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PubMed1994

Mechanisms of tizanidine action on spasticity.

This investigation estimated the mechanisms of tizanidine action on spasticity using a battery of neurophysiological methods. Thirty patients with old post-stroke spastic hemiparesis took part in the investigation. They were treated with tizanidine-mean daily dose 15.8 +/- 5.6 mg for a mean of 23.3 +/- 4.8 days. A questionnaire for assessment of subjective improvement after treatment used a 5-point scale. For standardization of the neurological examination 5-point scales were used to assess muscle tone, muscle force and tendon reflexes. A battery of neurophysiological methods was used to analyze different mechanisms of spasticity: for alpha motoneuron excitability--the F wave parameters; for presynaptic inhibition--the ratio of H reflex amplitudes before and after vibration of the achilles tendon (Hvibr/Hmax); for common interneuron activity--the flexor reflex parameters. Our results revealed that tizanidine reduces spastically increased muscle tone, but has no influence on muscle force, tendon reflexes, Babinski sign and ankle clonus. Tizanidine is supposed to act by increasing the presynaptic inhibition and decreasing of alpha motoneuron excitability. When spasticity has decreased presynaptic inhibition and increased motoneuron excitability, it is better to treat with tizanidine.

Adult↗
PubMed1984

Tension development and muscle activation in the leg during gait in spastic hemiparesis: independence of muscle hypertonia and exaggerated stretch reflexes.

In 15 patients with spastic hemiparesis the development of tension of calf muscles in relation to their electrical activation and their stretching period was studied on both sides during locomotion. Only in the spastic leg did isolated small biphasic potentials appear in the gastrocnemius E.M.G. with monosynaptic latency at the beginning of the stance phase, while the remaining gastrocnemius activation was reduced compared to the unaffected side. Perturbations of gait were followed in the spastic leg by a large monosynaptic response, while the polysynaptic reflex response was reduced. In the unaffected leg only a strong polysynaptic response appeared, which suggests a reciprocal modulation of monosynaptic and polysynaptic reflex responses. Tension development paralleled the gastrocnemius E.M.G. in the unaffected leg, while in the spastic leg tension was more closely correlated to muscle stretch. It is concluded that in spasticity the exaggerated monosynaptic reflexes represent only a small part of leg extensor activation during gait and that the tension development does not depend on these reflexes.

Adult↗
PubMed1996

Lasting reduction of severe spasticity after ending chronic treatment with intrathecal baclofen.

OBJECTIVE: To investigate whether the dose of intrathecal baclofen necessary for a sufficient reduction of muscle tone and spasms changes during treatment of severe spasticity. METHODS: A group of 27 patients received intrathecal baclofen for 61 (SD 18) months. RESULTS: Spasticity remained absent or strongly reduced after stopping the intrathecal baclofen infusion in seven patients. The dose of baclofen could be reduced to 40% of that dose which was originally necessary in 10 patients. The dose remained the same or increased slightly in 10 patients. Possible reasons for the continuing reduction of spasticity after terminating long term intrathecal baclofen infusion in some patients could be: lasting morphological changes in spinal cord neurons by second messenger controlled modulation of gene expression, a toxic effect of baclofen on spinal neurons, muscular atrophy, inflammation due to the catheter, or progression of multiple sclerosis. CONCLUSIONS: A higher initial daily dose of intrathecal baclofen might lead to a faster, lasting suppression of spasticity and the development of spastic symptoms might even be prevented by pre-emptive treatment with baclofen in patients with newly acquired lesions of the spinal cord.

Adult↗
PubMed1996

Use of botulinum toxin in stroke patients with severe upper limb spasticity.

OBJECTIVES: Spasticity can contribute to poor recovery of upper limb function after stroke. This is a preliminary evaluation of the impact of botulinum toxin treatment on disability caused by upper limb spasticity after stroke. METHODS: Seventeen patients with severe spasticity and a non-functioning arm were treated with intramuscular botulinum A neurotoxin (median age at treatment 54.5 years; median time between onset of stroke and treatment 1.5 years). Baseline and assessments two weeks after treatment were compared to assess efficacy. The duration of improvement in disability was documented. Outcome measures used were; passive range of movement at the shoulder, elbow, wrist, and fingers; modified Ashworth scale to assess spasticity of biceps and forearm finger flexors; an eight point scale to assess the degree of difficulty experienced by the patient or carer for each functional problem defined before treatment; the presence of upper limb pain. The biceps, forearm finger flexors, and flexor carpiulnaris were treated with intramuscular botulinum toxin. Up to a total dose of 400-1000 mouse units (MU) of Dysport (Speywood) or 100-200 MU of BOTOX (Allergan) was used in each patient. RESULTS: Functional problems reported by the patients before treatment were difficulty with cleaning the palm, cutting fingernails, putting the arm through a sleeve, standing and walking balance, putting on gloves, and rolling over in bed. Hand hygiene improved in 14 of 17 patients; difficulty with sleeves improved in four of 16; standing and walking balance improved in one of four; shoulder pain improved in six of nine; wrist pain improved in five of six. Passive range of movement at shoulder, elbow, and wrist improved after treatment. Benefit was noted within two weeks and lasted one to 11 months. No adverse effects occurred. CONCLUSION: This preliminary study suggests that intramuscular botulinum toxin is a safe and effective treatment for reducing disability in patients with severe upper limb spasticity.

Adolescent↗
PubMed2002

Quantitative analysis of the velocity related pathophysiology of spasticity and rigidity in the elbow flexors.

OBJECTIVE: To quantify velocity dependent and position related properties of increased muscle tone measured during a constant velocity stretch. METHODS: Elbow flexors were vertically stretched under four different velocities (40, 80, 120, and 160 degrees /s) through a 75 degrees range of motion in 12 patients with hemiparesis, 16 with parkinsonism, and 12 normal controls. From reactive torque measurement, a linear second order model was adopted to dissociate velocity dependent viscous and velocity independent elastic components. The averaged speed dependent reflex torque (ASRT)--defined as the deviation of measured torque from baseline torque--was used to quantify the viscous component of hypertonia. Velocity sensitivity of ASRT (VASRT) and segmented ASRT (SASRT), derived from the slope of the regression line among ASRT velocity plots and from segmentations of reactive torque, respectively, were used to differentiate the increased muscle tone of spasticity and rigidity. RESULTS: ASRT and VASRT were significantly higher in both spasticity and rigidity than in normal controls. SASRT analysis showed three different position related patterns among spasticity, rigidity, and normal groups: spasticity showed progressively increasing muscle tension relative to position; rigidity showed increased (relative to the norm) but constant muscle tone over the entire stretch range; the normal control group showed a consistently low reactive torque over the entire range. CONCLUSIONS: Velocity dependence analysis indicates that rigidity and spasticity have approximately equal velocity dependent properties. For differentiating these two types of hypertonia, position dependent properties my be employed.

Adult↗
PubMed2004

Spastic long-lasting reflexes in the awake rat after sacral spinal cord injury.

Following chronic sacral spinal cord transection in rats the affected tail muscles exhibit marked spasticity, with characteristic long-lasting tail spasms evoked by mild stimulation. The purpose of the present paper was to characterize the long-lasting reflex seen in tail muscles in response to electrical stimulation of the tail nerves in the awake spastic rat, including its development with time and relation to spasticity. Before and after sacral spinal transection, surface electrodes were placed on the tail for electrical stimulation of the caudal nerve trunk (mixed nerve) and for recording EMG from segmental tail muscles. In normal and acute spinal rats caudal nerve trunk stimulation evoked little or no EMG reflex. By 2 wk after injury, the same stimulation evoked long-lasting reflexes that were 1) very low threshold, 2) evoked from rest without prior EMG activity, 3) of polysynaptic latency with >6 ms central delay, 4) about 2 s long, and 5) enhanced by repeated stimulation (windup). These reflexes produced powerful whole tail contractions (spasms) and developed gradually over the weeks after the injury (< or =52 wk tested), in close parallel to the development of spasticity. Pure low-threshold cutaneous stimulation, from electrical stimulation of the tip of the tail, also evoked long-lasting spastic reflexes, not seen in acute spinal or normal rats. In acute spinal rats a strong C-fiber stimulation of the tip of the tail (20 x T) could evoke a weak EMG response lasting about 1 s. Interestingly, when this C-fiber stimulation was used as a conditioning stimulation to depolarize the motoneuron pool in acute spinal rats, a subsequent low-threshold stimulation of the caudal nerve trunk evoked a 300-500 ms long reflex, similar to the onset of the long-lasting reflex in chronic spinal rats. A similar conditioned reflex was not seen in normal rats. Thus there is an unusually long low-threshold polysynaptic input to the motoneurons (pEPSP) that is normally inhibited by descending control. This pEPSP is released from inhibition immediately after injury but does not produce a long-lasting reflex because of a lack of motoneuron excitability. With chronic injury the motoneuron excitability is increased markedly, and the pEPSP then triggers sustained motoneuron discharges associated with long-lasting reflexes and muscle spasms.

Anesthesia↗
PubMed2003

Spasticity in a child with myelomeningocele treated with continuous intrathecal baclofen.

Patients with myelomeningocele may often suffer from severe spasticity. Surgical treatment of the underlying pathology such as hydromyelia and tethered cord may be successful, but failures are not uncommon. Those cases may offer a surgical challenge since further therapeutic options are limited. We present the case of a 7-year-old boy with myelomeningocele and related conditions suffering from severe spasticity and pain in his lower limbs. Surgical efforts with untethering and posterior fossa decompression failed to improve the symptoms. A test with 25 microg intrathecally delivered baclofen showed a total relief of spasticity and pain so that a pump for continuous baclofen delivery was implanted. During 32 months of follow-up, his spasticity has been under excellent control on 55-157 microg baclofen per day. Continuous delivery of intrathecal baclofen may be a surgical option to consider in patients with myelomeningocele and severe spasticity.

Baclofen↗
PubMed1992

Neurosurgical treatment of spasticity: selective posterior rhizotomy and intrathecal baclofen.

The pathophysiology of spasticity and the history of posterior rhizotomies are reviewed. The rationale for selective posterior rhizotomies is that electrical stimulation identifies afferent posterior rootlets that terminate on relatively uninhibited alpha motoneurons; if these uninhibited rootlets are divided, spasticity can be alleviated without loss of other posterior root functions. Indications, technique, and results of selective posterior rhizotomies are presented. The use of continuous intrathecal baclofen (CITB) is summarized. CITB at doses of approximately 300 micrograms/day consistently reduces lower extremity spasticity and diminishes or alleviates muscle spasms in adults with spasticity of spinal origin. Single doses of intrathecal baclofen significantly decrease lower extremity muscle tone in children with cerebral palsy, and the effects can be maintained in these patients by CITB infusions which diminish muscle tone not only in the lower extremities, but in the upper extremities as well. CITB is best accomplished via an externally programmable pump that allows titration of the daily dose to attain the desired reduction in spasticity. Factors influencing the decision for rhizotomy or CITB are presented.

Adolescent↗
PubMedDate not supplied

Familial spastic paraparesis: a case of a mitochondrial disorder.

Familial spastic paraparesis is characterized by progressive gait disturbance without associated sensory, cerebellar, or cranial nerve deficits. Mitochondrial disorders are associated with heterogenic clinical presentations, though not with spastic paraparesis. A patient with familial spastic paraparesis had deficiencies of respiratory chain enzyme complex I, III, and IV. Progressive spasticity was arrested after treatment with coenzyme Q, carnitine, vitamin C and K. Familial spastic paraparesis may represent a mitochondrial disorder.

Biopsy↗
PubMed1995

Effects of continuous intrathecal baclofen infusion and selective posterior rhizotomy on upper extremity spasticity.

This study was performed to compare the effects of continuous intrathecal baclofen infusion (CIBI) and selective posterior rhizotomy (SPR) on upper extremity (UE) spasticity and range of motion in children with cerebral palsy. Spasticity was assessed with the Ashworth scale of muscle tone and range of motion was evaluated. Thirty-eight patients who had been treated with CIBI for at least 6 months were paired, according to pretreatment UE muscle tone and functional status, with 38 patients who had undergone SPR. The CIBI dosage had been titrated to reduce over lower extremity spasticity and improve lower extremity function, rather than to improve UE tone. The pretreatment muscle tone in the two groups was virtually identical. The UE tone of children treated with CIBI decreased from 2.07 prior to treatment to 1.66 after 1 year (p < 0.01). The tone of children treated with SPR decreased from 2.03 to 1.70 after 1 year (p = 0.005). In that group, the likelihood of a clinically significant reduction in muscle tone (one point or greater) was greater in children with a higher pretreatment UE muscle tone. There was no correlation between the percentage of posterior lumbar roots divided in SPR and the subsequent reduction in UE tone. There were no significant changes in the range of motion in any UE joint, at either 6 or 12 months, after either CIBI or SPR. We conclude that both CIBI and SPR significantly reduce UE spasticity, in addition to the previously documented reduction in lower extremity spasticity.

Arm↗
PubMed1997

Botulinum toxin type A for the treatment of arm and hand spasticity in stroke patients.

BACKGROUND: Focal spasticity can be a major drawback in the rehabilitation of stroke patients. Previous studies suggest a beneficial effect for botulinum toxin A (BTX-A) for relief of spasticity. OBJECTIVE: To evaluate the safety and efficacy of BTX-A in the treatment of spasticity in a homogeneous group of stroke patients. METHODS: In this phase III open label trial 19 stroke patients stable for at least six months were enrolled (mean age 53.1 (SD 3.27) years; range 26-72). There were 16 males and 4 females. ASSESSMENTS: Clinical (Ashworth spasticity rating scale, scores for joint mobility, pain and frequency of spasms, Frenchay arm test (FAT)) and subjective (semi-quantitative rating scale filled out by the patient). Only hand and finger flexors were injected. The maximum dosage was 150 U BOTOX (25 U/muscle), the mean dosage was 92.1 +/- 31.6 U BOTOX. RESULTS: Ashworth rating scale and joint mobility scores improved from a median value of 2 at baseline to a median value of 1 one month after treatment, FAT scores also improved from a median value of 0 at baseline to a median value of 1 one month after treatment (Kruskall-Wallis test p < 0.01). Two-thirds of the patients rated their functional improvement as none or mild. CONCLUSIONS: Our study confirmed that BTX-A has an anti-spastic effect but its functional impact needs further evaluation.

Adult↗
PubMed1996

A comparison of clinical and laboratory measures of spasticity.

Clinical evaluation of spasticity was performed in lower extremities in 35 ambulatory multiple sclerosis patients and compared with the soleus stretch reflex and the Hoffman reflex. There was no relation between the muscle tone score of dorsiflexion of the foot and the biomechanical/electrophysiological parameters. In contrast, the Achilles tendon reflex score was significantly related to the amplitude (rho = 0.411, P < 0.05) and the slope of the stretch reflex (rho = 0.523, P < 0.01). The clinical examination at the ankle joint revealed 33% normal reflex examinations but only 7% normal muscle tone examinations. In contrast, the number of normal examinations of patellar reflex and muscle tone at the knee joint were similar. It is concluded that the muscle tone score overestimates the amount of spasticity because of changes in the non-reflex properties of the spastic extremity and that a reflex score should be used as a clinical measure of spasticity. In addition, biomechanical/electrophysiological evaluation of spasticity at the ankle joint relates to the over-all total muscle tone and reflex scores of lower extremities in this group of MS patients.

Adult↗
PubMed2000

The effects of ipsilateral forearm movement and contralateral hand grasp on the spastic hand opened by electrical stimulation.

The purpose of this study was to investigate the effects of ipsilateral arm movement and contralateral hand grasp on the spastic hand opened by open-loop electrical stimulation. The major problem of applying proper electrical stimulation is variable spasticity, the intensity of which changes with posture and movements of other parts of the body. Electrical stimulation was applied to extensor digitorum communis and ulnar nerve to open the affected hand. Different procedures were then used to assess the effects of moving the ipsilateral forearm and contracting the contralateral normal hand. Electrical stimulation opened the spastic hand in more than 95% of trials in all subjects, whether stimulation was applied before or after the movement of the forearm. Moving the ipsilateral forearm did have an effect on opening the hand, and making adjustment of stimulation intensities was necessary in all subjects. The stimulation opened the spastic hand during the contraction of the contralateral normal hand. Electrical stimulation could open the spastic hands most of the time, in the presence of ipsilateral forearm movement and contralateral normal hand contraction. If electrical stimulation was applied before the ipsilateral forearm was moved toward the target, stimulation intensities needed to be adjusted.

Adult↗
PubMed2001

The estimated cost of managing focal spasticity: a physician practice patterns survey.

The purpose of this study was to estimate the overall cost of managing focal spasticity after stroke (CVA) and traumatic brain injury (TBI) and the cost impact of individual treatments. Sixty physicians described management strategies over six treatment visits for four focal spasticity case studies (one upper and one lower extremity case for CVA and TBI). Mean and median per-case costs were determined across physicians; median per-case costs of physicians who did or did not report use of specific treatments were compared. Mean per-case costs of managing spasticity are as follows: CVA upper, $5,131; CVA lower, $5,384; TBI upper, $14,615; and TBI lower, $13,966. Median per-case costs for strategies including botulinum toxin type A (BTX-A) were less than those without BTX-A in CVA upper; median costs for strategies including oral baclofen were more than those without baclofen in CVA lower. Fewer total treatments were reported with BTX-A than without; more total treatments were reported with baclofen than without. No individual treatment had a significant impact on median treatment costs in TBI. Physician-reported spasticity management costs are substantial. Despite higher drug costs for BTX-A compared with oral therapies like baclofen, strategies for managing spasticity in CVA that include BTX-A may cost less than those without BTX-A.

Brain Injuries↗
PubMed2006

Botulinum toxin A injection for spasticity in diplegic-type cerebral palsy.

Botulinum toxin type A can be both safe and effective in relieving spasticity in pediatric patients with cerebral palsy. In our prospective study, we evaluated the functional effect of botulinum toxin A in spastic diplegic-type cerebral palsy. Patients were examined on enrollment and at 1, 3, and 6 months after injection. Passive dorsiflexion of the ankle joint was measured using a goniometer as an angle of possible maximal dorsiflexion with the knee extended and flexed. Spasticity was graded using the Modified Ashworth Scale. Selective motor control at the ankle was assessed, and observational gait analysis was done. The functional status of the patients was determined by using the gross motor classification system. Botulinum toxin A was injected into the gastrocnemius muscle in all patients, and in four patients with concomitant jump knee gait, a hamstring muscle injection was added. Fourteen patients were included in the study. The mean age was 58.81 +/- 15.34 months. Following injection, spasticity was clinically decreased and statistically significant improvement was noticed in all clinical parameters after 1, 3, and 6 months of injection. The improvement in the clinical parameters decreased after 6 months but not to the baseline. One patient was Level II, four patients were Level III, and six patients were Level IV according to the Gross Motor Function Classification System at baseline. Improvement in the gross motor classification system is continued after 6 months in 12 children. The main goal of spasticity treatment in cerebral palsy is functional improvement. In our study, most of our patients had functional improvement according to the gross motor function classification system and did not change at 6 months.

Botulinum Toxins, Type A↗
PubMed2004

Predicting spasticity after stroke in those surviving to 12 months.

OBJECTIVE: To measure muscle tone in a cohort of patients 12 months after stroke and develop a preliminary model, using data recorded routinely after stroke, to predict who will develop spasticity. DESIGN: A cohort study. SETTING: Initially hospitalized but subsequently community-dwelling stroke survivors in Liverpool, United Kingdom. SUBJECTS: One hundred and six consecutively presenting stroke patients surviving to 12 months. MAIN OUTCOME MEASURES: Spasticity measured at a range of joints using the Tone Assessment Scale. RESULTS: The Tone Assessment Scale revealed spasticity in 38 (36%) patients and more severe spasticity in 21 (20%) of the 106 patients. Logistic regression analysis revealed that lower day 7 Barthel Index score and early arm or leg weakness were significant predictors of abnormal muscle tone; and lower day 7 Barthel Index score, left-sided weakness and ever smoked to be significant predictors of more severe muscle tone. CONCLUSIONS: Using the models, it may be possible to predict whether or not spasticity will develop in patients 12 months after stroke. The utility of the models is aided by their use of predictor variables that are routinely collected as part of stroke care in hospital and which are easy to measure. The models need testing prospectively in a new cohort of patients in order to test their validity, reliability and utility and to determine if other data could improve their efficiency.

Aged↗
PubMed2006

The effect of botulinum toxin type A injection into the gastrocnemius muscle on sit-to-stand transfer in children with spastic diplegic cerebral palsy.

OBJECTIVE: To investigate the benefit of botulinum toxin type A injection into the ankle plantarflexor muscle on sit-to-stand transfer in children with spastic diplegic cerebral palsy. DESIGN: Case-control study. SETTING: Inpatients in a university-affiliated hospital. SUBJECTS: Forty spastic diplegic children aged from 2 to 6 years (18 children with botulinum toxin type A injection into both gastrocnemius muscles as an experimental group and 14 children without injection as a control group). MAIN MEASURES: Sit-to-stand transfer task was evaluated using a motion analyser (Vicon 370 MA with six infrared cameras). The tests were performed twice with a two- week interval. The changes in temporal, kinematic and kinetic parameters were investigated in each group. RESULTS: In the control group there were no significant changes in any of the measured parameters between the tests. In the experimental group, total duration (s) of sit-to-stand transfer was shortened after injection (4.35 +/- 2.49 to 2.89 +/- 1.48, P < 0.05). The maximal angles (degrees) of pelvic and hip joints were reduced (28.88 +/- 5.53 to 26.57 +/- 3.73 and 90.78+8.69 to 87.23 +/- 8.76) and the initial angle of ankle dorsiflexion was increased (4.41 +/- 6.16 to 7.08 +/- 6.09) after injection (P < 0.05). The maximal moments (Nm/kg) of the hip and knee joints (0.44 +/- 0.17 to 0.51 +/- 0.21 and 0.13 +/- 0.05 to 0.18 +/- 0.14) were increased while that of the ankle joint was reduced (0.32 +/- 0.09 to 0.28 +/- 0.10) after injection (P < 0.05). Only the cases with greater reduction of spasticity showed an improvement on kinematic and kinetic parameters. CONCLUSION: Botulinum toxin type A injection into spastic ankle plantarflexors led to better accomplishment of sit-to-stand transfer in children with spastic diplegic cerebral palsy.

Ankle↗
PubMed1999

A review of the properties and limitations of the Ashworth and modified Ashworth Scales as measures of spasticity.

BACKGROUND: The Ashworth Scale and the modified Ashworth Scale are the primary clinical measures of spast city. A prerequisite for using any scale is a knowledge of its characteristics and limitations, as these will play a part in analysing and interpreting the data. Despite the current emphasis on treating spasticity, clinicians rarely measure it. OBJECTIVES: To determine the validity and the reliability of the Ashworth and modified Ashworth Scales. STUDY DESIGN: A theoretical analysis following a structured literature review (key words: Ashworth; Spasticity; Measurement) of 40 papers selected from the BIDS-EMBASE, First Search and Medline databases. CONCLUSIONS: The application of both scales would suggest that confusion exists on their characteristics and limitations as measures of spasticity. Resistance to passive movement is a complex measure that will be influenced by many factors, only one of which could be spasticity. The Ashworth Scale (AS) can be used as an ordinal level measure of resistance to passive movement, but not spasticity. The modified Ashworth Scale (MAS) will need to be treated as a nominal level measure of resistance to passive movement until the ambiguity between the '1' and '1+' grades is resolved. The reliability of the scales is better in the upper limb. The AS may be more reliable than the MAS. There is a need to standardize methods to apply these scales in clinical practice and research.

Arm↗