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PubMed2002

The vegetative and minimally conscious states in children: spasticity, muscle contracture and issues for physiotherapy treatment.

The neuropathology of the vegetative (VS) and minimally conscious (MCS) states and the pathophysiology of spasticity are reviewed. Current treatment options available in the physical management of children in a low-level state and factors influencing the physiotherapy treatment of children in a low-level state will be discussed. The complex neuropathology of VS and MCS helps to explain the varied clinical presentations of children in VS and MCS. Spasticity and muscle contracture are common motor sequelae of VS and MCS. Loss of inhibition by descending motor pathways is thought to result in increased muscle tone or spasticity. However, secondary changes in muscle fibre structure and periarticular connective tissue may be an additional component to increased muscle tone. A multimodal approach combining physical, pharmacological and surgical interventions is likely to be the most effective. Knowledge of the likelihood of recovery from VS and MCS can be helpful in determining the frequency and intensity of physiotherapy. Ethical issues in the management of children in a low-level state include a consideration of the benefits to the child and the child's family and the costs to the health care team and the medical institution.

Adolescent↗
PubMed2006

Evaluation of spastic muscle in stroke survivors using magnetic resonance imaging and resistance to passive motion.

OBJECTIVE: To assess the feasibility of using magnetic resonance imaging (MRI) and resistance to passive movement to evaluate spastic muscle. DESIGN: T2-weighted MRI scans of the upper arm were obtained at rest and after the performance of upper-arm exercise. In addition, resistance to passive movement was measured subjectively (Modified Ashworth Scale [MAS]) and objectively by an isokinetic device while the arm was moved at varying speeds (stretch reflex torque). SETTING: Research laboratory. PARTICIPANTS: Six hemiplegic stroke survivors (single group) with spasticity in the elbow flexors and extensors. INTERVENTIONS: Not applicable. MAIN OUTCOME MEASURES: Strength, stretch reflex torque, MAS, MRI-derived muscle cross-sectional area (CSA), and transverse relaxation time (T2). RESULTS: The affected sides exhibited spasticity (as assessed through MAS), with the extensors displaying a range of 0 to 3, and the flexors between 1 and 1+. The affected muscle groups were significantly weaker than the unaffected muscle groups (extensors: 61% less, flexors: 65% less; P< or =.05). The affected CSA of the triceps was 25% smaller than that of the unaffected side (P=.01), but the biceps muscle group was similar (5% less on the affected side, P> or =.05). There was a tendency (P=.07; effect size, .48) for the resting T2 to be higher in affected versus unaffected biceps, but triceps values were similar (P> or =.05). Both muscle groups showed an increase in T2 after exercise ( approximately 30%, P< or =.05); however, the affected sides did not show an increase (P> or =.05). For both muscle groups, the affected side had a greater stretch reflex torque, with the range of torque values being greater than the range of MAS scores. CONCLUSIONS: MRI and quantitative resistance to passive movement may be useful in the evaluation of spasticity. This is clinically relevant for the development and evaluation of antispasticity treatments.

Arm↗
PubMed1991

The mechanism of spastic muscle hypertonus. Variation in reflex gain over the time course of spasticity.

The electromyographic (EMG) response of the initially passive biceps brachii muscle to imposed extension applied at the elbow was studied in 19 hemiparetic and 12 normal subjects. In relaxed normal subjects, the biceps muscle was found to respond only at displacement velocities above 175 deg/s, with a single early burst of activity in the biceps EMG. In contrast, the hemiparetic subjects, in addition to the early EMG activity, also showed considerable late activity, which persisted even with stretch velocities as low as 35 deg/s. This late activity is a stretch reflex, present in fully plegic arms. It was seen in all spastic subjects in whom the tone of the biceps had been clinically assessed to be raised, but was never observed in subjects with normal muscle tone. The mean level of this EMG response was highly correlated with displacement velocity and its duration to the duration of the applied displacement. It is suggested that this reflex EMG activity is the major factor in the genesis of spastic hypertonus in the arm and that it arises not from a reduction in the threshold of the stretch reflexes of the muscle, but from a pathological increase in stretch reflex gain. It is further shown that this activity is at a high level between the first and third months after the onset of spasticity and that the reflex gain is significantly reduced when spasticity is established for a year or more. It is concluded that, while changes in passive mechanical properties may play a role when spasticity has been established for more than a year, the major cause of spastic muscle hypertonus is a pathological increase in stretch reflex activity.

Adult↗
PubMed2005

Reflex contribution of spindle group Ia and II afferent input to leg muscle spasticity as revealed by tendon vibration in hemiparesis.

OBJECTIVE: Foot dorsiflexion evokes a short- (SLR) and a medium-latency EMG response (MLR) in the soleus of standing subjects. SLR is mediated by spindle group Ia, while group II fibres contribute to MLR through an oligosynaptic circuit. We studied the effects of Achilles' tendon vibration on both responses in spastic patients to disclose any abnormal excitability of these pathways. METHODS: SLR and MLR were evoked in 11 hemiparetics and 11 normals. The vibration-induced changes in both responses were correlated to the Ashworth score of the affected leg. RESULTS: There were no differences between normals and patients in the size of control SLR or MLR. Vibration decreased SLR to 70% in normal subjects, but increased it to 110% in patients, in both affected and unaffected leg. Vibration did not affect MLR in normals, but increased it to 165% on the affected and 120% on the unaffected side of patients. Ashworth score was solely correlated with the degree of vibration-induced increase of MLR. CONCLUSIONS: While the lack of inhibitory effect of vibration on SLR confirms a reduced inhibitibility of the monosynaptic reflex, the increased MLR indicates a disinhibition of group II pathway in patients, connected to the loss of descending control on group II interneurones. Spastic hypertonia depends on release of group II rather than group Ia reflex pathways. SIGNIFICANCE: These findings give a neurophysiological support for the pharmacological treatment of spastic hypertonia and suggest a method for the assessment of its effects.

Adult↗
PubMed2005

The effects of isotonic and isokinetic muscle stretch on the excitability of the spinal alpha motor neurones in patients with muscle spasticity.

To examine the effect of isotonic (with and without weight bearing) and isokinetic muscle stretch on the excitability of the spinal alpha motor neurones (alphaMN) in patients with spasticity and to establish whether this effect is maintained for at least 24 h after the intervention. A single 20-min session of isotonic muscle stretch (with or without weight bearing) or isokinetic stretch was delivered to the ankle plantar flexors in patients with post-stroke lower limb spasticity and healthy control subjects. The effect of these types of muscle stretch on the excitability of alphaMN was assessed 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 maximum action motor potential of the soleus muscle (M(max)). Sixty-six hemiplegic stroke patients and 21 healthy control subjects were recruited and completed the trial. The H(max):M(max) ratio was significantly higher in patients with spasticity than in healthy control subjects. However, there were no statistically significant differences in the H-reflex latency or the change in H(max):M(max) ratio between the baseline values and those recorded immediately after the therapy intervention or 24 h later for each type of muscle stretch. Similarly, there were no significant differences in these variables between the interventions. In the present study neither isotonic muscle stretch (with or without weight bearing) or isokinetic stretch had a statistically significant effect on the excitability of the alphaMN in patients with muscle spasticity. This suggests that the previously reported reduction in spasticity after muscle stretch is because of mechanisms other than the direct effect on alphaMN. However, the lack of a demonstrable benefit of treatment may be due the fact that we examined the effects of a single, rather than repeated treatment cycles.

Aged↗
PubMed2004

Efficiency of work production by spastic muscles.

The present study compared the muscular efficiency in spastic and healthy lower limbs producing the same mechanical work. Sixteen chronic post-stroke hemiparetic and spastic patients and 14 age-matched healthy subjects were submitted to a submaximal stepwise exercise testing on a bicycle ergometer, pedalling with only one lower limb. Net energetic expenditure was computed from oxygen consumption above resting values. Electrical activity of antagonistic muscles in the thigh and in the shank was recorded and co-contraction was defined as the percentage of the pedalling cycle when antagonistic muscles were activated simultaneously. The efficiency was calculated as the ratio between the mechanical work done on the ergometer and the net energetic expenditure. Spasticity was quantitatively evaluated by measuring passive ankle plantar flexor muscle stiffness. The working capacity of the patients' paretic lower limb was very low (<40W). The energy expenditure increased linearly as a function of work intensity, without statistical difference between the patients paretic lower limb (PPL), the patients healthy lower limb (PHL) and the healthy subjects lower limb (HSL). Shank co-contraction was 2.9 times greater in PPL (p<0.05) and 2.3 times greater in PHL (p<0.05) than in HSL. Thigh co-contraction was also 1.8 times greater in PPL than in HSL (p<0.05). The ankle plantar flexor muscle stiffness was statistically greater in PPL than in PHL and HSL (p<0.05). The efficiency was not statistically different between the three groups (p=0.155). In conclusion, the efficiency of work production by paretic and spastic lower limb muscles was normal ( congruent with 20%) despite significant neurological impairments.

Adult↗
PubMed2005

Spastic muscle properties are affected by length changes of adjacent structures.

Recent animal experiments have shown that up to 37% of muscle force may be transmitted to adjacent structures rather than reach the insertion of the muscle's tendon, and that the extent of such force transmission depends on the length and relative position of these structures. We tested whether the force-length characteristics of the distally tenotomized human flexor carpi ulnaris muscle (FCU) of nine patients with cerebral palsy varied with the change of relative length of adjacent structures induced by a change of wrist position. In four patients, the FCU exerted up to 40% more active force in a flexed wrist position at short FCU length, whereas the active force was not significantly higher in the other five. In the same manner, passive force-length characteristics of the spastic FCU changed upon changes in wrist position. Variability in myofascial force transmission may partly explain the variability in success of the FCU-transfer.

Adolescent↗
PubMed2003

Spastic muscle cells are shorter and stiffer than normal cells.

The mechanical properties of isolated single muscle fiber segments were measured in muscle cells obtained from patients undergoing surgery for correction of flexion contractures secondary to static perinatal encephalopathy (cerebral palsy). "Normal" muscle cells from patients with intact neuromuscular function were also mechanically tested. Fiber segments taken from subjects with spasticity developed passive tension at significantly shorter sarcomere lengths (1.84 +/- 0.05 microm, n = 15) than fibers taken from normal subjects (2.20 +/- 0.04 microm, n = 35). Elastic modulus of the stress-strain relationship in fibers from patients with spasticity (55.00 +/- 6.61 kPa) was almost double that measured in normal fibers (28.25 +/- 3.31 kPa). The fact that these muscle cells from patients with spasticity have a shorter resting sarcomere length and increased modulus compared with normal muscle cells suggests dramatic remodeling of intracellular or extracellular muscle structural components such as titin and collagen. Such changes in muscles of patients with spasticity may have implications for therapy.

Adult↗
PubMed1995

Botulinum toxin A for spasticity, muscle spasms, and rigidity.

We studied the effects of botulinum toxin A in 12 patients with spasticity and in eight patients with rigidity. The study design was a double-blind, placebo-controlled crossover trial with botulinum toxin A versus saline. Using the Ashworth Scale for spasticity and the Unified Parkinson's Disease Rating Scale for rigidity, we gave the patients a tone grade before and 2 weeks after treatment. Improvement in tone by two grades or more was considered clinically significant. In the spasticity group, botulinum toxin A reduced the tone of all patients significantly, improved functionality and nursing care in eight of 12 patients, and alleviated painful spasms in five of five patients. In the rigidity group, muscle tone was decreased in seven of eight patients, functionality improved in four of seven, and joint and muscle pain decreased in four of five. We conclude that botulinum toxin A is effective against the disabling effects of spasticity and rigidity. The treatment was well tolerated.

Adolescent↗
PubMedDate not supplied

The effect of physiotherapeutic ultrasound on muscle spasticity in patients with hemiplegia: a pilot study.

BACKGROUND: Spasticity is one part of the upper motor neuron syndrome. Untreated spasticity not only causes loss of motor control that results in functional disability, but can easily lead to joint contractures as well. Physical therapy plays an important role in the management of patients with spasticity. Among the modalities, Therapeutic ultrasound has become an important modality for treatment of various conditions including spasticity. OBJECTIVES: The aim of this study is to determine the effect of ultrasound on spasticity. METHODS: In this before-after study, four adult patients (mean age: 57.5 +/- 14.43) with first ever stroke and resulting in hemiplegia participated in the study. The outcome measures were the Ashworth Scale for the assessment of spasticity, ankle passive and active range of motion, and the Hmax: Mmax ratio. RESULTS: The mean of Ashworth scores, Hmax:Mmax ratio, and passive range of motion in ankle joint improved after treatment with ultrasound, but it was not statistically significant (p > 0.05). CONCLUSIONS: The study did not show a significant decrease in spasticity after ultrasound therapy. A study with a large number of patients and a control group would clarify the effects of ultrasound on spasticity.

Adolescent↗
PubMed1995

Treatment of acquired muscle spasticity using phenol peripheral nerve blocks.

The use of phenol motor nerve blocks is advantageous in the early period of acquired spasticity (ie, that occurring following traumatic brain injury or incomplete spinal cord injury), when increased muscle tone is often the most severe. Because acquired spasticity is dynamic and usually improves slowly, a temporary treatment method used to ameliorate increased muscle tone is desirable. Phenol nerve infiltration provides a temporary motor nerve block that lasts for weeks or months. It allows passive limb mobilization in a comprehensive rehabilitation program that attempts to prevent fixed soft tissue contractures. Permanent or irreversible methods such as operative tendon lengthening, muscle release or recession, or neurectomy are usually best delayed until the spasticity has become static, when the need for surgical correction becomes more firmly indicated, and outcomes of operative intervention are more predictable. Although phenol nerve blocks were initially administered at the spinal cord level to control spasticity, the potential side effects have caused a loss of popularity of this method of administration. The safer and more common use of phenol infiltration at the peripheral nerve level is now more accepted for brain injury and spinal cord injury patients. This report reviews the indications, current concepts, and development of the different methods used to administer phenol nerve blocks. Comparisons to other methods to control spasticity are discussed.

Animals↗