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1.
Annals of Rehabilitation Medicine ; : 328-335, 2013.
Article in English | WPRIM | ID: wpr-192341

ABSTRACT

OBJECTIVE: To prospectively investigate the long-term effects of botulinum toxin treatment on the upper limb function and performance of school age children with spastic bilateral cerebral palsy, who have limitations in performing activities of daily living and school activities, due to spasticity of the upper extremities. METHODS: Botulinum type A toxin (BoNT-A) was injected into 24 spastic upper limbs of 15 children. We used a Modified Ashworth Scale and a Modified Tardieu Scale for the evaluation of upper limb spasticity, and Quality of Upper Extremity Skills Test (QUEST), Canadian Occupational Performance Measure (COPM), and Test of Visual-Motor Skills-Revised (TVMS-R) for the evaluation of upper limb function and performance. RESULTS: Upper limb spasticity continuously decreased until the end of the one-year follow-up. Upper limb function on QUEST and COPM showed the best performance at 3 months and deteriorated slightly, but still showed a significantly better performance at 9 and 12 months than at pre-injection. In more functional nine subjects who could perform TVMS-R, the performance enhancement effects remained constant after 12 months, suggesting that the reduced spasticity led to the learning effect acquired by the repeated use of the affected upper limb. CONCLUSION: For school age children with bilateral spastic cerebral palsy whose upper limb functions are important, BoNT-A injections seem to be of help in the performance of school activities and activities of daily living.


Subject(s)
Child , Humans , Activities of Daily Living , Botulinum Toxins , Botulinum Toxins, Type A , Cerebral Palsy , Follow-Up Studies , Learning , Muscle Spasticity , Prospective Studies , Upper Extremity
2.
Korean Circulation Journal ; : 1141-1153, 1998.
Article in Korean | WPRIM | ID: wpr-47492

ABSTRACT

BACKGROUND: Purinergic and cholinergic agonists elicit negative-inotropic and chronotropic effects, anticip-ating their protective action from the damage of overloaded myocardium. However, the actions of the agents during the ischemic insults are not yet clearly informed. The aim of this study was to investigate the role of the purinergic and cholinergic agonists on the simulated ischemic myocardium of the rat atrial fiber preparations. METHOD: Various action potential parameters (maximum diastolic potential MDP;action potential amplitude APA;velocity of phase 0 depolarization dV/dtmax;action potential duration APD90) were measured and compared in electrically paced, normal (NPSS) and modified physiological salt solution (MPSS) superfused rat atrial fibers in vitro, using conventional 3M-KCl microelectrode technique. Ischemia-simulated modified physiologic solutions were prepared by changing the solution's composition. RESULTS: Hypoxic-and/or hyperkalemic-MPSS decreased all the action potential (AP) variables. However, no significant changes of the AP variables were developed by the acidic-or glucose-free MPSS. Adenosine (Ado) and cyclopentyladenosine (CPA) only decreased the APD90 in a dose-dependent manner. Acetylcholine (Ach) and carbachol (Cch) hyperpolarized the MDP, increased the dV/dtmax with certain doses, and decreased the APD90 dose-depen-dently. The potency for APD90-decrease was greater in order, CPA>Cch>Ach>Ado. Ado and CPA did not affect the hypoxic, hypokalemic MPSS-induced dV/dtmax-decrease. On the other hand, Ach and Cch sig-nificantly inhibited the dV/dtmax-decrease by the hypoxic hypokalemic-MPSS. Ado, CPA, Ach and Cch sig-nificantly augmented the hypoxic, hypokalemic MPSS-induced APD90-decrease. The inhibition by the Ach and Cch on the MPSS-induced dV/dtmax-decrease was not affected by DPCPX, but atropine significantly attenuated the inhibition by the cholinergic agonists. DPCPX inhibited the augmentation by the Ado and CPA on the MPSS induced APD90-decrease, and atropine inhibited the effect of the cholinergic agonists. CONCLUSION: Both purinergic and cholinergic agonists not only shorten the AP duration by themselves but also enhance the AP-shortening effect elicited by the ischemia, and therefore, it is inferred that both agonists prevent further tissue damage from the ischemic insults.


Subject(s)
Animals , Rats , Acetylcholine , Action Potentials , Adenosine , Atropine , Carbachol , Cholinergic Agonists , Hand , Ischemia , Microelectrodes , Myocardium
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