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PubMed2005

Changes in vesicular glutamate transporter 2, vesicular GABA transporter and vesicular acetylcholine transporter labeling of sacrocaudal motoneurons in the spastic rat.

Spasticity of the midline musculature can significantly hinder performing transfers and lead to development of pressure sores. Currently, significant gaps exist in our knowledge of the pathophysiology involved in spasticity development following SCI, especially regarding the axial musculature. The goals of this study were: (1) to determine the effects of S(2) transection on the number and distribution of glutamatergic, GABAergic and cholinergic inputs on more caudal motoneurons, (2) to correlate these changes with the development of spasticity within the tail musculature, which are the caudal counterparts to the axial musculature. Animals with S(2) spinal transection were tested behaviorally for the progression of spasticity within the tail musculature. At 1, 2, 4, or 12 weeks post-injury, the animals were sacrificed and temporal changes in glutamatergic, GABAergic, and cholinergic inputs to sacrocaudal motoneurons were assessed using antibodies for the specific vesicular transporter of each neurotransmitter and confocal microscopy. At 1 week post-injury, when the tail musculature demonstrated decreased responsiveness, an overall increase in the ratio of excitatory to inhibitory input to sacrocaudal motoneurons was observed. From 2 to 12 weeks post-injury, when the tail musculature demonstrated increased reflex behavior, an overall decrease in the ratio of excitatory to inhibitory inputs was observed. Additionally, from 2 to 12 weeks following spinal transection, a progressive loss of cholinergic labeling of sacrocaudal motoneurons was observed. The increase in the overall level of excitation with a concomitant loss of cholinergic influence following spinal transection could, in part, explain the development of spasticity within the tail musculature.

Animals↗
PubMed2006

VGLUT1 and GLYT2 labeling of sacrocaudal motoneurons in the spinal cord injured spastic rat.

Spasticity of the midline (axial) musculature may hinder (1) performing transfers, (2) efficient extremity and head movements, and (3) efficient respiration. Currently, gaps exist in our knowledge of the pathophysiology involved in spasticity development within the axial musculature. The goals of this study were (1) to study the effects of S(2) transection on the number and distribution of glutamatergic inputs, arising from primary afferents, and glycinergic inputs to sacrocaudal motoneurons; and (2) to correlate changes in these synaptic inputs with the development of spasticity within the tail musculature, which are the caudal counterparts to the trunk axial musculature. Animals with S(2) spinal transection were tested behaviorally using our established system. At 1, 2, 4, and 12 weeks post-injury, sacrocaudal motoneurons were retrogradely labeled with cholera toxin beta-subunit (CTB), and temporal changes in vesicular glutamate transporter 1 (VGLUT1) and glycine transporter 2 (GlyT2) inputs to CTB-labeled motoneurons were visualized using antibodies specific for each synaptic type and confocal microscopy. These time points correspond to each of 4 stages of spasticity development. There was no significant change in either VGLUT1 or GlyT2 labeling of sacrocaudal motoneurons at any of the time points examined. Spinal cord injury-induced spasticity, in the tail musculature, does not appear to involve either an increase in monosynaptic glutamatergic inputs from myelinated afferents or a decrease in glycinergic inputs to sacrocaudal motoneurons.

Animals↗
PubMed2005

The influence of spasticity in the lower limb muscles on gait pattern in children with sacral to mid-lumbar myelomeningocele: a gait analysis study.

Gait analysis and recording of standing position were performed in 38 ambulatory children with myelomeningocele. Thirty-four were independent ambulators and four required a walking aid. All subjects were assigned one of four muscle function groups based on muscle strength. They were also divided into subgroups based on the distinction between flaccid and spastic paresis in the lower limb joints. A comparison was made between the gait pattern of the children with spasticity and that of the children with flaccid paresis in each muscle function group. Spasticity in only the ankle joint muscles influenced the subject's gait and standing position compared to the subgroups with a flaccid paresis. Even larger deviations in gait and standing position were observed when spasticity occurred in muscles at the knee and hip joints. When setting ambulatory goals the presence of additional neurological symptoms such as spasticity and inadequate balance should be taken into consideration.

Adolescent↗
PubMed2006

Spinal anaesthesia in a patient with hereditary spastic paraplegia: case report and literature review.

We report the use of spinal anaesthesia in a patient with hereditary spastic paraplegia who presented for manual removal of placenta following a normal vaginal delivery. This 18-year-old primigravida had been diagnosed with hereditary spastic paraplegia at 8 years of age when neurological examination revealed mild bilateral lower limb spasticity. A 25-gauge Whitacre spinal anaesthetic needle was inserted at the L3-4 intervertebral space and 0.5% plain bupivacaine 2 mL plus fentanyl 25 microg administered. The procedure was uneventful. At 24 hours postoperatively, there was full neurological recovery to pre-anaesthetic levels. The hereditary spastic paraplegias are a group of neurological disorders characterised by a slowly progressing spastic paraparesis. The neurological disorder and its anaesthetic implications are reviewed.

Adolescent↗
PubMed2006

Development of baclofen tolerance in a rat model of chronic spasticity and rigidity.

Systemic or spinal treatment with baclofen has been associated with the development of tolerance in patients with chronic spasticity. In the present study, we used a rat model of spinal ischemia-induced spasticity to characterize the development of baclofen tolerance after chronic intrathecal (i.t.) baclofen infusion. Following the induction of spinal ischemia and the development of behavioral spasticity, animals were implanted with i.t. catheters connected to osmotic pumps to continuously infuse baclofen (1.0 microg/0.5 microl/h). Hindleg peripheral muscle resistance (PMR) was measured periodically after initiation of chronic infusion and after bolus i.t. baclofen injection (1.0 microg). Peripheral muscle resistance was significantly decreased at the onset of baclofen infusion, however, after 5-7 days of infusion a progressive return of spasticity was noted, where baseline PMR values returned to preinfusion levels. At the same time, the efficacy of bolus i.t. baclofen treatment also decreased, where after 5 days of baclofen infusion 1.0 microg (i.t.) baclofen only reduced PMR by 10% (compared to 40-50% preinfusion). Baclofen efficacy progressively returned once continuous infusion was stopped. These data demonstrate that transient spinal ischemia leads to the development of spasticity which is sensitive to spinal baclofen. Chronic i.t. infusion leads to a progressive development of tolerance. This model offers potential to study tolerance mechanisms after spinal injury, and aid in drug discovery for use in baclofen-tolerant patients.

Animals↗
PubMed2006

Botulinum toxin type A for the treatment of the spastic equinus foot in cerebral palsy.

Muscle overactivity, one of the cardinal features of spasticity, is a common sequel of cerebral palsy. In this group of patients spasticity is responsible for several limitations that interfere with gait, causing variable functional disability. Drugs such as baclofen, tizanidine, or benzodiazepines, or even definitive treatments such as orthopedics or neurosurgeries are generally prescribed with uncertain results. The use of botulinum toxin type A has been frequently suggested for the treatment of spastic equinus foot in cerebral palsy, but few studies with adequate methodology support this idea. The present paper reviews and summarizes the data of published double-blind, randomized clinical trials to assess, with a meta-analysis, if botulinum toxin type A is an adequate treatment for spasticity caused by cerebral palsy. The results reveal a statistical superiority of botulinum toxin type A over placebo on gait improvement, tested using the Physician Rating Scale and Video Gait Analysis (Peto odds ratio = 3.99, 95% confidence interval = 2.20-7.22) in patients with spastic equinus foot. The botulinum toxin group also presented better results in the subjective assessment than the placebo group (Peto odds ratio = 3.49, 95% confidence interval = 1.50-8.12). Adverse events were more frequently observed after the use of botulinum toxin type A, but they were considered mild and self-limited.

Adolescent↗
PubMed2003

Intrathecal baclofen in subjects with spastic hemiplegia: assessment of the antispastic effect during gait.

OBJECTIVE: To determine whether leg muscle stiffness is measurably reduced after intrathecal baclofen (ITB) in subjects with spastic hemiplegia. DESIGN: Nonrandomized trial. SETTING: Inpatient multidisciplinary rehabilitation unit in France. PARTICIPANTS: Seven consecutive subjects with spastic hemiplegia having Ashworth Scale scores for their quadriceps and triceps greater than 2. INTERVENTION: Subjects were given ITB by lumbar puncture after a dose-selecting test period. MAIN OUTCOME MEASURES: Triceps and quadriceps Ashworth scores, gait analysis at preferred and maximal speed measured by a motion analysis system with 2 forceplates, and electromyographic recording of leg muscles before and 4 hours after ITB. The slopes of the moment-angle curves were measured on the hemiplegic side at the onset of ankle and knee flexion to assess muscle stiffness during walking. Pre- and post-ITB spatiotemporal, kinetic, and kinematic data were compared by using a nonparametric test (Wilcoxon signed-rank test). RESULTS: Ashworth scores of the quadriceps and triceps of all subjects decreased significantly after ITB. Maximal walking speed increased significantly, with a significant increase in stride length, but the preferred walking speed was unchanged. Minimal knee extension and maximal ankle flexion were the only kinematic data significantly different (increased) after ITB. The slope of the ankle moment-angle curve decreased significantly after ITB at preferred gait speed; it also decreased at maximal gait speed in all but 1 subject. Of the 4 available moment-angle curves, 3 showed decreased knee extensor muscle stiffness. The duration of the bursts of spastic muscles decreased after ITB. CONCLUSION: Acute ITB improved walking and reduced muscle stiffness at both the ankles and knees on the spastic hemiplegic side of our subjects. Electromyographic findings suggest that some of the post-ITB reduction in muscle stiffness might be attributed to decreased spasticity.

Adult↗
PubMed2004

Selective blocks of the motor nerve branches to the soleus and tibialis posterior muscles in the management of the spastic equinovarus foot.

OBJECTIVE: To identify the location of the motor nerve branches to the soleus and tibialis posterior muscles in relation to anatomic surface landmarks for selective motor nerve blocks in the management of the spastic equinovarus foot. DESIGN: Descriptive study by computed tomography (CT) scan of 12 hemiplegic legs. SETTING: Spasticity group at a university hospital. PARTICIPANTS: Twelve patients with hemiplegia (6 men, 6 women) with spastic equinovarus foot. INTERVENTION: Three-dimensional location of the motor nerve branches to the soleus and tibialis posterior muscles with CT scan, followed by selective motor branch blocks with anesthetics. MAIN OUTCOME MEASURES: Vertical, horizontal, and deep coordinates determined by CT scan in relation to anatomic surface landmarks (upper extremity of the fibula and vertical metallic element). Soleus and tibialis posterior spasticity (Ashworth Scale), soleus H-wave maximum (Hmax)/M-wave maximum (Mmax) ratio, and sensory testing before and after the blocks. RESULTS: The mean coordinates +/- standard deviation for the soleus motor branch were 10+/-5 mm (vertical), 17+/-9 mm (horizontal), and 30+/-4 mm (deep); for the tibialis posterior motor branch they were 45+/-6mm (vertical), 17+/-8mm (horizontal), and 47+/-4 mm (deep). Spasticity and Hmax/Mmax ratio decreased after the blocks, confirming their efficiency. No subjects experienced additional sensory deficit. CONCLUSION: Our study determined the location of the motor nerve branches to the soleus and tibialis posterior muscles in relation to anatomic surface landmarks for selective motor branch blocks and neurolytic procedures. These coordinates allow us to perform selective motor blocks without CT scan.

Adult↗
PubMed2004

Alcohol neurolysis of tibial nerve motor branches to the gastrocnemius muscle to treat ankle spasticity in patients with hemiplegic stroke.

OBJECTIVE: To evaluate the effectiveness of alcohol neurolysis of tibial nerve motor branches to the gastrocnemius muscle for the treatment of ankle plantarflexor spasticity in patients with hemiplegic stroke. DESIGN: Case series. SETTING: Inpatient and outpatient clinics in the rehabilitation department of a university hospital. PARTICIPANTS: Twenty-two patients with hemiplegic stroke (mean age, 48y). INTERVENTIONS: Motor branch block (MBB) of the tibial nerve to the gastrocnemius muscle with 50% ethyl alcohol in cases of spastic ankle. MAIN OUTCOME MEASURES: The severity of spasticity was assessed using the Modified Ashworth Scale (MAS) score of ankle plantarflexor, clonus score of the ankle, and the passive range of motion (PROM) of ankle dorsiflexion. RESULTS: The MAS score was reduced in 17 (77%) of 22 patients during the 6-month follow-up, and spasticity reappeared at the level of the pre-MBB state in 5 patients (23%). The mean values of all parameters were significantly improved. The changes of mean values from the pre-MBB to the 6-month post-MBB stage were as follows: MAS score, 3.3+/-0.7 versus 1.7+/-1.1; clonus score, 1.6+/-0.7 versus 0.4+/-0.8; and PROM, 17.1 degrees +/-13.0 degrees versus 28.6 degrees +/-4.7 degrees. No serious complications were observed during the 6-month follow-up period. CONCLUSIONS: MBB of the tibial nerve to the gastrocnemius muscle is an effective and safe procedure for relieving localized spasticity of the ankle plantarflexors.

Adult↗
PubMed1996

Quantitative clinical measure of spasticity in children with cerebral palsy.

OBJECTIVE: This investigation developed an objective measure to quantify the degree of spasticity. DESIGN: Specifications included a single variable that integrated key elements characterizing spasticity: velocity, range of motion, and resistance to passive motion. A dynamometer at a children's hospital quantified the passive resistance of the hamstrings to knee extension for a range of motion at 4 different speeds for the prospective descriptive investigation. PATIENTS: A convenience sample of six children with able bodies and 17 children with spastic diplegic cerebral palsy volunteered. DATA PROCESSING: Torque-angle data were processed to calculate the work done by the machine on the children for each speed and then determine the slope of the work-velocity curves. This slope was considered to be the measure of spasticity and it was hypothesized that children with cerebral palsy would have a greater slope than children with able bodies. An independent test determined whether a significant difference existed between groups (p < .05). RESULTS: Torque-angle data for children with able bodies indicated little change in passive resistance as a function of speed. Similar data for children with cerebral palsy indicated larger resistive torques with increasing speed. Slope from the work-velocity data was close to zero for children with able bodies [.003 J/(degrees/sec)], while the corresponding slope for children with cerebral palsy was approximately 10 times greater [.031 J/(degrees/sec)] and significantly different (p < .05). CONCLUSION: The slope of the work-velocity data integrates three major components characterizing spasticity, it is a single number that can easily be evaluated and interpreted in a clinical setting, and it utilizes a machine that is available at many centers.

Adolescent↗
PubMed1997

Increased spasticity in a chronic spinal cord injury patient after scabies infestation: a case report.

Spasticity is a common feature of spinal cord injury (SCI). Spasticity exacerbation is commonly encountered with nociceptive and exteroceptive stimuli including bladder and bowel dysfunction, pressure sores, contracture, tight-fitting leg bags and clothing, and ingrown toenail. This report describes a patient with chronic SCI (T4 level) who complained of increasing spasticity of bilateral lower extremities for 5 weeks. He also had skin lesions on different parts of his body, accompanied by itching above the spinal cord lesion level. A clinical diagnosis of scabies was made and pharmacologic treatment was initiated. Following treatment, spasticity was significantly reduced and the skin rash with itching faded out. This report is the first of scabies skin infestation lesions triggering exacerbation of spasticity in an SCI patient.

Adult↗
PubMed1998

Cold effect on oxygen uptake, perceived exertion, and spasticity in patients with multiple sclerosis.

OBJECTIVE: To determine the effect of a cold bath (24 degrees C) on oxygen consumption and perceived exertion during ambulation and on spasticity in individuals with mild to moderate multiple sclerosis. DESIGN: A repeated-measures design with random assignment of experimental and control conditions. SETTING: Outpatient physical therapy department associated with an academic institution. PATIENTS: Fourteen individuals with clinically definite multiple sclerosis exhibiting spasticity and capable of ambulating at 0.7 m/sec on a motorized treadmill without handrail support. MEASUREMENT: Assessment of oxygen uptake, heart rate, and perceived exertion occurred during two 10-minute walks interspersed with a 30-minute rest on 2 separate days. Measurement of spasticity occurred three times during each session. RESULTS: Oxygen consumption and perceived exertion were unchanged. Spasticity was higher immediately (p < .05) after the cold bath. CONCLUSIONS: Increase in spasticity was statistically significant, but unlikely to be of any clinical importance. Contrary to our hypothesis, a cold bath (24 degrees C) for 20 minutes did not reduce oxygen consumption or rating of perceived exertion during ambulation.

Adult↗
PubMed1999

Neurolysis of the musculocutaneous nerve with alcohol to treat poststroke elbow flexor spasticity.

OBJECTIVE: To evaluate the effectiveness of alcohol in neurolysis of the musculocutaneous nerve for the treatment of elbow flexor spasticity in individuals with a stroke. DESIGN: Case series. SETTING: Outpatient clinic of a tertiary rehabilitation facility. PARTICIPANTS: Twenty patients with a mean age of 62.8 years and poststroke duration of 12.3 months with elbow flexor spasticity. INTERVENTION: Musculocutaneous nerve block of the hemiplegic upper extremity with 50% ethyl alcohol. OUTCOME MEASURES: The severity of spasticity as assessed by the modified Ashworth scale (MAS) score and the elbow passive range of motion (PROM). RESULTS: The mean baseline MAS score was 3.7 +/- 0.6, and this improved to 1.7 +/- 1.0, 2.0 +/- 0.8, and 2.1 +/- 0.8 at 4 weeks, 3 months, and 6 months postneurolysis, respectively. The elbow PROM was 87.3 degrees +/- 20.2 degrees, 104.3 degrees +/- 20.1 degrees, 103.8 degrees +/- 18.9 degrees, and 101.6 degrees +/- 19.7 degrees, respectively. These improvements were statistically significant (p < .05). Four subjects had concomitant improvement of finger flexor spasticity and another four had relief of shoulder pain. Three subjects developed temporary dysesthetic pain over the lateral forearm. CONCLUSION: Neurolysis of the musculocutaneous nerve with alcohol provides good relief of elbow flexion spasticity in hemiplegic individuals.

Elbow Joint↗
PubMed1999

Antidepressant exacerbation of spasticity.

Patients with spinal cord injury (SCI) may develop depression. This may be related to adjustment to living with an SCI in addition to dealing with complications of the injury, such as spasticity. Pharmacologic treatment of depression can be difficult because of neurochemical and receptor changes that are associated with SCI. Newer antidepressant agents are purported to have selective activity by alteration of serotonergic neurotransmission. A case report is presented that illustrates exacerbation of spasticity by this family of antidepressant medications. Mechanisms possibly explaining this exacerbation of spasticity are the effects of serotonin on motor neuron and reflex activity, denervation supersensitivity, and the serotonin syndrome. Understanding the relationship between serotonergic systems and spasticity can be important in treating depression in patients with spasticity.

Adjustment Disorders↗
PubMed2000

Hyper-reflexia without spasticity after unilateral infarct of the medullary pyramid.

Whether or not a lesion confined to the pyramidal tract produces spasticity in humans remains an unresolved controversy. We have studied a patient with an ischemic lesion of the right medullary pyramid, using objective measures of hyper-reflexia, spasticity, and weakness. Electromyographic activity (EMG) of the biceps muscles was recorded under the following conditions: (1) in response to a tendon tap with an instrumental reflex hammer, (2) in response to imposed quick stretch with motion analysis, and (3) during an isometric holding task. Hyper-reflexia of the involved arm in response to tendon tap was shown to be due primarily to an increase in the gain of the reflex arc. No velocity-dependent increase in the response to quick stretch of the involved arm was present. This was consistent with the absence of detectable spasticity on the clinical exam. These findings suggest that a lesion confined to the medullary pyramid can give rise to weakness and hyper-reflexia without causing spasticity. Moreover, these findings suggest that different anatomical substrates may underlie the clinical phenomena of hyper-reflexia and spasticity.

Aged↗
PubMed2001

[Reevaluation of physiological mechanisms generating the stretch reflex: new hypotheses on the physiopathology of spasticity].

INTRODUCTION: Spasticity has been defined as tendon reflex exaggeration and increased muscle reflex contraction in response to its stretch (Lance, 1980). It has been generally admitted that stretch reflex exaggeration was due to myotatic reflex hyperexcitability (Ia fibre-motoneurone synapses). This interpretation has been recently revisited taking into account neurophysiological data obtained in cat and recent data obtained in spastic patients. PROBLEMATICS: Myotatic reflex has been described in decerebrate cat in 1924 by Liddel and Sherrington. In 1943, Lloyd demonstrated that myotatic reflex was due to monosynaptic Ia fibre motoneurone alpha synapses. Almost all the following studies of stretch reflexes were devoted to monosynaptic reflexes both in animal and humans. In fact, the existence of group II fibres coming also from spindles and some restricted experiments performed in man have led to discuss the role of group II fibres in the static component of the stretch reflexes. RESULTS: Recent studies performed in humans have shown that group II fibres play an important role in the development of stretch reflexes in leg muscles and that in spastic hemiplegic patients group II fibres facilitatory effects was deeply increased. DISCUSSION: Results obtained both in humans and animals suggest that group II fibres play also a role in a stretch reflex and led to consider that the pathophysiological modifications of group II effects could contribute to spasticity. CONCLUSION: Modifications of network fed by group II fibres and modifications of muscular fibres intrinsic properties are likely to play a role in the developments of spasticity in humans.

Animals↗
PubMed1987

Management of intrinsic spasticity in the hand with phenol injection or neurectomy of the motor branch of the ulnar nerve.

Thirty-nine adults with acquired spastic disorders who had 21 phenol injections and 21 neurectomies of the motor branch of the ulnar nerve in Guyon's canal for control of intrinsic spasticity in the hand were reviewed. Follow-up averaged 25.8 months for the patients with phenol blocks and 24.3 months for those who had a neurectomy. Intrinsic spasticity was relieved in all hands postoperatively. After the phenol block, which is a temporizing procedure, 13 hands had return of spasticity in 6 months. Eight hands had little or no return of spasticity and required no further treatment. Neurectomy was performed in predominantly nonfunctional hands with severe hygiene problems and with no potential for further neurologic recovery. Hand function was improved in six hands after phenol block and in one hand after neurectomy. Hygiene was improved in all hands after phenol block and in all except one hand after neurectomy. Two wound infections and one wound dehiscence occurred.

Adolescent↗
PubMed1982

Biofeedback therapy for spastic dysphonia.

Spastic dysphonia is a disorder of phonation which is characterized by a strained, creaking, and choked vocal attack, a tense and squeezed voice sound. Spastic dysphonia in a functional voice disorder can be classified into two types from the viewpoint of activities of the extrinsic and intrinsic laryngeal muscle groups. A functional voice disorder pertaining to abnormal activities of the intrinsic and extrinsic laryngeal muscles results in spastic dysphonia. The adductor spastic dysphonia may be due to abnormal actions of the intrinsic laryngeal muscles as such is relieved by sectioning of the recurrent nerve, while spastic dysphonia mainly dealing with the extrinsic laryngeal muscles is relieved by relaxation on monitoring an electromyographic feedback system. Within 3 months we encountered two patients whose extrinsic laryngeal muscles were hyperactive on phonation. A trial on injection of lidocaine into extrinsic laryngeal muscles made their muscles relax. So, biofeedback therapy of relaxation was began using a monitoring system of EMG burst regarding to hypertonicity of the extrinsic laryngeal muscles. Normal vocal abilities were recovered using a biotrainer as a monitoring device of electromyographic feedback.

Adult↗