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PubMed2003

Spasticity in adults living in a developmental center.

OBJECTIVES: To ascertain the prevalence of spasticity among adults living in a developmental center and to document the development of spasticity treatment plans for this population. DESIGN: Descriptions of the clinical features of medical disorders and a prevalence survey. SETTING: Residential developmental center. PARTICIPANTS: One hundred three adults. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Characteristics described included the prevalence of spasticity in this population, the specific spasticity diagnosis, functional goals for spasticity treatment identified by the participants' multidisciplinary teams, and the specific treatment indicated by the neurologist. RESULTS: Of the 103 people diagnosed by the neurologist, 24 had diplegic spasticity, 4 had hemiplegic spasticity, 44 had quadriplegic spasticity, and 31 had no spasticity. Functional goals identified by multidisciplinary teams were undergarment change (46.3% of the persons for whom goals were identified), splinting hands (11%), dressing (57.4%), hygiene (20.4%), wheelchair positioning (25.9%), ambulation improvement (14.8%), and transfers (9.3%). After physical and occupational therapy, the first invasive treatments indicated for people with spasticity included botulinum toxin injections (60%), intrathecal baclofen (26.4%), orthopedic surgery (5.6%), and medication (1.4%). No treatment was recommended for 25% of the spasticity patients. CONCLUSIONS: The prevalence of spasticity was 35% in this developmental center population of 205 individuals. A multidisciplinary team approach to the evaluation of adults with spasticity who live in a developmental center makes it possible to identify functional goals that are amenable to spasticity treatment and minimizes treatment that does not target specific functional goals.

Activities of Daily Living↗
PubMed1999

Spasticity after traumatic spinal cord injury: nature, severity, and location.

OBJECTIVE: To assess spasticity in a prevalence population of persons with traumatic spinal cord injury (SCI), and determine the degree of correspondence between self-reported spasticity and investigator-elicited spasticity using the modified Ashworth scale. DESIGN: Survey of a near total (88%) prevalence population. SETTING: Outpatient clinic of a university hospital. PATIENTS: A total of 354 individuals with SCI. MAIN OUTCOME MEASURES: The survey includes self-reported symptoms, neurologic examination (American Spinal Injury Association [ASIA] classification), physical therapy examination, range of motion (ROM), and complications. RESULTS: Presence of problematic spasticity was significantly correlated with cervical incomplete (ASIA B-D) injury. Reports of beneficial effects of spasticity were significantly less common in women. Self-reported problematic spasticity was significantly correlated with extensor spasticity. Spasticity was elicitable by movement provocation in 60% of the patients reporting spasticity. Significant correlations were found between elicitable spasticity and limited ROM. CONCLUSION: Flexion, extension, and abduction movements performed with the patient placed in a standardized supine test position are suitable both for test of ROM and degree of spasticity. Spasticity was not elicitable by movement provocation on physical examination in 40% of the patients who reported spasticity, thus indicating that the patient's self-report is an important complement to the clinical assessment. A significant association between spasticity and contractures (reduced ROM) was seen.

Activities of Daily Living↗
PubMed1989

FES and spasticity.

A model of hemiplegic spasticity based on electromyographical and biomechanical parameters measured during passive muscle stretching is presented. Two components of spasticity can be distinguished--phasic and tonic. This classification depends on the pattern of stretch reflex activity which can be either phasic or tonic as well as on the muscle stretch/tension characteristic. Stretch reflex, as a control loop, is in phasic spasticity characterized by increased sensitivity to velocity of stretching. In tonic spasticity, sensitivity to length of stretching is increased. After the injury, phasic spasticity appears first and invokes monosynaptic reflex pathways. The intensity of tonic spasticity increases with the duration of disability and hence causes changes in muscle fiber biomechanical properties. The model mentioned above has been used to evaluate the effects of FES on spasticity. Hemiplegic patients with implanted peroneal nerve stimulator for gait correction were followed up for one year starting a week before implantation. Long-term use of FES resulted in decrease of tonic spasticity in both ankle joint antagonistic muscle groups. In stimulated tibialis anterior muscle, the phasic type of spasticity increased. To obtain the correlation between changes in spasticity and functional abilities of patients, the maximal voluntary isometric contraction of both muscle groups was also measured. An improvement in voluntary strength was also observed. This can be taken as additional evidence that tonic spasticity is of greater physiological and clinical significance than phasic spasticity. It may be concluded that use of FES can decrease tonic spasticity and, if applied early after the injury, can prevent the appearance of tonic spasticity.

Adult↗
PubMed1998

Abnormal development of biceps brachii phasic stretch reflex and persistence of short latency heteronymous reflexes from biceps to triceps brachii in spastic cerebral palsy.

Co-contraction of antagonist muscles is characteristic of spasticity arising from perinatal brain damage but not in spasticity occurring after brain damage in adulthood. Such co-contraction is a normal feature of early post-natal motor development. Heteronymous, monosynaptic Group Ia projections from biceps brachii to both the antagonist triceps brachii and to other synergist and non-synergist muscles of the upper limb occur in the newborn baby and become restricted during the first 4 years to motor neurons of primarily synergistic muscles. Longitudinal and cross-sectional studies have been performed to test the hypothesis that inappropriate heteronymous excitatory projections persist in children with perinatal brain damage who develop spasticity. Subjects with spasticity, from brain damage acquired in adulthood were also studied to determine if these projections simply become unmasked as part of spasticity, independent of the age of occurrence of the brain damage. Twenty-nine healthy newborn babies and 29 at high risk for cerebral palsy, 12 of whom developed spastic quadriparesis, were studied longitudinally for 4 years. Thirty-eight subjects, aged 8-30 years, with spasticity of perinatal origin (11 hemiplegic, 11 quadriplegic, 16 with Rett syndrome) and 11 subjects with stroke in adulthood and spastic hemiplegia were also studied. The results were compared with those obtained in 372 normal subjects aged from birth to 55 years. Small taps were delivered to the tendon of biceps brachii using an electromechanical tapper. Surface EMG was recorded from biceps and triceps brachii, pectoralis major and deltoid. In the longitudinal study, those developing spastic quadriparesis showed persistent low thresholds for the homonymous phasic stretch reflex, which had abnormally short onset latencies. There was persistence of short onset heteronymous excitatory responses in triceps brachii, while a normal pattern of restriction of heteronymous responses to pectoralis major and deltoid occurred. The same pattern was observed in older subject groups with spasticity of perinatal origin. In adults with hemiplegia following stroke the threshold of the homonymous phasic stretch reflex was low, but it had a normal onset latency. There was no evidence of abnormal heteronymous excitatory responses. In conclusion, exaggerated excitatory responses to primary muscle afferent input were observed in the homonymous (biceps brachii) and antagonist (triceps brachii) motor neurons in subjects with spasticity arising from perinatal brain damage. They are likely to play an important role in the predominant co-contraction of agonist/antagonist muscles during voluntary movement observed in subjects with spastic cerebral palsy.

Adolescent↗
PubMed2006

Spasticity and its association with functioning and health-related quality of life 18 months after stroke.

BACKGROUND: There is no consensus concerning the presence of spasticity or the relationship between spasticity and functioning and spasticity and health-related quality of life (HRQL) in the stable phase after stroke. OBJECTIVE: The aim of the present study was to describe, 18 months after stroke, the frequency of spasticity and its association with functioning and HRQL. METHODS: In a cohort of 66 consecutive patients with first-ever stroke, studied prospectively, the following parameters were assessed 18 months after stroke: spasticity, by the Modified Ashworth Scale (0-4 points with 1+ as the modification), muscle stiffness, by self-report, abnormal tendon reflexes, by physical examination, motor performance, by the Lindmark Motor Assessment Scale, mobility, by the Rivermead Mobility Index, activities of daily living, by the Barthel Index, and HRQL, by the Swedish Short Form 36 Health Survey Questionnaire (SF-36). RESULTS: Of 66 patients studied, 38 were hemiparetic; of these, 13 displayed spasticity, 12 had increased tendon reflexes, and 7 reported muscle stiffness 18 months after stroke. Weak (r < 0.5) to moderate (r = 0.5-0.75) correlations were seen between spasticity and functioning scores. Correlations between spasticity and HRQL were generally weak (r < 0.5). Hemiparetic patients without spasticity had significantly better functioning scores and significantly better HRQL on 1 of the 8 SF-36 health scales (physical functioning) than patients with spasticity. CONCLUSIONS: Few patients displayed spasticity 18 months after stroke. Spasticity might contribute to impairment of movement function and to limitation of activity, but seems to have a less pronounced effect on HRQL.

Activities of Daily Living↗
PubMedDate not supplied

Spasticity measurement in stroke: a pilot study.

The ability to objectively measure spasticity, related to cerebral stroke, is important in the rehabilitation therapies since many therapeutic modalities have been developed over the years to reduce spasticity. The unproven clinical expectation is that function would be improved were spasticity to be reduced. Unfortunately, the ability to measure spasticity to conduct efficacy studies of spasticity-reducing therapies is not possible. This relates to the multi-variable nature of the spastic syndrome with the result that no clinical measurement technique has been proven to be sensitive, valid and reliable. Therefore, it is important to develop a research-oriented spasticity measurement system to meet this need. We describe the current development of such a system. Details of our pilot study of a reflex excitability technique, designed to measure certain components of cerebral spasticity, are presented. The technique combined biomechanical and electrophysiological measures to investigate a homogenous stroke sample (n = 6); it incorporated the H-reflex in soleus, during passive ankle movements, as a measure of faulty neural inhibition. This component significantly (p < .05) differentiated the stroke sample from a matched, healthy control group (n = 6). Evocation of a cutaneous reflex in soleus was a condition that was problematic and it had to be dropped from the protocol. Joint stiffness, which is thought to affect measures of spasticity during passive movement, did not contaminate the measures. Further research in this direction is required to delineate and measure other neural components of spasticity while taking into account related non-neural variables. The final objective in this line of research is to develop a valid, reliable and sensitive spasticity measurement system that could be used to judge the efficacy of physical neurorehabilitation treatments currently employed to reduce spasticity following stroke.

Aged↗
PubMed1991

Trends in the pathophysiology and pharmacotherapy of spasticity.

Spasticity develops after supraspinal or spinal lesions of descending motor systems, with obligate involvement of the corticospinal tract. Spasticity is characterized by an increase in muscle tone, which, in contrast to many other types of enhanced muscle tone, shows a marked velocity-dependent increase when the muscle is passively stretched. The pathophysiological mechanisms underlying this spastic muscle tone remain obscure. Three major causes are currently considered possible: (1) changes in the excitability of spinal interneurones; (2) receptor hypersensitivity; (3) formation of new synapses by sprouting. The latter mechanism could account for the long time course over which spastic muscle tone develops in hemiplegic or paraplegic patients, but there is no experimental evidence for this hypothesis. The electromyographic (EMG) gait analysis of patients with spasticity has thrown doubt on the common belief that the velocity-dependent increase in spastic muscle tone is evoked by stretch reflex activity and has led to the idea that spastic muscle tone resides in the muscle fibres themselves. While such a mechanism may contribute to the slowness of active movements in spastic patients, recent experiments on patients with spastic arm paresis have confirmed the classical view that the spastic muscle tone is related to the EMG activity evoked in the passively stretched muscle. This pathological EMG activity is seen during the entire range of the dynamic phase of the stretch, during which a normal muscle exhibits only an early, phasic burst at the highest stretch velocities employed. For the pharmacological treatment of spasticity, substances with different central or peripheral actions are available. Their assumed receptor actions are described, together with their main indications and side-effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Electromyography↗
PubMed1994

Eccentric and concentric muscle performance in patients with spastic paresis secondary to motor neuron disease. A preliminary report.

This study investigated the potential value of eccentric (ECC) and concentric (CONC) isokinetic testing for quantifying motor deficit in patients with spastic paresis secondary to motor neuron disease. We hypothesized that, at a moderately fast (120 degrees s-1) angular velocity, spastic patients would demonstrate different ECC-CONC torque relationships from healthy controls or patients with non-spastic neuromuscular disorders. Eleven patients with motor neuron disease having clinical evidence of spasticity, and 11 disease-control patients (with non-spastic disorders, e.g. lower motor neuron disease or myopathy) underwent isokinetic testing. One healthy subject was matched to each of the 22 patients. The average torque generated during maximal voluntary ECC and CONC knee flexion (KF) and extension (KE) was measured using an isokinetic dynamometer (Kin-Com). Reliability was established (all ICC > or = 0.97) for patient torque measurements. Relative strength (% of control subject torque) in spastic patients was significantly higher for ECC than for CONC actions in both KF and KE; conversely, in non-spastic disease-control patients relative strength was not affected by the type of muscle action. The ECC/CONC average torque ratios for KE and KF at 120 degrees s-1 were significantly greater in spastic patients than controls, but did not differ from controls in non-spastic patients. In spastic patients the ECC-CONC imbalances were related to ambulatory dysfunction. In four spastic patients followed with serial testing, the disproportion between ECC and CONC voluntary capacity persisted over time.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1997

Microsurgical selective peripheral neurotomy in the treatment of spasticity in cerebral-palsy children.

Spasticity represents the most handicapping sequelae of cerebral palsy in children. In this study, 28 children with spastic cerebral palsy were treated over the last 4 years by microsurgical selective peripheral neurotomy: 28 times the posterior tibial nerve for spastic foot deformity, 3 times the ulnar and median nerves for spastic flexion of wrist and fingers, 2 times the sciatic nerve for spastic knee flexion associated with spastic foot deformity and 3 times obturator nerves for spastic adductors. Results on spasticity with follow-up ranging from 3 to 48 months were as follows: spastic foot deformity was corrected in all patients with pure spasticity, 2 out of the 3 children with ulnar and median neurotomy improved, knee flexion and hip adduction were improved in the other 5 patients. Selective peripheral neurotomy is an effective procedure in the treatment of segmental harmful spasticity after failure of a well-conducted conservative treatment associating physiotherapy and antispasmodic medications. It must be performed before the fixed deformities and other orthopedic complications arise.

Adult↗
PubMed2003

Spasticity after stroke: its occurrence and association with motor impairments and activity limitations.

BACKGROUND AND PURPOSE: There is no consensus concerning the number of patients developing spasticity or the relationship between spasticity and disabilities after acute stroke. The aim of the present study was to describe the extent to which spasticity occurs and is associated with disabilities (motor impairments and activity limitations). METHODS: Ninety-five patients with first-ever stroke were examined initially (mean, 5.4 days) and 3 months after stroke with the Modified Ashworth Scale for spasticity; self-reported muscle stiffness; tendon reflexes; Birgitta Lindmark motor performance; Nine Hole Peg Test for manual dexterity; Rivermead Mobility Index; Get-Up and Go test; and Barthel Index. RESULTS: Of the 95 patients studied, 64 were hemiparetic, 18 were spastic, 6 reported muscle stiffness, and 18 had increased tendon reflexes 3 months after stroke. Patients who were nonspastic (n=77) had statistically significantly better motor and activity scores than spastic patients (n=18). However, the correlations between muscle tone and disability scores were low, and severe disabilities were seen in almost the same number of nonspastic as spastic patients. CONCLUSIONS: Although spasticity seems to contribute to disabilities after stroke, spasticity was present in only 19% of the patients investigated 3 months after stroke. Severe disabilities were seen in almost the same number of nonspastic as spastic patients. These findings indicate that the focus on spasticity in stroke rehabilitation is out of step with its clinical importance. Careful and continual evaluation to establish the cause of the patient's disabilities is essential before a decision is made on the most proper rehabilitation approach.

Activities of Daily Living↗
PubMed2003

Spasticity in multiple sclerosis.

The objective of this article is to establish the prevalence of spasticity in a random selection of people with multiple sclerosis (MS) in the city of Newcastle upon Tyne in the Northeast of England. A secondary aim was to assess the adequacy of current pharmacological intervention for spasticity and assess the relationship between spasticity and overall disability. The study design was a simple comparison that examined differences in functional independence in 2 random groups of people with MS subdivided by the presence of clinically significant spasticity. A total of 68 adults with a diagnosis of clinically definite MS were included in the study. Their level of functional independence was assessed using the Newcastle Independence Assessment Form (NIAF), the Functional Independence Measure (FIM), and the Kurtzke Extended Disability Status Scale (EDSS). Spasticity was assessed using the Modified Ashworth Scale. A subjective analysis was made of the appropriateness of oral antispastic medication by a rehabilitation physician. Thirty-two people (47%) had clinically significant spasticity (Modified Ashworth Score of 2, 3, or 4). Seventy-eight percent of the population were receiving some oral antispastic medication, but 50% were deemed to require some drug adjustment or additional treatment. Individuals with spasticity were found to have significantly higher levels of disability than those who had no spasticity or clinically insignificant spasticity. This study has confirmed that spasticity is highly prevalent in the MS population and is significantly associated with a reduced level of functional independence. Treatment of spasticity is suboptimal in a large proportion of the population, and the need for further information and education to health professionals and to people with MS is highlighted.

Adult↗
PubMed1994

Inclusion of the S2 dorsal rootlets in functional posterior rhizotomy for spasticity in children with cerebral palsy.

Many neurosurgeons have made a practice of sectioning the S2 dorsal roots during selective posterior rhizotomy for the treatment of spasticity in children with cerebral palsy, but the efficacy of this treatment has not previously been proven. S2 afferents are involved in reflex arcs of the plantar flexors (PFs), so that S2 lesioning should in theory reduce PF spasticity. To test this assumption, we determined the frequency of postoperative residual spasticity in the PFs when S2 lesioning was or was not performed. We assessed 85 children for whom 6-month follow-up was available. Functional rhizotomy from L2-S1 was performed on 13 of them (26 legs with PF spasticity) and from L2-S2 on 72 (141 legs with PF spasticity). Rootlets were lesioned if there was an abnormal response to intraoperative electrical stimulation. In 20 patients, lesioning of the S2 rootlets was assisted by the "pudendal neurogram," a technique previously shown to prevent bladder dysfunction during sectioning of the sacral roots. When S2 roots were excluded from the lesioning process, residual PF spasticity was detected in 35% of the legs that had it preoperatively, leaving 5 (38%) of 13 children with functionally impairing spasticity. When S2 roots were included, 6% of legs that had PF spasticity retained it postoperatively (P < 0.001), leaving 8 (11%) of 72 patients with functionally limiting spasticity (P < 0.05). Thus, the addition of the S2 roots to the procedure resulted in an 81% reduction in the number of legs with residual PF spasticity and a 71% reduction in the number of patients with residual PF spasticity.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1998

Intrathecal baclofen infusion and subsequent orthopedic surgery in patients with spastic cerebral palsy.

UNLABELLED: Intrathecal baclofen infusion (IBI) is an effective treatment for spasticity secondary to cerebral palsy (CP). OBJECT: To assess the need for orthopedic surgery of the lower extremities in such cases, the authors retrospectively reviewed the outcome in 48 patients with spastic CP who were treated with IBI. METHODS: Pumps were placed in 40 patients (84%) suffering from spastic quadriplegia and eight patients (16%) with spastic diplegia. The patients' ages ranged from 5 to 43 years (mean 15 years). The mean follow-up period was 53 months (range 24-94 months). The mean baclofen dosage was 306 microg/day (range 25-1350 microg/day). At the time of pump placement, subsequent orthopedic surgery was planned in 28 patients (58%); however, only 10 (21%) underwent surgery after IBI therapy. In all 10 cases, the surgical procedure was planned at the time of initial evaluation for IBI therapy. In the remaining 18 patients, who did not subsequently undergo their planned orthopedic operation, it was believed that their lower-extremity spasticity had improved to the degree that intervention was no longer indicated. In addition, although six patients had undergone multiple orthopedic operations before their spasticity was treated, no patient required more than one operation after IBI treatment for spasticity. CONCLUSIONS: The authors conclude that IBI for treatment of spastic CP reduces the need for subsequent orthopedic surgery for the effects of lower-extremity spasticity. In patients with spastic CP and lower-extremity contractures, spasticity should be treated before orthopedic procedures are performed.

Adolescent↗
PubMed2001

[Botulinum toxin treatment of hip adductor spasticity in multiple sclerosis].

Spasticity results in a resistance to passive movement and decrease of passive mobility of the involved joints and is defined as a state of hypertonicity with exaggeration of tendon reflexes mediated by a loss of inhibitory control of upper motor neurons. In patients with severe stages of multiple sclerosis (MS) spasticity of the lower limbs often leeds to a spastic pattern with hip adduction resulting in decreased range-of-motion (ROM), increased pain, spasms, and functional disability (disturbed gait and sitting position) as well as difficulties with perineal hygiene. Local botulinum toxin type A (Btx-A) injections in spastic muscles offer a new treatment approach for managing spasticity and associated problems. Up to now Btx-A is approved for the treatment of blepharospasm and cervical dystonia and the treatment of equinous gait in children with cerebral palsy in Austria and Germany. Up to now only in Switzerland Botox is licensed for the treatment of focal spasticity. Btx-A is a neurotoxin derived from Clostridium botulinum. In most european countries Btx-A is available as Dysport (vial = 500 units) and Botox (vial = 100 units). In prospective studies a ratio of 1 unit Botox to 3-4 units Dysport was found. Following intramuscular injection Btx-A blocks the release of acetylcholine at the neuromuscular junctions, thereby inhibiting muscle contraction, and decreases spastic muscle tone and muscle spindles afferent information to the spinal cord. The spectrum of side effects includes local weakening of the injected and adjacent muscles as well as pain and haematoma at the injection site. At therapeutic doses side effects are local and transient. According to a double blind, placebo controlled, dose ranging study published by Hyman et al. (2000, Dysport in a dose of 500, 1000 and 1500 units reduced the degree of hip adductor spasticity associated with MS, and this benefit was evident despite concomitant use of oral antispasticity medication. According to the results of the study there was a clear trend towards greater efficacy and duration of effects with higher doses of Dysport. Taking efficacy and adverse events into account (incidence of muscle weakness was higher for the 1500 units group than for placebo) the optimal dose for hip adductor spasticity seems to be 1000 units Dysport divided between the adductor magnus, longus and brevis muscles and between both legs. To increase Btx-A effects following injection of hip adductors additional physiotherapy and casting or orthosis to increase passive hip-abduction is recommended. According to the literature anatomical localisation of the adductor muscles for injection and aspiration following insertion of the needle, to avoid injection of the toxin into a vessel, should be performed. A maximum dose of 1500 units Dysport (400 units Botox) per treatment session and 250 units Dysport (50 units Botox) per injection site is recommended. See table for dose-range of Dysport, and Botox in the treatment of adult patients with hip-adductor spasticity. For evaluation of treatment effects in hip adductor spasticity clinical examination with specific scales and measurements (see Appendix) at baseline, 4 and 12 weeks following BtxA injection is recommended:--Global rating of severity (0-4; patient's self assessment and physician's rating) --Global rating of response (-4 - +4; patient's self assessment and physician's rating)--Visual Analogue Scale (patient's self assessment of pain)--Active and passive ROM (manual goniometer)--Distance between the medial femur condyles in thigh extension (distance in cm)--Modified Ashworth scale (0-4)--Ten meter walking time (seconds)--Functional Ambulation Categories (0-5)--Score of perineal hygiene (0-5).

Adult↗
PubMed1975

Spasticity following spinal cord injury.

Spasticity is a hyper-excitable state of the reflex arcs in the spinal cord below the level of injury. Not only is the skeletal motor system affected, but bladder, bowel, blood pressure, and erection reflex mechanisms are also involved. Spasticity gradually emerges from the initial phase of spinal shock one to two months after the injury, and usually reaches a plateau of a mild to moderate degree in 3 to 4 months. Neurophysiological mechanisms indicate an increase in the alpha and gamma reflex systems and that central excitability through the interneurons is also involved in these systems. Excessive spasticity should be recognized as a substitute for pain in the spinal cord injured patient, as infections, calculi, pressure ulcers, and other normally painful conditions set off the hyper-sensitive reflexes causing more spasticity. Education and health maintenance is the best prevention of severe spasticity. Definitive treatment of incapacitating spasticity is to find and treat the underlying disease condition, as well as to introduce medication which will also suppress the spasm (Valium and/or Dantrolene). Muscle motor points and/or nerve blocks with neurolytic agents is perhaps the best technique for quietening excessive spasticity. Intrathecal neurolytic agents, anterior or posterior rhizotomies and cordectomies are not advocated even in severe incapacitating spasticity as they are too destructive. Selective longitudinal myelotomy is by far the best surgical technique for disrupting excessive spasticity, if any such procedure is to be done. Tendonotomies may be necessary in chronic contractures of joints after the muscle spasticity has been reduced. Excessive spasticity is not regarded as a normal state in the spinal cord injured patient. The cause should be sought and treated. Nerve destruction techniques should not be used unless medical and nursing techniques have failed. Prevention is so important and can be achieved by education, health maintenance, and especially motivation.

Adult↗
PubMed1993

Are H and stretch reflexes in hemiparesis reproducible and correlated with spasticity?

The measurement of spasticity has always presented a problem to clinicians and researchers alike. As yet, there is no literature addressing the reproducibility of the existing barrage of clinical evaluations of spasticity and reflex measurement. Also not clear is whether or not a systematic relationship might exist between these multiple indices of spasticity. After delineating the differences in spasticity scores and reflex functions between spastic and normal states, the aims of this study were to examine the reliability of these measurements in hemiparetic subjects, and the correlation between altered reflex functions and clinically measured spasticity. An aggregate of lower limb reflexes was compared between ten spastic hemiparetic and seven age-matched normal subjects. Lower limb reflexes examined were: (1) the ratio of maximal H reflex to M response (H/M ratio), (2) the inhibition of the H reflex during vibration (Hvib/Hctl ratio), and (3) soleus stretch reflexes (SR/M ratio). H and stretch reflex latencies were shorter (P < 0.05), and reflex amplitudes were significantly greater (H/M ratios, P < 0.05; SR/M areas, P < 0.005) in spastic subjects. While H/M ratios, Hvib/Hctl ratios, SR/M areas and SR onset angles were highly reproducible, only some physiological measurements showed consistent but non-significant relationships with clinical spasticity. The decreased reflex latencies and increased reflex responses in the hemiparetic subjects suggested that spasticity may be related to reduced reflex thresholds. The physiological measurements and clinically assessed tone were both valid and reproducible, indicating that they can be used to evaluate the long-term effects of therapeutic intervention.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed2003

Spastic velocity threshold constrains functional performance in cerebral palsy.

OBJECTIVES: To evaluate a quantitative, velocity-based assessment of spasticity in the quadriceps and hamstrings muscles of children with cerebral palsy (CP) and to show the effects of spasticity in constraining knee velocities during fast gait. DESIGN: A quantitative comparison of neuromuscular and biomechanical performance in patients with CP and controls without CP. SETTING: Movement analysis laboratory within a university clinical referral center. PARTICIPANTS: A convenience sample of 18 ambulatory patients with CP and 11 control subjects without CP. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Spastic threshold velocity recorded from electromyographic response during passive isovelocity knee movement was compared with knee angular velocity during fast walking, Gross Motor Function Measure (GMFM) scores, and Ashworth Scale score. RESULTS: Patients with measurable spasticity showed slower peak knee angular velocity during walking than patients without spasticity (P<.005). A significant correlation existed between spastic threshold velocity and peak knee angular velocity during fast walking (r=.85, P<.001). Spastic threshold velocity correlated significantly with GMFM (r=.58, P<.05) but not with Ashworth score. CONCLUSIONS: The velocity dependency of spasticity can be measured by electromyograph and dynamometer to determine spastic threshold velocity. Spastic threshold velocity correlated with limitations in joint angular velocity during walking and functional performance.

Adolescent↗
PubMed2002

Effect of cold air therapy in relieving spasticity: applied to spinalized rabbits.

STUDY DESIGN: Before-After trial measured prior to cold air therapy, immediately following, after 30 and 60 min. OBJECTIVE: To determine the effect of cold air therapy in relieving spasticity, the optimal intramuscular temperature, and the duration of spasticity relief attained by cold air therapy. SETTING: Clinical research laboratory, Seoul, Korea. SUBJECT: Forty-six spastic paraplegic rabbits with spinal cord injury. METHODS: Spastic paraplegia was induced by transection of spinal cord in 46 rabbits. Cold air was applied to triceps surae muscles for 30 min at three different intramuscular temperatures (25, 30 and 32.5 degrees C). Clinical parameters of spasticity (muscle tone, Babinski's sign, muscle stretch reflex and ankle clonus) and electrophysiologic parameters (F/M ratio and H/M ratio) were measured immediately following, after 30 and 60 min. RESULTS: In the 32.5 degrees C group, relief in spasticity lasted less than 30 min. In the 30 and 25 degrees C groups, the decrease in spasticity lasted for at least 30 min clinically. The spasticity relief was observed only immediately following treatment when measured electrophysiologically. However, six out of 16 cases (37.5%) in the 25 degrees C group showed complete motor conduction block. CONCLUSION: To relieve spasticity with cold air therapy, the intramuscular temperature should be maintained at 30 degrees C. The duration of spasticity relief lasted from between 30-60 min after cold air therapy. We certify that all applicable institutional and governmental regulations concerning the ethical use of animals were followed during the course of this research.

Animals↗