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1 e, disease severity, apathy, and exposure to antimuscarinics.
2  [1.09-2.43]), and more frequent exposure to antimuscarinics (3.07 [1.35-6.97]) (logistic regression)
3 ting T-cell subsets, and characterization of antimuscarinic acetylcholine receptor type 3 autoantibod
4  safety of AD109, a combination of the novel antimuscarinic agent aroxybutynin and the norepinephrine
5  antinicotinic agent mecamylamine (MECA) and antimuscarinic agent scopolamine (SCOP) and were tested
6  movements are reduced significantly with an antimuscarinic agent used clinically, and we identify ch
7          In particular, the finding that the antimuscarinic agent, scopolamine, exerts fast-onset and
8 h an inhaled corticosteroid or a long-acting antimuscarinic agent.
9                  The addition of long-acting antimuscarinic agents (LAMA) can improve the management
10            Studies have included a number of antimuscarinic agents (tolterodine, oxybutynin, propiver
11 clusions: A combination of noradrenergic and antimuscarinic agents administered orally before bedtime
12          Recent evidence suggests that newer antimuscarinic agents are not only superior to placebo,
13                         The use of selective antimuscarinic agents in patients with moderate-to-sever
14  the further investigation of the utility of antimuscarinic agents in targeting WM microstructure as
15 symptoms may not respond to monotherapy with antimuscarinic agents or alpha-receptor antagonists.
16   Inhaled bronchodilators (beta-agonists and antimuscarinic agents) and inhaled corticosteroids are i
17 ls have received FDA approval; these are the antimuscarinic and anticholinergic/direct smooth muscle
18 emonstrated improvement in OSA with combined antimuscarinic and noradrenergic drugs.
19 ower urinary tract symptoms, combinations of antimuscarinics and alpha1-adrenoceptor blockers have pr
20 of these phenotypes to inhaled beta-agonist, antimuscarinic, and corticosteroid therapy.
21                     In patients resistant to antimuscarinics, botulinum toxin may be an alternative--
22 rbations compared with the single longacting antimuscarinic bronchodilator glycopyrronium, with conco
23 ine, a Food and Drug Administration-approved antimuscarinic compound that has been shown to enhance m
24 hesis, we orally administered clemastine, an antimuscarinic compound that has been shown to enhance o
25 active molecules, we identified a cluster of antimuscarinic compounds that enhance oligodendrocyte di
26 severity following the administration of the antimuscarinic drug scopolamine hydrobromide (4 microg/k
27           The long duration of action of the antimuscarinic drug tiotropium and its kinetic subtype s
28                                              Antimuscarinic drugs affect bladder sensory symptoms suc
29 mized controlled trials have shown that both antimuscarinic drugs and alpha1-adrenoceptor blockers ca
30                              As a variety of antimuscarinic drugs are approved for clinical use again
31                                        These antimuscarinic drugs prevented or reversed indices of pe
32                                              Antimuscarinic drugs remain the first-line treatment of
33                        Pretreatment with the antimuscarinic drugs scopolamine and atropine was able t
34 tes remyelination and summarizes alternative antimuscarinic drugs that could be leveraged to treat MS
35 ture review confirms the rationale for using antimuscarinic drugs, and that the currently used drugs
36 n and elaborate on a collection of promising antimuscarinic drugs, consolidating the knowledge needed
37  catheterisation, and storage dysfunction by antimuscarinic drugs.
38 tine may still be targeted using alternative antimuscarinic drugs.
39 s indicate that drugs with noradrenergic and antimuscarinic effects improve genioglossus muscle activ
40        A new generation of bladder-selective antimuscarinics has graduated through phase-III randomiz
41  review will provide an update on the use of antimuscarinics, in combination with an alpha-blocker, i
42       Inhibition of bladder contraction with antimuscarinics is a common approach to treat bladder hy
43 e than 2.5-fold higher in cases treated with antimuscarinic medication in the long term compared with
44 inary incontinence are commonly treated with antimuscarinic medications, but many discontinue therapy
45 ent regimen employed, approach to the use of antimuscarinic medications, follow-up protocols, and mea
46 ergistic bronchodilation over either inhaled antimuscarinic or beta2-agonist monotherapy.
47 rine reuptake inhibitor (atomoxetine) and an antimuscarinic (oxybutynin) on OSA severity (apnea-hypop
48   Across secondary nodes (k = 28, n = 1821), antimuscarinics (RR = 2.26, 95% C.I. = 1.91-2.68), benza
49 apid, robust antidepressant responses to the antimuscarinic scopolamine occurred in currently depress
50 optimizing dopaminergic therapy and avoiding antimuscarinics should be considered.
51                          Monotherapy with an antimuscarinic therapy alone in this patient group has p
52 py with an alpha-blocker, the addition of an antimuscarinic therapy is worth considering.
53 ty to sham treatment and benefits similar to antimuscarinic therapy may be observed.
54 provements can be achieved by addition of an antimuscarinic therapy to an alpha-blocker.
55 olume should be measured prior to commencing antimuscarinic therapy to rule out baseline retention su
56 nce is more homologous to antinicotinic than antimuscarinic toxins, but it lacks three almost invaria
57 I and III scores (r = -0.50; P < .01) and no antimuscarinic use (r = -0.21; P < .01).
58 younger ones with less severe disease and no antimuscarinic use.