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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The current notion of spasticity as a velocity-dependent increase of muscle response to imposed stretch was mainly derived from studies performed under stationary experimental conditions. To address the issue of a spastic muscle behaviour under dynamic conditions, we conceived a novel approach, aimed at quantitatively assessing motor output over the lengthening periods which take place during unperturbed functional movements. Application to the analysis of overground walking in children with spastic cerebral palsy (CP) revealed that, for representative lower limb muscles, the relationship between EMG levels and estimated muscle lengthening rate displays either increased gain or reduced velocity threshold. Parallel measurement of gait kinetics frequently showed congruent increase of the mechanical resistance to joint rotation. Abnormalities preferentially targeted the lengthening contractions occurring around the ground contact period of the stride. The pathophysiological profile of what is clinically defined as 'spastic' gait in CP children did not only consist of dynamic spasticity, as described above. Most often it resulted from the simultaneous contribution of other factors, including paresis, co-contraction, immature and non-neural components.
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PMID:Spasticity and 'spastic' gait in children with cerebral palsy. 959 71

The author reviews the current opinions on the treatment of spasticity with special consideration given to the new method of treatment with local injections of botulinum toxin A into the spastic muscles. Botulinum toxin is the treatment of choice in focal dystonias and hemifacial spasm. The mechanism of action of the toxin is unique and is a result of dose-dependent and partial chemical denervation of the muscles, with preservation of tonus and thus its function. Recent reports have confirmed the safety and effectiveness of the method in spasticity, especially when it is focal, not diffuse or severe and without concomitant severe paresis. The author describes also the basic data of the pathophysiology of spasticity and reviews other therapeutic options and practical problems concerning the injections of botulinum toxin.
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PMID:[Botulinum toxin in spasticity treatment]. 960 56

Based on the results of several electrodiagnostic and biomechanical studies, the following classification of muscle dysfunction in spastic hemiplegia is proposed: changes in muscle activation (excess symptoms, e.g., spasticity, and deficit symptoms, e.g., paresis); changes in muscle stiffness; and changes in muscle length. The clinical significance of this classification is that different types of muscle dysfunction might require specific treatment. The authors have developed techniques to measure quantitatively each type of muscle dysfunction: free frequency repetitive movement (FFRM) and torque angle diagram (TAD). Surface EMGs of tibialis anterior, gastrocnemius, and soleus muscle are recorded during active (FFRM) and passive (TAD) ankle movements. EMG data are converted to parameters for abnormal muscle activation (excess and deficit symptoms). Parameters for muscle stiffness and muscle length are derived from the hysteresis curve of the TAD. This article describes the measurements and the results of a validation study. For the validation study, four hypotheses were formulated: 1) in nonimpaired control subjects, parameters expressing abnormal muscle activation are low; 2) in hemiplegic subjects, differences between the affected and the unaffected sides will be found for all types of parameters; 3) after local anaesthesia of the tibial nerve on the hemiplegic side, excess symptoms will decrease, while muscle stiffness remains unchanged; and 4) despite a uniform gait pattern, between-subject differences can be detected with regard to muscle activation, stiffness, and length. The first hypothesis was tested and confirmed in two controls; the remaining three were tested and confirmed in ten hemiplegic subjects (mean age 47.7 yrs, mean time since onset 10.7 yrs). However, the level of co-contraction of the gastrocnemius muscle was low, probably indicating that the clinical significance of this phenomenon might be limited. The results support the validity of the proposed classification and measurements.
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PMID:Measurement of impaired muscle function of the gastrocnemius, soleus, and tibialis anterior muscles in spastic hemiplegia: a preliminary study. 970 15

In this study the energy cost of level walking was measured in 23 patients with stationary spastic paresis before and after a two-week treatment (45 min daily) of hydro-kinesi therapy, the latter consisting of passive and active movements in warm (32 degrees C) sea water, free swimming and water immersion walking. Among the subjects (80.2 +/- 13.2 kg body mass; 56.0 +/- 14.6 years of age; 10.7 +/- 6.6 years of duration of spasticity), 12 were affected by hemiparesis, 4 by multiple sclerosis and 7 by spinal cord injury. The energy cost of level walking (Cw) was measured before and after therapy from the ratio of the overall steady-state oxygen consumption to the effective speed of progression. The differences in Cw due to the treatment, at matched speeds, were found to be negligible at speeds higher than 0.75 m.s-1 (less than 5%) but to increase, with decreasing speed, up to about 17% at 0.1 m.s-1. The treatment was therefore effective in improving the gait characteristics of the subjects, through a decrease of their Cw, mainly at low speeds of progression.
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PMID:The energy cost of level walking before and after hydro-kinesi therapy in patients with spastic paresis. 976 44

Spasticity, mental retardation, macrocephaly and distinct craniofacial appearance: confirmation of a new subtype of complicated spastic paraplegia?: In this report, we describe a 30-year-old female with mental retardation, spastic paresis, epilepsy, macrocephaly and distinct craniofacial appearance. Probably, she suffers from the same condition as the two sibs described by Fryns et al., in 1994 (2).
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PMID:Spasticity, mental retardation, macrocephaly and distinct craniofacial appearance: confirmation of a new subtype of complicated spastic paraplegia? 977 44

The paper presents the results of clinical and neurophysiologic study of muscular tonus in 94 patients aged 42-70 years in early recovery after ischemic stroke. Selective role of spasticity was estimated in clinical pattern of motor disorders in groups of the patients with different disorders of muscular tonus with the same degree of paresis. Efficiency of antispastic preparation sirdalud was analyzed in 28 patients from this group. Sirdalud in daily dose of 6-12 mg in patients with prevalence of a spasticity in a clinical picture of the paresis and with either moderate or manifested degree of paresis of the extremities has significant antispastic effect without any decrease of muscular strength, which, in turn, increases the degree of restoration of motor functions.
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PMID:[Disorders of muscle tonus and their treatment with sirdalud in patients in the early recovery period of ischemic stroke]. 981 84

An upper motor neuron syndrome often leads to the development of stereotypical patterns of deformity secondary to agonist muscle weakness, antagonist muscle spasticity and changes in the rheologic (stiffness) properties of spastic muscles. Identification of the spastic muscles that contribute to deformity across a joint allows therapeutic denervation to be implemented with the maximum likelihood of success. Identifying responsible muscles can be complex, since many muscles may cross the joint involved, and not all muscles with the potential to cause deformity will be spastic. Strategies including polyelectromyography and diagnostic blocks with local anesthetics can be used to test hypotheses regarding the deformity, providing information for more long-term denervation. In this review, we discuss frequently observed patterns of deformity associated with problematic spasticity, paresis, contracture, and impaired voluntary motor control.
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PMID:Common patterns of clinical motor dysfunction. 982 81

Major neurologic complications secondary to cyclosporine are well documented and are known to include confusion, cortical blindness, seizure, spasticity, paresis, ataxia and coma. Most previous reports attribute these to white matter central nervous system (CNS) lesions or white/grey matter border lesions. Many predisposing factors have been identified, including: elevated levels of cyclosporine, hypomagnesemia, hypocholesterolemia, aluminium toxicity, high dose steroids, hypertension and infection. However CNS events attributed to cyclosporine have been reported without any of these risk factors. We report a case of a child developing multiple white and grey matter thalamic and cortical lesions along with acute neurologic deterioration, and then review cyclosporine mediated CNS injury, including the roles of P-glycoprotein and cyclophilin.
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PMID:Cyclosporine-induced white and grey matter central nervous system lesions in a pediatric renal transplant patient. 1008 60

The aim of this study was the quantitative evaluation of the myotatic reflex in a group of 11 subjects affected by spastic paresis of the lower limbs (8 hemiplegic and 3 paraplegic patients) and, for comparison, in a group of 7 healthy subjects. The parameters taken into account were the gain of the reflex and the time delay between the input and the mechanical output. The gain was calculated as the ratio between: i) the peak value of the input force (FPH) measured by means of an instrumented hammer with which the patellar tendon was hit; and ii) the peak value of the corresponding reflex force of the quadriceps femoris (FPQ) measured by means of a load cell connected to the subject's ankle. The gain of the reflex (FPQ/FPH) was found to be 1.9 to 2.4 times larger in patients as compared to control subjects and, among the patients to be twice at low, as compared to high, levels of stimulation. Among the hemiplegic patients, significant differences were found in the time delay of the response between the affected and unaffected limbs. Since both the intensity of the reflex and its gain were found to depend on the mechanical energy input, both parameters must be taken in to account if a diagnosis of spasticity has to be made.
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PMID:Quantitative evaluation of the Myotatic Reflex in Hemiplegic and Paraplegic patients. 1035 68

Forty two hemiparetic patients after cerebrovascular accidents were trained to change the position of the center of pressure according to a target on the screen with the visual feedback control. The learning was substantially impaired in comparison with the group of healthy subjects. Patients with the right-hemispheric lesions showed somewhat greater learning deficit than patients with lesions in the left hemisphere. Lesion localization also affected the process of learning. The learning was disturbed to a greater extent in patients with lesions involving not only motor but also premotor and parietal cortical areas. In patients with parieto-temporal lesions the learning reached a very low level after three initial days of training, possibly, because of the deficit of sensory integration and of body scheme in the extra-personal space. Patients with combined lesions of the motor, premotor, and parietal areas showed the lowest results. The learning was shown to depend on the deficit of proprioception and extent of postural disturbances (asymmetry of body weight distribution and amplitude of the center of pressure oscillations) rather than on the extent of motor deficit (paresis and spasticity). However, the learning itself improved some motor disturbances.
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PMID:[Deficit of learning of posture voluntary control in patients with cortical lesions of various locations: cortical mechanisms of posture regulation]. 1092 80


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