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Query: UMLS:C0026838 (spasticity)
 6,471 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Damage to the corticospinal system after brain injury interferes with activities of daily living, mobility, and communication. The chief cause of this interference has to do with impairment to produce and regulate voluntary movement accompanied by the presence of spasticity. This review advocates that the evaluation of "spasticity" should focus on 3 issues: (1) identifying the clinical pattern of motor dysfunction and its source; (2) identifying the patient's ability to control muscles involved in the clinical pattern; and (3) the differential role of muscle stiffness and contracture as it relates to the functional problem. We have identified and described 6 clinical patterns of motor dysfunction affecting the lower limbs during gait, found in patients with traumatic brain injury and residual from upper motor neuron lesions. We have presented the use of dynamic electromyography to identify the voluntary and spastic characteristics of individual muscles in gait and the use of anesthetic nerve blocks to identify properties of stiffness and contracture in particular muscle groups. Treatment algorithms for these problems include identification of the muscles that contribute to the deformity across a joint; the stage of patient recovery; and most important, the clinical goals applicable to the patient. The treatment strategies based on the algorithm included in this article were focused on the use of chemodenervation of targeted muscles, neuro-orthopedic surgery, and other therapeutic strategies.
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PMID:Evaluation and management of spastic gait in patients with traumatic brain injury. 1524 22

Spasticity is a frequent consequence of upper motor neuron lesion and is associated with a variety of symptoms such as pain, muscle stiffness and reflex patterns that interfere with activities of daily living, dexterity and gait. As therapy strategies in managing spasticity-associated problems have been evolving there is an increasing need for a practicable documentation system which describes spasticity and related symptoms on different levels in order to evaluate especially the level of functioning. In daily routine the single-case-design reflects a useful technique to evaluate the status in terms of technical, functional and individual goals for treatment. However, there is no single tool to measure the different types of changes due to treatment, therefore a variety of selecting tests, based on the functional changes expected from the selected treatment, is recommended. The sensitivity of the selected tests should match the range of expected improvements related to the specific treatment. Technical goals should be evaluated by validated spasticity rating scales. As changes in technical measures of spasticity such as muscle tone, muscle length, range of motion or repetitive voluntary movements may not correlate with clinical improvements, individual functional goals should be defined. Those functional goals should reflect the patients' and care-givers' individual perception of the actual problem. A treatment diary is a useful tool to document subjective perception of changes over time. Some practical issues are adressed below. Reliable outcome measures enable patients and doctors to select further treatment strategies and gives health care providers information on treatment expectations in return for their investments.
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PMID:[Measuring outcome in spasticity rehabilitation]. 1550 46

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.
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PMID:Efficiency of work production by spastic muscles. 1627 15

Spasticity is most commonly defined as an inappropriate, velocity dependent, increase in muscle tonic stretch reflexes, due to the amplified reactivity of motor segments to sensory input. It forms one component of the upper motor neuron syndrome and often leads to muscle stiffness and disability. Spasticity can, therefore, be measured through electrophysiological, biomechanical and clinical evaluation, the last most commonly using the Ashworth scale. None of these techniques incorporate the patient experience of spasticity, nor how it affects people's daily lives. Consequently, we set out to construct a rating scale to quantify the perspectives of the impact of spasticity on people with multiple sclerosis. Qualitative methods (in-depth patient interviews and focus groups, expert opinion and literature review) were used to develop a conceptual framework of spasticity impact, and to generate a pool of items with the potential to convert this framework into a rating scale with multiple dimensions. This item pool was administered, in the form of a questionnaire, to a sample of people with multiple sclerosis and spasticity. Guided by Rasch analysis, we constructed and validated a rating scale for each component of the conceptual framework. Decisions regarding item selection were based on the integration and assimilation of seven specific analyses including clinical meaning, ordering of thresholds, fit statistics and differential item functioning. The qualitative phase (17 patient interviews, 3 focus groups) generated 144 potential scale items and a conceptual model with eight components addressing symptoms (muscle stiffness, pain and discomfort and muscle spasms,), physical impact (activities of daily living, walking and body movements) and psychosocial impact (emotional health, social functioning). The first postal survey was sent to 272 people with multiple sclerosis and had a response rate of 88%. Findings supported the development of scales for each component but demonstrated that five item response options were too many. The 144-item questionnaire, reformatted with four-item response options, was administered with four validating instruments to an independent sample of 259 people with multiple sclerosis (response rate 78%). From the responses, an 88-item instrument with eight subscales was developed that satisfied criteria for reliable and valid measurement. Correlations with other measures were consistent with predictions. The 88-item Multiple Sclerosis Spasticity Scale (MSSS-88) is a reliable and valid, patient-based, interval-level measure of the impact of spasticity in multiple sclerosis. It has the potential to advance outcomes measurement in clinical trials and clinical practice, and provides a new perspective in the clinical evaluation of spasticity.
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PMID:Getting the measure of spasticity in multiple sclerosis: the Multiple Sclerosis Spasticity Scale (MSSS-88). 1628 Mar 52

Reduced depression of transmitter release from Ia afferents following previous activation (post-activation depression) has been suggested to be involved in the pathophysiology of spasticity. However, the effect of this mechanism on the myotatic reflex and its possible contribution to increased reflex excitability in spastic participants has not been tested. To investigate these effects, we examined post-activation depression in Soleus H-reflex responses and in mechanically evoked Soleus stretch reflex responses. Stretch reflex responses were evoked with consecutive dorsiflexion perturbations delivered at different intervals. The magnitude of the stretch reflex and ankle torque response was assessed as a function of the time between perturbations. Soleus stretch reflexes were evoked with constant velocity (175 degrees /s) and amplitude (6 degrees) plantar flexion perturbations. Soleus H-reflexes were evoked by electrical stimulation of the tibial nerve in the popliteal fossa. The stretch reflex and H-reflex responses of 30 spastic participants (with multiple sclerosis or spinal cord injury) were compared with those of 15 healthy participants. In the healthy participants, the magnitude of the soleus stretch reflex and H-reflex decreased as the interval between the stimulus/perturbation was decreased. Similarly, the stretch-evoked torque decreased. In the spastic participants, the post-activation depression of both reflexes and the stretch-evoked torque was significantly smaller than in healthy participants. These findings demonstrate that post-activation depression is an important factor in the evaluation of stretch reflex excitability and muscle stiffness in spasticity, and they strengthen the hypothesis that reduced post-activation depression plays a role in the pathophysiology of spasticity.
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PMID:Post-activation depression of soleus stretch reflexes in healthy and spastic humans. 1793 63

Eperisone hydrochloride (4'-ethyl-2-methyl-3-piperidinopropiophenone hydrochloride) is an antispastic agent used for treatment of diseases characterized by muscle stiffness and pain. The aim of this research was to investigate the efficacy of eperisone in patients with acute low back pain and spasticity of spinal muscles. The study design was a randomized, double-blind (double-dummy) study in 160 patients with low back pain and no Rx finding of major spinal diseases, randomly assigned to a treatment with oral eperisone 100 mg three times daily (t.i.d.) or thiocolchicoside 8 mg twice daily (b.i.d.) for 12 consecutive days. Analgesic activity was evaluated by scoring "spontaneous pain" (VAS) and pain on movement and pression (4-digit scale), while muscle relaxant activity of the medication was evaluated by means of the "hand-to-floor" distance and the Lasegue's manoeuvre. All the measures were done at the inclusion day and after 3, 7 and 12 days of treatment. The two medications had comparable analgesic and muscle relaxant efficacy. Sponta-neous pain and pain on movement/pressure were significantly reduced by both treatments. Moreover, both eperisone- and thiocolchicoside-treated patients showed a clinically evident muscle relaxation as proved by a progressive reduction in the "hand-to-floor" distance and increase in the articular excursion (Lasegue's manoeuvre). Only 5% of eperisone-treated patients showed minor gastrointestinal side effects, while the incidence of side effects in the thiocolchicoside group was 21.25%. Moreover, in the thiocolchicoside-treated patients also diarrhoea was present, which reached a moderate intensity in some cases. In conclusions, eperisone represents a valuable and safer alternative to other muscle relaxant agents for treatment of low back pain.
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PMID:Efficacy and safety of eperisone in patients with low back pain: a double blind randomized study. 1872 54

Stiff knee gait (SKG) is common in hemiplegic patients. The main focus of treatment is rectus femoris (RF) spasticity. The aims of this study were to evaluate the effect of botulinum toxin injection (BTI) in the RF muscle on peak knee flexion during swing phase and its quantitative and functional impact on gait. We also wished to evaluate the correlation between the effects of nerve block and BTI on peak knee flexion. 10 adult hemiplegic subjects (>6 months post stroke or traumatic brain injury) with SKG and inappropriate RF EMG activity during mid-swing phase were included. 3D gait analysis, clinical and functional assessments (Timed Up and Go test, 10 m walk test, 6 min walk test and the time taken to ascend and descend a flight of stairs) were performed initially, 30 min after anaesthetic block of the RF nerve and one month post BTI. After BTI, there was a significant increase in knee flexion (8 degrees average) and a tendency towards improvement in gait and functional parameters. The effect of the nerve block on peak knee flexion was significantly correlated with the effect of BTI (11 degrees average increase in peak knee flexion after nerve block). We challenge the relevance of RF nerve blocks in this population when EMG and kinematic data are available. Our results indicate that BTI is an effective treatment for SKG in adult hemiplegic subjects, with a significant increase in peak knee flexion, no reduction in hip flexion and a tendency towards functional improvements.
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PMID:Relevance of botulinum toxin injection and nerve block of rectus femoris to kinematic and functional parameters of stiff knee gait in hemiplegic adults. 1877 25

Stiffness and spasticity are common neurologic symptoms that affect limb movements. We describe a patient who presented with ill-defined stiffness and an exaggerated startle response, who on serial examinations had variable degrees of stiffness and marked hyperreflexia but with plantar flexor signs. Stiff-person syndrome (SPS) was considered when axial stiffness became evident and was confirmed with highly elevated anti-GAD antibody titers. A favorable response to a short course of intravenous immunoglobulin treatment was sustained for more than 10 months, an unusual feature to the disease. We review the clinical features, pathologic mechanism, and treatment of this disorder.
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PMID:Stiffness, spasticity, or both: a case report of stiff-person syndrome. 1907 72

Spasticity is usually observed along with paralysis, hyperreflexia, Babinski sign and abnormal associated movements associated with dysfunction of central motor tracts. In spasticity, exaggeration of the stretch reflex results in increased resistance during passive movements. Therefore, spasticity is pathophysiologically described as increased muscle tone whose pathognomonic sign is decreased passivity. Resistance is more strongly felt during rapid passive movements than during slow movements. The resistance felt at the beginning of the passive movement abruptly diminishes, which is well known as the clasp-knife phenomenon. Another character of spasticity is the distribution of the increment in the muscle tone. Not only rigidity, dystonia, and muscle stiffness demonstrating increased muscle tone, but also Gegenhalten and contracture of joint with normal muscle tone should be differentiated. No neurophysiological parameters reflect the degree of spasticity in a strictly parallel fashion. However, neurophysiological examinations provide some supportive objective data. Surface electromyography is useful to distinguish spasticity from rigidity and other conditions with increase muscle tone. The increased amplitude ratio and the decreased threshold ratio of the H-wave to the M-wave, and increased amplitude and persistence of the F-wave are observed the patients with spasticity. Magnetic stimulation is a useful tool to detect corticospinal tract lesions that induce leading to spasticity. Transcranial magnetic stimulation, magnetic brainstem stimulation, and magnetic spinal motor root stimulation are used to examine the entire motor pathway. Since positive correlation between spasticity and shortening of the silent period is reported, many investigations including paired-pulse magnetic stimulation will be necessary for understanding pathophysiology of spasticity. Patients with mild and reversible spasticity are usually treated with medications. Significant variations exist in the use of these therapies, because the treatments often depend on the clinicians' experience. It will be necessary to clarify the action mechanism of drugs, to develop new effective drugs, and to perform randomized controlled trails so that clinicians can select the optimal medication based on evidence.
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PMID:[Clinical signs, neurophysiological evaluation, and medication of spasticity--review]. 1911 Jul 51

In recent years, part of the muscle resistance in spastic patients has been explained by changes in the elastic properties of muscles. However, the adaptive spinal mechanisms responsible for the exaggeration of stretch reflex activity also contribute to muscle stiffness. The available data suggest that no single spinal mechanism is responsible for the development of spasticity but that failure of different spinal inhibitory mechanisms (reciprocal IA inhibition, presynaptic inhibition, IB inhibition, recurrent inhibition) are involved in different patients depending on the site of lesion and the etiology of the spastic symptoms. A recent finding also shows no sign of exaggerated stretch reflexes in muscles voluntarily activated by the spastic patient in general. This is easily explained by the control of stretch reflex activity in healthy subjects. In healthy subjects, the stretch reflex activity is increased during voluntary muscle contraction in part because of depression of the inhibitory mechanisms that are affected in spasticity. In spastic patients, these inhibitory mechanisms are already depressed at rest and cannot be depressed further in connection with a contraction. In relation to most normal movements, antagonist muscles should remain silent and maximally relaxed. This is ensured by increasing transmission in several spinal inhibitory pathways. In spastic patients, this control is inadequate, and therefore stretch reflexes in antagonist muscles are easily evoked at the beginning of voluntary movements or in the transition from flexor to extensor muscle activity. This problem is contradicted by the fact that antispastic therapy to improve voluntary movements should be directed.
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PMID:Stretch reflex regulation in healthy subjects and patients with spasticity. 2215 83


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