Ipsilateral lower limb motor performance and its association with gait after stroke.

BACKGROUND AND PURPOSE: Motor deficits of the ipsilateral lower limb could occur after stroke and may be associated with walking performance. This study aimed to determine whether the accuracy and movement path of targeted movement in the ipsilateral lower limb would be impaired in the chronic stage of stroke and whether this impairment would contribution to gait. METHODS: Twenty adults with chronic stroke and 20 age-matched controls went through Mini Mental Status Examination (MMSE), and a series of sensorimotor tests. The targeted movement tasks were to place the big toe ipsilateral to the lesion at an external visual target (EXT) or a proprioceptive target (PRO, contralateral big toe) with eyes open (EO) or closed (EC) in a seated position. A motion analysis system was used to obtain the data for the calculation of error distance, deviation from a straight path, and peak toe-height during the targeted movement tasks and gait velocity, step length, step width and step length symmetry of the lower limb ipsilateral to the brain lesion during walking. RESULTS: The stroke group had significantly lower MMSE and poorer visual acuity on the ipsilateral side, but did not differ in age or other sensorimotor functions when compared to the controls. For the targeted movement performance, only the deviation in PRO-EC showed significant between-group differences (p = 0.02). Toe-height in both EXT-EO and in PRO-EO was a significant predictor of step length (R2 = 0.294, p = 0.026) and step length symmetry (R2 = 0.359, p = 0.014), respectively. DISCUSSION AND CONCLUSIONS: The performance of ipsilateral lower limb targeted movement could be impaired after stroke and was associated with step length and its symmetry. The training of ipsilateral targeted movement with unseen proprioceptive target may be considered in stroke rehabilitation.

Effects of Trunk Exercise on Unstable Surfaces in Persons with Stroke: A Randomized Controlled Trial.

Background: Improving balance-related ability is an important goal in stroke rehabilitation. Evidence is needed to demonstrate how this goal could be better achieved. Aim: Determine if trunk exercises on unstable surfaces would improve trunk control and balance for persons in the subacute stage of stroke. Design: An assessor-blind randomized controlled trial. Setting: Inpatients in the department of rehabilitation in a general hospital. Population: Patients who suffered a first-time stroke with onset from one to six months. Methods: Inpatients with stroke were assigned to upper limb exercises (control group, n = 17) or trunk exercises on unstable surfaces (experimental group, n = 18) to receive training twice a week for six weeks, in addition to their daily conventional stroke rehabilitation. Sensorimotor function tests, including hand grip, plantar sensitivity, stroke rehabilitation assessment of movement and Fugl-Meyer lower extremity motor scale, and clinical outcome assessments, including Trunk Impairment Scale and 6 m walk test, were conducted before and after six weeks of training. The center of the pressure area while maintaining static posture and peak displacement while leaning forward, as well as the average speed of raising the unaffected arm, were measured in sitting without foot support, sitting with foot support and standing to reflect trunk control, sitting balance and standing balance, respectively. Results: The between-group differences in the sensorimotor functions were nonsignificant before and after training. Compared with the control group, the experimental group had significantly greater forward leaning and faster arm raising in sitting without foot support, higher Trunk Impairment Scale total score, and shorter 6 m walking time after training, but not before training. Conclusion: Trunk exercises on unstable surfaces could further improve trunk control, the ability to raise the unaffected arm rapidly in sitting, and walking for persons in the subacute stage of stroke. This intervention may be considered to be included in stroke rehabilitation.

TXAS-deleted mice exhibit normal thrombopoiesis, defective hemostasis, and resistance to arachidonate-induced death.

Besides its well-recognized role in hemostasis and thrombosis, thromboxane A(2) synthase (TXAS) is proposed to be involved in thrombopoiesis and lymphocyte differentiation. To evaluate its various physiologic roles, we generated TXAS-deleted mice by gene targeting. TXAS(-/-) mice had normal bone marrow megakaryocytes, normal blood platelet counts, and normal CD4 and CD8 lymphocyte counts in thymus and spleen. Platelets from TXAS(-/-) mice failed to aggregate or generate thromboxane B(2) in response to arachidonic acid (AA) but produced increased prostaglandin-E(2) (PGE(2)), PGD(2), and PGF(2 alpha). AA infusion caused a progressive drop of mean arterial pressure (MAP), cardiac arrest, and death in wild-type (WT) mice but did not induce shock in TXAS(-/-) mice or in WT and TXAS(-/-) mice treated with antagonist to the thromboxane-prostanoid (TP) receptor. The TXAS(-/-) mice were able to maintain normal MAP upon AA insult when TP was present but were unable to do so when TP was blocked by an antagonist, suggesting a role of endoperoxide accumulation in influencing MAP. We conclude that TXAS is not essential for thrombopoiesis and lymphocyte differentiation. Its deficiency causes a mild hemostatic defect and protects mice against arachidonate-induced shock and death. The TXAS-deleted mice will be valuable for investigating the roles of arachidonate metabolic shunt in various pathophysiologic processes.