Effect of an exercise intervention on global cognition after transient ischemic attack or minor stroke: the MoveIT randomized controlled trial.

BACKGROUND: Patients with a transient ischemic attack (TIA) or ischemic stroke are at increased risk of developing cognitive impairment in the subacute phase. At present, the effects of exercise on cognitive functioning following a TIA or stroke are not fully known. The purpose of this trial was to investigate the effect of exercise on global cognition. METHODS: The MoveIT trial is a single-centre, observer-blinded, randomized controlled trial involving a 1-year exercise intervention consisting of a 12-week group exercise program, combined with three counselling visits to the physiotherapists over a 9-month period. The control group received standard care. The primary outcome was global cognitive functioning, assessed at one year, using the Montreal Cognitive Assessment (MoCA). Secondary outcomes included cardiorespiratory fitness, the cardiovascular profile, and attainment of secondary prevention targets, anxiety, depression and fatigue at one and two years. RESULTS: The experimental group consisted of 60 patients, while the control group consisted of 59 patients. The mean age was 64.3 years and 41% were female. No between-group differences were found on global cognitive functioning (MD, 0.7 out of 30, 95% CI, - 0.2 to 1.6) or on secondary outcome measures at 12 months. The only significant between-group difference was found for fatigue, in favour of the experimental group at 12 months (MD, 0.6 out of 63, 95% CI, 0.1 to 1.1). CONCLUSIONS: No benefit of this exercise intervention was found regarding global cognition. Future studies need to focus on optimizing rehabilitation strategies for this vulnerable group of patients. TRIAL REGISTRATION: http://www.trialregister.nl . Unique identifier: NL3721 . Date first registration: 06-03-2013.

Limited Efficacy of a Long-term Secondary Prevention Program in Ischemic Stroke and Transient Ischemic Attack Patients.

BACKGROUND: Few studies have focused on the quality of care with regard to long-term secondary prevention after transient ischemic attack (TIA) or ischemic stroke. The aim of this study was 2-fold: (1) to determine if ischemic stroke and TIA patients are motivated for a long-term secondary prevention program after hospital discharge and (2) to study the effect of this program on the attainment of guideline-recommended secondary prevention targets. METHODS: A single-center, cohort study of ischemic stroke and TIA patients. The number of visits to the long-term secondary prevention program and the number of patients whom achieved the composite end point of optimal medical therapy at their last visit to our outpatient clinic were assessed. RESULTS: Of the 237 included ischemic stroke and TIA patients, only 164 (69%) visited the long-term secondary prevention program at least once. Of these patients, 37% reached the primary end point of optimal medical treatment at their last visit to our outpatient clinic. We found a significant increase in secondary prevention target attainment for the primary outcome of optimal medical treatment and its individual components. CONCLUSIONS: Despite our systematic approach to care for patients after ischemic stroke or TIA, we observed that 31% of our patients did not visit our outpatient clinic for the long-term secondary prevention program at all. In addition, the long-term secondary prevention program alone, consisting of regular follow-up visits and a medication treatment algorithm, was not sufficient to reach guideline-recommended treatment targets in most of our ischemic stroke and TIA patients.

Achieving a door-to-needle time of 25 minutes in thrombolysis for acute ischemic stroke: a quality improvement project.

BACKGROUND: Providing intravenous thrombolysis with short door-to-needle time is the result of a complex process that requires specific work standards. To expedite care for acute ischemic stroke patients, close collaboration between all participating health care professionals is required. The aim of this project was to reduce in-hospital treatment delay for acute ischemic stroke patients through the introduction of a standard operating procedure and by creating higher and sustained awareness of the importance of intravenous thrombolysis. METHODS: This study was set up as a before-versus-after study, divided into a preintervention period, an immediate postintervention period, and a late postintervention period. During the study, a standard operating procedure was implemented that defined the targeted standard of care to be provided to all acute stroke patients. Involved health care professionals received regular feedback to create greater awareness of the importance of this time-driven protocol. RESULTS: The median door-to-needle time decreased significantly, from 60 minutes in the preintervention period to 30 minutes in the immediate postintervention period (P < .001), and compared with the immediate postintervention period it decreased significantly further, to 25 minutes, in the late postintervention period (P < .001). The proportion of patients with a door-to-needle time <30 minutes and <20 minutes increased significantly across the 3 study periods (P < .001). CONCLUSIONS: The door-to-needle time for acute ischemic stroke patients can be reduced through the introduction of a standard operating procedure and by creating higher and sustained awareness of the importance of intravenous thrombolysis among health care professionals involved.

Drug treatment for spinal muscular atrophy type I.

BACKGROUND: Spinal muscular atrophy (SMA) is caused by degeneration of anterior horn cells of the spinal cord, which leads to progressive muscle weakness. Children with SMA type I will never be able to sit without support and usually die by the age of two years. There are no known efficacious drug treatments that influence the course of the disease. This is an update of a review first published in 2009. OBJECTIVES: To evaluate whether drug treatment is able to slow or arrest the disease progression of SMA type I, and to assess if such therapy can be given safely. Drug treatment for SMA types II and III is the topic of a separate updated Cochrane review. SEARCH METHODS: We searched the Cochrane Neuromuscular Disease Group Specialized Register (8 March 2011), CENTRAL (The Cochrane Library 2011, Issue 1), MEDLINE (January 1991 to February 2011), EMBASE (January 1991 to February 2011) and ISI Web of Knowledge (January 1991 to 8 March 2011). We searched the Clinical Trials Registry of the U.S. National Institute of Health (www.ClinicalTrials.gov) (8 March 2011) to identify additional trials that had not yet been published. SELECTION CRITERIA: We sought all randomised or quasi-randomised trials that examined the efficacy of drug treatment for SMA type I. Participants had to fulfil the clinical criteria and have a deletion or mutation of the SMN1 gene (5q11.2-13.2) confirmed by genetic analysis.The primary outcome measure was time from birth until death or full time ventilation. Secondary outcome measures were development of rolling, sitting or standing within one year after the onset of treatment, and adverse events attributable to treatment during the trial period. DATA COLLECTION AND ANALYSIS: Two authors (RW and AV) independently reviewed and extracted data from all potentially relevant trials. For included studies, pooled relative risks and standardised mean differences were to be calculated to assess treatment efficacy. MAIN RESULTS: One small randomised controlled study comparing riluzole treatment to placebo for 10 SMA type 1 children was identified and included in the original review. No further trials were identified for the update in 2011. Regarding the primary outcome measure, three of seven children treated with riluzole were still alive at the ages of 30, 48 and 64 months, whereas all three children in the placebo group died; but the difference was not statistically significant. Regarding the secondary outcome measures, none of the children in the riluzole or placebo group developed the ability to roll, sit or stand, and no adverse effects were observed. For several reasons the overall quality of the study was low, mainly because the study was too small to detect an effect and because of baseline differences. Follow-up of the 10 included children was complete. AUTHORS' CONCLUSIONS: No drug treatment for SMA type I has been proven to have significant efficacy.

Drug treatment for spinal muscular atrophy types II and III.

BACKGROUND: Spinal muscular atrophy (SMA) is caused by degeneration of anterior horn cells, which leads to progressive muscle weakness. Children with SMA type II do not develop the ability to walk without support and have a shortened life expectancy, whereas children with SMA type III develop the ability to walk and have a normal life expectancy. There are no known efficacious drug treatments that influence the disease course of SMA. This is an update of a review first published in 2009. OBJECTIVES: To evaluate whether drug treatment is able to slow or arrest the disease progression of SMA types II and III and to assess if such therapy can be given safely. Drug treatment for SMA type I is the topic of a separate updated Cochrane review. SEARCH METHODS: We searched the Cochrane Neuromuscular Disease Group Specialized Register (8 March 2011), Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library 2011, Issue 1), MEDLINE (January 1991 to February 2011), EMBASE (January 1991 to February 2011) and ISI Web of Knowledge (January 1991 to March 8 2011). We also searched clinicaltrials.gov to identify as yet unpublished trials (8 March 2011). SELECTION CRITERIA: We sought all randomised or quasi-randomised trials that examined the efficacy of drug treatment for SMA types II and III. Participants had to fulfil the clinical criteria and have a deletion or mutation of the survival motor neuron 1 (SMN1) gene (5q11.2-13.2) that was confirmed by genetic analysis.The primary outcome measure was to be change in disability score within one year after the onset of treatment. Secondary outcome measures within one year after the onset of treatment were to be change in muscle strength, ability to stand or walk, change in quality of life, time from the start of treatment until death or full time ventilation and adverse events attributable to treatment during the trial period. DATA COLLECTION AND ANALYSIS: Two authors independently reviewed and extracted data from all potentially relevant trials. Pooled relative risks and pooled standardised mean differences were to be calculated to assess treatment efficacy. Risk of bias was systematically analysed. MAIN RESULTS: Six randomised placebo-controlled trials on treatment for SMA types II and III were found and included in the review: the four in the original review and two trials added in this update. The treatments were creatine (55 participants), phenylbutyrate (107 participants), gabapentin (84 participants), thyrotropin releasing hormone (9 participants), hydroxyurea (57 participants), and combination therapy with valproate and acetyl-L-carnitine (61 participants). None of these studies were completely free of bias. All studies had adequate blinding, sequence generation and reports of primary outcomes.None of the included trials showed any statistically significant effects on the outcome measures in participants with SMA types II and III. One participant died due to suffocation in the hydroxyurea trial and one participant died in the creatine trial. No participants in any of the other four trials died or reached the state of full time ventilation. Serious side effects were infrequent. AUTHORS' CONCLUSIONS: There is no proven efficacious drug treatment for SMA types II and III.

Drug treatment for spinal muscular atrophy type I.

BACKGROUND: Spinal muscular atrophy (SMA) is caused by degeneration of anterior horn cells, which leads to progressive muscle weakness. Children with SMA type I will never be able to sit without support and usually die by the age of two years. There are no known efficacious drug treatments that influence the disease course. OBJECTIVES: To evaluate if drug treatment is able to slow or arrest the disease progression of SMA type I, and to assess if such therapy can be given safely. Drug treatment for SMA type II and III will be will be the topic of a separate Cochrane review. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group Trials Register (September 30 2008, The Cochrane Library (Issue 3, 2008), MEDLINE (January 1966 to June 2008), EMBASE (January 1980 to June 2008), ISI (January 1988 to June 2008), and ACP Journal Club (January 1991 to June 2008). SELECTION CRITERIA: All randomized or quasi-randomized trials that examined the efficacy of drug treatment for SMA type 1 were sought. Participants had to fulfil clinical criteria and, in studies including genetic analysis to confirm the diagnosis, have a deletion or mutation of the SMN1 gene (5q11.2-13.2)The primary outcome measure was to be time from birth until death or full time ventilation. Secondary outcome measures were to be development of rolling, sitting or standing within one year after the onset of treatment, and adverse events attributable to treatment during the trial period. DATA COLLECTION AND ANALYSIS: Two authors (WB and AV) independently reviewed and extracted data from all potentially relevant trials. For included studies pooled relative risks and pooled weighted standardized mean differences were to be calculated to assess treatment efficacy MAIN RESULTS: One small randomized-controlled study comparing riluzole treatment to placebo for SMA type 1 was identified and included in the review. Regarding the primary outcome measure three of seven children treated with riluzole were still alive at the age of 30, 48 and 64 months, whereas all three children in the placebo group died, but the difference was not statistically significant. Regarding the secondary outcome measures none of the patients in the riluzole or placebo group developed the ability to roll, sit or stand, and no adverse effects were observed. AUTHORS' CONCLUSIONS: No drug treatment for SMA type I has been proven to have significant efficacy.

Drug treatment for spinal muscular atrophy types II and III.

BACKGROUND: Spinal muscular atrophy (SMA) is caused by degeneration of anterior horn cells, which leads to progressive muscle weakness. Children with SMA type II do not develop the ability to walk without support and have a shortened life expectancy, whereas children with SMA type III develop the ability to walk and have a normal life expectancy. There are no known efficacious drug treatments that influence the disease course of SMA. OBJECTIVES: To evaluate if drug treatment is able to slow or arrest the disease progression of SMA type II and III, and to assess if such therapy can be given safely. Drug treatment for SMA type I will be the topic of a separate Cochrane review. SEARCH STRATEGY: We searched the Cochrane Neuromuscular Disease Group Trials Register (September 30 2008), The Cochrane Library (Issue 3, 2008), MEDLINE (January 1966 to June 2008), EMBASE (January 1980 to June 2008), ISI (January 1988 to June 2008), and ACP Journal Club (January 1991 to June 2008). SELECTION CRITERIA: We sought all randomized or quasi-randomized trials that examined the efficacy of drug treatment for SMA type II and III. Participants had to fulfil the clinical criteria and, in studies including genetic analysis to confirm the diagnosis, have a deletion or mutation of the SMN1 gene (5q11.2-13.2)The primary outcome measure was to be change in disability score within one year after the onset of treatment. Secondary outcome measures within one year after the onset of treatment were to be change in muscle strength, ability to stand or walk, change in quality of life, time from the start of treatment until death or full time ventilation, and adverse events attributable to treatment during the trial period. DATA COLLECTION AND ANALYSIS: Two authors independently reviewed and extracted data from all potentially relevant trials. Pooled relative risks and pooled weighted standardized mean differences were to be calculated to assess treatment efficacy MAIN RESULTS: Four randomized placebo-controlled trials on treatment for SMA type II and III were found and included in the review. The treatments were creatine, phenylbutyrate, gabapentin and thyrotropin releasing hormone. None of these trials showed any effect on the outcome measures in patients with SMA type II and III. None of the patients in any of the four trials died or reached the state of full time ventilation and serious side effects were infrequent. AUTHORS' CONCLUSIONS: There is no proven efficacious drug treatment for SMA type II and III.