Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “GABA Modulators”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,747 records · Page 97Linked to original sources

Clonidine differentially modulates the release of endogenous GABA in various rat brain areas.

The effects of clonidine on the release of endogenous gamma-aminobutyric acid (GABA) have been studied in superfused synaptosomes prepared from rat hypothalamus, nucleus tractus solitarii (NTS) and cerebellum. Clonidine enhanced in a concentration-dependent manner the basal release of GABA from hypothalamus and NTS synaptosomes. In contrast, the imidazoline did not affect the release of the amino acid from the cerebellar preparation. The alpha 2-adrenoceptor antagonist yohimbine prevented the releasing effect of clonidine, while the alpha 1-adrenoceptor antagonist prazosin was ineffective. The results show that the release of GABA from hypothalamus or NTS nerve endings can be enhanced by clonidine through the activation of adrenoceptors of the alpha 2 subtype. The GABAergic nerve terminals of cerebellum do not seem to possess presynaptic adrenoceptors by which clonidine can regulate the basal outflow of the amino acid. The results suggest that some of the clonidine effects may occur through activation of the GABA system.

Animals↗

Estimation of the binding affinity constants of soluble ligand-receptor complexes by a rapid filtration technique: [3H]-flunitrazepam-bovine serum albumin as an example.

A method for determining the equilibrium dissociation constant (KA) of a soluble ligand (L) from a soluble receptor (A) in the presence of another solid phase receptor (R) for the same ligand was developed. The total and nonspecific binding of L to R was measured in the presence and in the absence of A. The separation of bound and free L was done by a rapid filtration technique so that only the complex RL, but not AL, was recovered. An apparent dissociation constant (KR,app) was calculated from the saturation curve obtained in the presence of A. The magnitude of KA could be determined from this KR,app and the value of the equilibrium dissociation constant of the complex R-L (KR) calculated from the saturation curve in the absence of A. The equality of the Bmax values obtained in the presence and in the absence of A assured the accuracy in the determination of KA so that the fulfillment of this condition could be used as an internal control. For the correct definition of nonspecific binding, the displacement agent (L1) should be used at concentrations within the range 10(2).KR < L1 < 10. K4. This fact constraints the applicability of the method to systems where KA/KR > 10(3). The highest sensitivity of the method can be attained when 0.33 < [At]/KA < 3. The equilibrium binding constant of [3H]-flunitrazepam to non-delipidized bovine serum albumin determined by the present approach (31 +/- 7 mumol/L) did not differ significantly from the literature.

Binding Sites↗

[Use of diazepam in the treatment of opioid neonatal abstinence syndrome].

INTRODUCTION: The fetal opiate exposure presents many risks for the newborn. One of the most important is the neonatal abstinence syndrome that associates neurological and digestive signs. In some cases the vital prognosis can be involved. The evaluation of the syndrome's severity is based on certificated scales. The mortality has been reduced by the improved management of these neonates. Diamorphine, phenobarbital, chlorpromazine and diazepam are the most currently used. However, there is no consensus on the treatment. The data concerning the treatment are controversial, especially for the use of diazepam. The aim of our study was to describe the effects of diazepam obtained in three different centers and to compare our results to those of the literature. POPULATION AND METHODS: Twenty-three neonates were included. They were all hospitalized for abstinence syndrome and treated by diazepam. The Finnegan scale was used to evaluate the symptom's severity and the effects of the diazepam. The principal evaluation criteria were the duration of treatment and hospitalization, the timing in recovery of birth weight and the percentage of birth weight loss. RESULTS: The average treatment duration was 7 days, the average hospitalization duration was 18 days, the birth weight was recovered at 10 days of life and the percentage of loss of birth weight was 6.5%. Diazepam treatment failed in only one case. No case of intense dehydration occurred. CONCLUSION: Due to the retrospective design of the study, the diazepam could not be compared to other drugs. Nevertheless, it argues against the "anti-diazepam" attitude. A controlled randomised prospective study is needed to evaluated the optimal therapeutic strategy.

Adult↗

Episodic representations support early semantic learning: evidence from midazolam induced amnesia.

Current controversy exists regarding the role of episodic representations in the formation of long-term semantic memories. Using the drug midazolam to induce temporary amnesia we tested participants' memories for newly learned facts in a semantic cue condition or an episodic and semantic cue condition. Following midazolam administration, memory performance was superior in the episodic and semantic condition, suggesting early semantic learning is supported by episodic representations.

Adult↗

Differences in affective behaviors and hippocampal allopregnanolone levels in adult rats of lines selectively bred for infantile vocalizations.

Allopregnanolone, 3 alpha-hydroxy-5 alpha-pregnan-20-one (3 alpha,5 alpha-THP), a progesterone metabolite, is an endogenous neurosteroid mediating affective behaviors via its positive modulation of GABA(A) receptors. In order to better understand the role of this neurosteroid in individual differences in affective behavior, we used an animal model based on selective breeding for an infantile affective trait, ultrasonic vocalizations (USV). Adult male and female (in either proestrus or diestrus) rats that had been bred for low (low line) or high (high line) rates of USV after maternal separation were tested in a series of affective behavioral tests: open field, emergence, social interaction, defensive freezing, and the Porsolt forced swim task. Concentrations of allopregnanolone in combined hippocampus and amygdala tissue were then measured. low line subjects showed significantly lower anxiety and depression responses in the emergence, open field, and Porsolt forced swim tasks than did high line subjects. Proestrus females exhibited less affective behaviors than diestrus females or males. Allopregnanolone levels in hippocampus/amygdala were significantly higher in low line subjects compared to high line subjects, and in proestrus females compared to diestrus females and males. These data indicate that: (1) affective behaviors in lines selectively bred for an infantile anxiety trait exhibit selection persistence into adulthood; and (2) levels of allopregnanolone in the limbic system parallel selected disparities in affective behavior, suggesting a selection for alterations in the neurosteroid/GABA(A) receptor system in these lines.

Animals↗

Reversal of prenatal diazepam-induced deficit in a spatial-object learning task by brief, periodic maternal separation in adult rats.

In the rat, prenatal exposure to diazepam (DZ) induces a permanent reduction in GABA/BZ receptor (R) function and behavioural abnormalities. Environmental modifications during early stages of life can influence brain development and induce neurobiological and behavioural changes throughout adulthood. Indeed, a subtle, periodic, postnatal manipulation increases GABA/BZ R activity and produces facilitatory effects on neuroendocrine and behavioural responses. We here investigated the impact of prenatal treatment with DZ on learning performance in adult 3- and 8-month-old male rats and the influence of a brief, periodic maternal separation on the effects exerted by prenatal DZ exposure. Learning performance was examined employing a non-aversive spatial, visual and/or tactile task, the "Can test". Behavioural reactivity, emotional state and fear/anxiety-driven behaviour were also examined using open field (OF), acoustic startle reflex (ASR) and elevated plus-maze (EPM) tests. A single daily injection of DZ (1.5mg/kg, s.c.), over gestational days (GD) 14-20, induced, in an age-independent manner, a severe deficit in learning performance, a decrease in locomotor and explorative activity and an increase in peak amplitude in the ASR. Furthermore, anxiety-driven behaviour in EPM was disrupted. Daily maternal separation for 15 min over postnatal days 2-21 exerted opposite effects in all the paradigms examined. Prenatally DZ-exposed maternal separated rats, in contrast to respective non-separated rats, showed an improvement in learning performance, a decrease in emotionality and a normalization of the exploratory behaviour in EPM. These results suggest that a greater maternal care, induced by separation, can serve as a source for the developing brain to enhance neuronal plasticity and to prevent the behavioural abnormalities induced by prenatal DZ exposure.

Acoustic Stimulation↗

Different systems in the posterior hypothalamic nucleus of rats control theta frequency and trigger movement.

Reduced frequency of theta activity is thought to compromise hippocampal function and so behavioural inhibition. The anxiolytic benzodiazepine chlordiazepoxide (CDP) reduces theta frequency when injected into the medial supramammillary nucleus (mSuM), posterior hypothalamic nucleus (PH) and dorsomedial hypothalamic nucleus (DMH). These hypothalamic effects on theta could underlie at least some behavioural effects of benzodiazepines. We have previously shown that in a fixed interval 60-s schedule (FI60), CDP injected into mSuM reduced both theta frequency and behavioural inhibition. The present experiments test the effect of injections into PH and DMH on theta and hippocampal-sensitive behaviour (FI60 and open field ambulation). Systemic CDP (5mg/kg i.p.) released, but PH/CDP (20microg in 0.5microl vehicle) suppressed FI responding, though they both reduced FI theta frequency. In the open field, both CDP i.p. and PH/CDP reduced ambulation, but only the systemic injection reduced ambulation theta frequency. Taken together with previous research, these results support a role for PH in the control of voluntary behaviour. They imply that this function may be suppressed, independently of theta, by benzodiazepines. An anxiolytic effect of PH/CDP in FI60 may, therefore, have been masked by a concurrent action of CDP on the PH motor system. DMH/CDP did not affect behaviour or theta in either experiment, despite the fact that this nucleus is involved in benzodiazepine mediation of risk assessment and the flight response. This suggests that, like the control of theta frequency by the hypothalamus, the neural mechanisms underlying anxiety are distributed in complex networks.

Animals↗

Early behavioural enrichment in the form of handling renders mouse pups unresponsive to anxiolytic drugs and increases NGF levels in the hippocampus.

Early life experiences, such as early handling, can influence neural development of rodents leading to changes in physiological and behavioural reactivity to stress. These effects are likely to be mediated by changes in maternal behaviour. This study analyzed the effects of different manipulations of the rearing environment on maternal behaviour and the behavioural and physiological response to mild challenges in CD-1 mouse pups early during development. Litters underwent either 15 min of neonatal handling (H) or were exposed briefly to an unfamiliar male intruder from postnatal (PND) days 2 to 14 (MI). Both groups were compared with litters which were not manipulated (NH). Compared to NH subjects, licking behaviour in the MI group was increased only on the first day of introduction of the male intruder, while the H group showed an increase in maternal behaviour on PND 10. On PND 8, pups ultrasonic vocalizations were recorded upon treatment with an anxiolytic drug (chlordiazepoxide 0, 2, or 7.5mg/kg). Results indicate that, although there were no differences among the groups when mice were injected with vehicle, handled subjects did not reduce their calling rate following drug administration, in contrast to the NH and MI groups. Following maternal separation and novelty exposure on PND 9, levels of hippocampal NGF increased significantly only in the H group. These data suggest that active pup manipulations in the form of handling favour behavioural and neural plasticity resulting in the maintenance of a high level of arousal and in increased neurotrophin levels in response to an acute manipulation. Changes in hippocampal levels of NGF might be involved in the appraisal of subtle changes in the early social environment.

Age Factors↗

MK-801 prevents the increased NMDA-NR1 and NR2B subunits mRNA expression observed in the hippocampus of rats tolerant to diazepam.

The chronic diazepam administration in rats has been show from our previous results, to produce an increased synaptic plasticity. Furthermore, this occurs with a concomitant over expression of the mRNA NR1 and NR2B N-methyl-D-aspartate receptor subunits. MK-801, a non-competitive antagonist of N-methyl-D-aspartate receptor, impairs both the development of conditioned tolerance to diazepam and the hippocampal long-term potentiation generation. In the present study, we have further investigated the hippocampal glutamatergic transmission in the development of tolerance to diazepam. Our results demonstrate that the development of tolerance to the hypolocomotive effect of diazepam, along with the increased hippocampal synaptic plasticity and the associated over expression of the mRNA NR1 and NR2B N-methyl-D-aspartate receptor subunits, were blocked by previous MK-801 administration. We suggest that the participation of hippocampal glutamatergic transmission is relevant to increased hippocampal synaptic plasticity, the latter being a neurobiological mechanism behind the development of the conditioned tolerance to diazepam.

Analysis of Variance↗

Learning deficits induced by sleep deprivation and recovery are not associated with altered [(3)H]muscimol and [(3)H]flunitrazepam binding.

Several studies have shown that sleep deprivation produces deficits in learning tasks, but mechanisms underlying these effects remain unclear. Other lines of evidence indicate an involvement of brain GABA systems in cognitive processes. Here, we investigated the possibility that alterations in GABA(A) or benzodiazepine (BDZ) receptor binding might underlie avoidance deficits induced by sleep deprivation. Rats were deprived of sleep for 96 h using the platform method and then trained in a step-through inhibitory avoidance task, or allowed to recover sleep for 24 h before training (sleep rebound group). Thirty minutes after training, animals were given a retention test. Both sleep-deprived and sleep-recovered animals showed a significant impairment in avoidance responding compared to cage controls, and the sleep-deprived group performed significant worse than the sleep-recovered group. A separate group of animals was sacrificed either immediately after 96 h of sleep deprivation or after 96 h of sleep deprivation followed by 24 h of sleep recovery. [(3)H]muscimol and [(3)H]flunitrazepam binding were examined by quantitative autoradiography in 42 brain regions, including areas involved in cognitive processes. No significant differences among groups were found in any brain region, except for a reduction in [(3)H]flunitrazepam binding in the frontal cortex of sleep-recovered animals. These results confirm the deleterious effects of sleep loss on inhibitory avoidance learning, but suggest that such deficits cannot be attributed to altered GABA(A) or BDZ binding in brain.

Animals↗

Acute and chronic administration of clorazepate modifies the cell surface regulation of mu opioid receptors induced by buprenorphine in specific regions of the rat brain.

The aim of the present study was to investigate the acute and chronic effects of clorazepate (CRZ) alone or in combination with buprenorphine (BPN) on binding of the selective mu opiate tritiated ligand [3H]-DAMGO in the rat brain. Using 0.1 to 5 nM [3H]-DAMGO concentrations and a beta-imager, Bmax (maximal receptor density) and K(D) (the dissociation constant) were directly determined at different regions of interest (ROI) in the brains of rats treated with BPN and/or CRZ administered either once or over 21 consecutive days. Differences in Bmax and K(D) were related to both treatment and location. Acute BPN induced a down-regulation (62% mean decrease in Bmax observed on the whole brain) of mu opiate receptors. CRZ induced a mean 39% decrease in Bmax associated with substantially decreased affinity, particularly after acute administration (136% mean K(D) increase). Addition of CRZ to BPN [mean Bmax decreases of 34% (acute) and 29% (chronic)] induced significantly less down-regulation than did BPN alone, while altering affinity. These changes were maximal in the amygdaloid nucleus. Significant and persistent decreases in Bmax and affinity were also detected in the hippocampus, hypothalamus and thalamus. In the thalamus, an opposite regulation of Bmax was observed that was maximal with the combination. As the regions where changes were greatest have been specifically implicated in memory and socio-emotional functions and/or vegetative and endocrine adaptations, there is reason to suspect that the addition of CRZ to BPN may have clinical consequences. On the one hand, it may have some impact on drug abuse and misuse behaviors towards treatments including heroin substitute and BZD, and on the other, amplify the BPN effect-particularly hedonic or toxic-mainly after sporadic BPN-BZD abuses. These pharmacodynamic findings may explain, at least in part, the well-established preference of patients for the BPN-benzodiazepine combination and the toxicity with which it is associated.

Animals↗

Region-, age-, and sex-specific effects of fetal diazepam exposure on the postnatal development of neurosteroids.

Fetal exposure to diazepam (DZ), a positive modulator of GABA(A) receptors and an agonist at mitochondrial benzodiazine receptors, induces long-term neural and behavioral effects. This study evaluated whether the early manipulation influenced the normal development of brain levels of neurosteroids or altered steroid action at GABA(A) receptors. Pregnant dams were injected over gestation days 14 through 20 with DZ (2.5 mg/kg) or the vehicle. Male and female offspring were analyzed at five postnatal ages. The levels of progesterone (P), dihydroprogesterone (DHP), 3alpha-hydroxy-5alpha-pregnan-20-one (3alpha,5alpha-THP), testosterone (T), dihydrotestosterone, and 5alpha-androstan-3alpha,17beta diol were measured in the cerebral cortex and diencephalon. The results indicated that development of brain steroid levels and the impact of fetal DZ exposure were region- and sex-specific. Age-related changes in brain steroids did not mirror associated changes in circulating P and T. Age regulated the levels of all 3 progestins in the cerebral cortex, and fetal DZ exposure interacted with the development of P and DHP. The development of 3alpha,5alpha-THP in the cortex was markedly influenced by sex, with levels in males decreasing over postnatal development whereas they increased over postpubertal development in females. An adolescent surge in T levels was observed in male cortex and fetal DZ exposure prevented that surge. Steroid levels in the diencephalon were altered by age mainly in females, and DZ exposure had little effect in this region. The data support region-specific regulation of brain steroid synthesis. Only in the cerebral cortex are relevant mechanisms readily modifiable by fetal DZ exposure. However, neither sex nor fetal DZ exposure altered the response of GABA(A) receptors in adult cortex to neurosteroid.

Animals↗

Lorazepam and MK-801 effects on behavioral and electrographic indices of alcohol withdrawal sensitization.

Repeated cycles of chronic ethanol exposure and withdrawal result in sensitization of withdrawal-related CNS hyperexcitability that generally reflects an imbalance in activity of GABA and glutamate systems. Many pharmacological treatments for ethanol withdrawal target neuroadaptive changes in GABA and glutamate neurotransmission. The present study utilized a mouse model of repeated withdrawals to evaluate the ability of lorazepam and MK-801 treatments to antagonize behavioral and electroencephalographic (EEG) measures of sensitized withdrawal seizure activity. Adult male C3H/He mice received chronic intermittent ethanol vapor exposure in inhalation chambers (16 h/day) and during each withdrawal cycle, separate groups of mice were evaluated for handling-induced convulsions (HIC) or abnormal EEG (high-voltage "brief spindle episodes" (BSE)) activity. Lorazepam (0.5-1.0 mg/kg) or MK-801 (0.1-0.3 mg/kg) treatment at 1 h into each of three withdrawal cycles reduced behavioral (HIC) and electrographic (BSE) signs of seizure activity in a dose-related fashion compared to vehicle-treated mice. During a subsequent untreated withdrawal, mice previously treated with lorazepam or MK-801 for earlier withdrawals exhibited reduced HIC activity during the acute phase but exacerbated HIC activity during the protracted phase of this final (fourth) withdrawal cycle. Both lorazepam and MK-801 treatment conditions resulted in enhanced BSE activity during the entire fourth (untreated) withdrawal episode. Collectively, these results suggest that while treatment of repeated ethanol withdrawals with a benzodiazepine (lorazepam) or an NMDA receptor antagonist (MK-801) may have some initial benefits in ameliorating the development of sensitized withdrawal excitability, such treatment may also render subjects more vulnerable to seizure activity at later time points.

Animals↗

Clinical features of 35 patients with Parkinson's disease displaying REM behavior disorder.

OBJECTIVE: To assess and compare the disease severity, the treatment properties and the frequency of motor complications in the patients with Parkinson's disease (PD) having and not having REM sleep behavior disorder (RBD). PATIENTS AND METHODS: Based on chart review, patients with Parkinson's disease whose bed partners have reported prominent motor activity while dreaming were identified. Standard questionnaires assessing the presence of RBD have been addressed to these patients and their informants. Obtained data fulfilled clinical diagnostic criteria of probable RBD in 35 patients (RBD group) with the mean age at symptom onset was 61.8 years. Of them 77% were men. Clinical features of these patients concerning Hoehn-Yahr stage of PD, the severity of PD according to the Unified Parkinson's disease rating scale (UPDRS), the mean dose and duration of levodopa (LD) therapy, the presence of motor complications were compared with those of gender and age at PD-onset matched 35 PD patients without RBD (NRBD group). RESULTS: The mean values of PD duration, Hoehn-Yahr stage and UPDRS scores did not differ between groups. The duration of LD therapy was significantly longer in RBD group in comparison to NRBD group (6.2 years versus 3.05 years, respectively, P<0.005) and also mean actual dose of LD was higher (460.3 mg/day versus 320.3 mg/day respectively, P<0.02). The dose and duration of dopamine agonists did not differ between groups. In RBD group, wearing-off phenomenon was significantly common (P<0.01), its duration was longer (P<0.005), and LD-related dyskinesias were more frequent (P<0.01). CONCLUSION: In the current study, when compared with NRBD group, the patients with RBD required higher doses of LD treatment at an earlier stage of PD which eventually led to motor complications. In these patients, dopaminergic treatment restored UPDRS scores, but did not prevent the occurrence of RBD.

Age Factors↗

Age and gender effects on the pharmacokinetics and pharmacodynamics of triazolam, a cytochrome P450 3A substrate.

Sixty-one healthy men and women, aged 20 to 75 years, received single 0.25-mg doses of triazolam, a cytochrome P450 (CYP) 3A substrate benzodiazepine, and placebo in a double-blind crossover study. Among women, age had no significant effect on area under the triazolam plasma concentration curve (AUC) (Spearman r=0.14, P=.44) or clearance (r =-0.09, P=.62). Among men, AUC increased (r=0.43, P <.02) and clearance declined (r=-0.42, P <.02) with increasing age. Gender differences in triazolam kinetics were not apparent. Compared with placebo, triazolam impaired digit-symbol substitution test performance, increased observer-rated sedation, impaired delayed recall of information learned at 1.5 hours after dosing, and increased electroencephalographic beta amplitude. Among men, mean values of relative digit-symbol substitution test decrement (P <.002) and observer-rated sedation (P <.05) were significantly greater in elderly subjects compared with young subjects. Age-dependent differences among women reached significance for observer-rated sedation (P <.02). A combination of higher plasma levels and increased intrinsic sensitivity explained the greater pharmacodynamic effects of triazolam in elderly subjects. Although the findings are consistent with reduced clearance of triazolam in elderly men, individual variability was large and was not explained by identifiable demographic or environmental factors.

Adult↗

Use of microdosing to predict pharmacokinetics at the therapeutic dose: experience with 5 drugs.

OBJECTIVES: A volunteer trial was performed to compare the pharmacokinetics of 5 drugs--warfarin, ZK253 (Schering), diazepam, midazolam, and erythromycin--when administered at a microdose or pharmacologic dose. Each compound was chosen to represent a situation in which prediction of pharmacokinetics from either animal or in vitro studies (or both) was or is likely to be problematic. METHODS: In a crossover design volunteers received (1) 1 of the 5 compounds as a microdose labeled with radioactive carbon (carbon 14) (100 microg), (2) the corresponding (14)C-labeled therapeutic dose on a separate occasion, and (3) simultaneous administration of an intravenous (14)C-labeled microdose and an oral therapeutic dose for ZK253, midazolam, and erythromycin. Analysis of (14)C-labeled drugs in plasma was done by use of HPLC followed by accelerator mass spectrometry. Liquid chromatography-tandem mass spectrometry was used to measure plasma concentrations of ZK253, midazolam, and erythromycin at therapeutic concentrations, whereas HPLC-accelerator mass spectrometry was used to measure warfarin and diazepam concentrations. RESULTS: Good concordance between microdose and therapeutic dose pharmacokinetics was observed for diazepam (half-life [t((1/2))] of 45.1 hours, clearance [CL] of 1.38 L/h, and volume of distribution [V] of 90.1 L for 100 microg and t((1/2)) of 35.7 hours, CL of 1.3 L/h, and V of 123 L for 10 mg), midazolam (t((1/2)) of 4.87 hours, CL of 21.2 L/h, V of 145 L, and oral bioavailability [F] of 0.23 for 100 microg and t((1/2)) of 3.31 hours, CL of 20.4 L/h, V of 75 L, and F of 0.22 for 7.5 mg), and development compound ZK253 (F = <1% for both 100 microg and 50 mg). For warfarin, clearance was reasonably well predicted (0.17 L/h for 100 microg and 0.26 L/h for 5 mg), but the discrepancy observed in distribution (67 L for 100 microg and 17.9 L for 5 mg) was probably a result of high-affinity, low-capacity tissue binding. The oral microdose of erythromycin failed to provide detectable plasma levels as a result of possible acid lability in the stomach. Absolute bioavailability for the 3 compounds examined yielded excellent concordance with data from the literature or data generated in house. CONCLUSION: Overall, when used appropriately, microdosing offers the potential to aid in early drug candidate selection.

Administration, Oral↗

Cortical bases of speech perception: evidence from functional lesion studies.

Functional lesion studies have yielded new information about the cortical organization of speech perception in the human brain. We will review a number of recent findings, focusing on studies of speech perception that use the techniques of electrocortical mapping by cortical stimulation and hemispheric anesthetization by intracarotid amobarbital. Implications for recent developments in neuroimaging studies of speech perception will be discussed. This discussion will provide the framework for a developing model of the cortical circuitry critical for speech perception.

Amobarbital↗

Treatment options for status epilepticus.

Status epilepticus is a neurological emergency requiring prompt pharmacological intervention. Recent advances in the treatment of this condition include the introduction of treatment algorithms that are tailored more specifically to clinical situations, a trend towards more aggressive therapies if initial treatment with front-line agents fail, and a better understanding of the role of treatment for patients in status epilepticus in the out-of-hospital setting.

Adult↗