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Medicine May 2019Sedation with etomidate or propofol alone during gastroscopy has many side effects. A systematic review and meta-analysis were conducted to evaluate the safety and... (Comparative Study)
Comparative Study Meta-Analysis
BACKGROUND
Sedation with etomidate or propofol alone during gastroscopy has many side effects. A systematic review and meta-analysis were conducted to evaluate the safety and efficacy of the combined use of propofol and etomidate for sedation during gastroscopy.
METHODS
PubMed, Embase, Medline (via Ovid SP), Cochrane library databases, CINAHL (via EBSCO), China Biology Medicine disc (CBMdisc), Wanfang, VIP, and China National Knowledge Infrastructure (CNKI) databases were systematically searched. We included randomized controlled trials (RCTs) comparing the combined use of propofol and etomidate vs etomidate or propofol alone for sedation during gastroscopy. Data were pooled using the random-effects models or fixed-effect model based on heterogeneity.
RESULTS
Fifteen studies with 2973 participants were included in the analysis. Compared to propofol alone, the combined use of propofol and etomidate possibly increased recovery time (SMD = 0.14, 95% CI = 0.04-0.24; P = .005), and the risk for myoclonus (OR = 3.07, 95% CI = 1.73-5.44; P < .001), injection pain, and nausea and vomiting. Furthermore, compared to propofol alone, the combination of propofol and etomidate produced an apparent beneficial effect for mean arterial pressure (MAP) after anesthesia (SMD = 1.32, 95% CI = 0.38-2.26; P = .006), SPO2 after anesthesia (SMD = 0.99, 95% CI = 0.43-1.55; P < .001), apnea or hypoxemia (OR = 0.16, 95% CI = 0.08-0.33; P < .001), injection pain, and body movement. Further, compared to etomidate alone, the combination of propofol and etomidate reduced the risk for myoclonus (OR = 0.15, 95% CI = 0.11-0.22; P < .001), body movement, and nausea and vomiting.
CONCLUSION
The combination of propofol and etomidate might increase recovery time vs that associated with propofol, but it had fewer side effects on circulation and respiration in patients undergoing gastroscopy. The combined use of propofol and etomidate can improve and produce an apparent beneficial effect on the adverse effects of propofol or etomidate alone, and it was safer and more effective than propofol or etomidate alone.
Topics: Anesthetics, Combined; Anesthetics, Intravenous; Arterial Pressure; China; Etomidate; Female; Gastroscopy; Humans; Hypoxia; Injection Site Reaction; Male; Myoclonus; Nausea; Propofol; Randomized Controlled Trials as Topic; Risk; Vomiting
PubMed: 31096522
DOI: 10.1097/MD.0000000000015712 -
Nature Reviews. Neurology Dec 2015Myoclonus is a hyperkinetic movement disorder characterized by brief, involuntary muscular jerks. Recognition of myoclonus and determination of the underlying aetiology... (Review)
Review
Myoclonus is a hyperkinetic movement disorder characterized by brief, involuntary muscular jerks. Recognition of myoclonus and determination of the underlying aetiology remains challenging given that both acquired and genetically determined disorders have varied manifestations. The diagnostic work-up in myoclonus is often time-consuming and costly, and a definitive diagnosis is reached in only a minority of patients. On the basis of a systematic literature review up to June 2015, we propose a novel diagnostic eight-step algorithm to help clinicians accurately, efficiently and cost-effectively diagnose myoclonus. The large number of genes implicated in myoclonus and the wide clinical variation of these genetic disorders emphasize the need for novel diagnostic techniques. Therefore, and for the first time, we incorporate next-generation sequencing (NGS) in a diagnostic algorithm for myoclonus. The initial step of the algorithm is to confirm whether the movement disorder phenotype is consistent with, myoclonus, and to define its anatomical subtype. The next steps are aimed at identification of both treatable acquired causes and those genetic causes of myoclonus that require a diagnostic approach other than NGS. Finally, other genetic diseases that could cause myoclonus can be investigated simultaneously by NGS techniques. To facilitate NGS diagnostics, we provide a comprehensive list of genes associated with myoclonus.
Topics: Algorithms; Diagnosis, Differential; Electrophysiology; High-Throughput Nucleotide Sequencing; Humans; Myoclonus; Nervous System; Neuroimaging
PubMed: 26553594
DOI: 10.1038/nrneurol.2015.198 -
Movement Disorders : Official Journal... Nov 2018Whipple's disease, affecting the CNS, can cause a wide variety of symptoms. Movement disorders are very prevalent, and some are pathognomonic of the disease. This... (Review)
Review
Whipple's disease, affecting the CNS, can cause a wide variety of symptoms. Movement disorders are very prevalent, and some are pathognomonic of the disease. This systematic review analyzed all published cases of movement disorders because of CNS Whipple's disease, providing detailed information on clinical and associated features. We have also attempted to address sources of confusion in the literature, particularly related to differing uses of the terminology of movement disorder. This comprehensive overview of Whipple's disease-induced movement disorders aims to aid neurologists in recognizing this very rare disorder and successfully reaching a laboratory-confirmed diagnosis in order to initiate appropriate therapy. © 2018 International Parkinson and Movement Disorder Society.
Topics: Databases, Bibliographic; Humans; Magnetic Resonance Imaging; Male; Middle Aged; Movement Disorders; Ocular Motility Disorders; Whipple Disease
PubMed: 30338868
DOI: 10.1002/mds.27419 -
Parkinsonism & Related Disorders Sep 2023The human immunodeficiency virus (HIV) causes movement disorders in persons living with HIV (PLH). (Review)
Review
BACKGROUND
The human immunodeficiency virus (HIV) causes movement disorders in persons living with HIV (PLH).
OBJECTIVES AND METHODS
We conducted a systematic review on the spectrum of movement disorders in PLH using standard terms for each of the phenomenologies and HIV.
RESULTS
Movement disorders in PLH were commonly attributed to opportunistic infections (OI), dopamine receptor blockade reactions, HIV-associated dementia (HAD), presented during seroconversion, developed due to drug reactions or antiretroviral therapy (ART) itself and lastly, movement disorders occurred as a consequence of the HIV-virus. Parkinsonism in ART naïve PLH was associated with shorter survival, however when Parkinsonism presented in PLH on ART, the syndrome was indistinguishable from Idiopathic Parkinson's disease and responded to therapy. Tremor was often postural due to HAD, drugs or OI. Generalized chorea was most frequent in HIV encephalopathy and toxoplasmosis gondii caused most cases of hemichorea. Ataxia was strongly associated with JCV infection, ART efavirenz toxicity or due to HIV itself. Dystonia was reported in HAD, secondary to drugs and atypical facial dystonias. Both cortical/subcortical and segmental/spinal origin myoclonus were noted mainly associated with HAD. In patients with HIV related opsoclonus-myoclonus-ataxia-syndrome, seroconversion illness was the commonest cause of followed by IRIS and CSF HIV viral escape phenomenon.
CONCLUSIONS
Aetiology of movement disorders in PLH depend on the treatment state. Untreated, PLH are prone to develop OI and HAD and movement disorders. However, as the number of PLH on ART increase and survive longer, the frequency of ART and non-AIDS related complications are likely to increase.
Topics: Humans; HIV; Myoclonus; Movement Disorders; HIV Infections; Parkinson Disease; Parkinsonian Disorders; Ataxia
PubMed: 37532621
DOI: 10.1016/j.parkreldis.2023.105774 -
Neuroscience and Biobehavioral Reviews Sep 2015The variant amyloid deposits (VAD) include cotton wool plaques and diffuse plaques, which are associated with various motor deficits (e.g. spastic paraparesis,... (Review)
Review
BACKGROUND
The variant amyloid deposits (VAD) include cotton wool plaques and diffuse plaques, which are associated with various motor deficits (e.g. spastic paraparesis, myoclonus, parkinsonism and ataxia). VADs have been repeatedly identified in presenilin 1 (PSEN1) mutations. It is still unknown the effect of VAD on the motor deficits as well as on the course of Alzheimer's disease (AD).
METHODS
We conducted a systematic review of the literature using MEDLINE, AD&FTDMDB and China National Knowledge Infrastructure database.
RESULTS
A total of 46 studies on 84 patients were included. We found that the odds ratio of the motor deficits in the VAD group (56 patients) was 4.231 times of the non-VAD group (28 patients). Moreover, VAD group displayed older age of onset (42.80±9.12 years) and longer duration (9.05±4.75 years) of the diseases.
CONCLUSIONS
These results suggested that the VADs might be associated with the increased occurrence of the motor deficits. Moreover, the VADs might act as a protective modifier of the disease course of AD.
Topics: Alzheimer Disease; Databases, Factual; Humans; Movement Disorders; Mutation; Plaque, Amyloid; Presenilin-1
PubMed: 26165445
DOI: 10.1016/j.neubiorev.2015.07.003 -
Journal of the Academy of... 2023The clinical spectrum of stiff-person syndrome (SPS) encompasses a wide range of signs including psychiatric symptoms (PS). (Review)
Review
BACKGROUND
The clinical spectrum of stiff-person syndrome (SPS) encompasses a wide range of signs including psychiatric symptoms (PS).
OBJECTIVE
Our objective was to provide an overview of the spectrum of PS in SPS through a systematic literature search and 2 illustrative case reports.
METHODS
We reported 2 anti-glutamic acid decarboxylase-positive SPS cases that presented with phobic disorder, and we performed a systematic review by following the 2020 Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines. Articles published in PubMed, MEDLINE on Ovid, Embase, and via a manual search before October 20, 2020, were selected by 2 independent reviewers. Original studies, case reports, editorials, commentaries, and letters to the editor reporting cases of SPS with PS were all included. Conference abstracts, reviews and book chapters, unavailable articles, and those not reporting SPS cases or PS were excluded. Quantitative summary data were calculated.
RESULTS
In addition to our 2 cases, we identified 237 cases of SPS with PS from 74 additional included publications totaling 239 patients. Anxiety (56%) and depression (45%) were the most common PS in SPS. Mean diagnostic delay was 4.7 years. Among the 3 SPS phenotypes, the classic form was predominant (77%), followed by stiff-limb syndrome (13%) and progressive encephalomyelitis with rigidity and myoclonus (10%). The most frequent etiology of SPS with PS was autoimmune (90%), followed by cryptogenic (7%) and paraneoplastic forms (7%). These patients were mainly treated with immune-mediated therapies and GABAergic drugs.
CONCLUSIONS
Our review revealed that the most common PS of SPS are anxiety and depression occurring mostly in autoimmune and classic forms, allowing a clearer understanding of this entity, which may lead to earlier diagnosis and better outcome.
Topics: Humans; Stiff-Person Syndrome; Delayed Diagnosis; Autoantibodies; Encephalomyelitis
PubMed: 35940576
DOI: 10.1016/j.jaclp.2022.07.005 -
Sleep Aug 2012A systematic literature review and meta-analyses (where appropriate) were performed to update the previous AASM practice parameters on the treatments, both dopaminergic... (Meta-Analysis)
Meta-Analysis Review
The treatment of restless legs syndrome and periodic limb movement disorder in adults--an update for 2012: practice parameters with an evidence-based systematic review and meta-analyses: an American Academy of Sleep Medicine Clinical Practice Guideline.
A systematic literature review and meta-analyses (where appropriate) were performed to update the previous AASM practice parameters on the treatments, both dopaminergic and other, of RLS and PLMD. A considerable amount of literature has been published since these previous reviews were performed, necessitating an update of the corresponding practice parameters. Therapies with a STANDARD level of recommendation include pramipexole and ropinirole. Therapies with a GUIDELINE level of recommendation include levodopa with dopa decarboxylase inhibitor, opioids, gabapentin enacarbil, and cabergoline (which has additional caveats for use). Therapies with an OPTION level of recommendation include carbamazepine, gabapentin, pregabalin, clonidine, and for patients with low ferritin levels, iron supplementation. The committee recommends a STANDARD AGAINST the use of pergolide because of the risks of heart valve damage. Therapies for RLS secondary to ESRD, neuropathy, and superficial venous insufficiency are discussed. Lastly, therapies for PLMD are reviewed. However, it should be mentioned that because PLMD therapy typically mimics RLS therapy, the primary focus of this review is therapy for idiopathic RLS.
Topics: Academies and Institutes; Benzothiazoles; Cabergoline; Carbamates; Dopamine Agents; Ergolines; Evidence-Based Medicine; Humans; Indoles; Levodopa; Nocturnal Myoclonus Syndrome; Pergolide; Peripheral Nervous System Diseases; Pramipexole; Restless Legs Syndrome; Sleep Medicine Specialty; United States; Venous Insufficiency; gamma-Aminobutyric Acid
PubMed: 22851801
DOI: 10.5665/sleep.1988 -
Orphanet Journal of Rare Diseases Aug 2021Lafora disease (LD) is a rare fatal autosomal recessive form of progressive myoclonus epilepsy. It affects previously healthy children or adolescents, causing... (Meta-Analysis)
Meta-Analysis
BACKGROUND
Lafora disease (LD) is a rare fatal autosomal recessive form of progressive myoclonus epilepsy. It affects previously healthy children or adolescents, causing pharmacoresistant epilepsy, myoclonus and severe psychomotor deterioration. This work aims to describe the clinical course of LD and identify predictors of outcome by means of a prognostic systematic review with individual participant data meta-analysis.
METHODS
A search was conducted on MEDLINE and Embase with no restrictions on publication date. Only studies reporting genetically confirmed LD cases were included. Kaplan-Meier estimate was used to assess probability of death and loss of autonomy. Univariable and multivariable Cox regression models with mixed effects (clustered survival data) were performed to evaluate prognostic factors.
RESULTS
Seventy-three papers describing 298 genetically confirmed LD cases were selected. Mean age at disease onset was 13.4 years (SD 3.7), with 9.1% aged ≥ 18 years. Overall survival rates in 272 cases were 93% [95% CI 89-96] at 5 years, 62% [95% CI 54-69] at 10 years and 57% [95% CI 49-65] at 15 years. Median survival time was 11 years. The probability of loss of autonomy in 110 cases was 45% [95% CI 36-55] at 5 years, 75% [95% CI 66-84] at 10 years, and 83% [95% CI 74-90] at 15 years. Median loss of autonomy time was 6 years. Asian origin and age at onset < 18 years emerged as negative prognostic factors, while type of mutated gene and symptoms at onset were not related to survival or disability.
CONCLUSIONS
This study documented that half of patients survived at least 11 years. The notion of actual survival rate and prognostic factors is crucial to design studies on the effectiveness of upcoming new disease-modifying therapies.
Topics: Adolescent; Child; Humans; Lafora Disease; Prognosis
PubMed: 34399803
DOI: 10.1186/s13023-021-01989-w -
The Journal of Neuropsychiatry and... 2021The relationship between idiopathic and inherited (monogenic) forms of isolated and combined dystonia and psychiatric disorders remains unclear. In the present review,...
OBJECTIVE
The relationship between idiopathic and inherited (monogenic) forms of isolated and combined dystonia and psychiatric disorders remains unclear. In the present review, the authors aimed to provide increased clarity on this association through a systematic review of all controlled quantitative studies using a structured or semi-structured psychiatric interview to diagnose psychiatric disorders in individuals with these conditions.
METHODS
Three databases were searched to identify 20 eligible studies, with a total of 1,275 participants fulfilling inclusion criteria. Eligible articles were quality appraised and divided into four sections (idiopathic forms of dystonia [N=11], early-onset torsion dystonia [N=2], gene mutation positive myoclonus dystonia; DYT-SGCE [N=6], and rapid-onset dystonia-parkinsonism [N=1]).
RESULTS
For each study, results were grouped into subcategories (overall psychiatric comorbidity, anxiety disorders, mood disorders, substance misuse, and other [personality disorder and cognitive impairment]). For idiopathic dystonia, higher rates of psychiatric comorbidity, including mood and anxiety disorders, were noted when cases were compared with both healthy control subjects and control groups with a medical comorbidity. However, for major depressive disorder and obsessive-compulsive disorder (OCD) specifically, no differences were seen between groups. Study subjects with DYT-SGCE appeared to be at higher risk of psychiatric comorbidity, major depressive disorder, OCD, and alcohol dependence than control populations.
CONCLUSIONS
Overall, the prevalence of psychiatric comorbidity appears to be increased in individuals with idiopathic and inherited (monogenic) forms of isolated and combined dystonia compared with control subjects. This finding is not consistent for all comparisons, and further research is required to understand the nature of these associations and the underlying causative etiologies.
Topics: Anxiety Disorders; Comorbidity; Dystonia; Humans; Mood Disorders; Mutation
PubMed: 34280321
DOI: 10.1176/appi.neuropsych.20110293 -
Movement Disorders : Official Journal... Jan 2022Complex parkinsonism is the commonest phenotype in late-onset PLA2G6-associated neurodegeneration.
BACKGROUND
Complex parkinsonism is the commonest phenotype in late-onset PLA2G6-associated neurodegeneration.
OBJECTIVES
The aim of this study was to deeply characterize phenogenotypically PLA2G6-related parkinsonism in the largest cohort ever reported.
METHODS
We report 14 new cases of PLA2G6-related parkinsonism and perform a systematic literature review.
RESULTS
PLA2G6-related parkinsonism shows a fairly distinct phenotype based on 86 cases from 68 pedigrees. Young onset (median age, 23.0 years) with parkinsonism/dystonia, gait/balance, and/or psychiatric/cognitive symptoms were common presenting features. Dystonia occurred in 69.4%, pyramidal signs in 77.2%, myoclonus in 65.2%, and cerebellar signs in 44.6% of cases. Early bladder overactivity was present in 71.9% of cases. Cognitive impairment affected 76.1% of cases and psychiatric features 87.1%, the latter being an isolated presenting feature in 20.1%. Parkinsonism was levodopa responsive but complicated by early, often severe dyskinesias. Five patients benefited from deep brain stimulation. Brain magnetic resonance imaging findings included cerebral (49.3%) and/or cerebellar (43.2%) atrophy, but mineralization was evident in only 28.1%. Presynaptic dopaminergic terminal imaging was abnormal in all where performed. Fifty-four PLA2G6 mutations have hitherto been associated with parkinsonism, including four new variants reported in this article. These are mainly nontruncating, which may explain the phenotypic heterogeneity of childhood- and late-onset PLA2G6-associated neurodegeneration. In five deceased patients, median disease duration was 13.0 years. Brain pathology in three cases showed mixed Lewy and tau pathology.
CONCLUSIONS
Biallelic PLA2G6 mutations cause early-onset parkinsonism associated with dystonia, pyramidal and cerebellar signs, myoclonus, and cognitive impairment. Early psychiatric manifestations and bladder overactivity are common. Cerebro/cerebellar atrophy are frequent magnetic resonance imaging features, whereas brain iron deposition is not. Early, severe dyskinesias are a tell-tale sign. © 2021 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
Topics: Age of Onset; Atrophy; Dystonia; Genotype; Group VI Phospholipases A2; Humans; Mutation; Parkinsonian Disorders; Pedigree; Phenotype
PubMed: 34622992
DOI: 10.1002/mds.28807