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PubMed2006

Fibre type-specific increase in passive muscle tension in spinal cord-injured subjects with spasticity.

Patients with spasticity typically present with an increased muscle tone that is at least partly caused by an exaggerated stretch reflex. However, intrinsic changes in the skeletal muscles, such as altered mechanical properties of the extracellular matrix or the cytoskeleton, have been reported in response to spasticity and could contribute to hypertonia, although the underlying mechanisms are poorly understood. Here we examined the vastus lateralis muscles from spinal cord-injured patients with spasticity (n = 7) for their passive mechanical properties at three different levels of structural organization, in comparison to healthy controls (n = 7). We also assessed spasticity-related alterations in muscle protein expression and muscle ultrastructure. At the whole-muscle level in vivo, we observed increased passive tension (PT) in some spasticity patients particularly at long muscle lengths, unrelated to stretch reflex activation. At the single-fibre level, elevated PT was found in cells expressing fast myosin heavy chain (MyHC) isoforms, especially MyHC-IIx, but not in those expressing slow MyHC. Type IIx fibres were present in higher than normal proportions in spastic muscles, whereas type I fibres were proportionately reduced. At the level of the isolated myofibril, however, there were no differences in PT between patients and controls. The molecular size of the giant protein titin, a main contributor to PT, was unchanged in spasticity, as was the titin : MyHC ratio and the relative desmin content. Electron microscopy revealed extensive ultrastructural changes in spastic muscles, especially expanded connective tissue, but also decreased mitochondrial volume fraction and appearance of intracellular amorphous material. Results strongly suggest that the global passive muscle stiffening in spasticity patients is caused to some degree by elevated PT of the skeletal muscles themselves. We conclude that this increased PT component arises not only from extracellular matrix remodelling, but also from structural and functional adaptations inside the muscle cells, which alter their passive mechanical properties in response to spasticity in a fibre type-dependent manner.

Adult↗

PubMed2001

Physiologic and clinical monitoring of spastic hypertonia.

Spasticity has been defined as "a motor disorder characterized by a velocity-dependent increase in tonic stretch reflexes with exaggerated tendon jerks, resulting from hyperexcitability of the stretch reflex, as one component of the upper motor neuron syndrome." Increased motor neuron excitability and enhanced stretch-evoked synaptic excitation of motor neurons are potential neurophysiologic mechanisms to explain this phenomenon. The relative contribution of these two distinct mechanisms likely varies depending on the location of the lesion in the central nervous system. The patient history is an important component of the clinical evaluation focusing on potential nociceptive inputs that can worsen spasticity (e.g., urinary tract infections, skin breakdown). Assessment of the impact of the spasticity on function (positive and negative), position, care of the patient, and pain should be pursued. Clinical examination of spasticity is performed using methods to evoke and quantify spastic reflex responses to muscle stretch stimuli and to observe the patient performing functional tasks to note the impact of spasticity on their performance. Treatment is based on the negative impact of the spasticity on the patient, severity of the problems, and whether the hypertonicity is focal or diffuse in distribution (see article by Elovic elsewhere in this issue). First-line treatments include elimination of nociceptive stimuli, range of motion, seating and positioning, and other physical modalities. If additional intervention is necessary, oral medications are implemented for widespread spasticity, whereas focal problems are treated with prolonged stretching and splinting or casting to maintain muscle stretch and optimal positioning. In more severe cases, invasive procedures may be needed to supplement other treatments. Neurolytic procedures are pursued for focal tone problems. For generalized hypertonicity, intrathecal pump administration of medications or surgical interruption of reflex pathways has been helpful. Ultimately, the clinician must systematically approach the evaluation and treatment of spasticity. As decisions regarding moving from less to more invasive treatments are discussed, the potential risks and side effects of treatment options must be weighed versus the potential benefits that the patient might receive to maintain a rational approach to the management of spasticity.

Anti-Dyskinesia Agents↗

PubMed1987

Spasticity.

Spasticity has been defined as velocity-dependent hyperactivity of stretch reflexes; it is therefore only one aspect of the complex syndrome produced by a lesion of the upper motoneuron. Although spasticity may be partially responsible for joint contractures, it does not produce most of the functional disability experienced by patients with upper motoneuron lesions. Paresis, fatigability, lack of dexterity, etc., account for most of these patients' complaints. The pathophysiology of spasticity is poorly understood but appears to be related to an increased excitatory state at the segmental spinal level; there is no evidence for increased sensitivity of muscle spindles in spastic patients. Several mechanisms for this increased excitability within the spinal cord have been proposed. There are different types as well as degrees of spasticity. Clinical neurophysiologic recordings of reflex activity in patients with spasticity provide the means to differentiate among the various types of spasticity, to select the therapy most likely to be effective in a particular patient, and to see the results of its employment objectively. The latter will prove whether a specific therapy is useful or not. Ablative treatment at the level of the peripheral nerve or dorsal root may be useful, particularly when spasticity is severe. Drugs such as baclofen or diazepam relieve flexor spasms but are not particularly effective against spasticity itself. Dantrolene acts to weaken muscles, but that is not often helpful. Rarely do any of these therapies increase function; there are no effective cures for paresis or related negative manifestations of chronic spasticity.

Combined Modality Therapy↗

PubMed2003

Enhanced regional washout of technetium-99m-sestamibi in patients with coronary spastic angina.

BACKGROUND: Reverse redistribution and rapid washout of 99mTc-sestamibi are observed in patients with acute myocardial infarction and may indicate viable myocardium. However, the clinical significance of this phenomenon has not been rigorously examined in other cardiac diseases. Thus, we investigated whether reverse redistribution and washout of 99mTc-sestamibi could be used in the diagnosis and follow-up of patients with coronary spastic angina. METHODS: Thirty patients diagnosed as coronary spastic angina were examined. During coronary arteriography, spasm was induced by provocation test with ergonovine, and only total or subtotal occlusion was considered positive. Myocardial perfusion tomography was obtained 45 min (early) and 3 hr (delayed) after 99mTc-sestamibi injection. Segmental defect score was visually graded from 0 (normal) to 4 (defect), and a total defect score was determined as the sum of defect scores for all segments. Washout rate of 99mTc-sestamibi from the myocardium was calculated for each segment. After medical treatment with calcium antagonists and nitrates for 3 months, 99mTc-sestamibi imaging was repeated. RESULTS: Out of 30 patients, on the early images 17 (57%) patients demonstrated decreased 99mTc-sestamibi uptake in spastic segments; on the other hand, 24 (80%) patients did decreased 99mTc-sestamibi uptake in spastic segments on delayed images. Total defect scores in delayed images were higher than those in early images (6.9 +/- 0.3 vs. 3.6 +/- 0.4, p < 0.01). Reverse redistribution of 99mTc-sestamibi was observed in 17 out of 30 patients (57%) with coronary spastic angina. Washout rate of 99mTc-sestamibi from spastic segments was higher than that from non-spastic segments (16 +/- 2% vs. 11 +/- 5%, p < 0.01). After medical treatment, washout rate from spastic segments was decreased to 10 +/- 4 (p < 0.01), and left ventricular ejection fraction was increased from 63 +/- 8% to 73 +/- 4% (p < 0.01). CONCLUSION: Rapid washout of 99mTc-sestamibi was observed in patients with coronary spastic angina and might indicate that the ability of myocyte to retain the tracer was impaired due to repetitive brief ischemia by coronary spasm. The early and delayed 99mTc-sestamibi imaging provides useful information for the diagnosis and responses to the treatment in patients with coronary spastic angina.

Adult↗

PubMed2005

A comparison of spastic diplegic and tetraplegic cerebral palsy.

The aim of this study was to compare spastic diplegic and tetraplegic cerebral palsy. Thirty-eight children had spastic diplegic cerebral palsy and 48 spastic tetraplegic cerebral palsy. Risk factors of cerebral palsy, seizures, severity of cerebral palsy, electroencephalogram, and magnetic resonance imaging findings were analyzed. Gestational history, low birth weight, and perinatal pathologies were present in similar percentages in both groups. Lower values of the Apgar score were recorded more often in the tetraplegic cerebral palsy group than the diplegic group. The children with spastic diplegia were classified more frequently into levels I and II of the Gross Motor Function Classification System, but patients with spastic tetraplegia were classified more frequently into levels IV and V. Similarly, mental retardation was observed more frequently in the patients with spastic tetraplegia. In magnetic resonance imaging, periventricular leukomalacia was detected in a higher proportion of children with spastic diplegia than in patients with tetraplegia. Cerebral atrophy occurred more frequently in the tetraplegic group compared with diplegic patients. Twenty-four (50.0%) children with spastic tetraplegia had epilepsy compared with six children with spastic diplegia. The incidence of intractable epilepsy was higher in the tetraplegic patients than in the children with spastic diplegia.

Adolescent↗

PubMed2005

Tail muscles become slow but fatigable in chronic sacral spinal rats with spasticity.

Paralyzed skeletal muscle sometimes becomes faster and more fatigable after spinal cord injury (SCI) because of reduced activity. However, in some cases, pronounced muscle activity in the form of spasticity (hyperreflexia and hypertonus) occurs after long-term SCI. We hypothesized that this spastic activity may be associated with a reversal back to a slower, less fatigable muscle. In adult rats, a sacral (S2) spinal cord transection was performed, affecting only tail musculature and resulting in chronic tail spasticity beginning 2 wk later and lasting indefinitely. At 8 mo after injury, we examined the contractile properties of the segmental tail muscle in anesthetized spastic rats and in age-matched normal rats. The segmental tail muscle has only a few motor units (<12), which were easily detected with graded nerve stimulation, revealing two clear motor unit twitch durations. The dominant faster unit twitches peaked at 15 ms and ended within 50 ms, whereas the slower unit twitches only peaked at 30-50 ms. With chronic injury, this slow twitch component increased, resulting in a large overall increase (>150%) in the fraction of the peak muscle twitch force remaining at 50 ms. With injury, the peak muscle twitch (evoked with supramaximal stimulation) also increased in its time to peak (+48.9%) and half-rise time (+150.0%), and decreased in its maximum rise (-35.0%) and decay rates (-40.1%). Likewise, after a tetanic stimulation, the tetanus half-fall time increased by 53.8%. Therefore the slow portion of the muscle was enhanced in spastic muscles. Consistent with slowing, posttetanic potentiation was 9.2% lower and the stimulation frequency required to produce half-maximal tetanus decreased 39.0% in chronic spinals. Interestingly, in spastic muscles compared with normal, whole muscle twitch force was 81.1% higher, whereas tetanic force production was 38.1% lower. Hence the twitch-to-tetanus ratio increased 104.0%. Inconsistent with overall slowing, whole spastic muscles were 61.5% more fatigable than normal muscles. Thus contrary to the classical slow-to-fast conversion that is seen after SCI without spasticity, SCI with spasticity is associated with a mixed effect, including a preservation/enhancement of slow properties, but a loss of fatigue resistance.

Animals↗

PubMed2003

Inferior mechanical properties of spastic muscle bundles due to hypertrophic but compromised extracellular matrix material.

The passive mechanical properties of small muscle fiber bundles obtained from surgical patients with spasticity (n = 9) and patients without neuromuscular disorders (n = 21) were measured in order to determine the relative influence of intracellular and extracellular components. For both types of patient, tangent modulus was significantly greater in bundles compared to identical tests performed on isolated single cells (P < 0.05). However, the relative difference between bundles and single cells was much greater in normal tissue than spastic tissue. The tangent modulus of normal bundles (462.5 +/- 99.6 MPa) was 16 times greater than normal single cells (28.2 +/- 3.3 MPa), whereas the tangent modulus of spastic bundles (111.2 +/- 35.5 MPa) was only twice that of spastic muscle cells (55.0 +/- 6.6 MPa). This relatively small influence of the extracellular matrix (ECM) in spastic muscle was even more surprising because spastic muscle cells occupied a significantly smaller fraction of the total specimen area (38.5 +/- 13.6%) compared to normal muscle (95.0 +/- 8.8%). Based on these data, normal muscle ECM is calculated to have a modulus of 8.7 GPa, and the ECM from spastic muscle of only 0.20 GPa. These data indicate that spastic muscle, although composed of cells that are stiffer compared to normal muscle, contains an ECM of inferior mechanical strength. The present findings illustrate some of the profound changes that occur in skeletal muscle secondary to spasticity. The surgical implications of these results are discussed.

Adult↗

PubMed1989

A dynamic EMG profile index to quantify muscular activation disorder in spastic paretic gait.

Spasticity is a complex phenomenon that interferes with motor control. Existing clinical and physiological measures of spasticity have mainly focused on the evaluation of clonus and reflexes. Subjected to the limitation of testing in a resting position, the results may not necessarily reflect the extent of functional impairment caused by spasticity. To evaluate spasticity in a dynamic, voluntary movement such as locomotion, a task-specific approach is essential. A dynamic index, I, derived from the EMG activity obtained during treadmill walking in human subjects, is therefore proposed as a functionally relevant measurement of spasticity in locomotion. I, defined as the ratio of integrated EMG in the pre-determined 'off' window of the normalized gait cycle to that in the 'on' window, would indicate the degree of abnormal activation of locomotor muscles from their normally relaxed state as compared to the total recruitment in the active state during walking. The present study done on 5 normal and 8 spastic paraparetic subjects showed that I was homogeneously low in the normal group but abnormally high and variable in the spastic group. A case study has further demonstrated that I is sensitive to the alteration in locomotor spasticity with pharmacological intervention, and the change in I parallels the improvement in the kinematics observed. This preliminary study indicates that the proposed index appears to be a functionally relevant and dynamic measurement of spastic locomotor disorder.

Adult↗

PubMed1976

Action of dantrolene sodium in spasticity with low dependence on fusimotor drive.

The effects of dantrolene sodium, an anti-spasticity drug with a site of action within the muscle fibres, were studied in 19 patients with spastic paresis. Oral doses were successively increased from 100 mg/day to a maximal tolerated level or up to 800 mg/day. Trial periods were 8-13 weeks. The responses of stretch reflexes to local cooling over the spastic muscles were used to differentiate alpha and gamma spasticity. In the knee extensor and flexor muscle groups, cryo-negative alpha-spasticity was seen in 25 and cryo-positive gamma-spasticity in 4 muscle groups. Ankle clonus was cryo-positive in 14 of 15 cases. Resistance to passive knee joint movements, ankle clonus and isometric or isokinetic muscle strength was determined quantitatively. The gait was recorded by intermittent-light photography and the muscle activation patterns in gait were studied in recordings of the average EMG from limb muscles. Functional disability and spasms were assessed from clinical examinations and interviews. Passive resistance at slow (6%/sec) and fast (30 degrees/sec) knee joint movements decreased by 32% in the extensor muscles (p = 0.005 resp. 0.001) and by 23-26% in the flexor muscles (not significant). Reduced passive resistance was observed in 16 of the muscles with alpha-spasticity and in all 4 of the muscle groups with gamma-spasticity. Clonus was diminished or abolished in 14 of 15 patients with this sign. Maximal isometric or isokinetic muscle strength was unaltered in the majority of the patients. In a few the strength was increased, in some it was decreased. The averaged EMG activity during walking as studied in 10 patients were increased in 35 of the 57 muscle groups examined. In some muscle groups, exaggerated activity attributable to spastic reflexes was reduced. Motor disability was decreased significantly in 10 patients. It was not significantly changed in 5 and deteriorated in 4 patients. Drowsiness and subjective muscle weakness were the most frequent side-effects. SGOT and SGPT were increased in 3 cases.

Adult↗

PubMed2005

A physiologically based clinical measure for spastic reflexes in spinal cord injury.

OBJECTIVE: To test the validity of the Spinal Cord Assessment Tool for Spastic reflexes (SCATS), a clinical tool intended to rate spastic motor behavior after spinal cord injury (SCI). DESIGN: By using correlational analyses, the SCATS was validated using concurrent measurements of kinematics and electromyograms and traditional assessments of spasms and spastic hypertonia. SETTING: Research laboratory (kinematics and electromyography) and outpatient medical clinic (traditional measures of spastic hypertonia). PARTICIPANTS: Eleven people with SCI were used for kinematic and electromyographic measurements. Seventeen people with SCI were used for comparison with other clinical scales. INTERVENTIONS: Not applicable. Main outcome measures Kinematic and surface electromyographic measurements of the tested lower extremity were used to quantify magnitude and/or duration of motor behaviors, and the Penn Spasm Frequency Scale (PSFS) and the Ashworth Scale were used to measure spasm frequency and resistance to joint movement for the hip flexors, knee flexors, and ankle plantarflexors, respectively. Concurrently, the SCATS was used to assess the clonus response to an imposed ankle dorsiflexion, the flexion response to a stimulus to the foot, and the knee extensor activity in response to an imposed leg extension. Each component of the SCATS was compared with the Ashworth Scale, the PSFS, and kinematic and electromyographic measurements by using the Spearman rank correlation test. RESULTS: Clonus, flexor spasm, and extensor spasm responses measured by using the SCATS correlated significantly with kinematic and electromyographic recordings (P<.01). Significant correlations were also observed between the SCATS extensor spasms and the Ashworth scores for hip and knee flexors and for ankle plantarflexors (rho=.98, .88, .61, respectively). Also, SCATS flexor spasms and SCATS clonus scores correlated significantly with some of the Ashworth scores. Only SCATS clonus scores correlated significantly with spasm frequency measures (rho=.59, P<.05). CONCLUSIONS: The SCATS produced a valid measure of 3 distinct types of spastic motor behaviors in SCI and may provide a complementary tool for measuring spastic hypertonia. Such a measure is valuable because current assessment tools do not differentiate between the different types of spastic motor behaviors that manifest after SCI. Distinguishing the 3 spastic reactions using an efficient and valid clinical tool may help guide management of spastic hypertonia in SCI.

Adolescent↗

PubMed2002

[Evaluation of pendulum testing of spasticity].

OBJECTIVES: To identify valid measurements of spasticity derived from the pendulum test of the leg in a representative population of spastic patients. MATERIAL AND METHODS: Pendulum testing was performed in 15 spastic and 10 matched healthy subjects. The reflex-mediated torque evoked in quadriceps femoris, as well as muscle mechanical parameters (viscosity and elasticity), were calculated using mathematical modelling. Correlation with the two main measures derived from the pendulum test reported in the literature (the Relaxation Index and the area under the curve) was calculated in order to select the most valid. RESULTS, DISCUSSION: Among mechanical parameters, only viscosity was found to be significantly higher in the spastic group. As expected, the computed integral of the reflex-mediated torque was found to be larger in spastics than in healthy subjects. A significant non-linear (logarithmic) correlation was found between the clinically-assessed muscle spasticity (Ashworth grading) and the computed reflex-mediated torque, emphasising the non-linear behaviour of this scale. Among measurements derived from the pendulum test which are proposed in the literature for routine estimation of spasticity, the Relaxation Index exhibited an unsuitable U-shaped pattern of variation with increasing reflex-mediated torque. On the opposite, the area under the curve revealed a linear regression, which is more convenient for routine estimation of spasticity. CONCLUSION: The pendulum test of the leg is a simple technique for the assessment of spastic hypertonia. However, the measurement generally used in the literature (the Relaxation Index) exhibits serious limitations, and would benefit to be replaced by more valid measures, such as the area under the goniometric curve, especially for the assessment of therapeutics.

Adult↗

PubMed2006

Effect on spasticity after performance of dynamic-repeated-passive ankle joint motion exercise in chronic stroke patients.

Spasticity associated with abnormal muscle tone is a common motor disorder following stroke, and the spastic ankle may affect ambulatory function. The purpose of this study was to investigate the short-term effect of dynamic-repeated-passive ankle movements with weight loading on ambulatory function and spastic hypertonia of chronic stroke patients. In this study, 12 chronic stroke patients with ankle spasticity and inefficient ambulatory ability were enrolled. Stretching of the plantar-flexors of the ankle in the standing position for 15 minutes was performed passively by a constant-speed and electrically powered device. The following evaluations were done before and immediately after the dynamic-repeated-passive ankle movements. Spastic hypertonia was assessed by the Modified Ashworth Scale (MAS; range, 0-4), Achilles tendon reflexes test (DTR; range, 0-4), and ankle clonus (range, 0-5). Improvement in ambulatory ability was determined by the timed up-and-go test (TUG), the 10-minute walking test, and cadence (steps/minute). In addition, subjective experience of the influence of ankle spasticity on ambulation was scored by visual analog scale (VAS). Subjective satisfaction with the therapeutic effect of spasticity reduction was evaluated by a five-point questionnaire (1 = very poor, 2 = poor, 3 = acceptable, 4 = good, 5 = very good). By comparison of the results before and after intervention, these 12 chronic stroke patients presented significant reduction in MAS and VAS for ankle spasticity, the time for TUG and 10-minute walking speed (p < 0.01). The cadence also increased significantly (p < 0.05). In addition, subjective satisfaction with the short-term therapeutic effect was mainly good (ranging from acceptable to very good). In conclusion, 15 minutes of dynamic-repeated-passive ankle joint motion exercise with weight loading in the standing position by this simple constant-speed machine is effective in reducing ankle spasticity and improving ambulatory ability.

Adult↗

PubMed2007

Control of spasticity in a multiple sclerosis model is mediated by CB1, not CB2, cannabinoid receptors.

BACKGROUND AND PURPOSE: There is increasing evidence to suggest that cannabis can ameliorate muscle-spasticity in multiple sclerosis, as was objectively shown in experimental autoimmune encephalomyelitis models. The purpose of this study was to investigate further the involvement of CB1 and CB2)cannabinoid receptors in the control of experimental spasticity. EXPERIMENTAL APPROACH: Spasticity was induced in wildtype and CB1-deficient mice following the development of relapsing, experimental autoimmune encephalomyelitis. Spastic-hindlimb stiffness was measured by the resistance to flexion against a strain gauge following the administration of CB1 and CB2 agonists. KEY RESULTS: As previously suggested, some CB2-selective agonists (RWJ400065) could inhibit spasticity. Importantly, however, the anti-spastic activity of RWJ400065 and the therapeutic effect of non-selective CB1/CB2 agonists (R(+)WIN55,212-2 and CP55, 940) was lost in spastic, CB1-deficit mice. CONCLUSIONS AND IMPLICATIONS: The CB1 receptor controls spasticity and cross-reactivity to this receptor appears to account for the therapeutic action of some CB2 agonists. As cannabinoid-induced psychoactivity is also mediated by the CB1 receptor, it will be difficult to truly dissociate the therapeutic effects from the well-known, adverse effects of cannabinoids when using cannabis as a medicine. The lack of knowledge on the true diversity of the cannabinoid system coupled with the lack of total specificity of current cannabinoid reagents makes interpretation of in vivo results difficult, if using a purely pharmacological approach. Gene knockout technology provides an important tool in target validation and indicates that the CB1 receptor is the main cannabinoid target for an anti-spastic effect.

Animals↗

PubMed2002

The effect of spasticity on cortical somatosensory-evoked potentials: changes of cortical somatosensory-evoked potentials after botulinum toxin type A injection.

OBJECTIVE: To evaluate the changes in cortical somatosensory-evoked potentials (SEPs) after botulinum toxin type A injection to determine what effect spasticity has on cortical SEPs. DESIGN: Intervention study and before-after trial. SETTING: University-affiliated hospital in Korea. PARTICIPANTS: Twelve children with spastic hemiplegic cerebral palsy (CP), 7 children with spastic diplegic CP, and 8 patients with traumatic brain injury. INTERVENTION: All participants had botulinum toxin type A injected into the muscles of the spastic limb. MAIN OUTCOME MEASURES: SEPs were recorded before and 7 days after the botulinum toxin type A injection. Spasticity of the affected spastic limb was also measured. The short latency and amplitude of waves in SEPs were measured. The SEP results were divided into 3 groups: flat (no evoked potential), abnormal (evoked but delayed in latency), and normal (clear waveform with normal latency). RESULTS: The normal response of cortical SEP increased after injection. The SEPs exhibited more frequent improvement in the limbs, with greater improvement of spasticity in grade (>1.0 grade) and in patients of younger age (<3y) after injection (P<.05). CONCLUSION: The observed improvement of cortical SEPs with associated reduction of spasticity that occurred after the botulinum toxin type A injection indicates that spasticity itself can be considered a factor affecting cortical SEPs.

Adolescent↗

PubMedDate not supplied

Theoretical and methodological considerations in the measurement of spasticity.

PURPOSE: To discuss the measurement of spasticity in the clinical and research environments, make recommendations based on the SPASM reviews of biomechanical, neurophysiological and clinical methods of measuring spasticity and indicate future developments of measurement tools. METHOD: Using the results of the systematic reviews of the biomechanical, neurophysiological and clinical approaches, methods were evaluated across three dimensions: (1) validity, reliability and sensitivity to change; (2) practical quality such as ease of use and (3) qualities specific to the measurement of spasticity, for example ability to be applied to different muscle groups. Methods were considered in terms of applicability to research and clinical applications. RESULTS: A hierarchy of measurement approaches was identified from highly controlled and more objective (but unrelated to function) to ecologically valid, but less objective and subject to contamination from other variables. The lack of a precise definition of spasticity may account for the problem of developing a valid, reliable and sensitive method of measurement. The reviews have identified that some tests measure spasticity per se, some phenomena associated with spasticity or consequential to it and others the effect of spasticity on activity and participation and independence. CONCLUSIONS: Methods appropriate for use in research, particularly into the mechanism of spasticity did not satisfy the needs of the clinician and the need for an objective but clinically applicable tool was identified. A clinical assessment may need to generate more than one 'value' and should include evaluation of other components of the upper motor neurone syndrome. There is therefore a need for standardized protocols for 'best practice' in application of spasticity measurement tools and scales.

Electromyography↗

PubMed2006

The construct validity of a spasticity measurement device for clinical practice: an alternative to the Ashworth scales.

INTRODUCTION: Spasticity is a significant cause of disability in people with an upper motor neurone lesion, but there is a paucity of appropriate outcome measures to evaluate this phenomenon. The aim was to test the construct validity of a clinically relevant, non-invasive measure of spasticity. METHODS: A cross-section study design in which participants with elbow flexor spasticity and capable of providing written informed consent were recruited. RESULTS: Fourteen stroke patients participated (six female and eight male). Median age was 61 years and the median time post stroke was 48 months. Six patients had a MAS grading of '1+', three a grade of '2' and five a grade of '3'. The velocity of the brisk stretch was significantly higher than that of the slow stretch (p < 0.05: median difference, 34 degrees /s: IQR, 20 - 46). Flexor muscle activity during the brisk stretch was significantly higher than that of the slow stretch (p < 0.05: median difference, 2.0 microV; IQR, 0.4 - 8.4). In contrast the RPE was not significantly different between the slow and the fast stretches (p > 0.1: median difference, 0.07 N/deg; IQR, - 0.09 - 0.16). There were no patterns of association between the MAS, elbow flexor muscle activity and RPE. Other important observations, in some patients, were: continuous background muscle activation consistent with descriptions of spastic dystonia; muscle activity at the slow velocity stretch; muscle activation patterns consistent with the clasp-knife phenomenon. CONCLUSIONS: The measurement system was capable of measuring spasticity as defined by Lance (1980; In: Lance et al., editors. Spasticity: disordered motor control. Chicago, IL: Year Book. p 185 - 204). In addition, it enabled various other clinical phenomena associated with spasticity to be measured. Assessing spasticity by measuring changes in resistance to passive movement only may not be sufficient, as the latter is influenced by many factors of which spasticity may only be one. Further work is now required to investigate repeatability and sensitivity.

Biomechanical Phenomena↗

PubMed1996

Spasticity and muscle contracture following stroke.

It has become increasingly recognized that the major functional deficits following brain damage are largely due to "negative' features such as weakness and loss of dexterity rather than spasticity. A variety of studies suggest that spasticity is a distinct problem and separate from the loss of dexterity, but that it may be implicated in the formation of muscle contracture and even in the recovery of strength. In order to address these issues, we examined the relationship between spasticity, contracture, strength and dexterity in the affected upper limb following stroke. Spasticity was measured both as increased tonic stretch reflexes and increased resistance to passive stretch (hypertonia). Twenty-four patients were recruited non-selectively from three rehabilitation units within 13 months of their stroke. Few patients exhibited increased tonic reflexes but half were found to have muscle contracture, the earliest at 2 months following stroke. Hypertonia was associated with contracture but not with reflex hyperexcitability. Increased tonic stretch reflexes were observed only in a subgroup of those with contracture and where present could usually be elicited only at the end of muscle range. This findings suggests that instead of spasticity causing contracture, contracture may actually potentiate spasticity in some patients. However, the majority of patients with contracture did not have increased tonic stretch reflexes. In addition, we found no relationship between spasticity and either weakness or loss of dexterity. Therefore, while hypertonia remains an important problem following cerebral lesions, it would appear that the amount of attention directed to reflex hyperexcitability associated with spasticity is out of proportion with its effects. Consequently, hypertonia needs to be clearly distinguished from reflex hyperexcitability in patients with spasticity.

Adult↗

PubMedDate not supplied

Outcome assessment for spasticity management in the patient with traumatic brain injury: the state of the art.

The objective of this article was to (1) review the engineering and medical literature to structure the available information concerning the assessment of spasticity in the neurological population; (2) to discuss the strengths and weaknesses of the different methods currently in use in spasticity assessment; and (3) make recommendations for future efforts in spasticity outcome assessment. Spasticity textbooks, Web sites, and OVID, IEEE, and Medline searches from 1966 through 2003 of spasticity, quantitative measure, or outcome assessment in the rehabilitation population were used as data sources. Over 500 articles were reviewed. Articles that discussed outcome measures used to assess interventions and evaluation of spasticity were included. Authors reviewed the articles looking at inclusion criteria, data collection, methodology, assessment methods, and conclusions for validity and relevance to this article. Issues such as clinical relevance, real-world function and lack of objectivity, and time consumed during performance are important issues for spasticity assessment. Some measures such as the Ashworth Scale remain in common use secondary to ease of use despite their obvious functional limitations. More functional outcome goals are plagued by being more time consuming and a general inability to demonstrate changes after an intervention. This may be secondary to the other factors that combine with spasticity to cause dysfunction at that level. Quantitative metrics can provide more objective measurements but their clinical relevance is sometimes problematic. The assessment of spasticity outcome is still somewhat problematic. Further work is necessary to develop measures that have real-world functional significance to both the individuals being treated and the clinicians. A lack of objectivity is still a problem. In the future it is important for clinicians and the engineers to work together in the development of better outcome measures.

Activities of Daily Living↗