Among those studies using sustained stretching, there was no justification given by the authors14,17,18,21 regarding the duration of stretching chosen. A duration of 30 minutes stretching was the most commonly chosen in the studies14,17,18,21 which may be based on previous animal studies.5
LIMITATIONS

The significant limiting factor of this review is that the selection of studies was done by one person. Two or more reviewers should reduce the risk of selection bias in future. Another limitation of this body of evidence is the small number of participants in each study and their heterogeneity, which has already been identified as a major barrier in research, particularly in children with CP 22 The childrens ages varied at the . point of investigation, implying variability in their growth rate and their stage of neuronal plasticity, which, in turn, affects the influence of different interventions.22 None of the studies reported if the power of the sample size was calculated a priori. As the power of these studies was unknown, it is suggested that readers interpret the statistically non-significant results as inconclusive, rather than indicative of there being no effect from passive stretching.7 Most of the studies were in the middle range in the total PEDro score. It appears that there is a need to carry out well-designed trials for evaluation of the effects of passive stretching in children with CP . Due to the limitations in the methodology of these studies, it was difficult to make definite recommendations regarding the current clinical practice for children with CP . Conclusion The current level of evidence to support the effectiveness of passive stretching in children with spastic CP remains weak. The main limitations are the inadequate rigorousness of the research designs and the small number of the participants involved. There are a few conclusions that can be drawn from the existing evidence: (1) there appears to be some evidence favouring passive stretching in increasing range of movements in children with CP although the effect size remained , small; (2) there is some favourable evidence indicating that passive stretching may reduce spasticity in children with CP although the effect size and clinical merit remain limited; and (3) there is some evidence to indicate that sustained stretching is preferable to manual stretching in improving range of movement and reducing spasticity in targeted joints and muscles in studies of children with spasticity.
CLINICAL IMPLICATIONS

ing the effects of passive stretching by including it in the daily routine of patients. As there appears to be some evidence to show that sustained stretching is more effective than manual stretching of short duration in improving range of motion and reducing spasticity, perhaps emphasis should be placed on the optimum positioning of patients (both daytime and night-time positioning) so as to maximize the effects of passive stretching. Equipment such as orthoses, splinting, and serial casting can be used as alternatives to sustained stretching. However, this needs to be verified by studies of more rigorous methodological quality and of larger sample size. There are substantial gaps in this existing evidence related to passive stretching that need to be addressed by future research. More rigorous, well-controlled trials are required to investigate the impact of passive stretching in children with CP particularly with regard to functional limitation/activity , and participation. Studies that aim to investigate the optimal duration and frequency of passive stretching to obtain the desirable clinical changes in patients are necessary.
DOI: 10.1017/S0012162206001836 Accepted for publication 14th July 2006. Acknowledgement This review was an outcome of the Evidence-based Practice project funded by the Community Development Services in the Cerebral Palsy Association of Western Australia in Perth, Australia between 2000 and 2003. References 1. Mutch L, Alberman E, Hagberg B, Kodama K, Perat MV (1992) . Cerebral palsy epidemiology: where are we now and where are we going? Dev Med Child Neurol 34: 547551. 2. Rang M, Silver R, De la Gracia J. (1990) Cerebral Palsy. In: Lovell WW , Winter RB, editors. Pediatric Orthopaedics. 3rd edn. Philadelphia: JB Lippincott & Co. p 465506. 3. Farmer SE, James M. (2001) Contractures in orthopaedics and neurological conditions: a review of causes and treatment. Disabil Rehabil 23: 549558. 4. Massagli TL. (1991) Spasticity and its management in children. Phys Med Rehabil Clin N Am 2: 867889. 5. Gracies J-M. (2001) Pathophysiology of impairment in patients with spasticity and use of stretch as a treatment of spastic hypertonia. Phys Med Rehabil Clin N Am 12: 747768. 6. De Deyne PG. (2001) Application of passive stretch and its implications for muscle fibers. Phys Ther 81: 819827. 7. Butler C. (1999) AACPDM methodology for developing evidence tables and reviewing treatment outcome research. http://www.aacpdm.org (Accessed 19 June 2006) 8. PEDro. (2000) The Physiotherapy Evidence Database (PEDro) frequently asked questions: how are trials rated? http://www.cchs.usyd.edu.au/pedro (Accessed 19 June 2006) 9. Maher CG, Sherrington C, Herbert RD, Moseley AM, Elkins M. (2003) Reliability of the PEDro scale for rating quality of randomized controlled trials. Phys Ther 83: 713721. 10. Sackett DL, Richardson WS, Rosenberg W Haynes RB. (1997) , Evidence-Based Medicine: How to Practice and Teach EBM. New York: Churchill Livingstone. 11. Herbert R. (2000) How to estimate treatment effects from reports of clinical trials. I: continuous outcomes. Aust J Physiother 46: 229235. 12. Leong B. (2002) Critical review of passive muscle stretch: implications for the treatment of children in vegetative and minimally conscious states. Brain Inj 16: 169183. 13. Nash J, Neilson PD, ODwyer NJ. (1989) Reducing spasticity to control muscle contracture of children with cerebral palsy. Dev Med Child Neurol 31: 471480. 14. ODwyer N, Neilson P Nash J. (1994) Reduction of spasticity in , cerebral palsy using feedback of the tonic stretch reflex: a

The findings of this review prompt clinicians to rethink the use of passive stretching in their clinical settings. Clinically there are many children with CP particularly those profoundly , impaired, who like passive stretching as they feel it prevents muscle cramps and gives them a chance to change their position. Parents of these children also like passive stretching as they feel that they are doing something for their children. If there is no definite evidence to indicate that passive stretching has an effect on improving range of motion and reducing spasticity, perhaps passive stretching should only be used as an adjunct to other treatment techniques, rather than solely on its own. In addition, clinicians should investigate ways of prolong-

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controlled study. Dev Med Child Neurol 36: 770786. 15. Tardieu C, Lespargot A, Tabary C, Bret MD. (1988) For how long must the soleus muscle be stretched each day to prevent contracture? Dev Med Child Neurol 30: 310. 16. Miedaner JA, Renander J. (1987) The effectiveness of classroom passive stretching programs for increasing or maintaining passive range of motion in non-ambulatory children: an evaluation of frequency. Phys Occup Ther Pediatr 7: 3543. 17. Richards CL, Malouin F, Dumas F. (1991) Effects of a single session of prolonged plantarflexor stretch on muscle activations during gait in spastic cerebral palsy. Scand J Rehabil Med 23: 103111. 18. Tremblay F, Malouin F, Richards CL, Dumas F. (1990) Effects of prolonged muscle stretch on reflex and voluntary muscle activations in children with spastic cerebral palsy. Scand J

Rehabil Med 22: 171180. 19. Lespargot A, Renaudin E, Khouri N, Robert M. (1994) Extensibility of hip adductors in children with cerebral palsy. Dev Med Child Neurol 36: 980988. 20. Fragala MA, Goodgold S, Dumas HM. (2003) Effects of lower extremity passive stretching: pilot study of children and youth with severe limitations in self-mobility. Pediatr Phys Ther 15: 16775. 21. McPherson JJ, Arends TG, Michaels MJ, Trettin K. (1984) The range of motion of long term knee contractures of four spastic cerebral palsied children: A pilot study. Phys Occup Ther Pediatr 4: 1734. 22. Stanley F, Blair E, Alberman E. (2000) Cerebral palsies: Epidemiology & Causal Pathways. Clinics in Developmental Medicine No. 151. London: Mac Keith Press.

Book Review
Autism: A Neurological Disorder of Early Brain Development International Review of Child Neurology Series Edited by Roberto Tuchman and Isabelle Rapin London: Mac Keith Press (for the International Child Neurology Association), 2006, pp 354, 65.00, $US115.00 ISBN 1 898683 49 2 (Hardback) The title of this book highlights the essence of the revolution in ideas concerning the nature of autistic conditions. In the 1940s and 50s, the prevailing view was that autism was due to the cold, distant, child-rearing practices of parents, especially mothers. From the 1960s onwards the hypothesis that autistic conditions are developmental disorders with a neurological basis has evolved and is now generally accepted. The editors and contributors agree with the concept of a spectrum of autistic conditions that is much wider than Kanners original description of early infantile autism. The term autism is used in the book and in this review to refer to the whole spectrum. There are chapters discussing each of the major clinical features the social deficit, language and communication problems, stereotypies and repetitive behaviour, unusual sensory responses, motor problems, and sleep disorders. Other chapters deal in detail with research in the neurobiology of autistic spectrum disorders, including genetics and the relationship of epilepsy with the basic neuropathology. The concepts underlying neuropsychological assessment, methods used, and the value of such assessments in clinical work have a chapter to themselves, as does the epidemiology of autism. The editors focus the first chapter on Where are we now and the final one on What we have learned and where we need to go, both of which are informative summaries. The book provides a comprehensive overview of current research and theoretical ideas on the neurological basis of autistic spectrum disorders. It is refreshing to find that the contributors are able to criticise and look beyond conventional views when they deem this to be necessary. For example, the editors, in their first chapter, discuss the disadvantages of the categorical nature of the diagnostic criteria laid down in the Diagnostic and Statistical Manual of Mental Disorders, 4th edition (1994) and the ICD-10

Classification of Mental and Behavioural disorders. Diagnostic Criteria for Research 10th revision (1993). They point out that a dimensional approach is far more appropriate and emphasize that behaviour is inherently dimensional, creating problems in defining subgroups within the spectrum. Reliable and valid definitions of subgroups will be possible only when the underlying neuropathologies of different types of autism are understood. The editors also emphasize the overlap of autistic disorders with other developmental and psychiatric conditions, especially as manifested in more able individuals. The authors of the chapter on stereotypies do not agree with the currently popular hypothesis that they are a form of self-stimulation. They consider that the movements are involuntary, due to an immature and aberrant central nervous system. Yet another example of a willingness to take an unconventional view can be found in Martha Bridge Dencklas preface. She points out that the overly conventional approaches within neuropsychology, while emphasizing the neuropathological basis of autism, have had the disadvantage of focusing on cortical functions. This is not appropriate for a disorder starting early in life, probably in most cases before birth, with diverse developmental consequences which include, but are by no means limited to, functions affiliated with the cerebral cortex. Dr Denckla notes that many of the chapters in the book indicate the need to investigate subcortical systems that are basic to the development of the socialemotional brain. In a book that is so comprehensive and detailed it is surprising that there is no mention of the catatonia-like problems causing deterioration of movement and behaviour that affect around 10% or more of adolescents and adults with autistic disorders.1 However, apart from this small criticism, this book is to be recommended to researchers and professional workers engaged in clinical work in the field. It would also be of interest to parents and carers who want to broaden their understanding of the fascinating and mysterious conditions making up the autistic spectrum. Lorna Wing
DOI: 10.1017/S0012162206001848 Reference 1. Wing L, Shah A. (2000) Catatonia in autistic spectrum disorders. Br J Psychiatry 176: 357362.

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