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PubMed1997

Flow-mediated, endothelium-dependent dilatation of the brachial arteries is impaired in patients with coronary spastic angina.

Coronary spasm is induced by acetylcholine, serotonin, ergonovine, or histamine, all of which cause vasodilation when the endothelium is intact, and is promptly relieved by nitroglycerin, which vasodilates through the direct action on smooth muscle. Endothelial dysfunction is therefore possibly involved in the pathogenesis of coronary artery spasm. The aim of this study was to determine whether endothelium-dependent vasodilation is impaired in the peripheral arteries of patients with coronary spastic angina. Flow-dependent vasodilation of the brachial arteries during reactive hyperemia after the transient arterial occlusion was examined by using the high-resolution ultrasound technique in 35 patients with coronary spastic angina and 35 controls. Flow-dependent vasodilation of the brachial arteries was impaired in patients with coronary spastic angina compared with controls (5.9% +/- 4.2% vs 9.6% +/- 3.4%, p < 0.001) although the percent increase in blood flow during reactive hyperemia was not different between the two groups. The dilator response to nitroglycerin was preserved in patients with coronary spastic angina compared with controls (18.6% +/- 5.1% vs 16.2% +/- 3.9%, p < 0.04). The results indicate that endothelium-dependent vasodilation of the brachial arteries is impaired in patients with coronary spastic angina. Thus endothelial vasomotor dysregulation may also be present in the systemic arteries as well as coronary arteries in patients with coronary spastic angina.

Adult↗
PubMed2006

The use of tiagabine in pediatric spasticity management.

Tiagabine, developed as an anti-epileptic medication, has the potential to reduce spasticity. The purpose of the present study was to assess the effectiveness of tiagabine in decreasing spasticity and improving the functional abilities of children with spastic cerebral palsy (CP). Nine children (seven females, two males) with CP (six spastic quadriplegia, three moderate to severe spastic diplegia) were treated with tiagabine for a mean of 7.2 months. Median age was 4y 5mo (range 3y 2mo-10y). All children were non-ambulatory. According to the Gross Motor Function Classification System, six were Level IV and three were Level V. Only one child showed a median decrease >or=1.0 grade on the modified Ashworth scale in upper extremities, lower extremities, and overall. Another child had significant improvement in the Pediatric Evaluation of Disability Inventory Self-care score and improved feeding. None of the participants was found to have a significant improvement in motor function or a decrease in the number of motions (passive range of motion and muscle length test) that were limited. Reduction of nocturnal awakenings from painful spasms was reported in one child. Eight of the nine children experienced adverse side-effects during treatment. Although tiagabine was not found to be effective in decreasing children's spasticity or improving their function, its potential use in the relief of painful spasms associated with neurological conditions in the pediatric population warrants further investigation.

Anticonvulsants↗
PubMed1982

Diadochokinetic syllable rate and regularity in normal and in spastic and ataxic dysarthric subjects.

Rate and regularity of diadochokinetic syllable repetitions of /p/, /t/, and /k/ in 30 normal subjects, 30 subjects with spastic dysarthria, and 30 subjects with ataxic dysarthria were measured by computer. Normal subjects had rates (syllables per second) of 6.4, 6.1, and 5.7; spastic dysarthric subjects, 4.6, 4.2, and 3.5; and ataxic dysarthric subjects, 3.8, 3.9, and 3.4 for /p/, /t/, and /k/, respectively. Spastic and ataxic subjects were significantly slower and more variable than normal subjects and ataxic subjects were significantly more variable than spastic subjects. The significantly slower than normal rate of repetition in the ataxic subjects and the significantly more variable than normal rhythm of repetition in the spastic subjects were unexpected findings and are in contrast with results from perceptually based investigations of dysarthria. The study demonstrates that slowness of syllable repetition is not restricted to spastic dysarthria and that dysrhythmia of syllable repetition is not restricted to ataxic dysarthria, thus suggesting the need for additional quantitative measurements of acoustic features on which certain notions about the dysarthrias are currently based.

Aged↗
PubMed1995

Use of a hand-held dynamometer and a Kin-Com dynamometer for evaluating spastic hypertonia in children: a reliability study.

BACKGROUND AND PURPOSE: Studies in subjects with spastic hypertonia indicate that the higher resistance to stretch in the spastic muscles is not only due to hyperactive stretch reflexes but also to changes in the muscle-tendon unit (nonreflex components). The aim of this study was to compare the test-retest reliability of two methods: hand-held dynamometry and isokinetic dynamometry for the evaluation of nonreflex and reflex-mediated resistive force in the plantar flexors of young children with spastic cerebral palsy (CP). SUBJECTS: Ten children 2 to 7 years of age with a diagnosis of spastic CP (either diplegia [n = 7] or hemiplegia [n = 3]) participated in the study. METHODS: The resistive force recorded at 0 degrees of dorsiflexion during passive ankle dorsiflexions executed at low and high velocities was evaluated twice at a 1-month interval with a Penny and Giles myometer (a hand-held dynamometer) and a Kin-Com dynamometer. The electromyographic activity of the soleus and tibialis anterior muscles was recorded during Kin-Com testing to detect unwanted activity during low-velocity tests and to identify trials with a reflex response during high-velocity tests. RESULTS: High intraclass correlation coefficients (ICCs) for the resistive force values recorded at the test and retest were computed for both the myometer (ICCs = .79 and .90) and the Kin-Com (ICCs = .84 and .84) at low and high velocities, respectively. Coefficients of variation for force values measured at a 1-month interval at low and high velocities were 13.9% and 13.2% with the myometer and 11.8% and 12.8% with the Kin-Com. CONCLUSION AND DISCUSSION: The results suggest that the myometer can provide a measure of spastic hypertonia with a reproducibility and a variation in the measures that compare to those of a computer-controlled dynamometer. From a clinical point of view, the myometer is simpler and cheaper to use given the lower cost and the little time required for testing and data analysis. Care must be taken to select a velocity that is low enough not to evoke a stretch reflex (to isolate nonreflex components) and another that is high enough to elicit a reflex response, so that it becomes possible to differentiate the reflex and non-reflex components involved in spasticity. Such a distinction is important for the choice of treatment procedures.

Ankle Joint↗
PubMedDate not supplied

Orally delivered baclofen to control spastic hypertonia in acquired brain injury.

To determine if oral/systemic delivery of baclofen can effectively decrease spastic hypertonia due to acquired brain injury (traumatic brain injury, stroke, anoxia, or encephalopathy). Tertiary care outpatient rehabilitation center directly attached to a university hospital. Patients were a convenience sample recruited consecutively who had been referred for treatment of their spastic hypertonia to our spasticity clinic over a 5-year period. The spastic hypertonia was due to an acquired brain injury by either traumatic brain injury (TBI), stroke, or anoxic brain injury. All patients were more than 6 months postinjury or illness. Retrospective review of patients before and after initiation of treatment with oral baclofen, per standardized clinical data sheets. Thirty-five patients (22 TBI patients) were started on oral baclofen and were reevaluated between 1 to 3 months after initiation of treatment. Data for motor tone (Ashworth scores), spasm scores (Penn spasm frequency score), and deep tendon reflex scores were collected on the affected upper extremity (UE) and lower extremity (LE) side(s). Normal extremities were not assessed. Differences over time were assessed via descriptive statistics and Wilcoxon signed-rank. After 1 to 3 months of treatment when subjects had reached their maximal tolerated dosage, the average LE Ashworth score in the affected lower extremities (LEs) decreased from 3.5 to 3.2 (P =.0003), the reflex score decreased from 2.5 to 2.2 (P =.0274), and there was no statistical difference in the spasm score (P >.05). When the 22 TBI patients are analyzed separately, the average LE Ashworth score decreased from 3.5 to 3.2 (P =.0044) and the reflex score decreased from 2.7 to 2.0 (P =.0003). There was no statistically significant change in UE tone, spasm frequency, or reflexes after 1 to 3 months of treatment (P >.05). The average dosage at follow-up was 57 mg/day of baclofen (range 15-120 mg/day). There was a 17% incidence of somnolence that limited the maximum daily dosage of the medication. The oral delivery of baclofen is capable of reducing LE spastic hypertonia resulting from acquired brain injury. The lack of effect upon the upper extremities may be due to receptor specificity issues. GABA-B receptors may be less involved in the modulation of UE spastic hypertonia.

Administration, Oral↗
PubMed2006

Selective tibial neurotomy in the treatment of spastic equinovarus foot: a 2-year follow-up of three cases.

OBJECTIVE: To objectively assess the decrease in spasticity and the improvement in gait after tibial nerve neurotomy performed to treat spastic equinovarus foot. DESIGN: Before-after trial with a 2-yr follow-up. Three hemiplegic patients with spastic equinovarus foot were treated with a selective peripheral neurotomy of the tibial motor nerve branches (soleus, lateral and medial gastrocnemius and tibialis posterior nerves). Evaluation included clinical assessment of spasticity (Ashworth scale), maximal Hoffmann reflex (H(max))/compound muscle action potential (M(max)) ratio measurement, gait analysis, and muscle stiffness evaluation performed before and 2 mos, 1 yr, and 2 yrs after the neurotomy. RESULTS: Spasticity, muscle stiffness, and H(max)/M(max) ratio decreased after neurotomy. The kinematic (ankle dorsal flexion and knee recurvatum) and kinetic variables (maximum ankle muscle moment and external work) of the gait were permanently improved after neurotomy. Interestingly, kinetic variables seemed to gradually improve with time after the neurotomy. CONCLUSION: Tibial neurotomy is an effective and durable treatment for spastic equinovarus foot.

Aged↗
PubMed1992

Receptive field organization of retinal ganglion cells in the spastic mutant mouse.

1. We examined the receptive field properties of retinal ganglion cells in the isolated, superfused retinae of spastic mutant mice (B6C3Fe-spa/spa) that did not have the retinal degeneration (rd) phenotype. Glycine receptor density in the spastic mutant is greatly reduced in all areas of the CNS that have been examined. Phenotypically normal litter-mates were used as controls. Radial sections from the retinae of both spastic and normal animals were examined with light and electron microscopy and no differences were observed. The planimetric density of the cell bodies in the inner nuclear layer did not differ between the normal and mutant animals, about 400 cm-2. The absolute dark-adapted sensitivity of spastic ganglion cells was greater (271 +/- 69.0 impulses quanta-1 rod-1) than that of normal ganglion cells (47.7 +/- 10.4 impulses quanta-1 rod-1; P < 0.01). 2. Extracellular recordings of retinal ganglion cell responses to circular and annular stimuli, centred on the receptive field, were used to construct peri-stimulus-time histograms. In normal retinae, an annular stimulus elicited a response that was characteristic of the surround response mechanism of receptive fields with antagonistic centre-surround organization. In the mutant retina, annular stimuli did not elicit a surround-type response; instead, a centre-type response was recorded. 3. Illumination of the receptive field periphery attenuated centre-type responses in ganglion cells from both spastic and normal retinae. Centred circular stimuli of various areas (14, 35, 78, 122, 235, 783 deg2) were presented to the receptive fields. For mutant and normal ganglion cells, the response to the largest stimulus was smaller than that to an intermediate-sized stimulus. 4. The effect of strychnine, a glycine receptor antagonist, on the response to circular stimuli was examined. Very low concentrations of strychnine attenuated the light response in mutant retinae (apparent inhibitory binding constant KI = 8.1 x 10(-13) M). In normal animals, the light response was also attenuated by strychnine, but the apparent KI was much higher (apparent KI = 1 x 10(-7) M). 5. In normal ganglion cells, the sustained component of the light response was much more attenuated by strychnine than was the transient component. Interestingly, ganglion cells from spastic retinae did not exhibit a sustained component, even at stimulus luminances that evoked responses near threshold.(ABSTRACT TRUNCATED AT 400 WORDS)

Adaptation, Ocular↗
PubMed1996

A randomised, double blind, placebo controlled trial of botulinum toxin in the treatment of spastic foot in hemiparetic patients.

OBJECTIVE: To confirm the apparent effectiveness of botulinum toxin (BTX) in hemiparetic patients with ankle plantar flexors and foot invertor spasticity. METHODS: Twenty three hemiparetic patients with spasticity of the ankle plantar flexors and foot invertors were included in a randomised double blind, placebo controlled study with BTX. Patients were examined on days 0, 30, 90, and 120 and received one injection of BTX and one of placebo in a random order at day 0 and day 90. RESULTS: Patients reported a clear subjective improvement in foot spasticity after BTX (P = 0.0014) but not after placebo. Significant changes were noted in Ashworth scale values for ankle extensors (P < 0.0001) and invertors (P = 0.0002), and for active ankle dorsiflexion (P = 0.0001). Gait velocity was slightly but not significantly (P = 0.0731) improved after BTX injections. The severity of spasticity did not modify treatment efficacy, but BTX was less effective in patients with longer duration of spasticity (P = 0.0081). CONCLUSION: The efficacy of BTX injections in the treatment of spastic foot suggests that BTX may be particularly useful during the first year after a stroke.

Adult↗
PubMed2000

Contribution of thixotropy, spasticity, and contracture to ankle stiffness after stroke.

OBJECTIVES: Increased resistance to stretch of muscles after stroke may be the result of centrally mediated neural factors such as spasticity or local, peripheral factors such as muscle contracture or thixotropy. The aim was to investigate evidence for an abnormal thixotropic response and compare this with two other factors-contracture and spasticity-which could potentially contribute to muscle stiffness after stroke. METHODS: Thirty patients with stroke whose calf muscles were assessed clinically as stiff and 10 neurologically normal subjects were recruited. To measure thixotropy, their calf muscles were stretched through two cycles after two prestretch conditions: one in which the muscles were maintained in a shortened position and one in which they were maintained in a lengthened position. Spasticity was defined as the presence of tonic stretch reflexes in relaxed muscles. Contracture was defined as being present when maximum passive ankle dorsiflexion fell at least 2 SD below the mean value of the control subjects. RESULTS: Both controls and patients with stroke exhibited a thixotropic response but this was no greater in the patients than the controls. About one third of the patients displayed muscle contracture and most exhibited spasticity. Contracture made a significant contribution (p=0.006) to the clinical measure of calf muscle stiffness while spasticity made a significant contribution (p=0.004) to the laboratory measure of calf muscle stiffness. CONCLUSIONS: Measuring thixotropy at the level of joint movement was sufficiently sensitive to determine the thixotropic response in both neurologically normal subjects and patients impaired after stroke. The thixotropic response was not higher than normal after stroke, suggesting that whereas thixotropy may produce enough immediate resistance to impede movement in those who are very weak, it is not a substantial contributor to long term muscle stiffness. Contracture did significantly contribute to muscle stiffness, supporting the importance of prevention of contracture after stroke. Spasticity contributed to muscle stiffness only when the limb was moved quickly.

Aged↗
PubMed2001

Glutathione attenuates coronary constriction to acetylcholine in patients with coronary spastic angina.

This study examined the effect of reduced glutathione (GSH), an important antioxidant that restores intracellular redox imbalance and prevents inactivation of endothelial-derived nitric oxide, on the abnormal vasomotor reactivity in spastic coronary arteries. The responses of epicardial diameter of the left coronary arteries to intracoronary infusion of acetylcholine (ACh; 50 microg/min) were measured by quantitative coronary angiography before and during combined intracoronary infusion of GSH (50 mg/min for 6 min) or saline as a placebo in 24 patients with coronary spastic angina and in 28 control patients. All of the spastic coronary arteries showed constrictor response to ACh, whereas the control coronary arteries as a whole showed only minimal diameter changes to ACh. GSH infusion suppressed constrictor response of epicardial diameter to ACh in patients with coronary spastic angina, whereas it had no significant effect in control subjects. Saline infusion did not have any effects. The results indicate that GSH attenuated the constrictor response to ACh in epicardial coronary arteries of patients with coronary spastic angina. GSH may have an important role in the regulation of coronary vasomotor function in patients with coronary spastic angina.

Acetylcholine↗
PubMed2001

Increased autoantibodies against oxidized low-density lipoprotein in coronary circulation in patients with coronary spastic angina.

Oxidized low-density lipoproteins are important in the progression of atherosclerosis. Autoantibodies against malondialdehyde-modified low-density lipoproteins have been reported to be predictive of the progression of atherosclerosis. This study sought to examine whether plasma levels of autoantibodies against oxidized low-density lipoprotein increase in the coronary circulation in patients with coronary spastic angina. The authors examined plasma antioxidized low-density lipoprotein antibody levels (activity unit values (AcU)/mL) simultaneously in the coronary sinus and the aortic root in 20 patients with coronary spastic angina, 23 patients with stable exertional angina, and 15 control subjects by measuring plasma levels of immunoglobulin G (IgG) autoantibodies against malondialdehyde-modified low-density lipoproteins by enzyme-linked immunosorbent assay. The plasma antioxidized low-density lipoprotein antibody levels (AcU/mL) in the coronary sinus increased in coronary spastic angina (38 +/- 16) compared with stable exertional angina (23 +/- 7) and control subjects (20 +/- 6) (p < or = 0.0001). The levels (AcU/mL) in the aortic root also increased in coronary spastic angina (33 +/- 12) compared with stable exertional angina (23 +/- 7) and control subjects (20 +/- 6) (p < 0.005). Furthermore, the coronary sinus-arterial differences of the levels (AcU/mL) were also higher in coronary spastic angina (5 +/- 9) than in stable exertional angina (0 +/- 6) and healthy subjects (-1 +/- 5) (p < 0.05). The generation of malondialdehyde-modified low-density lipoproteins is reported to be associated with atherothrombosis. These findings suggest that elevated levels of autoantibodies against malondialdehyde-modified oxidized low-density lipoproteins in coronary circulation are associated with the development of atherothrombosis from the progression of atherosclerosis rather than with the extent of coronary atherosclerosis in patients with coronary spastic angina.

Acetylcholine↗
PubMed2000

Intrathecal baclofen for management of spastic cerebral palsy: multicenter trial.

Intrathecal baclofen infusion has demonstrated effectiveness in decreasing spasticity of spinal origin. Oral antispasticity medication is minimally effective or not well tolerated in cerebral palsy. This study assessed the effectiveness of intrathecal baclofen in reducing spasticity in cerebral palsy. Candidates were screened by randomized, double-blind, intrathecal injections of baclofen and placebo. Responders were defined as those who experienced an average reduction of 1.0 in the lower extremities on the Ashworth Scale for spasticity. Responders received intrathecal baclofen via the SynchroMed System and were followed for up to 43 months. Fifty-one patients completed screening and 44 entered open-label trials. Lower-extremity spasticity decreased from an average baseline score of 3.64 to 1.90 at 39 months. A decrease in upper extremity spasticity was evidenced over the same study period. Forty-two patients reported adverse events. Most common reports were hypotonia, seizures (no new onset), somnolence, and nausea or vomiting. Fifty-nine percent of the patients experienced procedural or system-related events. Spasticity in patients with cerebral palsy can be treated effectively by continuous intrathecal baclofen. Adverse events, although common, were manageable.

Adolescent↗
PubMed2002

[Spasticity treated with selective posterior rhizotomy].

BACKGROUND: Spasticity is often seen in patients with central nervous lesions. Some patients with severe spasticity are not optimally treated with physiotherapy and medication. MATERIAL AND METHODS: We present a case history of a 41-year-old woman with multiple sclerosis and severe painful spasticity in her lower limbs. Her spasticity did not respond to treatment with physiotherapy, spasmolytic medication, botulinum toxin A, intrathecal baclofen or epidural spinal cord stimulation. RESULT: The patient was treated with selective posterior rhizotomy S1-L1. Section of 60% of the rootlets on the right side and 40% on left the side resulted in a good outcome with less spasticity and pain. Finally her contractures were treated with tenotomy and myotomy, also with good functional result. INTERPRETATION: Patients suffering from severe painful spasticity and who do not respond to physiotherapy in combination with other spasmolytic medication should be considered for surgical treatment. In some patients posterior rhizotomy is the treatment of choice.

Adult↗
PubMed2004

Modulation of the transmission in group II heteronymous pathways by tizanidine in spastic hemiplegic patients.

OBJECTIVE: To investigate the effect of tizanidine (an alpha(2) noradrenergic agonist) on transmission in the interneuronal pathway coactivated by group I and group II afferents in post-stroke patients with spastic hemiplegia. METHODS: Early and late facilitation of the quadriceps H reflex elicited in the common peroneal nerve--attributed to non-monosynaptic group I and group II excitation, respectively--was investigated in 14 spastic hemiplegic patients. All received a single dose of tizanidine (150 microg/kg) or placebo in randomised order at 10 day intervals. Repeated measurements were made at baseline (T0), 45-90 min, and 120 min after drug intake. Spasticity was assessed by modified Ashworth score in the quadriceps muscle and by a leg tone score calculated by the sum of the modified Ashworth score in five muscle groups. RESULTS: On the spastic side a decrease in late group II and, to a lesser extent, early group I common peroneal nerve induced quadriceps H reflex facilitation occurred with tizanidine (group II, mean (SEM) difference T0-T90: 34.3 (10.2)%, p<0.001; group I, T0-T120: 19.8 (9)%, p<0.05), but not with placebo (group II, difference T0-T90: 12.5 (8)%, NS; group I, T0-T120: 3.2 (7)%, NS). Tizanidine but not placebo decreased the quadriceps muscle and global lower limb Ashworth scores (2.9 (0.2) to 1.9 (0.3), p<0.001; and 12 (0.7) to 9.5 (0.8), p<0.0001, respectively). CONCLUSIONS: Enhancement of group II-group I facilitation of the quadriceps motor neurones on the spastic side of hemiplegic patients is modulated by alpha(2) noradrenergic agonists. This strengthens the view that late facilitation of quadriceps motor neurones is mediated by group II afferents and suggests that group II pathways may be involved in lower limb spasticity.

Administration, Oral↗
PubMed2005

Range of motion in children with spastic diplegia, GMFCS I-II compared to age and gender matched controls.

Measurements of passive range of motion are often used to define the degree of muscle shortening in children with spastic diplegic cerebral palsy. However, little is known about the expected values of passive range of motion measurements in children with spastic diplegia and how these might differ from age and gender matched norms taken from the same population. Therefore, the purpose of this study was to compare eight lower limb measurements of sagittal plane passive range of motion in 22 children with spastic diplegia, GMFCS I to II, with 22 matched controls. Children with spastic diplegia had minimal hip extension loss, but reduced hamstring length, with popliteal angle averaging -59.2+/-10.6 degrees (control -38.8+/-13.4 degrees, p < 0.001) and SLR averaging 52.7+/-10.2 degrees (control 75.8+/-11.1 degrees, p < 0.001). Ankle dorsiflexion with knee extension averaged -2.5+/-8.4 degrees in children with spastic diplegia (control 8.6+/-6.8 degrees, p < 0.001). These data confirmed that children with mild spastic diplegia had some restriction in passive range of motion compared to controls but that there was considerable variability between individuals.

Adolescent↗
PubMed1991

[A new type of complicated form of hereditary spastic paraplegia showing mental deterioration, quadriplegia with muscular atrophy, sensory disturbance, extrapyramidal disorders, and epilepsy].

UNLABELLED: This study proposes a new type of complicated form of hereditary spastic paraplegia (HSP) and some problems on a clinico-pathological classification of HSP. The present study includes three male and two female patients from two families (A and B). In the family A, four siblings (two males and two females) were affected. Spastic paraplegia developed as an initial symptom. In the family B, a man was affected with spastic paraplegia which had started at the age of eleven. His two half-sisters are normal. All parents in two pedigrees are healthy. The parents in the family B are first cousins. CLINICAL FEATURES: Their physical development was normal, but all of them showed mild mental retardation. Gait disturbance due to spastic paraplegia and mental deterioration developed at the age of high teens. At the age of high 20's, they became unable to walk, because of progressive spastic paraplegia and other complicated neurological impairments including pyramidal disorders in the upper limbs, generalized neurogenic muscular atrophy, sensory disturbance and bradykinesia. Some cases showed rigidity and/or spasticity. At the age of high 30's, they became bed-ridden, because of quadriplegia with generalized muscular atrophy. Three cases in the family A suffered from convulsions which started at the high 30's. Mild athetoid movement in the face and neck was observed in three cases in the family A. All patients became apathetic and indifferent at least by the age of 40. Laboratory findings and data: CT scan yielded brain atrophy and dilatation of the lateral ventricles, atrophy of the corpus callosum and hyperostosis of the cranium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1996

[Therapeutic effect of "Ueda" method for a case of spastic paraplegia as a sequela of transverse myelitis].

This paper showed the therapeutic effect of the "Ueda" method (UM) for one case with spastic paraplegia as a sequela of transverse myelitis. The effects of UM was dramatic. Two weeks after the beginning of UM, spastic gait improved moderately and inner rotation of lower extremities on supine posture changed to external rotation. Transitionally the fast stretch ROM by the procedure of straight leg raising improved to the level of the normal range four months after the beginning of UM. Although UM was originally designed for cerebral palsy, it was effective for spasticity due to transverse myelitis. Spasticity showed reversible changes depending on UM. Therapists will be able to reduce and control spasticity by means of UM. This result suggests that spasticity treated by UM does not depend on the maturity of central nervous system (CNS) or recovery of the CNS lesion, but is caused by the lesions of the spinal loop.

Child, Preschool↗
PubMed1997

Spastic disorders of the esophagus.

Spastic disorders of the esophagus are found in up to 50% of patients referred for manometry, therapy representing the most prevalent motility disorders in clinical practice. They share in common their manifestations of hypermotility, one of two principal types of esophageal motor dysfunction. Diffuse esophageal spasm is segregated from the nonspecific spastic disorders because of its demonstrated interference with bolus transit. However, the overlap among the spastic disorders in manifestation, course, and management is great; segregation of any disorder within this group is not of paramount importance. Spastic disorders, pain reproduction with provocative testing, and psychological abnormalities are coprevalent in patients with unexplained symptoms, but a cause-effect relationship of the motor abnormalities with the other findings is not established. The physician's charge in determining the relevance of a spastic disorder to the clinical presentation and for creating a treatment plan is to establish a direct relationship of motor dysfunction with symptoms-a task that may require correlation of transit abnormalities with symptoms using tests other than manometry. A variety of treatment options, invasive and noninvasive, are available today for patients who have spastic disorders, and each is effective in appropriately selected candidates.

Esophageal Motility Disorders↗