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1 olinergic receptors in the bladder (known as anticholinergics).
2 ntipsychotics, sedative-hypnotics, or strong anticholinergics).
3 tilation, and receipt of benzodiazepines and anticholinergics.
4 ojections, as produced by septal infusion of anticholinergics.
5 nd treatment centred on early institution of anticholinergics.
6  clinical trials on cognition with other OAB anticholinergics.
7 mpared with $9.78 (95% CI, $9.16-$10.42) for anticholinergics.
8 nasal decongestant, saline douches and nasal anticholinergics.
9 rected] of the patients treated with inhaled anticholinergics (2.1%) and 108 [corrected] of the contr
10 atients (1.9%) [corrected] receiving inhaled anticholinergics and 83 of 6661 [corrected] patients (1.
11 s between short-term cognitive safety of OAB anticholinergics and the long-term increased dementia ri
12 vention types included behavioral therapies, anticholinergics, and neuromodulation.
13 ee classes of bronchodilators-beta agonists, anticholinergics, and theophylline-are available and can
14                                      Inhaled anticholinergics are associated with a significantly inc
15    These studies provided good evidence that anticholinergics are effective at improving both urodyna
16  consists of medical therapy, primarily with anticholinergics as well as behavioral therapy to modify
17 response to botulinum toxin is not adequate, anticholinergics, benzodiazepines, baclofen and other me
18 dase type B inhibitors [MAOBIs], amantadine, anticholinergics, beta-blockers, or dopamine agonists) m
19               Current COPD therapy involving anticholinergics, beta2-adrenoceptor agonists and/or cor
20 s and medications including corticosteroids, anticholinergics, certain antidepressants, and topiramat
21 rent autonomic failure; dramatic response to anticholinergics; early or atypical L-dopa-induced dyski
22 veractive bladder detrusor muscle, including anticholinergics (eg, trospium) and beta3 agonists (eg,
23  evidence on the effectiveness and safety of anticholinergics for male lower urinary tract symptoms.
24 esting in children; enuresis topics included anticholinergics for treating monosyptomatic enuresis re
25                                              Anticholinergics have been associated with functional de
26 nts, antidepressants, fiber, probiotics, and anticholinergics have not been adequately studied.
27 tistically significantly more effective than anticholinergics in achieving cure or improvement (high
28        Safety data from larger studies using anticholinergics in patients with overactive bladders su
29 etylcholinesterase inhibitors and muscarinic anticholinergics in these patients.
30 nd new or broadened indications for existing anticholinergics, in treating the overactive bladder in
31 QSAR) study is presented for quaternary soft anticholinergics including two distinctly different clas
32                                      Inhaled anticholinergics (ipratropium bromide or tiotropium brom
33 ose with detrusor overactivity refractory to anticholinergics, is, however, evidenced increasingly.
34 lly evaluation of various inhaled therapies (anticholinergics, long-acting beta-agonists, and cortico
35 ation inhaled therapies (long-acting inhaled anticholinergics, long-acting inhaled beta-agonists, or
36 antihistamines, metoclopramide, domperidone, anticholinergics, loop diuretics, urologics, and ophthal
37 acting anticholinergics (n = 7), long-acting anticholinergics (n = 10), long-acting beta2-agonists (n
38 CTs examined inhaled therapies: short-acting anticholinergics (n = 7), long-acting anticholinergics (
39 pain control, minimizing benzodiazepines and anticholinergics, normalizing the sleep-wake cycle, prov
40 tention, because of the inhibitory effect of anticholinergics on bladder contraction in the presence
41                                   Given that anticholinergics only decrease mucus production, it is u
42   Pharmacologic interventions include use of anticholinergics or antipsychotic medications for dement
43 monotherapy using either long-acting inhaled anticholinergics or long-acting inhaled beta-agonists fo
44 ulation, high-risk ingestion, coingestion of anticholinergics or opioids, age younger than 6 years, p
45 g inhaled beta-agonists, long-acting inhaled anticholinergics, or inhaled corticosteroids.
46                    However, trials involving anticholinergics other than oxybutynin have not shown su
47 T3 receptor antagonists, antihistamines, and anticholinergics reduce the incidence of PONV, whereas m
48                                              Anticholinergics remain the first line in pharmacotherap
49                                         Yet, anticholinergics remain the predominant OAB medication p
50 components of the primary end point, inhaled anticholinergics significantly increased the risk of MI
51                                      Inhaled anticholinergics such as ipratropium bromide (IB), when
52  therapy with inhaled beta-agonists, inhaled anticholinergics, systemic corticosteroids, and intraven
53 ), phosphodiesterase inhibitors (tadalafil), anticholinergics (trospium), and beta3 agonists (mirabeg
54 MI, or stroke (2.9% of patients treated with anticholinergics vs 1.8% of the control patients; RR, 1.