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At least 667 records · Page 37Linked to original sources
PubMed1998

Bereitschaftspotential in amyotrophic lateral sclerosis (ALS): lower amplitudes in patients with hyperreflexia (spasticity).

In a pilot study the Bereitschaftspotential (BP) was investigated in 16 patients suffering from amyotrophic lateral sclerosis (mean age 58.6, mean severity of the illness according to Norris ALS score 76.4 points). Comparing the total ALS group (n=16) with matched controls no significant differences in the BP amplitude parameters were found. However, a subgroup of 7 ALS patients with signs of pronounced spasticity (hyperreflexia) differed significantly at the central midline from matched controls and significantly in addition from patients with a lower degree of spasticity. Controls as well as patients with a lower degree of spasticity had significantly higher BP amplitudes at the midline (electrode positions Cz and Pz, P<0.05, H-test). The correlation coefficient between the hyperreflexia Norris score and the various BP parameters for the total ALS sample (n=16) revealed a significant correlation especially over the midline. Stronger signs of spasticity (hyperreflexia) are associated with lower amplitudes of the BP.

Adolescent↗
PubMedDate not supplied

Treatment of muscle spasticity in patients with cerebral palsy using BTX-A: a pilot study.

This study was designed to verify the safety and efficacy of botulinum toxin type A (BTX-A) used as a neuromuscular block on spastic masticatory musculature of children with cerebral palsy. Six patients who had spastic-tetraplegic cerebral-palsy, aged 5 to 20 years were selected. All patients had spasticity of the jaw muscles, bruxism, lower lip trauma, limited mouth opening, and difficulties in cleaning the oral cavity. The patients were sedated under general anesthesia, while the dentist injected the masseter and temporalis muscles bilaterally with 150 and 75 units of BTX-A each. Clinical examinations were conducted at 7, 14, 30, and 90 days after the initial appointment. We found statistically significant decreases in muscle spasticity and bruxism (p = 0.002), improved inter-incisal opening (p = 0.002), improved oral hygiene (p = 0.031), and less lower lip trauma (p = 0.060) after the neuromuscular blocking.

Adolescent↗
PubMed1984

Changes in benzodiazepine receptor binding as seen autoradiographically in the central nervous system of the spastic mouse.

Quantitative light-microscope autoradiography has been used to compare the specific, clonazepam-displaceable binding of [3H]flunitrazepam, a photoaffinity label for the 1,4-benzodiazepine receptor, in different regions of the brain and spinal cord of spastic mice and their unaffected littermates. Specific binding of [3H]flunitrazepam in the central nervous system of the spastic mouse showed significant increases in the anterior colliculus and pretectal area and in all laminae of the grey matter in the lumbar spinal cord. These results confirm homogenate binding assays suggesting an increased number of benzodiazepine receptors in the spinal cord of the spastic mouse. Possible sites are therefore provided at which disorders of function could arise, associated with changes seen at the gamma-aminobutyric acid (GABA)-benzodiazepine receptor complex in spinal cord homogenates from the mutant mouse spastic.

Animals↗
PubMed1971

Radiofrequency cordotomy for the relief of spasticity in decerebrate cats.

The effectiveness of radiofrequency (RF) cordotomy of segmental motoneurone pools of the lumbosacral cord in reducing spasticity of decerebrate cats is evaluated. The need for a new form of therapy for clinical spasticity is based upon the limitations of contemporary methods, including surgical and pharmacological techniques. In man, spasticity of spinal origin may be treated effectively by intrathecal administration of hyperbaric phenol solutions. The advantages and disadvantages are described. Difficulty in controlling the lesion is emphasized. Tension and EMG-length curves of the spastic triceps surae muscle in acute and chronic animals show that RF lesions (fixed amperage and duration) of the segmental motoneurone pools reduces myotatic reflex activity in accordance with the number of segments cordotomized. Clinical examination including cinematography and electromyography complement the physiological interpretation. RF lesions of the internuncial pool induce spontaneous EMG discharges. This finding is related to similar observations of EMG discharges and alterations in muscle tone after asphyxiation of the spinal cord.

Action Potentials↗
PubMed1972

Tonic vibration reflex in spasticity, Parkinson's disease, and normal subjects.

The tonic vibration reflex (TVR) has been studied in the quadriceps and triceps surae muscles of 34 spastic, 15 Parkinsonism, and 10 normal subjects. The TVR of spasticity develops rapidly, reaching a plateau level within 2-4 sec of the onset of vibration. The tonic contraction was often preceded by a phasic spike which appeared to be a vibration-induced equivalent of the tendon jerk. The initial phasic spike was usually followed by a silent period, and induced clonus in some patients. No correlation was found between the shape of the TVR and the site of the lesion in the central nervous system. The TVR of normal subjects and patients with Parkinsonism developed slowly, starting some seconds after the onset of vibration, and reaching a plateau level in 20-60 sec. A phasic spike was recorded occasionally in these subjects, but the subsequent tonic contraction followed the usual time course. Muscle stretch increased the quadriceps TVR of all subjects, including those with spasticity in whom the quadriceps stretch reflex decreased with increasing stretch. It is suggested that this difference between the tonic vibration reflex and the tonic stretch reflex arises from the selective activation of spindle primary endings by vibration, while both the primary and the secondary endings are responsive to muscle stretch. The TVR could be potentiated by reinforcement in some subjects. Potentiation outlasted the reinforcing manoeuvre, and was most apparent at short muscle lengths. As muscle stretch increased, thus producing a larger TVR, the degree of potentiation decreased. It is therefore suggested that the effects of reinforcement result at least partially from the activation of the fusimotor system. Since reinforcement potentiated the TVR of patients with spinal spasticity in whom a prominent clasp-knife phenomenon could be demonstrated, it is suggested that the effects of reinforcement are mediated by a descending pathway that traverses the anterior quadrant of the spinal cord.

Electromyography↗
PubMed1977

C0-contraction and stretch reflexes in spasticity during treatment with baclofen.

Surface electromyograms were recorded from the quadriceps and hamstring muscles of 11 spastic patients during cyclical flexion and extension movements of the knee. A potentiometer strapped to the knee recorded the angle of the joint, the output signal being displayed on an oscilloscope. The patient used this signal to track a sine wave target for 20 cycles. The observer then moved the patient's limb through a further 20 cycles tracking the same target. Recordings were repeated at intervals for four hours after an oral dose of baclofen. Analysis of the recordings showed that the response of a spastic muscle to lengthening is not the same during passive movement as during voluntary movement. In mild spasticity stretch reflexes appear to be suppressed by voluntary effort whereas in severe spasticity they are enhanced. Baclofen suppressed the response to passive stretch by over 30% at plasma concentrations of over 250 ng/ml and by 50% at concentrations of over 400 ng/ml, but this effect was largely extinguised during voluntary movement.

Adolescent↗
PubMed1993

The limitations of the tendon jerk as a marker of pathological stretch reflex activity in human spasticity.

The motor disorders associated with human spasticity arise, partly from a pathological increase in the excitability of muscle stretch reflexes. In clinical practice, reflex excitability is commonly assessed by grading the reflex response to a blow delivered to the tendon of a muscle. This is a much simpler response than the complex patterns of activity which may be elicited following muscle stretch caused by active or passive movement. Changes in the biceps brachii tendon jerk response have been followed over the first year after stroke in a group of hemiparetic patients and compared with changes in short and medium latency reflex responses elicited by imposed elbow flexion of initially relaxed spastic muscle and with the development of the late reflex responses which contribute to spastic hypertonia. A progressive increase in tendon jerk responses occurred over the first year following stroke, whereas reflex responses to imposed displacement, in particular the late reflex responses contributing to muscle hypertonia, reached their peak excitability one to three months after stroke, with a subsequent reduction in activity. The tendon jerk reflex therefore provides an incomplete picture of the pathological changes in the reflex responses in spasticity.

Adult↗
PubMed1995

Treatment of chronic limb spasticity with botulinum toxin A.

The purpose of this open study was to find out whether botulinum toxin A (BTX-A) relieves the signs and symptoms of chronic limb spasticity. The study comprised 40 patients, aged 12-82 years, with moderate to severe spasticity of the upper (13) or lower limbs (27) refractory to conventional physical and medical treatments. Outcome measures were clinical and blinded videotape assessments of spasticity and motor function. Electromyography guided BTX-A injections were given in one or two sessions at total doses averaging 175 U in the upper limb (range 70-270 U) and 221 U in the lower limb (range 100-500 U). Thirty four patients (85%) derived worthwhile benefit, with improved limb posture and increased range of passive motion in 31, pain reduction in 28 of 31 with pain, and improved function in 16. Side effects were limited to local and usually mild discomfort from the injections (19), symptomatic local weakness (one), and local infection (one). Preliminary experience indicates that BTX-A is a promising adjunctive treatment for selected patients with spasticity.

Adolescent↗
PubMed1997

Physiological effects of selective tibial neurotomy on lower limb spasticity.

OBJECTIVES: To assess by electrophysiology the effect of tibial selective neurotomy on muscle imbalance of the spastic ankle. METHOD: The amplitudes of the H reflexes, M responses (muscle contractions recorded after stimulation of the tibial nerve), and Hmax:Mmax ratio were recorded in 12 patients with chronic lower limb spasticity, before and one month after tibial selective neurotomy. Recordings were done on medial and lateral gastrocnemius and soleus muscles. Clinical evaluation was done with both global (Held's score) and analytical tests (step measurements, gait velocity, and ankle angulation during active and passive movements). RESULTS: After neurotomy, gait improved in all patients. Held's score of spasticity was better in all patients. Active dorsiflexion of the ankle was unchanged in three patients, but the others improved by 5 degrees to 12 degrees. Hmax, Mmax, and Hmax:Mmax ratios were lower. The Hmax on the gastrocnemius muscle, clinical strength, Mmax of all the muscles, and Hmax:Mmax ratio for the soleus and lateral gastrocnemius muscle were significantly lower after surgery. CONCLUSION: There was an improvement of clinical and electrophysiological spastic indices after selective tibial neurotomy. Neurotomy acted not only on motor neurons by decreasing strength, but also the reflex enlargement by decreasing sensory afferents.

Adolescent↗
PubMed2000

Botulinum toxin (Dysport) treatment of hip adductor spasticity in multiple sclerosis: a prospective, randomised, double blind, placebo controlled, dose ranging study.

OBJECTIVE: To define a safe and effective dose of Dysport for treating hip adductor spasticity. METHODS: Patients with definite or probable multiple sclerosis, and disabling spasticity affecting the hip adductor muscles of both legs, were randomised to one of four treatment groups. Dysport (500, 1000, or 1500 Units), or placebo was administered by intramuscular injection to these muscles. Patients were assessed at entry, and 2, 4 (primary analysis time-point), 8, and 12 weeks post-treatment. RESULTS: A total of 74 patients were recruited. Treatment groups were generally well matched at entry. The primary efficacy variables-passive hip abduction and distance between the knees-improved for all groups. The improvement in distance between the knees for the 1500 Unit group was significantly greater than placebo (p = 0.02). Spasm frequency was reduced in all groups, but muscle tone was reduced in the Dysport groups only. Pain was reduced in all groups, but improvements in hygiene scores were evident only in the 1000 Unit and 1500 Unit groups. Duration of benefit was significantly longer than placebo for all Dysport groups (p<0.05). Adverse events were reported by 32/58 (55%) Dysport patients, and by 10/16 (63%) placebo patients. Compared with the two lower dose groups, twice as many adverse events were reported by the 1500 Unit group (2.7/patient). The incidence of muscle weakness was higher for the 1500 Unit group (36%) than for placebo (6%). The response to treatment was considered positive by two thirds of the patients in the 500 Unit group, and by about half the patients in the other groups. CONCLUSION: Dysport reduced the degree of hip adductor spasticity associated with multiple sclerosis, and this benefit was evident despite the concomitant use of oral antispasticity medication and analgesics. Although evidence for a dose response effect was not statistically significant, there was a clear trend towards greater efficacy and duration of effect with higher doses of Dysport. Dysport treatment was well tolerated, with no major side effects seen at doses up to 1500 Units. The optimal dose for hip adductor spasticity seems to be 500-1000 Units, divided between both legs.

Adult↗
PubMed2001

A large family with hereditary spastic paraparesis due to a frame shift mutation of the spastin (SPG4) gene: association with multiple sclerosis in two affected siblings and epilepsy in other affected family members.

Hereditary spastic paraparesis (HSP) is a clinically and genetically heterogeneous neurodegenerative disorder characterised by progressive lower limb spasticity and weakness. Some forms have been associated with white matter lesions and complex phenotypes. This study was prompted by the diagnosis of multiple sclerosis (MS) in two sisters from a large pedigree with hereditary spastic paraparesis. Twelve affected members of the extended family were examined (MRI and EEG were carried out and evoked potentials measured in five), and historical information was obtained from six affected deceased persons. The inherited disease phenotype was confirmed as autosomal dominant hereditary spastic paraparesis associated with epilepsy in four affected persons. None of the extended family had evidence of MS. Genetic analysis of the family has shown linkage to chromosome 2p and sequencing of the spastin gene has identified a 1406delT frameshift mutation in exon 10. This kindred demonstrates the clinical heterogeneity of HSP associated with spastin mutations. The possible relevance of the concurrence of HSP and MS in the sib pair is discussed.

Adenosine Triphosphatases↗
PubMed2003

The relation between Ashworth scale scores and the excitability of the alpha motor neurones in patients with post-stroke muscle spasticity.

BACKGROUND: The modified Ashworth scale (MAS) is the most widely used method for assessing muscle spasticity in clinical practice and research. However, the validity of this scale has been challenged. OBJECTIVES: To compare the MAS with objective neurophysiological tests of spasticity. METHODS: The MAS was recorded in patients with post-stroke lower limb muscle spasticity and correlated with the excitability of the alpha motor neurones. The latter was evaluated by measuring the latency of the Hoffmann reflex (H reflex) and the ratio of the amplitude of the maximum H reflex (H(max)) to that of the compound action motor potential of the soleus muscle (M(max)). RESULTS: Data on 24 randomly recruited patients were analysed. Patients were divided into two groups according to their MAS score: 14 had a MAS score of 1 (group A) and 10 scored 2 (group B). The two groups were comparable with respect to age and sex, but in group A there was a longer period since the stroke. The H reflex latency was reduced and the H(max):M(max) ratio was increased in both groups. The H(max):M(max) ratio values were higher for group B but the differences were not statistically significant. CONCLUSIONS: There is a relation between the MAS scores and alpha motor neurone excitability, although it is not linear. This suggests that the MAS measures muscle hypertonia rather than spasticity.

Action Potentials↗
PubMed2004

Spastic long-lasting reflexes of the chronic spinal rat studied in vitro.

Over the months following sacral spinal cord transection in adult rats, a pronounced spasticity syndrome emerges in the affected tail musculature, where long-lasting muscle spasms can be evoked by low-threshold afferent stimulation (termed long-lasting reflex). To develop an in vitro preparation to examine the neuronal mechanisms underlying spasticity, we removed the whole sacrocaudal spinal cord of these spastic chronic spinal rats (>1 mo after S(2) sacral spinal transection) and maintained it in artificial cerebral spinal fluid in a recording chamber. The ventral roots were mounted on monopolar recording electrodes in grease, and the reflex responses to dorsal root stimulation were recorded and compared with the reflexes seen in the awake chronic spinal rat. When the dorsal roots were stimulated with a single pulse, a long-lasting reflex occurred in the ventral roots, with identical characteristics to the long-lasting reflex in the awake spastic rat tail. The reflex response was low threshold (T), short latency, long duration ( approximately 2 s), and enhanced by repeated stimulation. Brief high-frequency stimulation trains (0.5 s, 100 Hz, 1.5 x T) evoked even longer duration responses (5-10 s), with repeated bursts of activity that were similar to the repeated muscle spasms evoked in awake rats with stimulation trains or manual skin stimulation. Stimulation of a given dorsal root evoked long-lasting reflexes in both the ipsilateral and contralateral ventral roots. Long-lasting reflexes did not occur in the sacrocaudal spinal cord of acute spinal rats (S(2) transection), which is similar to the areflexia seen in awake acute spinal rats. However, long-lasting reflexes could be made to occur in the acute spinal rat by altering K(+) (7 mM) or Mg(2+) (0 mM) concentrations, or by application of high doses of the neuromodulators norepinephrine (NE, >20 microM) or serotonin (5-HT, >20 microM). In chronic spinal rats, much lower doses of these neuromodulators (0.1 microM) enhanced the long-lasting reflexes, suggesting a denervation supersensitivity to 5-HT and NE following injury. Higher doses of NE or 5-HT produced a paradoxical inhibition of the long-lasting reflexes. The high dose inhibition by NE was mimicked by the alpha(2)-adrenergic receptor agonist clonidine but not the alpha(1)-adrenergic receptor agonist methoxamine. In summary, the sacral spinal in vitro preparation offers a new approach to the study of spinal cord injury and analysis of antispastic drugs.

Adrenergic alpha-Agonists↗
PubMed1994

Effects of conditioning cutaneomuscular stimulation on the soleus H-reflex in normal and spastic paretic subjects during walking and standing.

1. The modulation of the soleus H-reflex by a conditioning cutaneomuscular stimulation was investigated in 10 normal and 10 spastic paretic subjects who suffered from incomplete spinal cord lesions. The different motor tasks examined were standing, locomotion, and the maintenance of static limb postures to mimic critical gait events. The test soleus H-reflex was obtained by stimulating the tibial nerve in the popliteal fossa with a single 1-ms pulse at an intensity that produced a barely detectable M wave. The conditioning stimulus, consisting of an 11-ms train of three 1-ms pulses at 200 Hz, was delivered to the ipsilateral medial plantar arch, stimulating predominantly the medial plantar nerve, at an innocuous intensity of 2.5-3.0 X sensory threshold and at a conditioning-test delay of 45 ms. 2. During quiet standing, the H-reflex amplitude was inhibited only marginally by the conditioning cutaneomuscular stimulation, not reaching statistical significance in either the normal or spastic group of subjects. Although there was a trend of reflex inhibition in the normal subjects as the conditioning intensity was increased, a reversed trend of reflex facilitation was observed in the spastic patients. 3. During treadmill walking, the conditioned H-reflex was inhibited significantly during all phases in all the normal subjects and in one mildly impaired patient. In the moderately and severely impaired patients, cutaneomuscular stimulation selectively inhibited the soleus H-reflex in the early stance and swing phases, thereby producing a near normal phasic modulation pattern. Such modulatory effects were not present under static gait-mimicking conditions. 4. The task-specific and phase-dependent effects of cutaneomuscular stimulation on the soleus H-reflex in the spinal cord-injured patients revealed strong inhibitory influence on Ia afferents from cutaneomuscular inputs. It is plausible that inhibition occurs at both pre- and postsynaptic levels. 5. It is concluded that normal Ia modulatory mechanisms during locomotion are deficient in spastic spinal cord-injured patients and can partially and artificially be restored by cutaneomuscular stimulation applied to the sole of the foot. This can be used as a functional electrical stimulation (FES) regime in gait rehabilitation.

Adult↗
PubMed2002

The effect of intrathecal baclofen on muscle co-contraction in children with spasticity of cerebral origin.

AIM: Investigation of the effect of intrathecal baclofen administration on the time course of electrical patterns of muscle activation in patients with spasticity due to upper motor neuron syndrome. METHODS: Six children with clinical signs of upper motor neuron syndrome resulting from an acquired cerebral hypoxic injury were tested. Simultaneous multichannel acquisition of surface EMG activity from flexor/extensor muscle groups of the upper and lower limbs was recorded. Investigated muscle group pairs included biceps/triceps brachii, wrist flexors/extensors, rectus/biceps femoris and tibialis anterioris/gastrocnemius. Time-frequency analysis of EMG activity at rest and while eliciting a stretch reflex was performed. The non-linear cross-correlation coefficient and time lag estimation were computed between paired channel groups both for baseline and post-intrathecal baclofen injection conditions for epochs consisting of 2 s prior to and 2 s after voluntary contraction. The effect of baclofen was assessed 3 h following single-bolus intrathecal injections of 25 or 50 microg during the baclofen trial and 6 months after baclofen pump implantation. RESULTS: In the baseline condition, the stretch reflex resulted in a synchronous increase in spectral EMG power in both the agonist and the antagonist muscles. The mean correlation coefficient between agonist and antagonist muscles was 0.948 (SD = 0.034), and the mean time lag was 4.64 ms (SD = 1.84 ms). After intrathecal administration of baclofen, a dramatic decrease in the correlation coefficient between agonist and antagonists (mean value = 0.342) during voluntary contraction was observed. This corresponded to a significant reduction of tone and spasticity in all four limbs, and reduction of the Ashworth score by 2 points on average. CONCLUSION: After intrathecal baclofen administration, we observed a significant decrease in the co-contraction pattern typically associated with upper motor neuron spasticity. This was evident clinically and was quantitatively expressed by the significantly decreased degree of coupling in EMG activity of agonist/antagonist muscles. Although a relatively small sample was investigated in this study, we were able to demonstrate the efficacy of this procedure in restoring selective activation of agonists during voluntary contraction. This is one of the prerequisites of an improvement of motor function in patients with spasticity.

Adolescent↗
PubMed1989

Direct spinal effect of a benzodiazepine (midazolam) on spasticity in man.

The water-soluble benzodiazepine, midazolam, was administered epidurally over the lumbar enlargement 18 times to 9 patients with spasticity due to severe spinal cord injury. Doses of 1.25-3.75 mg produced a rapid decrease of spasticity which lasted 1 h. After the maximal reduction of spasticity, the patients became drowsy. While the results suggest a direct action of midazolam on the spinal cord to reduce spasticity, the effect does not contribute to its usefulness as a therapeutic tool.

Adult↗
PubMed1985

Microsurgical selective procedures in peripheral nerves and the posterior root-spinal cord junction for spasticity.

This review deals with the long-term results of selective peripheral neurotomy (SPN) of the tibial nerve and selective posterior rhizotomy (SPR) in 123 cases of severe spastic syndromes in the limbs. The microtechniques and preoperative electrostimulation for identification of the nervous structures responsible for the spastic components give to these methods an advantage of a substantial reduction of the harmful spasticity, without suppressing the useful muscle tone and impairing the residual motor and sensory functions. The results were effective, with a 1- to 13-year follow-up, in 89% of 47 SPN of the tibial nerve for spastic foot, in 92% of 53 SPR for paraplegia and in 87% of 23 SPR for hemiplegia.

Adolescent↗
PubMed2007

A randomized controlled study of botulinum toxin A in the treatment of hemiplegic shoulder pain associated with spasticity.

OBJECTIVES: To assess the effects of botulinum toxin A (BT-A) on hemiplegic shoulder pain associated with spasticity. DESIGN: Randomized, double-blind, placebo-controlled study. SETTING: Outpatient clinic of a rehabilitation department. PARTICIPANTS: Patients, more than three months post stroke, with hemiplegic shoulder pain associated with shoulder adductor and elbow flexor spasticity, randomly assigned to BT-A or placebo. INTERVENTION: One-time injection of BT-A (500 units) into the pectoralis major and biceps brachii on the hemiplegic side. MAIN MEASURES: Visual analogue scale of shoulder pain (0 -10), shoulder adductor and elbow flexor tone using the Ashworth Scale and passive range of shoulder abduction. These were assessed at baseline, four weeks, eight weeks and 12 weeks post injection. RESULTS: Seventeen patients were enrolled, eight in the BT-A group and nine in the placebo group. At baseline, the median visual analogue scale score for shoulder pain was 6, the median Ashworth Scale shoulder adductor and elbow flexor spasticity score was 2 and the median range of shoulder abduction 76 degrees. Subjects who received BT-A showed significantly greater improvements in median shoulder adductor and elbow flexor Ashworth Scale scores than placebo at week 4 (P B / 0.01) but not at week 8 and 12. For shoulder pain and passive shoulder abduction range, all subjects showed postinjection improvements and no difference could be demonstrated between the two groups. DISCUSSION: Possible reasons for the negative finding in this study include the small sample size and the presence of causes of shoulder pain not related to spasticity which could have confounded outcome.

Adult↗