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PubMedDate not supplied

The effect of physiotherapeutic ultrasound on muscle spasticity in patients with hemiplegia: a pilot study.

BACKGROUND: Spasticity is one part of the upper motor neuron syndrome. Untreated spasticity not only causes loss of motor control that results in functional disability, but can easily lead to joint contractures as well. Physical therapy plays an important role in the management of patients with spasticity. Among the modalities, Therapeutic ultrasound has become an important modality for treatment of various conditions including spasticity. OBJECTIVES: The aim of this study is to determine the effect of ultrasound on spasticity. METHODS: In this before-after study, four adult patients (mean age: 57.5 +/- 14.43) with first ever stroke and resulting in hemiplegia participated in the study. The outcome measures were the Ashworth Scale for the assessment of spasticity, ankle passive and active range of motion, and the Hmax: Mmax ratio. RESULTS: The mean of Ashworth scores, Hmax:Mmax ratio, and passive range of motion in ankle joint improved after treatment with ultrasound, but it was not statistically significant (p > 0.05). CONCLUSIONS: The study did not show a significant decrease in spasticity after ultrasound therapy. A study with a large number of patients and a control group would clarify the effects of ultrasound on spasticity.

Adolescent↗
PubMed1989

[Two cases of familial spastic paraparesis with amyotrophy of the hands].

Familial spastic paraparesis with amyotrophy of the hands was reported, and its significance in the literature was reviewed. Case 1: An 18 year-old boy, who had been suffering from spastic gait since 12 years old, noticed his hand muscle wasting distributed bilateral first interosseous muscle, thenar and hypothenar muscle at age 17. Case 2: A 20 year-old man, elder brother of case 1, who also walked in spastic manner from his childhood, developed bilateral hand muscle atrophy similar to case 1 at age 19. Clinical features of these two cases could be summarized as familial spastic paraparesis with amyotrophy characterized by hand muscle atrophy, spasticity of lower extremities with hyperreflexia and bilateral positive pathological reflexes and spastic gait. Their younger sister was also examined, who showed only minimal spastic paraparesis. The electrophysiological examination including EMG and SEP suggested the pathological process could involve not only lateral column, but also posterior column and anterior horn. Slight but generalized spinal cord atrophy was demonstrated on metrizamide CT myelography. The muscle biopsy performed from left gastrocnemius in case 2, confirmed neurogenic changes. Although the association of retinal degeneration, cataracta, mental retardation, pes cavus or even generalized amyotrophy has been reported in familial spastic paraparesis, only limited cases are available, dealing with the amyotrophy of limbs. As far the cases with amyotrophy localized to the hands are concerned, it is absolutely rare and only the cases reported by Silver could be regarded as similar or same clinical entities to our cases.

Adolescent↗
PubMed1984

[Spinal cord stimulation for post-apoplectic spastic hemiplegia].

Although the therapeutic effect of spinal cord stimulation (SCS) for spastic movement disorders is still controversial, its effect for multiple sclerosis has been supported by several authors. Among various clinical beneficial effects, reduction of the spasticity may be attractive for physical therapy of post-apoplectic patients. Two patients suffered from post-apoplectic spastic hemiplegia were selected for SCS. Electrodes of Medtronic's SCS system were placed at lower cervical or upper thoracic spinal cord extradura. Stimulation of 30-75 Hz in frequency and 0.3-0.5 in voltage continued for 12-14 hours during daytime every days. U.S., a 74-year-old man, suffered from cerebral infarction in the right internal capsule was treated by SCS at one year after the stroke . At the fourth day after SCS spasticity of the lower extremity reduced and his gait improved remarkably. Upper extremity also showed reduction of spasticity at the seventh day after SCS. H/M ratio before SCS was 0.85 and reduced to 0.77 at 68 th day after SCS. Recovery curve of H-wave also improved after SCS. Y.K., a 47-year-old man, suffered from pontine hemorrhage showed right spastic hemiplegia. He was treated by SCS at 13th month after the hemorrhage. Spasticity of the upper extremity reduced slightly and his gait improved obviously. H/M ratio which was 1.05 before SCS, reduced to 0.75 at 122 nd day after SCS. Recovery curve of H-wave improved remarkably after the treatment. It was obvious that the spasticity reduced after SCS and function of the extremities recovered to some extent in above patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMedDate not supplied

Ankle spasticity is inversely correlated with antagonist voluntary contraction in hemiparetic subjects.

The correlation between the severity of spasticity and residual muscular activity is unclear, yet the latter is often used to investigate the effects of therapeutic interventions in spastic movement disorders. Our objectives were to compare the EMG and force generated by the ankle plantar- and dorsi-flexors in normal and spastic hemiparetic subjects, and to investigate their reproducibility and their correlation with clinical spasticity. Thirteen spastic hemiparetic and seven age-matched normal subjects generated maximal isometric ankle plantar- and dorsi-flexing contractions. Maximal force was significantly decreased to 33% of the non-affected leg during dorsiflexion and to 59% during plantarflexion. Measurements of force parameters (onset and magnitude) during both dorsi- and plantar-flexion and the EMG co-contraction ratios during dorsiflexion were highly reproducible (r = 0.78 to 0.99). Our most interesting finding was that the EMG co-contraction ratio was inversely correlated with the amount of force produced by the paretic dorsiflexors (r = -0.91), and that the latter was in turn, inversely related to plantarflexor spasticity (r = -0.65). The high reproducibility of the force measurements suggested that they could be used to evaluate the long-term effects of therapeutic interventions. Furthermore, our findings demonstrated that the voluntary motor deficit in the paretic dorsiflexors but not the spastic plantarflexors was a reliable and valid indicator of the severity of ankle spasticity.

Adult↗
PubMed1993

Influence of cryotherapy on spasticity at the human ankle.

The application of cryotherapy to temporarily reduce spasticity is a widespread clinical practice. A method of quantifying spasticity, based on viscoelastic stiffness measurements at the ankle, was applied to objectively determine the efficacy of cryotherapy in reducing spasticity of the calf. Baseline, cryotherapy and one-hour postcryotherapy measurements of spasticity were performed in 25 subjects with clinical signs of spasticity secondary to traumatic brain injury, spinal cord injury, and stroke. A statistically significant reduction in spasticity occurred during cryotherapy. Postcryotherapy results were equivocal, although there was a tendency for diminished spasticity relative to the baseline measurement. Two subjects showed a clear aggravation of spasticity following cryotherapy, thus leading to the conclusion that dichotomous results are possible.

Adolescent↗
PubMed1985

The glycine receptor in the mutant mouse spastic (spa): strychnine binding characteristics and pharmacology.

There is a marked deficit in the binding of the glycine receptor antagonist strychnine to the CNS of the mutant mouse spastic. The characteristics and pharmacology of [3H]strychnine binding to washed homogenates of spastic and littermate control spinal cord and brainstem were investigated to determine the nature of this defect. The maximal binding of [3H]strychnine to spastic homogenates is approximately 20% the value obtained from littermate control homogenates; the affinity of [3H]strychnine binding is approximately 25% lower than littermate control values. The pharmacology of [3H]strychnine binding has the same rank order of potency in spastic and littermate control mice; however, there are small differences in the potency of several compounds in spastic vs littermate control animals. These results indicate that the glycine receptor alteration seen in the spastic mutant mouse is primarily due to a decrease in receptor number. They also suggest that the pharmacological characteristics of the glycine receptor in spastic are different from littermate control. The data do not permit a distinction between whether the strychnine binding sites found in spastic represent the same population seen in littermate control animals or are a subpopulation that is spared by the mutation.

Animals↗
PubMed2004

Biomechanic changes in passive properties of hemiplegic ankles with spastic hypertonia.

OBJECTIVE: To investigate quantitatively biomechanic changes in the passive properties of hemiplegic spastic ankles. DESIGN: Evaluation of spastic hypertonia by moving the ankle joint slowly between dorsiflexion and plantarflexion extreme positions under controlled joint torque and position. SETTING: Institutional research center. PARTICIPANTS: Twenty-four stroke patients with spastic ankles and 32 healthy controls. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Passive resistance torque at controlled dorsiflexion and plantarflexion positions, dorsiflexion and plantarflexion range of motion (ROM) at controlled torques, and quasistatic stiffness and energy loss in dorsiflexion and plantarflexion. RESULTS: Spastic hypertonic ankles showed significant alterations of the passive properties in plantarflexion (P=.041) as well as in dorsiflexion (P=.016) directions. Compared with healthy controls, spastic ankles showed higher resistance torque (9.51+/-4.79Nm vs 6.21+/-3.64Nm, P=.016), higher quasistatic stiffness (.54+/-.19Nm/deg vs .35+/-.20Nm/deg, P=.001) at 10 degrees of dorsiflexion, larger normalized dorsiflexion energy loss (.068+/-.04J/deg vs .04+/-.02J/deg, P=.037), and decreased dorsiflexion ROM at 10Nm of resistance torque (10.77 degrees +/-8.69 degrees vs 20.02 degrees +/-11.67 degrees , P=.014). The resistance torque, ROM, and stiffness of spastic hypertonic ankles in plantarflexion showed similar changes (P<.05) to those in dorsiflexion. The passive ROM, joint stiffness, and resistance torque at controlled positions correlated with each other and also correlated with the Modified Ashworth Scale (P<.01). CONCLUSIONS: Various biomechanic changes in both plantar- and dorsiflexors are associated with spastic hypertonia of chronic stroke patients, and they can be evaluated quantitatively under well-controlled conditions. With simplifications, the various measures in this study can potentially be used to obtain more comprehensive and quantitative evaluations of spastic hypertonia in a clinical setting.

Analysis of Variance↗
PubMed2004

Magnetic resonance imaging in 122 children with spastic cerebral palsy.

The interrelationship between magnetic resonance imaging findings, types of cerebral palsy, and gestation was studied. We analyzed the magnetic resonance imaging of brain in 122 children with spastic cerebral palsy. Forty-three patients had spastic hemiplegia, 61 had spastic diplegia, and 18 had spastic tetraplegia. Magnetic resonance imaging abnormalities were observed in 75% of patients. Periventricular leukomalacia accounted for 66% of abnormalities observed in patients with spastic diplegia; other types of brain lesions were uncommon. In patients with spastic tetraplegia, two types of magnetic resonance imaging abnormalities predominated: congenital brain anomalies and term-type brain injuries, 42% and 33% respectively. Types of magnetic resonance imaging abnormalities were more heterogeneous in patients with spastic hemiplegia. Preterm brain injuries (periventricular leukomalacia and posthemorrhagic porencephaly) were observed often in patients born at preterm but were also observed in patients born at term. Term-type brain injuries (term-type border-zone infarct, basal ganglia-thalamic lesion, subcortical leukomalacia, and multicystic encephalomalacia) were observed only in patients born at or near term. We conclude that magnetic resonance imaging findings for patients with spastic cerebral palsy were closely related to types of cerebral palsy and gestation at birth. Magnetic resonance imaging in patients with perinatal brain injury may reflect pathologic changes and is useful in understanding and evaluating cerebral palsy.

Cerebral Palsy↗
PubMed2001

Energy requirements of spasticity.

Direct measurement of energy expended by spasticity in children with severe spastic quadriparesis is difficult. Insertion of an intrathecal baclofen pump in a 13-year-old boy with severe spasticity and profound mental retardation resulted in an estimated 30 to 40% decrease in his spasticity. As he had been on a carefully calculated ketogenic diet and fed by gastrostomy, his precise caloric intake was known. Decrease in spasticity, on the same caloric intake, led to marked weight gain. Reduction of 100 calories intake resulted in new weight stability. It was possible therefore, to estimate indirectly energy used by his spasticity. This 100 calories, representing 34% of calories above his resting energy requirement, corresponded to an independently estimated 30 to 40% of caloric expenditure of his spasticity. It was concluded that when calculation of calories is critical, energy utilization by spasticity must be taken into consideration.

Adolescent↗
PubMed1987

Attenuation of endothelium-related relaxation and enhanced responsiveness of vascular smooth muscle to histamine in spastic coronary arterial segments from miniature pigs.

Mechanism of coronary spasm was examined regarding endothelium-related relaxation and contraction produced by smooth muscle cells of spastic vessels isolated from Göttingen miniature pigs. In these pigs, coronary artery spasm was documented angiographically in vivo three months after endothelial denudation, and spastic and control segments of the coronary artery were suspended in organ chambers at their optimal length for generating tension. Applications of KCl (118 mM), acetylcholine(10(-9) to 10(-4) M), and PGF2 alpha (10(-8) to 3 X 10(-5) M) produced similar tension, at the respective doses, in both the spastic and control coronary arteries. During increasing concentrations of histamine (10(-8) to 3 X 10(-4) M; n = 14) and serotonin (10(-9) to 10(-5) M; n = 13), the maximum tension of the spastic vessel was 136 +/- 6 and 97 +/- 4%, respectively, of the tension produced by 118 mM KCl. That is significantly larger than seen in the control vessels: 98 +/- 4 and 74 +/- 4%, respectively. The ED50 to histamine and serotonin was also significantly less in the spastic vessels. After mechanical removal of the endothelium, the tension generated during the cumulative administration of histamine (n = 8) but not serotonin (n = 8) was larger in the spastic than the control vessels, thereby suggesting the presence of augmented responses of the smooth muscle to histamine in the spastic vessels. The increase in maximum tension after mechanical denudation was greater in the control than the spastic vessels in cases of histamine and serotonin.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2004

Coronary spastic angina in patients with connective tissue disease.

BACKGROUND: Connective tissue disease, which is an inflammatory condition represented by C-reactive protein (CRP), is a risk factor for ischemic heart disease. The aim of the present study was to examine if there is a relationship between connective tissue disease and coronary spastic angina, and whether the inflammatory condition was associated with ischemic heart disease, even in patients with connective tissue disease. METHODS AND RESULTS: The study group comprised 73 consecutive patients with connective tissue disease who were admitted to the Department of Cardiovascular Medicine between April 2000 and March 2003. Of the 73 patients, 38 (19 men, 19 women) were diagnosed as having an ischemic heart disease (7 patients acute coronary syndrome, 19 patients coronary spastic angina, 12 patients stable exertional angina). In the present study, 19 (50.0%) of the 38 patients of ischemic heart disease were diagnosed as having coronary spastic angina. In the same study period, 151 (38.7%) of 390 patients with ischemic heart disease (without connective tissue disease) were diagnosed as having coronary spastic angina. The frequency of the patients with coronary spastic angina tended to be higher in patients with connective tissue disease than in patients without connective tissue disease. Among the study patients, serum CRP concentrations (mg/dl) were higher in patients with acute coronary syndrome (1.50 +/- 1.19, n=7) and those with coronary spastic angina (1.06 +/- 1.78, n=19) than in those with non-ischemia (0.35 +/- 0.40, n=35, p<0.05). CONCLUSIONS: Coronary spastic angina is a frequent complication in patients with connective tissue disease and the inflammatory condition is associated with coronary spastic angina and unstable angina in patients with connective tissue disease.

Aged↗
PubMed1991

Reflex activity and muscle tone during elbow movements in patients with spastic paresis.

Reflex behavior and tension development in upper limb muscles were analyzed and comparisons made between the unaffected and spastic sides of patients with spastic hemiparesis. During sinusoidal (0.3-Hz) isometric or isotonic elbow tracking, with a control either of joint position or of torque, randomly timed displacements were induced (at one of three velocities) stretching either the activated flexor or the extensor muscles. On the spastic side, exaggerated short-latency reflexes were apparent, but in contrast, the amplitude of long-latency electromyography (EMG) responses was reduced. The latter responses were differentially modulated on the unaffected side, predominantly by the acceleration signal during control of position and more by the velocity signal during control of torque, while the mode of muscle contraction (isometric or isotonic) had little influence on this behavior. This difference in reflex modulation was lost on the spastic side. The functional consequence of this reduced EMG modulation could be difficulty in performing finely controlled arm movements. The ratio of torque to EMG activity during displacements was higher for both background and reflex-induced EMG on the spastic limb than on the unaffected side. This effect was more pronounced for the flexor than for the extensor muscles. Consequently, the development of spastic muscle hypertonia cannot be attributed to an increase in EMG activity. It is suggested that secondary to a supraspinal lesion, mechanical muscle properties change in such a way that the activated spastic muscle develops more tension when it is stretched.

Adolescent↗
PubMed1995

Residual spasticity after selective posterior rhizotomy.

The technique used in performing selective posterior rhizotomies to treat spastic cerebral palsy remains controversial. One hundred nine children who had undergone selective posterior rhizotomies were studied 6 months after their surgery. Their residual spasticity was correlated to the number of roots and whether or not abnormally responding roots were left, in order to validate the surgical technique used to treat spastic cerebral palsy at most neurosurgical centers in North America. The children were divided into three groups (group A: children who had their L2-S1 roots tested and selectively lesioned, n = 15; group B: children who had their L2-S2 roots tested and selectively lesioned, n = 62; group C: children who had their L2-S2 roots tested and whose lesioning was directed both by the response to the stimulation and mapping of the S1-S3 dorsal roots for afferent pudendal nerve activity, n = 32). Clinically significant residual spasticity was present in the gastrocnemius in 33% of the group A children, 11% of the group B children, and 6% of the group C children. We found that there was no significant increase in residual spasticity in the group C children when abnormally responding roots were not cut in order to preserve pudendal nerve activity. This study shows that the inclusion of the S2 roots decreases the amount of residual spasticity (P < 0.01). It also shows that leaving abnormally responding S2 roots to preserve pudendal nerve activity does not affect the incidence of postoperative spasticity (P > 0.1).

Adolescent↗
PubMed1976

Sectorial posterior rhizotomy, a new technique of surgical treatment for spasticity.

After their experience of Foerster's operation and its technical modifications in 80 cases the authors report a new concept of analysis and treatment of spasticity in lower limbs. Spasticity of the different muscle groups is classified either as "useful spasticity" or "handicapping spasticity". The first has to be preserved, the second must be reduced. In order to achieve this purpose a new technique is presented, based on operative sectorial identification of the posterior rootlets subserving the "handicapping spasticity" by electrophysiological stimulation, muscle testing, and E.M.G. studies. The conus medullaris and cauda equina are exposed by T 11-L 1 laminectomy, performed in the lateral position. The clinical and E.M.G. evaluation of responses to stimulation enables the surgeon to establish a map of rootlet groups which are marked with coloured threads. Selective resection of "handicapping posterior rootlets" is then performed after several tests of the mapping. The rootlets subserving useful spasticity are carefully preserved. Ten cases are reported, comprising five cases of cerebral palsy operated upon since 1974 and five cases of posttraumatic spastic paraplegia from the same period. Pre and postoperative findings are summarized. The technical features of this procedure are discussed and compared with other surgical procedures. The problem of the rootlet reflex arch is considered in the light of the effects of stimulation of anterior and posterior rootlets at the same level.

Adolescent↗
PubMed1987

Spasticity and drug therapy.

An overview is presented of pathophysiology, classification and measurement of spasticity and of its treatment, especially with dantrolene and baclofen. In spasticity, the balance between excitatory and inhibitory neurotransmitters in the central nervous system is impaired by mechanisms that are for the greater part unknown. Spasticity includes various disorders of motor control, and classification is needed for a meaningful evaluation of antispastic therapy. Cerebral palsy is a specific disorder, sometimes also called spasticity. Measurement of spasticity is complicated and should include signs characteristic of spasticity and parameters for clinical improvement. Dantrolene and baclofen have established their place in the treatment of spastic disorders, but a preference for either drug is hard to give. For tizanidine it is still too early to determine its place in therapy. Dantrolene is a direct acting muscle relaxant which should be avoided in patients with pre-existing liver damage. Its mechanism of metabolism and excretion is for the greater part unknown. The GABAB agonist baclofen is a centrally acting muscle relaxant. In patients with impaired renal function the dose should be reduced. Abrupt withdrawal carries the risk of unwanted reactions. The R(-)-enantiomer has proved to be the active isomer. This means that human trials need reappraisal, especially those relating to the pharmacokinetics of the racemate.

Baclofen↗
PubMed1989

Recurrent inhibition in human spinal spasticity.

The study was performed on a group of 17 patients with spastic paraparesis: 12 with hereditary spastic paraparesis, 3 with cord compression and 2 with complete spinal transection. 10 healthy volunteers acted as controls. Recurrent inhibition of the soleus alpha-motoneurones was estimated at rest and during voluntary contraction of triceps surae. At rest, there was evidence for a substantial decrease in the excitability of Renshaw cells in 9 out of the 12 patients with hereditary spastic paraparesis; this was also observed in the 2 patients with complete spinal transection, while the 3 patients with cord compression exhibited a normal Renshaw cell activity. In 3 out of 4 patients with hereditary spastic paraparesis, the changes in Renshaw cell excitability expected to occur during voluntary contraction were not found, whereas in one patient with hereditary spastic paraparesis and one with spastic paraparesis due to cord compression recurrent inhibition was normally influenced by the motor command. Our results indicate that recurrent inhibition is likely to be differently affected according to the type and/or localization of the lesion. It is also suggested that the central nervous system might control the excitability of Renshaw cells at rest and during voluntary contraction via partly separate pathways. The role of recurrent inhibition in spasticity is discussed.

Adult↗
PubMed2003

Lower extremity spasticity as an early marker of ambulatory recovery following traumatic brain injury.

METHODS: A consecutive series of 107 children and young persons with traumatic brain injury (TBI) admitted to a hospital-based inpatient rehabilitation program was assessed to determine whether lower extremity spasticity could be utilized as an early clinical marker for recovery of ambulation. Presence of spasticity was determined by clinical examination at admission, and the ability to ambulate safely indoors (15.24 m) was evaluated at discharge. Sensitivity, specificity and positive and negative predictive values for spasticity were calculated. RESULTS: Lower extremity spasticity is a sensitive (71.4%) and specific (81.5%) predictor of the inability to ambulate at discharge. The absence of lower extremity spasticity, however, was a better predictor of ambulation recovery than the presence of spasticity was a predictor of nonambulatory status at hospital discharge. DISCUSSION: Implications for spasticity assessment and prognosis in terms of ambulation and recovery are discussed.

Adolescent↗
PubMed2003

Time course of the effect of a bolus dose of intrathecal baclofen on severe cerebral spasticity.

Continuous intrathecal administration of baclofen with implanted programmable pump systems is recommended in the treatment of severe spasticity of cerebral origin. Prior to pump implantation, a baclofen bolus test (BBT) is used to assess the effectiveness of intrathecal baclofen using clinical scales such as the Modified Ashworth Scale (MAS). In the literature, the time and period of maximum effect of a bolus dose of intrathecally administered baclofen in patients with cerebral spasticity is variously reported. The aim of the study was, therefore, to reveal the time course of the effect of a BBT on severe cerebral spasticity by the use of a recently described spasticity measurement method. Spasticity in knee joints of 13 patients with severe cerebral spasticity was repeatedly assessed using the MAS and also continuously recorded by the measurement of force under circular fibreglass casts. Force was recorded as nettorque by multiplying the force by the distance between sensor and joint axis, thus allowing inter-individual comparison. Half-hour time integrals (TI) of net-torque were determined 9 hours before and 22 hours after intrathecal baclofen administration. Post-BBT half-hour time integrals (TI(+0), TI(+0.5), to TI(+22)) were compared with the mean of 17 pre-BBT half-hour time integrals. Significantly lower post-BBT half-hour time integrals compared with were found between TI(+2) and TI(+8) (Dunnett adjusted p < 0.05). The median lowest TI after BBT of the 13 patients was TI(+4). The lowest mean MAS scores were found 4 hours after BBT. The findings suggest that the greatest effect of BBT on cerebral spasticity occurs between 2 and 8.5 hours, with a maximal effect at 4 hours after intrathecal baclofen injection. Clinical scales used to determine the effect of BBT should thus be carried out during this period-ideally at 4 hours after baclofen injection.

Adult↗