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

Spasticity has been defined as velocity-dependent hyperactivity of stretch reflexes; it is therefore only one aspect of the complex syndrome produced by a lesion of the upper motoneuron. Although spasticity may be partially responsible for joint contractures, it does not produce most of the functional disability experienced by patients with upper motoneuron lesions. Paresis, fatigability, lack of dexterity, etc., account for most of these patients' complaints. The pathophysiology of spasticity is poorly understood but appears to be related to an increased excitatory state at the segmental spinal level; there is no evidence for increased sensitivity of muscle spindles in spastic patients. Several mechanisms for this increased excitability within the spinal cord have been proposed. There are different types as well as degrees of spasticity. Clinical neurophysiologic recordings of reflex activity in patients with spasticity provide the means to differentiate among the various types of spasticity, to select the therapy most likely to be effective in a particular patient, and to see the results of its employment objectively. The latter will prove whether a specific therapy is useful or not. Ablative treatment at the level of the peripheral nerve or dorsal root may be useful, particularly when spasticity is severe. Drugs such as baclofen or diazepam relieve flexor spasms but are not particularly effective against spasticity itself. Dantrolene acts to weaken muscles, but that is not often helpful. Rarely do any of these therapies increase function; there are no effective cures for paresis or related negative manifestations of chronic spasticity.
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PMID:Spasticity. 358 84

Muscle strength for knee extension, both isokinetic and isometric, and walking capacity, maximum velocity and walking rate, were examined in 11 post-stroke hemiparetic patients. The degree of spasticity of the affected lower extremity was not related to the isokinetic and isometric torques, or to the walking capacity. Although both the isokinetic and isometric torques decreased on the affected side compared to the non-affected side, the rate of decrease was remarkable in isokinetic torque at fast velocities. The walking capacity was well correlated with isokinetic torque of the affected side at fast velocities but not isometric torques. These results suggest that reduction of muscle strength at rapid movements is an essential feature of spastic paresis and is primary cause of motor disabilities such as impaired locomotor function.
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PMID:Relationship of muscle strength for knee extension to walking capacity in patients with spastic hemiparesis. 400 20

EMG denervation activity was studied in patients without peripheral neuron disorder but with upper motor neuron lesions. The time course of such central denervation activity, the local distribution and the quantitative relationship between denervation activity and the degree of paresis and spasticity were also studied. A total of 101 patients, who had developed hemiplegia or hemiparesis as a result of a cerebral vascular accident, underwent needle electromyographic examination at regular intervals in proximal and distal muscle groups. The maximum observation time was 1 year. Denervation activity in cases of central paresis first occurred 2-3 weeks after stroke. This could be observed most frequently in the distal arm and hand muscles. In the course of weeks and months the frequency of the denervation activity decreased in parallel with the development of spasticity and the increasing voluntary innervation. The occurrence and the dynamic properties of the denervation activity in cases of central paresis support the assumption of a trans-synaptic degeneration of alpha-motoneurons and of a compensating segmental "sprouting" of afferents.
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PMID:Denervation activity in the EMG of patients with upper motor neuron lesions: time course, local distribution and pathogenetic aspects. 619 9

Activation of leg musculature on both sides following a unilateral displacement was studied during stance on separate see-saws, or on stable force-measuring platforms, in patients with spastic hemiparesis and paraparesis. During balancing the movements on the spastic side were damped and the degree of muscle activation reduced. Whereas in healthy subjects the tibialis anterior muscles of both sides were activated, following a unilateral displacement, with the same strength and latency (see-saws 55 ms, platforms 85 ms), in hemispastic patients the EMG responses were delayed (by about 20 to 30 ms) and of reduced strength on the spastic leg, irrespective of whether the unaffected or the spastic side was displaced. In addition, the compensatory movements on the spastic side were damped in both conditions, although the amplitude of displacement was the same bilaterally. Although there was no correlation between the delay and the reduction in EMG response, the latter was correlated with the severity of paresis. In patients with spastic paraparesis quite similar results were obtained with delayed and reduced EMG responses on both sides. It is concluded that in spasticity the impaired regulation of quick compensatory movements is due to a dysfunction of a spinal interneuronal system by which the early EMG responses are mediated. This could be explained by loss of supraspinal control. In addition to the impaired neural activation of leg muscles, changes in the mechanical properties of muscle can be assumed to contribute to the damped movements on the spastic side.
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PMID:Interlimb coordination of posture in patients with spastic paresis. Impaired function of spinal reflexes. 647 85

From 1972-1974, 228 children began treatment for acute lymphocytic leukemia and were prospectively assessed for neurologic complications. After CNS irradiation (2,400 rad) and intrathecal methotrexate (MTX), they received weekly intravenous maintenance therapy with MTX alone (40-60 mg/m2; 20 patients) or MTX (10-30 mg/m2) with other drugs (208 patients). Signs of leukoencephalopathy appeared in 11 children (nine without CNS leukemia) after 4-15 months of IV MTX alone, and included lethargy, seizures, spasticity, paresis, drooling, and dementia. Before or during the clinical onset, EEG frequencies slowed (all ten patients tested). Radionuclide scans showed periventricular accumulation of 99mTc (9/11 patients) and remained abnormal for greater than or equal to six months in eight patients. Cranial computed tomograms or neuropathology findings (five patients each) demonstrated leukoencephalopathy (nine patients) and radiation-related microangiopathy (ten patients). Severe neurologic and neuropsychologic dysfunctions were present in four long-term survivors.
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PMID:Progression of methotrexate-induced leukoencephalopathy in children with leukemia. 693 56

In spastic patients suffering from spastic paresis on one side the degree of spasticity on the background of isometric innervation was investigated with a new self-constructed torque motor. It offers the opportunity to analyze how external forces can be compensated automatically by reflex or reaction. In spastic patients M1, M2 and M3 were compared with the responses of the nonaffected normal side as a control. The effects of diazepam and baclofen are analyzed with this new technique.
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PMID:Quantification and documentation of changes produced by spinal cord stimulation. 702 51

Epidural spinal electrostimulation (ESES), as method in the treatment of patients with chronic pain or severe central motor disturbances, especially spastic paresis of spinal origin and bladder dysfunction, is indicated when conservative measures prove ineffectual and before surgical intervention is considered. The biochemical and innervation processes which are brought about by ESES are discussed, as well as the literature on the efficacy and possible complications of the method. Twenty cases were subjected to a test stimulation and in twelve of these the stimulation system was implanted. Spinal spasticity and the range of mobility were improved by 20 to 30% in 8 patients with multiple sclerosis and 3 other patients with myelopathy of varied aetiology. In addition, spastic cramps of abrupt onset, with or without pain, disappeared almost completely following ESES in all cases. Three cases with chronic pain, two after a caudal lesion and one with cervical radicular damage, were markedly improved.
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PMID:[Epidural spinal electrostimulation (ESES) in patients with chronic pain and central motor disturbances (author's transl)]. 732 83

Shoulder-hand syndrome developed in 36 (27%) of 132 hemiplegic patients in a prospective study. Subluxation, paresis of the shoulder girdle, moderate spasticity, and deficits in confrontation visual field testing were the major risk factors. In a placebo-controlled, nonblinded trial, 31 of the 36 patients became almost symptom free within 10 days' treatment with low doses of oral corticosteroids. Shoulder joint capsules taken at autopsy of 7 patients showed signs of previous trauma of the affected shoulder. In the second part of this study on another 86 patients, early awareness of potential injuries to shoulder joint structures reduced the frequency of shoulder-hand syndrome from 27 to 8%. These clinical findings suggest that shoulder-hand syndrome in hemiplegia is initiated by peripheral lesions. A self-perpetuating vicious cycle may be established, followed by the clinical picture of a "reflex sympathetic dystrophy." In the majority of stroke patients, this clinical phenomenon seems to be preventable by avoiding shoulder trauma.
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PMID:The shoulder-hand syndrome after stroke: a prospective clinical trial. 752 74

This study investigated the potential value of eccentric (ECC) and concentric (CONC) isokinetic testing for quantifying motor deficit in patients with spastic paresis secondary to motor neuron disease. We hypothesized that, at a moderately fast (120 degrees s-1) angular velocity, spastic patients would demonstrate different ECC-CONC torque relationships from healthy controls or patients with non-spastic neuromuscular disorders. Eleven patients with motor neuron disease having clinical evidence of spasticity, and 11 disease-control patients (with non-spastic disorders, e.g. lower motor neuron disease or myopathy) underwent isokinetic testing. One healthy subject was matched to each of the 22 patients. The average torque generated during maximal voluntary ECC and CONC knee flexion (KF) and extension (KE) was measured using an isokinetic dynamometer (Kin-Com). Reliability was established (all ICC > or = 0.97) for patient torque measurements. Relative strength (% of control subject torque) in spastic patients was significantly higher for ECC than for CONC actions in both KF and KE; conversely, in non-spastic disease-control patients relative strength was not affected by the type of muscle action. The ECC/CONC average torque ratios for KE and KF at 120 degrees s-1 were significantly greater in spastic patients than controls, but did not differ from controls in non-spastic patients. In spastic patients the ECC-CONC imbalances were related to ambulatory dysfunction. In four spastic patients followed with serial testing, the disproportion between ECC and CONC voluntary capacity persisted over time.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Eccentric and concentric muscle performance in patients with spastic paresis secondary to motor neuron disease. A preliminary report. 801 93

The relative importance of hyperreflexia and paresis in disturbances of voluntary arm movement was studied in a group of patients (n = 25) with spasticity arising from a unilateral ischemic cerebral lesion. Patient performance was evaluated against data obtained from normal subjects (n = 15). Spastic patients achieved lower maximum movement velocities during flexion or extension than did normal subjects. The more marked the paresis of the elbow flexor and extensor muscles of the patients, relative to the strength of the normal subjects, the greater was this reduction in maximum velocity. For a given velocity, however, the time taken to complete a movement and the time to reach the peak velocity were normal. No relationship was found between the degree of impairment of voluntary movement and the level of passive muscle hypertonia in the antagonist. Although overactivity of the antagonist muscle may play some role in disturbance of movements made at low velocities without an opposing load, antagonist activity during movements made against a load (i.e., under more natural conditions) was at or below normal levels, even in those patients with the most marked passive muscle hypertonia. It is concluded that agonist muscle paresis, rather than antagonist muscle hypertonia, plays the dominant role in the disturbance of voluntary elbow movement following stroke.
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PMID:Voluntary movement at the elbow in spastic hemiparesis. 808 Feb 47


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