European Journal of Neurology 2010, 17: 720725

doi:10.1111/j.1468-1331.2009.02915.x

Location and severity of spasticity in the rst 12 weeks and at 3 and 18 months after stroke
n Holmqvista,d and D. K. Sommerfelda,e A.-K. Welmera,b,c, L. Wide
a

Department of Neurobiology, Care Sciences and Society, Division of Physiotherapy, Karolinska Institutet Huddinge, Stockholm; Department of Neurobiology, Care Sciences and Society, Aging Research Center (ARC), Karolinska Institutet, Stockholm; cKarolinska

University Hospital, Stockholm; dDivision of Neurology, Department of Clinical Sciences Karolinska Institutet Huddinge, Stockholm; and
e

Department of Geriatric Medicine, Danderyd Hospital, Stockholm, Sweden

Keywords:

age, location, muscle spasticity, severity, stroke

Received 22 May 2009 Accepted 11 November 2009

Background and purpose: There is no consensus concerning the location or severity of spasticity, or how this changes with time after stroke. The purpose was to describe: the location and severity of spasticity, in dierent muscle groups, during the rst 12 weeks and at 3 and 18 months after stroke; the association between the severity of spasticity and control of voluntary movements; and the occurrence of spasticity in younger versus older patients. Methods: In a cohort of consecutive patients, the following parameters were assessed during the rst 12 weeks (n = 109) and at 3 (n = 95) and 18 (n = 66) months after rst-ever stroke: spasticity, by the Modied Ashworth Scale in dierent muscle groups; plantar-exor clonus, by physical examination; and movement function, by the Lindmark Motor Assessment Scale. Results: During the rst 12 weeks and at 3 months after stroke, spasticity was most common in the anti-gravity muscles. The severity of upper extremity spasticity increased over time (P < 0.05). Upper extremity spasticity and movement scores were moderately associated (r = )0.61, P < 0.05). At 3 months, spasticity was more common amongst the younger patients (P < 0.05). Conclusions: The results conrm that spasticity is most common in the anti-gravity muscles and is associated with the control of voluntary movements. As the severity of spasticity also increased after 3 months, when neurally mediated spasticity is expected to have passed its peak, intrinsic muscle changes may play a larger role than neural components with the passage of time after stroke.

Introduction
Impairments resulting from damage to the upper motor neuron (UMN), including lesions in the pyramidal and parapyramidal tracts, exhibit positive and negative features [1]. The positive features are characterized by muscle over-activity, of which spasticity is one example [2]. The negative features are weakness and loss of dexterity [1]. Spasticity is dened as a velocity-dependent increase in tonic stretch reexes experienced by a clinician attempting to ex or extend a limb in patients with UMN lesions [3]. Spasticity may be exacerbated by

Correspondence: A.-K. Welmer, Department of Neurobiology, Care Sciences and Society, Aging Research Center (ARC), Karolinska Institutet, Ga vlegatan 16, S-113 30 Stockholm, Sweden (tel.: +46 70 745 18 18; fax: +46 8 690 58 19; e-mail: anna-karin.welmer@ki.se).

muscle contracture, because when a muscle and its spindles shorten as a result of contracture, a stretch of the muscle may increase the size of the tonic stretch reex [1]. The neural component of spasticity has been shown to reach its peak 13 months after stroke [4]. We recently investigated the occurrence of clinically assessed spasticity and its impact on functioning during the rst 12 weeks [5], and at 3 [5] and 18 months [6] after rst-ever stroke. Twenty-one per cent of all the 95 consecutive patients exhibited spasticity in the rst 12 weeks, 19% did so at 3 months and 20% of remaining 66 patients did so at 18 months after stroke. Amongst the hemiparetic patients, 26%, 28% and 34% exhibited spasticity at the respective assessments. These ndings were in accordance with those of ODwyer et al. [1], who found electromyography-veried spasticity amongst 21% of hemiparetic patients assessed 13 months after stroke, and with Lundstro m et al. [7],
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who found clinically assessed spasticity 1 year after rst-ever stroke in 17% of all patients with stroke. Another study has found that as many as 39% of all stroke patients suer from spasticity 12 months after rst-ever stroke [8]; however, in that study, non-velocity-dependent resistance to passive stretch, i.e. shortened muscle length, was also regarded as evidence of spasticity. Much focus in stroke care is placed on reducing spasticity [9]. Yet, details on which muscles are most commonly aected by spasticity, how severely they are aected, and how this changes over time from the onset of stroke have been poorly documented in the stroke literature [10]. Our earlier articles [5,6] show that patients with spasticity show impaired voluntary movement functions, i.e. hemipareses. However, hemiparesis and severe activity limitations also occurred without the presence of spasticity [5,6]. The correlations between spasticity and other functioning was low at 3 months [5] and low to moderate at 18 months after stroke [6]. Another study suggests that spasticity may help patients to support body weight during ambulation [11], implying that spasticity might be advantageous for some patients. The extent to which the severity of spasticity is associated with voluntary movements has, so far, been poorly documented. It has been suggested that tendon reexes decrease with age [12]. Further, it has been suggested that disabling spasticity is more common amongst the younger than the older patients at 1 year post-stroke [7]. From an epidemiological perspective, it seems important to ascertain whether spasticity is an impairment aecting mostly younger patients with stroke. However, whether the occurrence of any spasticity diers between younger and older patients has not been described. The following questions were to be answered by the study: (i) in which muscle groups does spasticity most commonly occur and how severely are these muscle groups aected by spasticity in the rst 12 weeks and at 3 and 18 months after stroke? (ii) How many muscle groups are aected by spasticity in the rst 12 weeks and at 3 and 18 months after stroke? (iii) What is the association between the severity of spasticity and control of voluntary movements? (iv) How common is spasticity in younger versus older patients?

criteria were patients residing in Stockholm who presented with an acute, rst-ever stroke (unless characterized by subarachnoid haemorrhage or a cerebellar lesion), in the absence of other diagnoses aecting muscle tone and who were conscious and agreed to participate in the study.
Outcome measures

Spasticity It was assessed by the Modied Ashworth Scale [13]. If a patients score was above 0 for any of the tested muscle groups, he or she was deemed to exhibit spasticity. The Modied Ashworth Scale was computed to a scale ranging from 0 to 5 to include the score 1+. Reliability studies of the Modied Ashworth Scale indicate that a high inter-rater reliability can be achieved, but is not achieved in all conditions [14]. The lack of standard guidelines for positioning and performance may contribute to the variability of results [14]. The muscle groups evaluated in the upper extremity were arm adductors, elbow exors and extensors, wrist exors and extensors, and nger exors (tested in the sitting position, if possible); and in the lower extremity: hip adductors, knee exors and extensors, and plantar exors (tested in the supine position). Plantar-exor clonus was also evaluated by counting the number of clonic beats. Inexhaustible clonus was dened as more than 10 beats. Severe spasticity was dened as a Modied Ashworth Scale score 2 in one muscle group or more, or inexhaustible clonus. Control of voluntary movements It was assessed using part one of the seven-part Lindmark Motor Assessment Scale [15] (upper extremity movements, 057 points and lower extremity movements, 036 points; the higher the score, the better). The scale is derived from the Fugl-Meyer Assessment [16] but involves both sides and is considered valid and reliable for assessment of movement impairments in stroke patients [15]. The patients were assessed during the rst 12 weeks and at 3 and 18 months after acute stroke. All tests were performed either in the hospital or in the patients home by four purpose-trained physiotherapists. To improve the inter-rater reliability between the therapists involved, more than one-third of the assessments were performed by at least two of the physiotherapists. When more than one therapist assessed a patient, one of the therapists conducted the actual assessment and the other therapist/therapists noted the scores. The score noted represented a consensus reached by the therapists involved in the assessment. All tests were performed in a predened order.

Methods
Participants

All consecutive stroke patients were recruited from the stroke unit of Danderyd Hospital in Stockholm, Sweden, between June 2001 and March 2002. Inclusion

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Data analysis

Results
In the rst 12 weeks, 109 patients 67 women and 42 men, with a median age on recruitment of 79 years (inter-quartile range [IQR] 7384, range 4493) were enrolled in the study. Ninety-ve patients 60 women and 35 men, with a median age on recruitment of 80 years (IQR 7385, range 4493) were still enrolled on/in the study at the end of the 3-month follow-up period; and 66 patients 44 women and 22 men, with a median age on recruitment of 78.5 years (IQR 7283, range 44 to 93) still participated at the end of the 18month follow-up period. Twenty-two patients showed spasticity in the rst 12 weeks after stroke (median age 74 years, IQR 6578, range 4490); 18 patients did at 3 months (median age 75.5 years, IQR 5681, range 4490); and 13 patients did so at 18 months (median age 77, IQR 7281, range 5590). When only the 66 patients who were followed up after 18 months were analysed, 10 patients showed spasticity in the rst 12 weeks after stroke, and 13 patients did so at 3 months.
Location of spasticity and severity of spasticity in the affected muscle groups

Descriptive statistics were used to present the numbers of patients with spasticity in each of the tested muscle groups. Median, interquartile ranges (IQRs) and ranges were calculated for the number of muscle groups with spasticity in each patient and Modied Ashworth Scale scores, for each of the tested muscle groups. The occurrence of spasticity in younger (<65 years) versus older (65 years) patients was calculated using the chisquared test. Friedmans ANOVA was used to analyse dierences in spasticity scores and the number of muscle groups with spasticity over time, i.e. all three assessments were included in each analysis. Spearmans correlation coecient was used to establish the relation of the Modied Ashworth Scale with the Lindmark Motor Assessment Scale. All spasticity scores for the upper and lower extremities, respectively, were added together for the analyses. Correlation coecients with absolute values below 0.5 were referred to as low: between 0.5 and 0.75, as moderate to good; and coecients with values greater than 0.75, as high [17]. The signicance level was set at P < 0.05. Data were analysed using STATISTICA 7.0 for Windows (Stat Soft. Inc, Tulsa, OK, USA).
Ethics

The study was approved by the Regional Ethical Review Board in Stockholm. Informed consent was obtained from all participants.

Table 1 shows the number of patients and the percentage of all patients with spasticity in each of the tested muscle groups, the median and range of the spasticity scores, in the rst 12 weeks and at 3 and 18 months after stroke as well as P-values for the

Table 1 Number of patients and percentage of all patients with spasticity assessed with the Modied Ashworth Scale (MAS) in each of the tested muscle groups; median and range of the scores, in the rst 12 weeks and at 3 and 18 months after stroke as well as P-values for the differences in MAS scores over time The rst 12 weeks n = 109 Number of spastic patients (%) Upper extremity Arm adductors Elbow exors Elbow extensors Wrist exors Wrist extensors Finger exors Lower extremity Hip adductors Knee exors Knee extensors Plantar exors MAS Median (range) 3 months after stroke n = 95 Number of spastic patients (%) MAS Median (range) 18 months after stroke n = 66 Number of spastic patients (%) MAS Median (range)

P-value

2 (1.8) 18 (16.5) 8 (7.3) 7 (6.4) 0 (0) 5 (4.6) 6 5 4 0 (5.5) (4.6) (3.7) (0)c

1 (11) 1 (12) 1 (11.5) 1 (11.5) NA 1 (11.5) 1 (12) 1.5 (12) 1 (11.5) NA

7 (7.4) 15 (15.8) 10 (10.5) 6 (6.3) 2 (2.1) 8 (8.4) 5 7 8 1 (5.3) (7.4) (8.4) (1.1)d

1 (13) 1 (13) 1.25 (13) 1 (13)a 2 (13)a 1 (12)b 2 2 1 3 (13) (13) (13) (33)

4 (6.1) 9 (13.6) 9 (13.6) 10 (15.2) 4 (6.1) 8 (12.1) 3 6 5 3 (4.5) (9.1) (7.6) (4.5)d

1.5 (13) 1.5 (13) 1.5 (13) 2 (13) 2 (23) 2.5 (13) 3 (23) 1.5 (13) 2 (13) 3 (13)

0.142 0.956 0.005 0.034 0.037 0.040 0.273 0.607 0.424 0.504

NA, not applicable; aMissing data for four patients (because of pain n = 3); bOne patient not tested because of pain; cNine additional patients had clonus; dSix additional patients had clonus; bold values indicate P-values < 0.05.

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dierence in spasticity scores over time. The severity of spasticity increased over time for elbow extensors, wrist exors and extensors, and nger exors (P < 0.05). When adding the Modied Ashworth Scale scores for all tested muscle groups, the severity of spasticity increased for the upper but not for the lower extremities (P = 0.004 and P = 0.128, respectively. In the rst 12 weeks after stroke, severe spasticity was present in two (9%) of the 22 patients, in six (33%) of the 18 patients at 3 months and in 11 (85%) of the 13 patients at 18 months. Of these patients, two had inexhaustible clonus at 3 months and four had at 18 months. When analysing only the 66 patients who were followed up after 18 months, severe spasticity was present in one (10%) of the 10 patients in the rst 12 weeks, and in ve (38%) of the 13 patients at 3 months.
Number of spastic muscle groups

Scale for the lower extremities was not statistically signicant.

Occurrence of spasticity in younger versus older patients

Table 2 shows median, IQR and range for the number of muscle groups with spasticity amongst the six muscle groups assessed in the upper extremity and the four muscle groups assessed in the lower extremities, in patients with spasticity in the rst 12 weeks and at 3 and 18 months. It also shows the P-values for the dierences in the number of muscle groups with spasticity over time.
Association between the severity of spasticity and control of voluntary movements

Of all 109 patients assessed in the rst 12 weeks after stroke, 10 were below 65 years of age and nine of these were followed up at 3 and 18 months. Five of these younger patients showed spasticity both in the rst 12 weeks (50%) and at 3 months (56%), and three patients did so at 18 months after stroke (33%). Of the older patients (65 years) (n = 99 in the rst 12 weeks; n = 86 at 3 months; and n = 57 at 18 months), 17 (17%) patients showed spasticity in the rst 12 weeks after stroke, 13 (14%) did so at 3 months and 10 (18%) at 18 months after stroke. The dierences between the numbers of younger versus older patients with spasticity tended to be statistically signicant in the rst 12 weeks (P = 0.067) and were statistically signicant at 3 months (P = 0.031) but not at 18 months (P = 0.386).

Discussion
In the present study, we focused on the location and severity of spasticity, in dierent muscle groups, in the rst 12 weeks and at 3 and 18 months after stroke, on the association between the severity of spasticity and voluntary movements, and on the occurrence of spasticity in younger versus older patients. To our knowledge, this is the rst study investigating which muscles are aected by spasticity as well as how severely these muscles are aected, and how this changes over time in a consecutive sample of patients with rst-ever stroke. Our ndings from the assessments in the rst 12 weeks and at 3 months are in accordance with the general assumption that spasticity is most

For the 17 patients with upper extremity spasticity at 3 months, the correlation between the Modied Ashworth Scale for the upper extremities and the Lindmark Motor Assessment Scale for the upper extremities was moderate (r = )0.61, P < 0.05). For the 10 patients with lower extremity spasticity at 3 months, the correlation between the Modied Ashworth Scale for the lower extremities and the Lindmark Motor Assessment

Table 2 Median, (IQR), [range] of the number of muscle groups with Modied Ashworth Scale-assessed spasticity, in the upper and lower extremity, respectively, of all patients with spasticity, in the rst 12 weeks (n = 22) and at 3 (n = 18) and 18 months (n = 13) after stroke and Pvalues for the differences in number of spastic muscle groups over time The rst 12 weeks n; median number of muscle groups with spasticity (IQR) [range] Upper extremity, Six muscle groups assessed Lower extremity, four muscle groups assessed n = 20; 1 (13) [15] n = 8a; 2 (12.5) [13] 3 months after stroke n; median number of muscle groups with spasticity (IQR) [range] n = 17; 3 (23) [16] n = 10b; 2 (13) [14] 18 months after stroke n; median number of muscle groups with spasticity (IQR) [range] n = 13; 4 (24) [16] n = 10b; 1.5 (12) [13]

P-values 0.114 0.549

n = number of patients with spasticity; IQR, interquartile ranges; aNine patients had clonus; bSix patients had clonus.

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common in muscles resisting gravity, i.e. the arm exors and leg extensors [18]. It has been suggested that this phenomenon is because of dierences in muscle mass in favour of the anti-gravity muscles [19]. Alternatively, it may be attributed to a dierential control of exor and extensor muscles of upper and lower limbs by supraspinal centres, with a larger inuence of proprioceptive reexes in the lower limb [20]. However, the result of the 18-month assessment was not in accordance with this assumption. This may be explained by diminished tonic stretch reexes at 18 months after stroke, which are most evident 13 months after stroke [4]. In the rst 12 weeks, 2 was the highest spasticity score, and at 3 and 18 months, 3 was the highest spasticity score, i.e. no patient scored 4 on the Modied Ashworth Scale on any occasion. The increase in the severity of spasticity in some muscles between the rst assessment and at 3 months may be explained by neural changes, i.e. increased tonic stretch reexes [4]. Further, the increase in spasticity between 3 and 18 months may be explained by intrinsic muscle changes rather than by neural changes [1,4]. Because patients with spasticity may be more prone to develop muscle contracture and muscle contracture may exacerbate spasticity [1], it is reasonable to assume that the severity of Modied Ashworth Scale-assessed spasticity is often aggravated over time, as shown by the present study. The occurrence of inexhaustible clonus also increased over time. It has been suggested that the underlying mechanism of clonus is hyperactive phasic stretch reexes [2], or an interaction of central and peripheral events [21]. The analyses of changes over time are limited by the small number of patients, which makes it dicult to discover statistically signicant changes. This is a limitation of the study. The severity of Modied Ashworth Scale-assessed spasticity was analysed in comparison with control of voluntary movements only at 3 months after stroke. This was performed because the tonic stretch reex reaches its peak at this time after stroke [4]. The severity of upper extremity spasticity was associated with the severity of impaired upper extremity voluntary movements, but this was not the case for the lower extremities. These dierences between the upper and lower extremities may be explained by dierences in supraspinal control as the upper limb normally functions predominantly under voluntary control whilst movements of the lower limb are inuenced to a larger extent by spinal locomotor centres [20]. Our study does not give information on whether spasticity limits the patients movements or whether both spasticity and impaired movements reect the general neurological status of the patient, which may constitute a limitation of the study.

Spasticity was signicantly more common amongst the younger patients at 3 months and borderline statistically signicant during the rst 12 weeks after stroke. If reex decrease with increasing age, as seen in the tendon reexes [12], is attributable also to the tonic reexes, this might be a plausible explanation for the dierences between younger and older patients found in the present study and also in another study [7]. The fact that this dierence was not signicant at the 18-month assessment may be explained by diminished neural components of spasticity and a greater inuence of intrinsic muscle changes at that time point after stroke [4]. Although the study sample was small and few patients were spastic, our nding supports that of Lundstro m et al. [7], who found that disabling spasticity was more common amongst the younger stroke patients than amongst the older patients at 1 year post-stroke. Intrinsic muscle changes, associated with immobility, may be more common amongst the older patients [4]. Weaknesses of the study include the relatively small sample sizes as well as the decreased sample size at each measurement time, leading to a less representative sample of the initial population, which limits generalization of the results. The higher minimum age in the 18-month group may have aected the number of patients with spasticity at the 18-month assessment. Further, the fact that more spasticity tests were performed on exor muscles than on extensor muscles may have biased the results by showing a larger proportion of spastic exor muscles. The exclusion of patients with recurrent strokes further limits the generalization of the results to patients with one stroke. Studies with larger samples, or a systematic review with a meta-analysis, are required to establish the exact location and severity of spasticity over time from stroke onset. However, the present study provides important information for those who plan similar, larger trials, both observational and treatment studies. Finally, the validity of the Modied Ashworth Scale can be criticized because the scale does not distinguish between reexogenic and peripheral contributions to the resistance to stretch [22]. It has also been shown that the Modied Ashworth Scale may confounded by contractures [23]. However, the Modied Ashworth Scale is one of the most commonly used clinical measures of muscle tone. In summary, spasticity was more common in the upper than the lower extremities. In the rst 12 weeks and at 3 months after stroke, spasticity was most common in the anti-gravity muscles. The severity of spasticity continued to increase until 18 months after stroke for the upper extremity, suggesting that intrinsic muscle changes, rather than neural components, i.e. the tonic stretch reex, play a larger role with the passage

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of time after stroke [1,4]. However, this was not signicant for the lower extremity. The severity of upper, but not lower, extremity spasticity was associated with the severity of impaired control of voluntary movements, perhaps because of a larger inuence of spinal locomotor centres in the lower extremity [20]. Together with those of others [7], our results indicate that spasticity is more common amongst the younger than the older patients at 3 months after stroke, suggesting that neurally mediated spasticity is more probably to occur in the younger stroke population.

Acknowledgements
This study was supported by grants from Karolinska Institutet and Karolinska University Hospital. We thank physiotherapists Helena Vesterlin and Elsy Eek for assessing the patients, and Magnus von Arbin, MD, PhD, for constructive advice.

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