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Canadian Journal of Psychiatry. Revue... Jun 2019Tardive dyskinesia is a movement disorder characterised by irregular, stereotyped, and choreiform movements associated with the use of antipsychotic medication. We aim...
BACKGROUND
Tardive dyskinesia is a movement disorder characterised by irregular, stereotyped, and choreiform movements associated with the use of antipsychotic medication. We aim to provide recommendations on the treatment of tardive dyskinesia.
METHODS
We performed a systematic review of studies of the treatment of tardive dyskinesia. Studies were rated for methodological quality using the American Academy of Neurology Risk of Bias Classification system. Overall level of evidence classifications and grades of recommendation were made using the Scottish Intercollegiate Guidelines Network framework.
RESULTS
Preventing tardive dyskinesia is of primary importance, and clinicians should follow best practice for prescribing antipsychotic medication, including limiting the prescription for specific indications, using the minimum effective dose, and minimising the duration of therapy. The first-line management of tardive dyskinesia is the withdrawal of antipsychotic medication if clinically feasible. Yet, for many patients with serious mental illness, the discontinuation of antipsychotics is not possible due to disease relapse. Switching from a first-generation to a second-generation antipsychotic with a lower D2 affinity, such as clozapine or quetiapine, may be effective in reducing tardive dyskinesia symptoms. The strongest evidence for a suitable co-intervention to treat tardive dyskinesia comes from tests with the new VMAT inhibitors, deutetrabenazine and valbenazine. These medications have not been approved for use in Canada.
CONCLUSION
Data on tardive dyskinesia treatment are limited, and the best management strategy remains prevention. More long-term safety and efficacy data are needed for deutetrabenazine and valbenazine, and their routine availability to patients outside of the USA remains in question.
Topics: Adrenergic Uptake Inhibitors; Antipsychotic Agents; Humans; Tardive Dyskinesia; Tetrabenazine; Valine
PubMed: 30791698
DOI: 10.1177/0706743719828968 -
CA: a Cancer Journal For Clinicians May 2016Answer questions and earn CME/CNE The American Cancer Society Head and Neck Cancer Survivorship Care Guideline was developed to assist primary care clinicians and other... (Review)
Review
Answer questions and earn CME/CNE The American Cancer Society Head and Neck Cancer Survivorship Care Guideline was developed to assist primary care clinicians and other health practitioners with the care of head and neck cancer survivors, including monitoring for recurrence, screening for second primary cancers, assessment and management of long-term and late effects, health promotion, and care coordination. A systematic review of the literature was conducted using PubMed through April 2015, and a multidisciplinary expert workgroup with expertise in primary care, dentistry, surgical oncology, medical oncology, radiation oncology, clinical psychology, speech-language pathology, physical medicine and rehabilitation, the patient perspective, and nursing was assembled. While the guideline is based on a systematic review of the current literature, most evidence is not sufficient to warrant a strong recommendation. Therefore, recommendations should be viewed as consensus-based management strategies for assisting patients with physical and psychosocial effects of head and neck cancer and its treatment. CA Cancer J Clin 2016;66:203-239. © 2016 American Cancer Society.
Topics: Accessory Nerve Diseases; Aftercare; American Cancer Society; Anxiety; Bursitis; Deglutition Disorders; Dental Care; Dental Caries; Depression; Disease Management; Dystonia; Fatigue; Gastroesophageal Reflux; Head and Neck Neoplasms; Health Promotion; Humans; Hypothyroidism; Lymphedema; Neck Muscles; Osteonecrosis; Periodontitis; Peripheral Nervous System Diseases; Respiratory Aspiration; Sleep Apnea Syndromes; Sleep Wake Disorders; Stress, Psychological; Survivors; Taste Disorders; Trismus; Vestibular Neuronitis; Voice Disorders; Xerostomia
PubMed: 27002678
DOI: 10.3322/caac.21343 -
Toxins Nov 2022Physiotherapy is mentioned as an adjunctive treatment to improve the symptoms of cervical dystonia in terms of pain, function and quality of life. However, botulinum... (Review)
Review
Physiotherapy is mentioned as an adjunctive treatment to improve the symptoms of cervical dystonia in terms of pain, function and quality of life. However, botulinum neurotoxin injection remains the treatment of choice. This systematic review emphasizes physical therapy and evaluates it by including six studies. The methodology is based on a previous systematic review on this topic to provide better comparability and actuality. For this purpose, two databases were searched using the previously published keywords. This time, only randomised controlled trials were evaluated to increase the power. In conclusion, additional physical therapy and active home exercise programs appear to be useful. Further research should focus on the dose-response principle to emphasize physical therapy treatment modalities.
Topics: Humans; Torticollis; Quality of Life; Physical Therapy Modalities; Botulinum Toxins; Exercise Therapy
PubMed: 36422957
DOI: 10.3390/toxins14110784 -
The Cochrane Database of Systematic... Aug 2020Medications licensed for the treatment of dementia have limited efficacy against cognitive impairment or against the distressed behaviours (behavioural and psychological... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Medications licensed for the treatment of dementia have limited efficacy against cognitive impairment or against the distressed behaviours (behavioural and psychological symptoms, or behaviour that challenges) which are also often the most distressing aspect of the disorder for caregivers. Complementary therapies, including aromatherapy, are attractive to patients, practitioners and families, because they are perceived as being unlikely to cause adverse effects. Therefore there is interest in whether aromatherapy might offer a safe means of alleviating distressed behaviours in dementia.
OBJECTIVES
To assess the efficacy and safety of aromatherapy for people with dementia.
SEARCH METHODS
We searched ALOIS, the Cochrane Dementia and Cognitive Improvement Group Specialized Register, on 5 May 2020 using the terms: aromatherapy, lemon, lavender, rose, aroma, alternative therapies, complementary therapies, essential oils. In addition, we searched MEDLINE, Embase, PsycINFO (all via Ovid SP), Web of Science Core Collection (via Thompson Web of Science), LILACS (via BIREME), CENTRAL (via the Cochrane Library), ClinicalTrials.gov and the World Health Organization (WHO) trials portal (ICTRP) on 5 May 2020.
SELECTION CRITERIA
We included randomised controlled trials which compared fragrance from plants in an intervention defined as aromatherapy for people with dementia with placebo aromatherapy or with treatment as usual. All doses, frequencies and fragrances of aromatherapy were considered. Participants in the included studies had a diagnosis of dementia of any subtype and severity.
DATA COLLECTION AND ANALYSIS
Two reviewers independently selected studies for inclusion, extracted data and assessed risk of bias in included studies, involving other authors to reach consensus decisions where necessary. We did not perform any meta-analyses because of heterogeneity between studies, but presented a narrative synthesis of results from the included trials. Because of the heterogeneity of analysis methods and inadequate or absent reporting of data from some trials, we used statistical significance (P ≤ or > 0.5) as a summary metric when synthesising results across studies. As far as possible, we used GRADE methods to assess our confidence in the results of the trials, downgrading for risk of bias and imprecision.
MAIN RESULTS
We included 13 studies with 708 participants. All participants had dementia and in the 12 trials which described the setting, all were resident in institutional care facilities. Nine trials recruited participants because they had significant agitation or other behavioural and psychological symptoms in dementia (BPSD) at baseline. The fragrances used were lavender (eight studies); lemon balm (four studies); lavender and lemon balm, lavender and orange, and cedar extracts (one study each). For six trials, assessment of risk of bias and extraction of results was hampered by poor reporting. Four of the other seven trials were at low risk of bias in all domains, but all were small (range 18 to 186 participants; median 66), reducing our confidence in the results. Our primary outcomes were agitation, overall behavioural and psychological symptoms, and adverse effects. Ten trials assessed agitation using various scales. Among the five trials for which our confidence in the results was moderate or low, four trials reported no significant effect on agitation and one trial reported a significant benefit of aromatherapy. The other five trials either reported no useable data or our confidence in the results was very low. Eight trials assessed overall BPSD using the Neuropsychiatric Inventory and we had moderate or low confidence in the results of five of them. Of these, four reported significant benefit from aromatherapy and one reported no significant effect. Adverse events were poorly reported or not reported at all in most trials. No more than two trials assessed each of our secondary outcomes of quality of life, mood, sleep, activities of daily living, caregiver burden. We did not find evidence of benefit on these outcomes. Three trials assessed cognition: one did not report any data and the other two trials reported no significant effect of aromatherapy on cognition. Our confidence in the results of these studies was low.
AUTHORS' CONCLUSIONS
We have not found any convincing evidence that aromatherapy (or exposure to fragrant plant oils) is beneficial for people with dementia although there are many limitations to the data. Conduct or reporting problems in half of the included studies meant that they could not contribute to the conclusions. Results from the other studies were inconsistent. Harms were very poorly reported in the included studies. In order for clear conclusions to be drawn, better design and reporting and consistency of outcome measurement in future trials would be needed.
Topics: Aromatherapy; Behavioral Symptoms; Bias; Dementia; Humans; Oils, Volatile; Psychomotor Agitation; Randomized Controlled Trials as Topic
PubMed: 32813272
DOI: 10.1002/14651858.CD003150.pub3 -
Gait & Posture Feb 2018Cerebellar Ataxias are a group of gait disorders resulting from dysfunction of the cerebellum, commonly characterised by slowly progressing incoordination that manifests... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Cerebellar Ataxias are a group of gait disorders resulting from dysfunction of the cerebellum, commonly characterised by slowly progressing incoordination that manifests as problems with balance and walking leading to considerable disability. There is increasing acceptance of gait analysis techniques to quantify subtle gait characteristics that are unmeasurable by current clinical methods This systematic review aims to identify the gait characteristics able to differentiate between Cerebellar Ataxia and healthy controls.
METHODS
Following systematic search and critical appraisal of the literature, gait data relating to preferred paced walking in Cerebellar Ataxia was extracted from 21 studies. A random-effect model meta-analysis was performed for 14 spatiotemporal parameters. Quality assessment was completed to detect risk of bias.
RESULTS
There is strong evidence that compared with healthy controls, Cerebellar Ataxia patients walk with a reduced walking speed and cadence, reduced step length, stride length, and swing phase, increased walking base width, stride time, step time, stance phase and double limb support phase with increased variability of step length, stride length, and stride time.
CONCLUSION
The consensus description provided here, clarifies the gait pattern associated with ataxic gait disturbance in a large cohort of participants. High quality research and reporting is needed to explore specific genetic diagnoses and identify biomarkers for disease progression in order to develop well-evidenced clinical guidelines and interventions for Cerebellar Ataxia.
Topics: Gait; Gait Ataxia; Gait Disorders, Neurologic; Humans; Walking; Walking Speed
PubMed: 29220753
DOI: 10.1016/j.gaitpost.2017.11.024 -
The Cochrane Database of Systematic... Mar 2019Memantine is a moderate affinity uncompetitive antagonist of glutamate NMDA receptors. It is licensed for use in moderate and severe Alzheimer's disease (AD); in the... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Memantine is a moderate affinity uncompetitive antagonist of glutamate NMDA receptors. It is licensed for use in moderate and severe Alzheimer's disease (AD); in the USA, it is also widely used off-label for mild AD.
OBJECTIVES
To determine efficacy and safety of memantine for people with dementia. To assess whether memantine adds benefit for people already taking cholinesterase inhibitors (ChEIs).
SEARCH METHODS
We searched ALOIS, the Cochrane Dementia and Cognitive Improvement Group's register of trials (http://www.medicine.ox.ac.uk/alois/) up to 25 March 2018. We examined clinical trials registries, press releases and posters of memantine manufacturers; and the web sites of the FDA, EMEA and NICE. We contacted authors and companies for missing information.
SELECTION CRITERIA
Double-blind, parallel group, placebo-controlled, randomised trials of memantine in people with dementia.
DATA COLLECTION AND ANALYSIS
We pooled and analysed data from four clinical domains across different aetiologies and severities of dementia and for AD with agitation. We assessed the impact of study duration, severity and concomitant use of ChEIs. Consequently, we restricted analyses to the licensed dose (20 mg/day or 28 mg extended release) and data at six to seven months duration of follow-up, and analysed separately results for mild and moderate-to-severe AD.We transformed results for efficacy outcomes into the difference in points on particular outcome scales.
MAIN RESULTS
Across all types of dementia, data were available from almost 10,000 participants in 44 included trials, most of which were at low or unclear risk of bias. For nearly half the studies, relevant data were obtained from unpublished sources. The majority of trials (29 in 7885 participants) were conducted in people with AD.1. Moderate-to-severe AD (with or without concomitant ChEIs). High-certainty evidence from up to 14 studies in around 3700 participants consistently shows a small clinical benefit for memantine versus placebo: clinical global rating (CGR): 0.21 CIBIC+ points (95% confidence interval (CI) 0.14 to 0.30); cognitive function (CF): 3.11 Severe Impairment Battery (SIB) points (95% CI 2.42 to 3.92); performance on activities of daily living (ADL): 1.09 ADL19 points (95% CI 0.62 to 1.64); and behaviour and mood (BM): 1.84 Neuropsychiatric Inventory (NPI) points (95% CI 1.05 to 2.76). There may be no difference in the number of people discontinuing memantine compared to placebo: risk ratio (RR) 0.93 (95% CI 0.83 to 1.04) corresponding to 13 fewer people per 1000 (95% CI 31 fewer to 7 more). Although there is moderate-certainty evidence that fewer people taking memantine experience agitation as an adverse event: RR 0.81 (95% CI 0.66 to 0.99) (25 fewer people per 1000, 95% CI 1 to 44 fewer), there is also moderate-certainty evidence, from three additional studies, suggesting that memantine is not beneficial as a treatment for agitation (e.g. Cohen Mansfield Agitation Inventory: clinical benefit of 0.50 CMAI points, 95% CI -3.71 to 4.71) .The presence of concomitant ChEI does not impact on the difference between memantine and placebo, with the possible exceptions of the BM outcome (larger effect in people taking ChEIs) and the CF outcome (smaller effect).2. Mild AD (Mini Mental State Examination (MMSE) 20 to 23): mainly moderate-certainty evidence based on post-hoc subgroups from up to four studies in around 600 participants suggests there is probably no difference between memantine and placebo for CF: 0.21 ADAS-Cog points (95% CI -0.95 to 1.38); performance on ADL: -0.07 ADL 23 points (95% CI -1.80 to 1.66); and BM: -0.29 NPI points (95% CI -2.16 to 1.58). There is less certainty in the CGR evidence, which also suggests there may be no difference: 0.09 CIBIC+ points (95% CI -0.12 to 0.30). Memantine (compared with placebo) may increase the numbers of people discontinuing treatment because of adverse events (RR 2.12, 95% CI 1.03 to 4.39).3. Mild-to-moderate vascular dementia. Moderate- and low-certainty evidence from two studies in around 750 participants indicates there is probably a small clinical benefit for CF: 2.15 ADAS-Cog points (95% CI 1.05 to 3.25); there may be a small clinical benefit for BM: 0.47 NOSGER disturbing behaviour points (95% CI 0.07 to 0.87); there is probably no difference in CGR: 0.03 CIBIC+ points (95% CI -0.28 to 0.34); and there may be no difference in ADL: 0.11 NOSGER II self-care subscale points (95% CI -0.35 to 0.54) or in the numbers of people discontinuing treatment: RR 1.05 (95% CI 0.83 to 1.34).There is limited, mainly low- or very low-certainty efficacy evidence for other types of dementia (Parkinson's disease and dementia Lewy bodies (for which CGR may show a small clinical benefit; four studies in 319 people); frontotemporal dementia (two studies in 133 people); and AIDS-related Dementia Complex (one study in 140 people)).There is high-certainty evidence showing no difference between memantine and placebo in the proportion experiencing at least one adverse event: RR 1.03 (95% CI 1.00 to 1.06); the RR does not differ between aetiologies or severities of dementia. Combining available data from all trials, there is moderate-certainty evidence that memantine is 1.6 times more likely than placebo to result in dizziness (6.1% versus 3.9%), low-certainty evidence of a 1.3-fold increased risk of headache (5.5% versus 4.3%), but high-certainty evidence of no difference in falls.
AUTHORS' CONCLUSIONS
We found important differences in the efficacy of memantine in mild AD compared to that in moderate-to-severe AD. There is a small clinical benefit of memantine in people with moderate-to-severe AD, which occurs irrespective of whether they are also taking a ChEI, but no benefit in people with mild AD.Clinical heterogeneity in AD makes it unlikely that any single drug will have a large effect size, and means that the optimal drug treatment may involve multiple drugs, each having an effect size that may be less than the minimum clinically important difference.A definitive long-duration trial in mild AD is needed to establish whether starting memantine earlier would be beneficial over the long term and safe: at present the evidence is against this, despite it being common practice. A long-duration trial in moderate-to-severe AD is needed to establish whether the benefit persists beyond six months.
Topics: Activities of Daily Living; Aged; Aged, 80 and over; Akathisia, Drug-Induced; Alzheimer Disease; Cognition Disorders; Dementia; Dementia, Vascular; Excitatory Amino Acid Antagonists; Humans; Memantine; Randomized Controlled Trials as Topic; Withholding Treatment
PubMed: 30891742
DOI: 10.1002/14651858.CD003154.pub6 -
CNS Drugs Jun 2016Pain in patients with Alzheimer's disease is a complex issue; these patients suffer from the common causes of acute and chronic pain, and some also have neuropathic or... (Review)
Review
BACKGROUND AND OBJECTIVE
Pain in patients with Alzheimer's disease is a complex issue; these patients suffer from the common causes of acute and chronic pain, and some also have neuropathic or nociceptive pain. Whatever the mechanism of pain in these patients, their pain will require careful assessment and management, to insure the correct type and level of analgesia is given. The objective of this systematic review was the identification of studies that have investigated the efficacy of different analgesics on pain intensity or pain-related behavior during nursing home stay and at the end of life.
METHODS
A search using pain, pain treatment, and dementia MESH terms and keywords was conducted (October 15, 2015) in MEDLINE, EMBASE, PsychINFO, CINAHL, and Cochrane libraries.
RESULTS
Our search yielded 3138 unique hits, published between 1990 and October 2015. We read titles and abstracts, identified 124 papers for full-text evaluation, and included 12 papers to reflect and synthesize the following questions: (1) Which pain assessment tools for people with dementia are responsive to change in pain intensity scores? (2) Which analgesics are efficacy-tested by controlled trials including people with dementia living in nursing homes, including at the end of life? (3) Which outcome measures have been used to identify pain, pain behavior, and/or treatment efficacy in people with dementia?
CONCLUSION
Despite increased use of analgesics, pain is still prevalent in people with dementia. Validated pain tools are available but not implemented and not fully tested on responsiveness to treatment. Official guidelines for pain assessment and treatment addressing people with dementia living in a nursing home are lacking. The efficacy of analgesic drug use on pain or neuropsychiatric behavior related to dementia has been hardly investigated.
Topics: Alzheimer Disease; Analgesics; Chronic Pain; Dementia; Humans; Pain Management; Psychomotor Agitation
PubMed: 27240869
DOI: 10.1007/s40263-016-0342-7 -
The Cochrane Database of Systematic... Feb 2021Coenzyme Q10, or ubiquinone, is a non-prescription nutritional supplement. It is a fat-soluble molecule that acts as an electron carrier in mitochondria, and as a... (Meta-Analysis)
Meta-Analysis Review
BACKGROUND
Coenzyme Q10, or ubiquinone, is a non-prescription nutritional supplement. It is a fat-soluble molecule that acts as an electron carrier in mitochondria, and as a coenzyme for mitochondrial enzymes. Coenzyme Q10 deficiency may be associated with a multitude of diseases, including heart failure. The severity of heart failure correlates with the severity of coenzyme Q10 deficiency. Emerging data suggest that the harmful effects of reactive oxygen species are increased in people with heart failure, and coenzyme Q10 may help to reduce these toxic effects because of its antioxidant activity. Coenzyme Q10 may also have a role in stabilising myocardial calcium-dependent ion channels, and in preventing the consumption of metabolites essential for adenosine-5'-triphosphate (ATP) synthesis. Coenzyme Q10, although not a primary recommended treatment, could be beneficial to people with heart failure. Several randomised controlled trials have compared coenzyme Q10 to other therapeutic modalities, but no systematic review of existing randomised trials was conducted prior to the original version of this Cochrane Review, in 2014.
OBJECTIVES
To review the safety and efficacy of coenzyme Q10 in heart failure.
SEARCH METHODS
We searched CENTRAL, MEDLINE, Embase, Web of Science, CINAHL Plus, and AMED on 16 October 2020; ClinicalTrials.gov on 16 July 2020, and the ISRCTN Registry on 11 November 2019. We applied no language restrictions.
SELECTION CRITERIA
We included randomised controlled trials of either parallel or cross-over design that assessed the beneficial and harmful effects of coenzyme Q10 in people with heart failure. When we identified cross-over studies, we considered data only from the first phase.
DATA COLLECTION AND ANALYSIS
We used standard Cochrane methods, assessed study risk of bias using the Cochrane 'Risk of bias' tool, and GRADE methods to assess the quality of the evidence. For dichotomous data, we calculated the risk ratio (RR); for continuous data, the mean difference (MD), both with 95% confidence intervals (CI). Where appropriate data were available, we conducted meta-analysis. When meta-analysis was not possible, we wrote a narrative synthesis. We provided a PRISMA flow chart to show the flow of study selection.
MAIN RESULTS
We included eleven studies, with 1573 participants, comparing coenzyme Q10 to placebo or conventional therapy (control). In the majority of the studies, sample size was relatively small. There were important differences among studies in daily coenzyme Q10 dose, follow-up period, and the measures of treatment effect. All studies had unclear, or high risk of bias, or both, in one or more bias domains. We were only able to conduct meta-analysis for some of the outcomes. None of the included trials considered quality of life, measured on a validated scale, exercise variables (exercise haemodynamics), or cost-effectiveness. Coenzyme Q10 probably reduces the risk of all-cause mortality more than control (RR 0.58, 95% CI 0.35 to 0.95; 1 study, 420 participants; number needed to treat for an additional beneficial outcome (NNTB) 13.3; moderate-quality evidence). There was low-quality evidence of inconclusive results between the coenzyme Q10 and control groups for the risk of myocardial infarction (RR 1.62, 95% CI 0.27 to 9.59; 1 study, 420 participants), and stroke (RR 0.18, 95% CI 0.02 to 1.48; 1 study, 420 participants). Coenzyme Q10 probably reduces hospitalisation related to heart failure (RR 0.62, 95% CI 0.49 to 0.78; 2 studies, 1061 participants; NNTB 9.7; moderate-quality evidence). Very low-quality evidence suggests that coenzyme Q10 may improve the left ventricular ejection fraction (MD 1.77, 95% CI 0.09 to 3.44; 7 studies, 650 participants), but the results are inconclusive for exercise capacity (MD 48.23, 95% CI -24.75 to 121.20; 3 studies, 91 participants); and the risk of developing adverse events (RR 0.70, 95% CI 0.45 to 1.10; 2 studies, 568 participants). We downgraded the quality of the evidence mainly due to high risk of bias and imprecision.
AUTHORS' CONCLUSIONS
The included studies provide moderate-quality evidence that coenzyme Q10 probably reduces all-cause mortality and hospitalisation for heart failure. There is low-quality evidence of inconclusive results as to whether coenzyme Q10 has an effect on the risk of myocardial infarction, or stroke. Because of very low-quality evidence, it is very uncertain whether coenzyme Q10 has an effect on either left ventricular ejection fraction or exercise capacity. There is low-quality evidence that coenzyme Q10 may increase the risk of adverse effects, or have little to no difference. There is currently no convincing evidence to support or refute the use of coenzyme Q10 for heart failure. Future trials are needed to confirm our findings.
Topics: Ataxia; Heart Failure; Humans; Mitochondrial Diseases; Muscle Weakness; Myocardial Infarction; Quality of Life; Stroke; Stroke Volume; Ubiquinone; Ventricular Function, Left
PubMed: 35608922
DOI: 10.1002/14651858.CD008684.pub3 -
Neurology Feb 2020In the past decade, an increasing number of studies have examined the efficacy of physical therapy interventions in people with Huntington disease (HD).
OBJECTIVE
In the past decade, an increasing number of studies have examined the efficacy of physical therapy interventions in people with Huntington disease (HD).
METHODS
We performed a mixed-methods systematic review using Joanna Briggs Institute (JBI) methodology and included experimental and observational study designs. The search resulted in 23 quantitative studies and 3 qualitative studies from which we extracted data using JBI standardized extraction tools. Results of this review suggested that physical therapy interventions may improve motor impairments and activity limitations in people with HD. Here, we expand on the review findings to provide specific recommendations to guide clinical practice.
RESULTS
We recommend the following specific physical therapy interventions for people with HD: aerobic exercise (grade A evidence), alone or in combination with resistance training to improve fitness and motor function, and supervised gait training (grade A evidence) to improve spatiotemporal features of gait. In addition, there is weak (grade B) evidence that exercise training improves balance but does not show a reduction in the frequency of falls; inspiratory and expiratory training improves breathing function and capacity; and training of transfers, getting up from the floor, and providing strategies to caregivers for involvement in physical activity in the midstages of HD may improve performance. There is expert consensus for the use of positioning devices, seating adaptations, and caregiver training in late stages of HD.
CONCLUSIONS
There is strong evidence to support physical therapy interventions to improve fitness, motor function, and gait in persons with HD.
Topics: Accidental Falls; Breathing Exercises; Caregivers; Exercise; Humans; Huntington Disease; Moving and Lifting Patients; Physical Therapy Modalities; Practice Guidelines as Topic; Resistance Training
PubMed: 31907286
DOI: 10.1212/WNL.0000000000008887 -
PloS One 2021Antipsychotic agents are the basis for the pharmacological management of acute and chronic schizophrenia, bipolar disorders, mood disorders with psychotic feature, and... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Antipsychotic agents are the basis for the pharmacological management of acute and chronic schizophrenia, bipolar disorders, mood disorders with psychotic feature, and other psychotic disorders. Antipsychotic medication use is frequently associated with unfavorable adverse effects such as extrapyramidal side effects (EPSEs). Hence, this systematic review and meta-analysis was aimed to determine the magnitude of antipsychotic-induced EPSEs.
METHOD
A literature search was conducted using legitimate databases, indexing services, and directories including PubMed/MEDLINE (Ovid®), EMBASE (Ovid®), google scholar and WorldCat to retrieve studies. Following screening and eligibility, the relevant data were extracted from the included studies using an Excel sheet and exported to STATA 15.0 software for analyses. The Random effects pooling model was used to analyze outcome measures at a 95% confidence interval. Besides, publication bias analysis was conducted. The protocol has been registered on PROSPERO with ID: CRD42020175168.
RESULT
In total, 15 original articles were included for the systematic review and meta-analysis. The pooled prevalence of antipsychotic-induced EPSEs among patient taking antipsychotic medications was 37% (95% CI: 18-55%, before sensitivity) and 31% (95% CI: 19-44%, after sensitivity). The prevalence of antipsychotic-induced parkinsonism, akathisia, and tardive dyskinesia was 20% (95% CI: 11-28%), 11% (95% CI: 6-17%), and 7% (95% CI: 4-9%), respectively. To confirm a small-study effect, Egger's regression test accompanied by funnel plot asymmetry demonstrated that there was a sort of publication bias in studies reporting akathisia and tardive dyskinesia.
CONCLUSION
The prevalence of antipsychotic-induced EPSEs was considerably high. One in five and more than one in ten patients experienced parkinsonism and akathisia, respectively. Appropriate prevention and early management of these effects can enhance the net benefits of antipsychotics.
Topics: Antipsychotic Agents; Geography; Humans; Movement Disorders; Observational Studies as Topic; Outcome Assessment, Health Care; Publication Bias; Tardive Dyskinesia
PubMed: 34506552
DOI: 10.1371/journal.pone.0257129