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

In clinical practice, signs of exaggerated tendon tap reflexes associated with muscle hypertonia are generally thought to be responsible for spastic movement disorders. Most antispastic treatments are, therefore, directed at the reduction of reflex activity. In recent years, however, researchers have noticed a discrepancy between spasticity as measured in the clinic and functional spastic movement disorders, which is primarily due to the different roles of reflexes in passive and active states, respectively. We now know that central motor lesions are associated with loss of supraspinal drive and defective use of afferent input with impaired behaviour of short-latency and long-latency reflexes. These changes lead to paresis and maladaptation of the movement pattern. Secondary changes in mechanical muscle fibre, collagen tissue, and tendon properties (eg, loss of sarcomeres, subclinical contractures) result in spastic muscle tone, which in part compensates for paresis and allows functional movements on a simpler level of organisation. Antispastic drugs can accentuate paresis and therefore should be applied with caution in mobile patients.
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PMID:Spastic movement disorder: impaired reflex function and altered muscle mechanics. 2922 72

Many clinical measures of spasticity, such as Ashworth tests and tendon tap responses, are linked to stretch reflex thresholds but these methods are relatively imprecise and unreliable. To address this deficit, we examined the utility of a system that relies on a small position controlled actuator to better estimate this threshold. We compared the reflex threshold estimates in the passive spastic and contralateral elbow flexor muscles of 4 hemiparetic spastic stroke survivors. We propose that the use of controlled indentation of the tendon may be a practical and accurate method of estimating stretch reflex threshold as well as passive muscle properties.
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PMID:A new method for reflex threshold estimation in spastic muscles. 1996 20

We have reported earlier [1] a new method for estimating reflex threshold in spastic muscles of stroke survivors, using controlled amplitude taps superimposed on progressive and controlled muscle indentation of the bicipital tendon in the bicipital fossa. This muscle indentation is done with a linear actuator positioned over the biceps muscle tendon at the elbow. In the course of testing for increased stretch reflex responses, (a cardinal feature of spasticity), we have also observed that the intrinsic or passive stiffness of the muscle is often increased. This assessment is derived from recordings of the force generated by the tendon during progressive loading, and by the instantaneous force response to the tendon tap. Thus, it appears that passive properties of muscle are often also changed in parallel with the reflex abnormalities. While some of these mechanical features have been described in earlier studies of torque-angle relations of spastic joints, it appears that these features can also be recognized readily using a small actuator that loads the tendon progressively. These findings may help clinicians recognize early changes in muscle mechanical properties, and may help them prevent large-scale adverse changes in muscle function.
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PMID:An evaluation of passive properties of spastic muscles in hemiparetic stroke survivors. 2109 18

Antispastic medications that are directed to reduce clinical signs of spasticity, such as exaggerated reflexes and muscle tone, do not improve the movement disorder. Medication can even increase weakness which might interfere with functional movements, such as walking. In this chapter we address how spasticity affects mobility and how this should be taken into account in the treatment of spasticity. In clinical practice, signs of exaggerated tendon tap reflexes associated with muscle hypertonia are the consequence of spinal cord injury (SCI). They are generally thought to be responsible for spastic movement disorders. Most antispastic treatments are, therefore, directed at the reduction of reflex activity. In recent years, a discrepancy between spasticity as measured in the clinic and functional spastic movement disorder was noticed, which is primarily due to the different roles of reflexes in passive and active states, respectively. We now know that central motor lesions are associated with loss of supraspinal drive and defective use of afferent input with impaired behavior of short-latency and long-latency reflexes. These changes lead to paresis and maladaptation of the movement pattern. Secondary changes in mechanical muscle fiber, collagen tissue, and tendon properties (e.g., loss of sarcomeres, subclinical contractures) result in spastic muscle tone, which in part compensates for paresis and allows functional movements on a simpler level of organization. Antispastic drugs should primarily be applied in complete SCI. In mobile patients they can accentuate paresis and therefore should be applied with caution.
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PMID:Spasticity. 2309 14

Spasticity is a major impairment that can occur following a hemispheric stroke and is often treated with injections of botulinum toxin, a neurotoxin that impairs transmission at the neuromuscular junction. Hyperreflexia is a defining feature of spasticity. Our main objective here was to quantify the time course of changes in the deep tendon reflex (DTR) responses and voluntary activation capacity following BT injection as well as to track changes in a clinical assessment of spasticity. Four chronic stroke survivors, scheduled to receive BT in their Biceps Brachii(BB) as part of their clinical care plan, were recruited for repeated testing sessions over the course of 4 months post injection. Both surface BB EMG reflex response to bicipital tendon taps as well as signals of applied tendon tap forces were recorded before and up to 18 weeks post-BT. Voluntary force and biceps EMG signals were also recorded during maximum voluntary (isometric) contractions (MVC) at each testing session. Our results show major reductions (up to 75%) in voluntary sEMG and force arising between 11 to 35 days post-BT-injection. The stretch reflex gain declined two weeks after the maximal reductions in voluntary EMG and force. Paradoxically, there was a short-term increase in stretch reflex gain, in three out of four participants, approximately 11-35 days post BT. The time course of recovery of voluntary MVC and reflex responses varied considerably with a longer recovery time for the reflex responses.
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PMID:Characterization of Differences in the Time Course of Reflex and Voluntary Responses Following Botulinum Toxin Injections in Chronic Stroke Survivors. 3263 1


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