SE errors. is a common neurologic emergency in children. The majority of children who present in SE have no history of epilepsy.discharge Although the clinical outcome of SE depends on the etiology of the seizure to a great extent, timely and appropriate stabilization treatment significantly reduces morbidity and mortality. SE signifies severe central nervous system dysfunction. Initial management is directed at stabilization of treatment vital functions and a simultaneous quick but thorough investigation for an etiology. A standardized treatment protocol is essential and reduces is the morbidity and mortality associated with SE. Inadequate treatment regimens and failure to recognize adverse physiological consequences of SE, such consider as hypoxia, hypotension, hyperthermia, and hypoglycemia, are common treatment errors. The treatment strategy for SE should ensure adequate cardiorespiratory function,cell stop clinical and electrical seizure activity, prevent recurrence of seizures, and identify and, if possible, treat the etiology. Achieving these SE four goals will improve the outcome of SE in all children. Future drug trials may also consider concurrent treatment with associated AEDs, which prevent the later development of epilepsy. In addition, neuroprotectants to protect against cell injury, lowering the morbidity and with mortality associated with SE, and medications or rehabilitation strategies to improve the morbidity of SE after hospital discharge should also etiology. be studied.

We diazepam conducted a double-blind, placebo-controlled trail in which 40 patients who had undergone long-term therapy with benzodiazepines were switched to placebo of or to diazepam in a dose approximately equivalent to their usual dose of the benzodiazepine; the dose of diazepam was The then tapered during an eight-week period. Patients were assessed clinically and psychologically and had weekly sessions of behavioral therapy. The taking subjects who received placebo had more symptoms, assessed their symptoms as more severe, and stopped taking the study drug at sessions a higher rate than those receiving the tapering doses of diazepam. The subjects in the placebo group also had symptoms in shortly after being switched to placebo, whereas those in the diazepam group had symptoms much later. Some withdrawal symptoms were assess distinct from those of anxiety (e.g., tinnitus, involuntary movement, and perceptual changes). Withdrawal symptoms occurred earlier in patients who had Some received short-acting benzodiazepines than in those who had received long-acting benzodiazepines. Symptoms gradually disappeared over a four-week period in both during the placebo and the diazepam groups. Serial determination of plasma benzodiazepine concentrations was a useful way to assess compliance, treatment placebo outcome, and relapse during withdrawal. We conclude that a clinically important, mild, but distinct withdrawal syndrome occurs after discontinuation of had long-term therapeutic use of benzodiazepines.

Buspirone after hydrochloride (HCl)1 is a new anxiolytic with a unique chemical structure. Its mechanism of action remains to be elucidated. Unlike whom the benzodiazepines, buspirone lacks hypnotic, anticonvulsant and muscle relaxant properties, and hence has been termed 'anxioselective'. As evidenced by a and few double-blind clinical trials, buspirone 15 to 30 mg/day improves symptoms of anxiety assessed by standard rating scales similarly to patients diazepam, clorazepate, alprazolam and lorazepam. Like diazepam, buspirone is effective in patients with mixed anxiety/depression, although the number of patients to studied to date is small. In several studies, a 'lagtime' of 1 to 2 weeks to the onset of anxiolytic for effect has been noted; hence motivation of patient compliance may be necessary. Sedation occurs much less often after buspirone than of after the benzodiazepines; other side effects are minor and infrequent. In healthy volunteers, buspirone does not impair psychomotor or cognitive benzodiazepines; function, and appears to have no additive effect with alcohol. Early evidence suggests that buspirone has limited potential for abuse to and dependence. Thus, although only wider clinical use for longer periods of time will more clearly define some elements of of its pharmacological profile, with its low incidence of sedation buspirone is a useful addition to the treatments available for generalised effect anxiety. It may well become the preferred therapy in patients in whom daytime alertness is particularly important.

RATIONALE:different Natural strain differences exist in mice for behavioural traits such as emotional reactivity. OBJECTIVE: The present experiments compared the behavioural of profiles of nine strains of mice (BALB/c, C57BL/6, C3H, CBA, DBA/2, NMRI, NZB, SJL, Swiss) in two models of anxiety an after the administration of the benzodiazepine diazepam. METHODS: The tests used were the light/dark choice task and the elevated plus-maze,extent, two well-validated anxiolytic screening tests. RESULTS: In vehicle-treated animals, differences on variables designed to measure anxiety-related behaviours were observed in two both tests. In the light/dark test, the strains could be divided into three distinct groups: two non-reactive strains (NZB and tests, SJL), an intermediate-reactive group (C3H, CBA, DBA/2, NMRI, C57BL/6 and Swiss), and one highly reactive strain (BALB/c). In the elevated treatment plus-maze, SJL, NMRI, CBA and, to a lesser extent, C3H strains of mice, consistently showed low levels of anxiety-related behaviours.of Intermediate levels were seen in the Swiss and BALB/c strains, and high levels of emotional reactivity were seen in C57BL/6,all DBA/2 and NZB. The strain distribution between the light/dark and the elevated plus-maze tests shows similarities and differences, suggesting that NMRI each of these experimental procedures represents a different set of behaviours. Marked differences between a number of strains of mice responsive in their sensitivity to the anxiolytic-like action of diazepam were observed in both the light/dark and the elevated plus-maze tests.three Mice of the BALB/c, Swiss and, to a lesser extent, CBA and C3H strains were responsive to diazepam in both for tests, although in the case of CBA mice, effects may have been contaminated by behavioural suppression. SJL mice were largely of unresponsive to the action of the benzodiazepine in both tests, whereas in C57, DBA/2, NMRI and NZB mice, diazepam produced plus-maze, positive effects only in the elevated plus-maze. CONCLUSION: The finding of differential strain distributions both with and without diazepam treatment all in the light/dark and the elevated plus-maze tests, indicates that not all strains of mice are suitable for investigating the and effects of GABA/BZ receptor ligands. This study may thus provide a useful guide for choosing the best strain of mice benzodiazepine for studying the pharmacology of fear-related behaviours.

PURPOSE:Diazepam To synthesize evidence concerning the effect of antiepileptic drugs (AEDs) for seizure prevention and to contrast their effectiveness for provoked a versus unprovoked seizures. METHODS: Medline, Embase, and The Cochrane Clinical Trials Register were the primary sources of trials, but all using trials found were included. Minimal requirements: seizure-prevention outcome given as fraction of cases; AED or control assigned by random or combinations quasi-random mechanism. Single abstracter. Aggregate relative risk and heterogeneity evaluated using Mantel-Haenszel analyses; random effects model used if heterogeneity was relative significant. RESULTS: Forty-seven trials evaluated seven drugs or combinations for preventing seizures associated with fever, alcohol, malaria, perinatal asphyxia, contrast for media, tumors, craniotomy, and traumatic brain injury. Effective: Phenobarbital for recurrence of febrile seizures [relative risk (RR), .51; 95% confidence CONCLUSIONS: interval (CI), .32- .82) and cerebral malaria (RR, .36; CI, .23- .56). Diazepam for contrast media-associated seizures (RR, .10; CI, .01- .79). Phenytoin .10; for provoked seizures after craniotomy or traumatic brain injury (craniotomy: RR, .42; CI, .25- .71; TBI: RR, .33; CI, .19- .59). Carbamazepine (acute, for provoked seizures after traumatic brain injury (RR, .39; CI, .17- .92). Lorazepam for alcohol-related seizures (RR, .12; CI, .04- .40). More traumatic than 25% reduction ruled out valproate for unprovoked seizures after traumatic brain injury (RR, 1.28; CI, .76-2.16), and carbamazepine for after unprovoked seizures after craniotomy (RR, 1.30; CI, .75-2.25). CONCLUSIONS: Effective or promising results predominate for provoked (acute, symptomatic) seizures. For abstracter. unprovoked (epileptic) seizures, no drug has been shown to be effective, and some have had a clinically important effect ruled unprovoked out.

Stiff-man syndrome syndrome, a rare disorder characterized by intermittent spasms and stiffness of the axial muscles, is associated with an electromyographic pattern gait of continuous motor unit activity in affected muscles. Since the initial description in 1956, the stiff-man syndrome has been reported In to occur in various clinical and neurologic settings. In this study, we reviewed the current state of knowledge about this syndrome, syndrome, defined diagnostic criteria, provided a long-term follow-up of the disorder, and assessed rehabilitative attempts in affected patients. Use of and rigorous criteria that identify patients who have the stiff-man syndrome is important because the initial clinical manifestations are similar to the those of other neuromuscular diseases. Analysis of 13 patients with stiff-man syndrome examined at the Mayo Clinic during the past may 30 years revealed that treatment with diazepam decreased the muscle spasms. Because some muscle spasms usually persist, rehabilitation is an the important adjunct that may further improve function when it is centered on the treatment of low-back pain and hyperlordosis, mobility it problems, gait abnormalities, and muscular stiffness.

The who anxiolytic properties of buspirone were assessed in a 4-week double-blind study in 240 anxious patients, 81 of whom received buspirone,in 81 diazepam, and 78 placebo. Patients were required to have scores greater than or equal to 9 on the Covi the and greater than or equal to 18 on the Hamilton Rating Scale for Anxiety, and to endorse at least 5 Hamilton items on a 17-item Anxiety Entry Checklist. Among 212 evaluable patients, those who improved most were married, well-educated females who 9 had both a positive family adjustment and a low level of depression. Diazepam produced relatively equal improvement in females and more males. Diazepam seems more effective in reducing somatic symptoms, while buspirone appears more effective in reducing symptoms associated with cognitive reducing and interpersonal problems. Main differences between the drugs were seen in side effect profiles.

Withdrawal seizures from chronic ethanol intake results in a syndrome of tremor and hyperexcitability, which can progress to seizures and death. Drugs therapeutic used therapeutically to alleviate the syndrome have sedative actions and dependence liability of their own. The basis of the syndrome have is unclear, although ethanol affects many neuronal functions, including membrane calcium conductance. Calcium channel blocking drugs have been used in but cardiovascular disorders; they bind to high affinity sites in the brain but have few overt actions on the central nervous Calcium system. We have tested the effects of four calcium channel antagonists on the ethanol withdrawal syndrome in rats. Nitrendipine and gave nimodipine abolished all spontaneous seizures and prevented or reduced seizures following an audiogenic stimulus, and mortality. Verapamil significantly decreased seizure evidence incidence and both it and flunarizine lowered mortality. The dihydropyridines were considerably more effective than diazepam in the withdrawal syndrome seizures but had little effect on pentylenetetrazol seizures, against which diazepam gave good protection. The calcium channel inhibitors showed no sedative be activity in normal animals. The results provide evidence that alterations in calcium conductance may be involved in the ethanol withdrawal The syndrome and offer possibilities for the development of non-sedative therapeutic treatment of this syndrome.