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At least 685 records · Page 38Linked to original sources
PubMed2001

Pathophysiology of impairment in patients with spasticity and use of stretch as a treatment of spastic hypertonia.

Paralysis, muscle shortening, and muscle overactivity are the three main disabling factors in patients with spasticity. Occurring after most central lesions, muscle overactivity and shortening are not equally spread throughout all muscles of the body. In an agonist-antagonist couple, there is invariably "greater" overactivity and shortening of one versus the other. This is the rationale for the use of targeted local treatments that train the weaker agonist and stretch and partially block the more overactive and shorter antagonist. Central paralysis, muscle shortening, and muscle overactivity are intertwined, and the three corresponding therapies, motor training, stretch, and local partial blocks, should be implemented in combination. This triple treatment is the main condition for any functional recovery. Muscle shortening occurs acutely after a central nervous system lesion; therefore its treatment should be implemented as rapidly as possible.

Casts, Surgical↗
PubMed2006

Treatment of shoulder pain in spastic hemiplegia by reducing spasticity of the subscapular muscle: a randomised, double blind, placebo controlled study of botulinum toxin A.

OBJECTIVE: This randomised, double blind, placebo controlled, two parallel group study was conducted to assess the beneficial effect of injection of botulinum toxin A (Dysport) into the subscapularis muscle on shoulder pain in stroke patients with spastic hemiplegia. METHODS: A single dose of botulinum toxin A (500 Speywood units) or placebo was injected into the subcapularis muscle. Pain was assessed using a 10 point verbal scale. Subscapularis spasticity was assessed by the change in passive shoulder lateral rotation and abduction. Upper limb spasticity was assessed using the Modified Ashworth Scale for shoulder medial rotators, and elbow, wrist and finger flexors. Assessments were carried out at baseline and at weeks 1, 2 and 4. RESULTS: Twenty patients (10 patients per group), 11 with ischaemic stroke and 9 with haemorrhagic stroke, completed the study. Pain improvement with botulinum toxin A was observed from week 1; score difference from baseline at week 4 was 4 points versus 1 point with placebo (p = 0.025). Lateral rotation was also improved, with a statistically significant difference compared with placebo at week 2 (p = 0.05) and week 4 (p = 0.018). A general improvement in upper limb spasticity was observed; it was significant for finger flexors at week 4 (p = 0.025). CONCLUSIONS: Subscapularis injection of botulinum toxin A appears to be of value in the management of shoulder pain in spastic hemiplegic patients. The results confirm the role of spasticity in post-stroke shoulder pain.

Botulinum Toxins, Type A↗
PubMed2005

Starting position and stretching velocity effects on the reflex threshold angle of stretch reflex in the soleus muscle of normal and spastic subjects.

BACKGROUND AND PURPOSE: Although both starting position and stretching velocity play an important role in reflex response, their interaction with stretch reflexes has not been thoroughly investigated. This study examined the interaction effect of starting position and stretching velocity on the reflex threshold angle (RTA) of the stretch reflex in the soleus muscle of normal and spastic subjects. METHODS: The spastic group included 11 ankles from 7 subjects with a history of upper motor neuron lesions. Their ages ranged from 22 to 40 years. Another 10 healthy subjects served as the control group. RTAs of the stretch reflex in the soleus muscle were measured for a matrix of starting positions and stretching velocities. The matrix design enabled the use of a 2-way analysis model to investigate the effect of starting position and stretching velocity on the RTA. RESULTS: No interaction effect was found in either the phasic stretch reflex (PSR) or the tonic stretch reflex (TSR) in the spastic group, or in the PSR in the normal group. The RTA of the PSR in both spastic and normal groups was significantly affected by starting position but not by stretching velocity. In contrast, the RTA of the TSR in the spastic group was affected by both starting position and stretching velocity. Stretching velocity and starting position played independent roles in determining the RTA of both the PSR and the TSR of the spastic group and in the PSR of the normal group. CONCLUSIONS: The lack of interaction between length-sensitive and velocity-sensitive muscle spindles in both normal and spastic subjects supports the hypothesis that they independently modulate the stretch reflex. Results for the RTA of the TSR demonstrated that spasticity results in disinhibition of motoneuron excitability with different thresholds.

Adult↗
PubMed1993

Determinants of muscle function in the spastic lower extremity.

The upper motor neuron lesion that causes hemiplegia impairs the patient's selective control and exposes primitive modes of muscle activation. Significant inconsistency between the clinical findings and the patient's gait may result. Dynamic electromyography revealed the primitive mechanisms leading to these inconsistencies. The rate of stretch does not differentiate spasticity from contracture, since either a quick or slow stretch frequently causes a sustained muscle response. Using knee flexion to differentiate gastrocnemius and soleus spasticity is not reliable, since the change in neurologic input with flexion may inhibit the extensor muscle's response to stretch so that the soleus is also relaxed. The change in body position from lying supine to sitting can double the intensity of soleus spasticity, and standing further increases the tone. Primitive patterns of mass extension and flexion, while voluntary, inhibit normal progression during walking. Simultaneous activation of the soleus and gastrocnemius with the knee's quadriceps causes premature ankle plantar flexion as the limb is loaded in stance. The primitive flexion synergy between the hip, knee, and ankle (dorsiflexion) inhibits terminal swing knee extension while the hip remains flexed. Consequently, surgical planning for the hemiparetic limb must rely heavily on gait analysis findings (systematic observation or by instrumentation).

Adolescent↗
PubMed1991

Trends in the pathophysiology and pharmacotherapy of spasticity.

Spasticity develops after supraspinal or spinal lesions of descending motor systems, with obligate involvement of the corticospinal tract. Spasticity is characterized by an increase in muscle tone, which, in contrast to many other types of enhanced muscle tone, shows a marked velocity-dependent increase when the muscle is passively stretched. The pathophysiological mechanisms underlying this spastic muscle tone remain obscure. Three major causes are currently considered possible: (1) changes in the excitability of spinal interneurones; (2) receptor hypersensitivity; (3) formation of new synapses by sprouting. The latter mechanism could account for the long time course over which spastic muscle tone develops in hemiplegic or paraplegic patients, but there is no experimental evidence for this hypothesis. The electromyographic (EMG) gait analysis of patients with spasticity has thrown doubt on the common belief that the velocity-dependent increase in spastic muscle tone is evoked by stretch reflex activity and has led to the idea that spastic muscle tone resides in the muscle fibres themselves. While such a mechanism may contribute to the slowness of active movements in spastic patients, recent experiments on patients with spastic arm paresis have confirmed the classical view that the spastic muscle tone is related to the EMG activity evoked in the passively stretched muscle. This pathological EMG activity is seen during the entire range of the dynamic phase of the stretch, during which a normal muscle exhibits only an early, phasic burst at the highest stretch velocities employed. For the pharmacological treatment of spasticity, substances with different central or peripheral actions are available. Their assumed receptor actions are described, together with their main indications and side-effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Electromyography↗
PubMed1976

Familial spastic paraplegia with distal muscle wasting in the Old Order Amish; atypical Troyer syndrome or "new" syndrome.

The Troyer syndrome was found by Cross & McKusick (1967) in 20 members of 12 Old Order Amish families in Holmes County, Ohio; it is a form of hereditary spastic paraplegia combined with distal muscle wasting, i.e. signs of involvement of lower motor neurons. The condition usually begins at 1 to 2 years and progresses at variable rates. Further manifestations include growth retardation, delayed speech development with dysarthria and drooling, and cerebellar signs; mental functions are usually not affected but severe emotional lability is a common finding. Brothers in a Wisconsin Old Order Amish family are reported with spastic diplegia, mental retardation, behavioral disorder and shortness of stature; the condition apparently is not progressive, and may be a "new" syndrome but could also represent a variant of the Troyer syndrome. Autosomal recessive inheritance is most likely, although consanguinity of the parents could not be proven. Another child in this family suffers from focal scleroderma (morphea) which is not related to the neurological syndrome.

Adolescent↗
PubMed2004

Validation of portable muscle tone measurement device for quantifying velocity-dependent properties in elbow spasticity.

The objective of this study is to develop a portable device for quantifying the velocity-dependent properties of spastic elbow muscles. Based on a motor-driven system, validation tests of the portable system such as accuracy and response of sensors were first examined. Furthermore, simulated modules (inertia, damper and spring) as well as elbow joints (15 control and 15 hemiplegic subjects) were manually stretched under four different frequencies (1/3, 1/2, 1 and 3/2 Hz) through 60 degrees range of motion. Joint resistance and displacement during sinusoidal stretch were collected for further analysis. Two quantitative parameters (i.e., viscous components under each frequency and averaged viscosity across four frequencies) were derived to estimate the velocity-dependent properties of elbow joint. Tests of simulated modules confirm the manual stretch protocol and data analysis are valid in estimating the velocity-dependent component during a sinusoidal stretch. Compared to normal control, viscous component in each stretch frequency and averaged viscosity were significantly higher in subjects with spasticity (P < 0.001). The viscous component and averaged viscosity were found highly correlated with the modified Ashworth scale. These findings suggest that measurements of viscous component and averaged viscosity during manual sinusoidal stretching using the portable device could be clinically useful in evaluating spasticity.

Elasticity↗
PubMed2002

Intramuscular distribution of nerves in the human triceps surae muscle: anatomical bases for treatment of spastic drop foot with botulinum toxin.

Recent progress has been made in selective functional treatment of hypertonia of spastic origin by local injection of botulinum toxin into the muscles responsible for equinus foot dynamic deformation. The technical aspect of the intervention requires a strategy adapted to the individual patient. Good practice is founded on precise knowledge of the intramuscular nerve distribution of end plate zones, since the target organ of the toxin is the motor end plate. Knowledge about the location of motor end plates, which differs according to the structure of the muscle in question, remains rather poor. Through macroscopic and stereoscopic microscopic dissection of the nerve courses in the triceps surae muscular group in 40 legs, we have ascertained in more detail the distribution of motor end plates, which appear to be more numerous in certain zones of the muscle bellies. These zones were measured morphometrically and divided into segments which are expressed in percentages of a standard leg length. We maintain that these zones are the injection sites most likely to guarantee the best treatment efficacy.

Anti-Dyskinesia Agents↗
PubMed2002

Spasticity causes a fundamental rearrangement of muscle-joint interaction.

Sarcomere length was measured in flexor carpi ulnaris (FCU) muscles from patients with severely spastic wrist flexion contractures (n = 6), as well as from patients with radial nerve injury and a normally innervated FCU (n = 12). Spastic FCU muscles had extremely long sarcomere lengths with the wrist fully flexed (3.48 +/- 0.44 microm) compared to the FCU muscles of patients with radial nerve injury (2.41 +/- 0.31 microm). In three of the patients with spastic wrist flexion contractures, the slope of the FCU sarcomere length-joint angle relationship was measured and found to be, essentially, normal (0.017 +/- 0.005 microm/degree, n = 3) suggesting that serial sarcomere number (and therefore muscle fiber length) was unchanged in spite of the dramatic absolute sarcomere length change. These results indicate that spasticity results in a major alteration of normal muscle-joint anatomical relationships that has not previously been recognized to our knowledge. We hypothesize that the results are explained either by the inability of muscle fibers to add serial sarcomeres in response to growth, or the selective loss of FCU muscle length secondary to the central nervous system lesion.

Adaptation, Physiological↗