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Comparison of pelvic floor muscle training, electromyography biofeedback, and neuromuscular electrical stimulation for bladder dysfunction in people with multiple sclerosis: a randomized pilot study.
McClurg, D, Ashe, RG, Marshall, K, Lowe-Strong, AS
Neurourology and urodynamics. 2006;(4):337-48
Abstract
AIM: Bladder dysfunction affects up to 90% of the multiple sclerosis (MS) population. Interventions such as Pelvic Floor Training and Advice (PFTA), Electromyography (EMG) Biofeedback, and Neuromuscular Electrical Stimulation (NMES) have received limited research attention within this population. This study aimed to determine the effectiveness of a combined programme of PFTA, EMG Biofeedback, and NMES for bladder dysfunction in MS. METHODS Females (n = 30) who fulfilled strict inclusion/exclusion criteria were recruited. Outcome measures (weeks 0, 9, 16, and 24) included: 3-day Voiding Diary; 24 hr Pad-Test; Uroflowmetry; Pelvic Floor Muscle Assessment; Incontinence Impact Questionnaire (IIQ); Urogenital Distress Inventory (UDI); King's Health Questionnaire (KHQ), and the Multiple Sclerosis Quality of Life-54 Instrument (MSQoL-54). Following baseline (week 0) assessment, participants were randomly allocated, under double blind conditions, to one of the three groups: Group 1 (PFTA); Group 2 (PFTA and EMG Biofeedback); and Group 3 (PFTA, EMG Biofeedback, and NMES). Treatment was for 9 weeks. RESULTS Baseline severity (measured by number of leaks and pad weight) showed some variation between groups, although not statistically significant (P > 0.05); with the caveat that this baseline imbalance makes interpretation difficult, a picture emerges that at week 9, Group 3 demonstrated superior benefit as measured by the number of leaks and pad test than Group 2, with Group 1 showing less improvement when compared to week 0; this was statistically significant between Groups 1 and 3 for number of leaks (P = 0.014) and pad tests (P = 0.001), and Groups 1 and 2 for pad tests (P = 0.001). A similar pattern was evident for all other outcome measures. CONCLUSION Results suggest that these treatments, used in combination, may reduce urinary symptoms in MS. Further research will establish the effectiveness of these interventions.
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Comparison of the effects of acetyl L-carnitine and amantadine for the treatment of fatigue in multiple sclerosis: results of a pilot, randomised, double-blind, crossover trial.
Tomassini, V, Pozzilli, C, Onesti, E, Pasqualetti, P, Marinelli, F, Pisani, A, Fieschi, C
Journal of the neurological sciences. 2004;(1-2):103-8
Abstract
Treatment with acetyl L-carnitine (ALCAR) has been shown to improve fatigue in patients with chronic fatigue syndrome, but there have been no trials on the effect of ALCAR for treating fatigue in multiple sclerosis (MS). To compare the efficacy of ALCAR with that of amantadine, one of the drugs most widely used to treat MS-related fatigue, 36 MS patients presenting fatigue were enrolled in a randomised, double-blind, crossover study. Patients were treated for 3 months with either amantadine (100 mg twice daily) or ALCAR (1 g twice daily). After a 3-month washout period, they crossed over to the alternative treatment for 3 months. Patients were rated at baseline and every 3 months according to the Fatigue Severity Scale (FSS), the primary endpoint of the study. Secondary outcome variables were: Fatigue Impact Scale (FIS), Beck Depression Inventory (BDI) and Social Experience Checklist (SEC). Six patients withdrew from the study because of adverse reactions (five on amantadine and one on ALCAR). Statistical analysis showed significant effects of ALCAR compared with amantadine for the Fatigue Severity Scale (p = 0.039). There were no significant effects for any of the secondary outcome variables. The results of this study show that ALCAR is better tolerated and more effective than amantadine for the treatment of MS-related fatigue.
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3.
Liver injury associated with the beta-interferons for MS: a comparison between the three products.
Tremlett, HL, Yoshida, EM, Oger, J
Neurology. 2004;(4):628-31
Abstract
A population-based retrospective chart review of the biochemical liver tests of 844 patients with multiple sclerosis prescribed a beta-interferon (IFNbeta) product in British Columbia, Canada was performed between 1995 and 2001. Overall, 36.9% (243/659) of patients developed new elevations of alanine aminotransferase. All the IFNbetas caused elevated aminotransferase levels compared with pretreatment levels (p < 0.005) and were higher than reported in clinical trials. Their relative effect on aminotransferases can be approximated as IFNbeta-1b(subcutaneous [SC]) = IFNbeta-1a(SC) > IFNbeta-1a(IM).
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4.
Influence of creatine monohydrate ingestion on muscle metabolites and intense exercise capacity in individuals with multiple sclerosis.
Lambert, CP, Archer, RL, Carrithers, JA, Fink, WJ, Evans, WJ, Trappe, TA
Archives of physical medicine and rehabilitation. 2003;(8):1206-10
Abstract
OBJECTIVE To evaluate the effectiveness of ingesting creatine monohydrate in elevating intramuscular creatine stores and improving exercise capacity in individuals with multiple sclerosis (MS). DESIGN Randomized, double-blind, placebo-controlled, pre-posttrial. SETTING A university-based exercise physiology laboratory. PARTICIPANTS Sixteen individuals with relapsing-remitting MS (median Expanded Disability Status Scale score, 4.75; range, 1.5-6.0). INTERVENTION Eight individuals with MS were randomized to the creatine group (20g/d of creatine monohydrate for 5d), and 8 others were randomized to the placebo group. Needle biopsies were performed on the vastus lateralis at rest before and after treatment. Subjects performed 3 bouts of 30 maximal knee extensions and flexions at 180 degrees /s with 1 minute of recovery between bouts before and after treatment. MAIN OUTCOME MEASURES Intramuscular total creatine, phosphocreatine, free creatine, and total work output. RESULTS Creatine ingestion did not significantly elevate intramuscular total creatine, phosphocreatine, or free creatine or improve total work production. CONCLUSION Creatine ingestion had no significant effect on muscle creatine stores or high-intensity exercise capacity in individuals with MS.
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5.
A randomized clinical trial of a wellness intervention for women with multiple sclerosis.
Stuifbergen, AK, Becker, H, Blozis, S, Timmerman, G, Kullberg, V
Archives of physical medicine and rehabilitation. 2003;(4):467-76
Abstract
OBJECTIVE To examine the effects of a wellness intervention program for women with multiple sclerosis (MS) on health behaviors and quality of life (QOL). DESIGN Randomized clinical trial. SETTING Community setting in the southwestern United States. PARTICIPANTS Convenience sample of 113 women with physician-confirmed MS (mean age, 45.79y). INTERVENTIONS The 2-phase intervention program included lifestyle-change classes for 8 weeks, then telephone follow-up for 3 months. Participants were followed over an 8-month period. MAIN OUTCOME MEASURES A series of self-report instruments to measure barriers, resources, self-efficacy for health behaviors, health promotion behaviors, and health-related QOL were completed at baseline, 2 months (after the classes), 5 months (after telephone follow-up), and at 8 months. Principal outcomes measures were health-promoting behaviors (scores on the Health Promoting Lifestyle Profile II) and QOL (scores on the Medical Outcomes Study 36-Item Short-Form Health Survey [SF-36] scales). RESULTS Hierarchical linear modeling techniques revealed a statistically significant group by time effect for self-efficacy for health behaviors, health-promoting behaviors, and the mental health and pain scales of the SF-36. CONCLUSION These data provide initial support for the positive effects of wellness interventions to improve health behaviors and selected dimensions of QOL for women with MS.
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The physiological basis of conduction slowing in ALS patients homozygous for the D90A CuZn-SOD mutation.
Weber, M, Eisen, A, Stewart, HG, Andersen, PM, Hirota, N
Muscle & nerve. 2001;(1):89-97
Abstract
Familial amyotrophic lateral sclerosis (ALS) with the autosomal-recessively inherited D90A CuZn-superoxide dismutase (CuZn-SOD) mutation is characterized by a stereotypic slowly progressive, distinctive phenotype and very slow central motor conduction. To determine the basis of this slowing, we assessed corticomotoneuronal function using peristimulus time histograms (PSTHs) in 8 ALS patients homozygous for the D90A CuZn-SOD mutation. The results were compared with findings in 10 patients with multiple sclerosis (MS), in which slowing of central motor conduction is common, and 11 healthy subjects. PSTHs were constructed from 3-7 different, voluntarily recruited motor units recorded in each patient from the extensor digitorum communis muscle (EDC). In D90A and MS patients, the stimulus threshold, onset latency, number of excess bins, duration, amplitude, and synchrony of the primary peak differed significantly from controls (P < 0.0004). The mean onset latency of the primary peak in D90A patients was 35.3 ms, compared to 23.6 ms for MS patients and 19.3 ms for normal subjects (P < 0.0001). In the D90A patients, the onset latencies of the primary peak had a bimodal distribution, whereas in MS the distribution showed a continuum. Loss of synchrony was similar in D90A and MS patients, but the threshold, number of excess bins, and duration differed significantly (P < 0.0057), which suggests that either axonal loss or demyelination can result in delayed and desynchronized primary peaks. We propose that conduction slowing in the D90A homozygotes results from selective loss of fast-conducting large pyramidal cells with preservation of slow-conducting mono- or polysynaptic corticomotoneuronal connections.