[Spastic hypertonia in clinical medicine].
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We studied the short term effects of a single session of prolonged muscle stretch (PMS) on reflex and voluntary muscle activations in 22 children with spastic cerebral palsy (CP) assigned to an experimental (n = 12) and a control group (n = 10). Children of the experimental group underwent PMS of the triceps surae (TS) by standing with the feet dorsiflexed on a tilt-table for 30 min, whereas children of the control group were kept at rest. The effects were determined by measuring the associated changes in torque and in electromyographic (EMG) activity of the TS and tibialis anterior (TA) muscles during both passive ankle movements and maximal static voluntary contractions. The results indicate that PMS led to reduced spasticity in ankle muscles as demonstrated by the significant reductions (p less than 0.05) of the neuromuscular responses (torque and EMG) to passive movement. These inhibitory effects lasted up to 35 min after cessation of PMS. In addition, the capacity to voluntarily activate the plantar flexors was significantly (p less than 0.05) increased post-PMS, but the capacity to activate the dorsiflexors was apparently not affected. These findings suggest that repeated sessions of PMS may have beneficial effects in the management of spasticity in children with CP.
PRIMARY OBJECTIVE: Spastic equinovarus deformity of the ankle in adults with acquired brain injury can severely limit the achievement of rehabilitation goals. This study examined changes in triceps surae muscle extensibility, passive resistive torque and soleus stretch reflex responses in 10 adult brain injured subjects undergoing serial casting to correct ankle equinovarus deformity. METHOD: Goniometric measurement of maximal passive dorsiflexion was used to evaluate extensibility of the triceps surae muscles. Computer controlled ankle dynamometry and surface electromyography were used to identify passive resistive torque and soleus stretch reflex onset angle in response to stretches at two velocities. RESULTS: The mean casting period was 5 weeks. Casting was discontinued in one subject due to failure to achieve measurable gain in ankle range over three consecutive cast changes. Median improvements in maximal ankle dorsiflexion, with the knee flexed or extended, of 30 degrees and 15 degrees, respectively, were achieved in the remaining nine subjects (p < 0.0001). The median passive ankle range in response to a displacing torque of 10 Nm increased 4.3 degrees over the intervention period (p < 0.0001). Consistent soleus reflex activity in response to passive stretches at 25 degrees x s(-1) was elicited in only four subjects. A trend for the stretch reflex onset to move further into the available range was demonstrated in these subjects. CONCLUSION: In the present study, serial casting contributed to significant change in triceps surae extensibility and passive resistive torque, corresponding with improved maximal passive ankle dorsiflexion range and an increase in the angle achieved with a displacing torque of 10 N.m. Increased stretch reflex threshold was observed in some subjects. The use of pre-determined outcome criteria and careful measurement of responses to this intervention were important to prevent premature discontinuation of casting when gains were slower than expected.
The effect of the alpha-adrenergic blocking agent thymoxamine by intravenous administration was studied in 25 patients with spastic paraplegia and uninhibited neurogenic bladder. By cystometry a shift to the right of the first desire to void, the threshold of the first uninhibited contraction and a reduction of the pressures of the uninhibited contractions was found, but the bladder capacity was unchanged. The urethral pressure profile studied in 10 patients showed reduction in most and the peak value in all the patients. EMG from the external urethral sphincter in five patients showed damping of anal reflexes in all cases and in basic activity and cough reflexes when appropriate for studies. The site of action on the bladder is most likely adrenergic receptors in the bladder and the unchanged bladder capacity may be related to a too-short duration of the effect of thymoxamine. The effect on the spastic striated pelvic sphincters may be central, whereas the effect on the smooth muscle may be peripheral. Feedback from the drug relaxed proximal part of the urethra to the bladder might also be of importance.
Lesions of the upper motor neurons cause a spastic syndrome and a central paresis. The consequence of these "plus" and "minus" symptoms on locomotor function is a spastic movement disorder. Strategies of physical therapy for the spastic movement disorders are discussed in relation to research findings in neurophysiology and muscle physiology. The main therapeutic technics are physiotherapy, functional electrical stimulation (FES) and biofeedback training (BFB). Various methodological problems which arise in carrying out and evaluating therapeutic studies are described. Valid prognostic criteria are essential in order to achieve an optimal use of the different therapeutic procedures. This review underlines the need for further research, since some important questions remain open.
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