ObjectiveTo evaluate the effect of extracorporeal shock wave therapy (ESWT) on lower limb spasticity in subacute stroke patients.MethodsWe studied thirty hemiplegic subacute stroke patients with ankle plantar flexor spasticity. ESWT was applied for 1 session/week, with a total of 3 sessions at the musculotendinous junction of medial and lateral gastrocnemius muscles. Patients were evaluated both clinically and biomechanically at baseline, after sham stimulation, and at immediately 1 week and 4 weeks after ESWT. For clinical assessment, Modified Ashworth Scale (MAS), clonus score, passive range of motion of ankle, and Fugl-Myer Assessment for the lower extremity were used. A biomechanical assessment of spasticity was conducted by an isokinetic dynamometer. Two parameters, peak eccentric torque (PET) and torque threshold angle (TTA), were analyzed at the velocities of 60°/sec, 180°/sec, and 240°/sec.ResultsAfter sham stimulation, there were no significant changes between each assessment. MAS and PET (180°/sec and 240°/sec) were significantly improved immediately and 1 week after ESWT. However, these changes were not significant at 4 weeks after ESWT. PET (60°/sec) and TTA (60°/sec, 180°/sec, and 240°/sec) were significantly improved immediately after ESWT. Yet, these changes were not significant at 1 week and 4 weeks after ESWT as well.ConclusionLower limb spasticity in subacute stroke patients was significantly improved immediately after ESWT. Although the therapeutic effect of ESWT reduced with time and therefore was not significant at 4 weeks after ESWT, the degree of spasticity was lower than that of the baseline. Future studies with a larger sample of patients are warranted in order to verify the protocols which can optimize the effect of ESWT on spasticity.
Background:Certain metabolic factors have been proposed as risk factors for a posterosuperior rotator cuff tear. Although metabolic syndrome is of increasing concern in industrialized societies, little information exists regarding its association with posterosuperior rotator cuff tears. The purpose of this study was to determine the risk factors for an atraumatic posterosuperior rotator cuff tear, including metabolic factors and metabolic syndrome.Methods:This study involved 634 subjects (634 shoulders) drawn from a cohort of rural residents. Posterosuperior rotator cuff tear diagnoses were based on magnetic resonance imaging (MRI) findings. Logistic regression analysis was used to determine the odds ratios (ORs) and 95% confidence intervals (CIs) for various demographic, physical, and social factors, including age, sex, dominant-side involvement, body mass index (BMI), and participation in manual labor; the comorbidities of diabetes, hypertension, dyslipidemia, thyroid dysfunction, ipsilateral carpal tunnel syndrome, and metabolic syndrome; and the serum metabolic parameters of serum lipid profile, glycosylated hemoglobin A1c, and level of thyroid hormone. Two multivariable analyses were performed: the first excluded metabolic syndrome while including diabetes, hypertension, BMI, and hypo-high-density lipoproteinemia (hypo-HDLemia), and the second included metabolic syndrome while excluding the formerly included variables.Results:Age, BMI, waist circumference, dominant-side involvement, manual labor, diabetes, hypertension, metabolic syndrome, ipsilateral carpel tunnel syndrome, HDL (high-density lipoprotein), and hypo-HDLemia were significantly associated with posterosuperior rotator cuff tears in univariate analyses (p ≤ 0.035). In the first multivariable analysis, age (OR. 1.86 [95% CI, 1.47 to 2.35]), BMI (OR, 1.09 [95% CI, 1.02 to 1.18]), dominant-side involvement (OR, 2.04 [95% CI, 1.38 to 3.01]), manual labor (OR, 9.48 [95% CI, 5.13 to 17.51]), diabetes (OR, 3.38 [95% CI, 1.98 to 5.77]), and hypo-HDLemia (OR, 2.07 [95% CI, 1.30 to 3.29]) were significantly associated with posterosuperior rotator cuff tears (p ≤ 0.019). In the second multivariable analysis, age (OR, 1.85 [95% CI, 1.48 to 2.31]), dominant-side involvement (OR, 1.83 [95% CI, 1.26 to 2.67]), manual labor (OR, 7.71 [95% CI, 4.33 to 13.73]), and metabolic syndrome (OR, 1.98 [95% CI, 1.35 to 2.91]) were significantly associated with posterosuperior rotator cuff tears (p ≤ 0.002).Conclusions:The metabolic factors of diabetes, BMI, hypo-HDLemia, and metabolic syndrome were significant independent factors associated with the development of posterosuperior rotator cuff tears.Level of Evidence:Prognostic Level III. See Instructions for Authors for a complete description of levels of evidence.
It is not common for a patient who survives cardiac arrest to experience significant neurologic impairment such as acute and chronic post-hypoxic myoclonus, known as Lance-Adams syndrome. This syndrome is predominantly characterized by myoclonus that starts days to weeks after cardiopulmonary resuscitation in patients who regained consciousness. Although several cases of LAS were reported, the decisive treatment method has not been established. We report a 43 year old man with Lance-Adams syndrome who showed long-term improvement through treatment with anti-myoclonic agents and participation in a rehabilitation program.
The proliferation, migration, cytokine release, and contraction of airway smooth muscle cells are key events in the airway remodeling process that occur in lung disease such as asthma, chronic obstruction pulmonary disease, and cancer. These events can be modulated by a number of factors, including cigarette smoke extract (CSE). CSE-induced alterations in the viability, migration, and contractile abilities of normal human airway cells remain unclear. This study investigated the effect of CSE on cell viability, migration, tumor necrosis factor (TNF)-α secretion, and contraction in normal human bronchial smooth muscle cells (HBSMCs). Treatment of HBSMCs with 10% CSE induced cell death, and the death was accompanied by the generation of reactive oxygen species (ROS). CSE-induced cell death was reduced by N-acetyl-l-cysteine (NAC), an ROS scavenger. In addition, CSE reduced the migration ability of HBSMCs by 75%. The combination of NAC with CSE blocked the CSE-induced reduction of cell migration. However, CSE had no effect on TNF-α secretion and NF-κB activation. CSE induced an increase in intracellular Ca2+ concentration in 64% of HBSMCs. CSE reduced the contractile ability of HBSMCs, and the ability was enhanced by NAC treatment. These results demonstrate that CSE treatment induces cell death and reduces migration and contraction by increasing ROS generation in normal HBSMCs. These results suggest that CSE may induce airway change through cell death and reduction in migration and contraction of normal HBSMCs.
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