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1 -benzyl-2-acetamidoacetamides (2) are potent anticonvulsants.
2 tics, class I antiarrhythmic drugs, and some anticonvulsants.
3 ccupied by traditional local anesthetics and anticonvulsants.
4 nce seizure generation and responsiveness to anticonvulsants.
5 acting drugs, including antidepressants and anticonvulsants.
6 t spontaneous convulsions (>1 per hour) with anticonvulsants.
7 g-sensitive (BS) mutants as a tool to screen anticonvulsants.
8 by hypoxia can be refractory to conventional anticonvulsants.
9 logical conditions and is the target of some anticonvulsants.
10 Its pharmacology seems unaffected by anticonvulsants.
11 40 (5.6%) of 716 patients received anticonvulsants.
12 (p=0.26) was found among patients receiving anticonvulsants.
13 lopmental quotient (DQ) > 30 did not require anticonvulsants.
14 ng effects on block by local anesthetics and anticonvulsants.
17 to the hypothesis that lithium and antimanic anticonvulsants act by targeting parts of the "arachidon
19 i); and Bn, Et (7j)] are also very effective anticonvulsants against seizures induced by maximal elec
20 psychotropic classes (e.g., antidepressants, anticonvulsants), although they may be safer options.
21 ues in patients treated with enzyme-inducing anticonvulsants, although this did not reach statistical
24 ly important compounds, including diuretics, anticonvulsants and antidepressants, many of which have
25 ation suggest that concurrent treatment with anticonvulsants and dexamethasone enhances drug clearanc
26 er combinations appear to be the mixtures of anticonvulsants and lithium, particularly valproate plus
30 es occur frequently, are often refractory to anticonvulsants, and are associated with considerable mo
32 low-potency phenothiazines, lithium, certain anticonvulsants, and benzodiazepines may increase the re
33 mptomatic treatment with corticosteroids and anticonvulsants, and definitive therapy in the form of w
37 neurological symptoms, with gabapentin-type anticonvulsants, and is among the first in nonepileptic
40 r-bipolar subtype (N = 15) for whom lithium, anticonvulsants, and neuroleptics had been ineffective,
42 reatments include tricyclic antidepressants, anticonvulsants, and opioids, depending on the severity
43 Their therapeutic potential as anxiolytics, anticonvulsants, and sedative/hypnotics is limited by ra
44 utic drugs and supportive-care drugs-such as anticonvulsants, antiemetics, uric-acid-lowering compoun
45 esthetics, antiarrhythmics, antidepressants, anticonvulsants, antihistamines, antihypertensives, anti
46 17-3.81; P for trend < .001), whereas use of anticonvulsants, antipsychotics, or antidepressants was
47 ulate GABAA receptors have potential uses as anticonvulsants, anxiolytics, and sedative-hypnotic agen
53 s to specific treatments, including sedative anticonvulsants (barbiturates and benzodiazepines) and E
55 de: antidepressants, anti-adrenergic agents, anticonvulsants, benzodiazepines, atypical antipsychotic
56 dditional commonly used Na(+) channel-acting anticonvulsants, both in control and epileptic animals.
57 ies and other risk factors, among individual anticonvulsants compared with topiramate and secondarily
59 .80-3.42; P for trend < .001), as was use of anticonvulsants (definite CKD, 1-2 prescriptions: HR = 1
60 unds represent novel leads in the search for anticonvulsants devoid of sedative, ataxic, and amnestic
61 zyl-3-ethyl lactam 7j are the most effective anticonvulsants (ED50 = 46 and 42 mg/kg, respectively) a
62 d in patients receiving p450 enzyme-inducing anticonvulsants (EIACs) by 73%, 47%, and 50%, respective
63 aging or EEG), prophylactic antipyretics and anticonvulsants far outweigh their potential benefits.
64 sia and eclampsia; and short-term parenteral anticonvulsants for seizures associated with encephalopa
66 ll have surprisingly high in vivo potency as anticonvulsants in a mouse maximal electroshock-induced
67 ncy O-methylated analogue 18 are both potent anticonvulsants in a mouse maximal electroshock-induced
70 ge underlying precipitant causes, administer anticonvulsants in rapid succession until seizures have
71 ation, and for prophylactic antipyretics and anticonvulsants, in the majority of children with simple
73 the most teratogenic of commonly prescribed anticonvulsants, increasing the risk in humans of major
74 ds, acetaminophen, anti-inflammatory agents, anticonvulsants, ketamine, clonidine, mexiletine, antide
76 re antidepressants, atypical antipsychotics, anticonvulsants, lithium, and other medications used in
80 sed to assess the prognostic significance of anticonvulsants on event-free survival and risk of haema
81 ds for chronic noncancer pain, compared with anticonvulsants or cyclic antidepressants, was associate
82 for long-acting opioids or either analgesic anticonvulsants or low-dose cyclic antidepressants (cont
83 ) or were nonambulatory and either receiving anticonvulsants or not; all had developmental delays.
85 psychotics, combinations of antidepressants, anticonvulsants, or "other") for >/=60 consecutive days
86 , which was similar to that observed for the anticonvulsants phenytoin (slowly binds to the fast-inac
88 eceived treatment for 30 days or longer with anticonvulsants (phenytoin, phenobarbital, carbamazepine
91 ng at very high rates, suggesting that these anticonvulsants should cause impaired GABAergic inhibiti
92 TCAs (SMD, -0.78 [CrI, -1.24 to -0.33]), and anticonvulsants (SMD, -0.67 [CrI, -0.97 to -0.37]) were
93 epinephrine reuptake inhibitors (SNRIs) than anticonvulsants (standardized mean difference [SMD], -0.
94 ng-term relapse prevention; the evidence for anticonvulsants such as divalproex and lamotrigine is le
95 lectroencephalographic response to GABAergic anticonvulsants such as phenobarbital and benzodiazepine
97 CBZ) and oxcarbazepine (OXC) are widely used anticonvulsants that are extensively metabolized in the
98 activity in the cortex is not suppressed by anticonvulsants that block the transmission of seizure a
99 tribute to resistance of seizure activity to anticonvulsants that increase GABAergic function, and ma
103 des because of the increased availability of anticonvulsants, the ketogenic diet has re-emerged as a
104 yl-N'-(4-methoxynaphth-1-yl)guanidine (3) as anticonvulsants through blockade of sodium channels.
107 to treatment with tricyclic antidepressants, anticonvulsants (topiramate), coenzyme Q-10, and L-carni
108 differences in sex distribution or number of anticonvulsants used between patients with bruising/blee
109 , attempted suicides, and violent deaths for anticonvulsants used in at least 100 treatment episodes
111 reased rate of end-stage CKD, whereas use of anticonvulsants was (1-2 prescriptions, HR = 0 [95% CI,
113 rtication at age 8.5 years and withdrawal of anticonvulsants when he was more than 9 years old, Alex
114 nonketotic hyperglycinemia required multiple anticonvulsants, whereas patients with developmental quo
115 ribute an important component to binding for anticonvulsants, which compensates energetically for the
116 ical conditions, such as antidepressants and anticonvulsants, which were found empirically to be effe
117 compound was directed to identifying potent anticonvulsants with a long duration of action and a fav
118 tassium channels, we have docked these three anticonvulsants with residues identified by mutagenesis
119 mnolence and dizziness with TCAs, SNRIs, and anticonvulsants; xerostomia with TCAs; and peripheral ed
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