A comparison of the residual effects of zaleplon and zolpidem following administration 5 to 2 h before awakening

Danjou,; Paty,; Fruncillo,; Worthington,; Unruh,; Cevallos,; [], Martin

doi:10.1046/j.1365-2125.1999.00024.x

Cited by 106 publications

(74 citation statements)

References 27 publications

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“…[17][18][19][20] Zolpidem produces impairment of memory, motor, and cognitive functions. [21][22][23] Profound impairment of driving ability is present 4 hours after ingestion of both 10 and 20 mg doses, and lasts perhaps as long as 6 hours. [24][25][26][27] However, most studies of the effect of zolpidem on driving have examined the next day residual effect and have shown no impairment when conducted eight or nine hours after ingestion.…”

Section: Legal Case 4 April 2009mentioning

confidence: 99%

Zolpidem Ingestion, Automatisms, and Sleep Driving: A Clinical and Legal Case Series

Poceta

2011

Journal of Clinical Sleep Medicine

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study Objectives: To describe zolpidem-associated complex behaviors, including both daytime automatisms and sleeprelated parasomnias. Methods: A case series of eight clinical patients and six legal defendants is presented. Patients presented to the author after an episode of confusion, amnesia, or somnambulism. Legal defendants were being prosecuted for driving under the infl uence, and the author reviewed the cases as expert witness for the defense. Potential predisposing factors including comorbidities, social situation, physician instruction, concomitant medications, and patterns of medication management were considered. Results: Patients and defendants exhibited abnormal behavior characterized by poor motor control and confusion. Although remaining apparently interactive with the environment, all reported amnesia for 3 to 5 hours. In some cases, the episodes began during daytime wakefulness because of accidental or purposeful ingestion of the zolpidem and are considered automatisms. Other cases began after ingestion of zolpidem at the time of going to bed and are considered parasomnias. Risk factors for both wake and sleep-related automatic complex behaviors include the concomitant ingestion of other sedating drugs, a higher dose of zolpidem, a history of parasomnia, ingestion at times other than bedtime or when sleep is unlikely, poor management of pill bottles, and living alone. In addition, similar size and shape of two medications contributed to accidental ingestion in at least one case. Conclusions s C i e n T i F i C i n V e s T i g a T i O n sT he ingestion of zolpidem and other hypnotic sedative medications for the treatment of insomnia has been associated with sleepwalking and other complex behaviors including sleep eating and sleep driving.1-5 When ingested during the daytime, hypnotic sedatives impair cognition, memory, and motor performance. 6 There are also reports of a high frequency of blood levels of hypnotic sedatives in drivers apprehended for driving under the infl uence (DUI).7-9 An advisory letter was sent and change in package insert information occurred on March 14, 2007, alerting physicians and the public to the possibility of complex behaviors with all hypnotic sedatives.According to the prescribing information for Ambien and Ambien CR, zolpidem is an imidazopyridine chemical class agent available in the US since 1992. It is chemically unrelated to benzodiazepine and barbiturate hypnotic sedatives. Zolpidem in vitro binds the BZ1 receptor of the GABA(A) complex with high affi nity ratio for the alpha1/alpha5 subunits. Mean peak concentrations were 59 (range 29 to 113) after ingestion of the 5 mg tablet and 121 (range 58 to 272) after ingestion of the 10 mg tablet (ng/mL). Time to maximum concentration was 1.6 h for both doses (but 2.2 h if taken with food) with a half-life of approximately 2.6 h (range 1.4 to 4.5) The zolpidem extended release formulation 12.5 mg tablets produced a maximum concentration of 134 (69 to 197) at 1.5 hours. Co-administration with fl uoxetine increased ha...

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Section: Legal Case 4 April 2009mentioning

confidence: 99%

Zolpidem Ingestion, Automatisms, and Sleep Driving: A Clinical and Legal Case Series

Poceta

2011

Journal of Clinical Sleep Medicine

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“…Psychoactive drugs and caffeine tend to increase and sedatives tend to decrease CFF, as does exhaustive physical exercise. 28,31,[38][39][40][41] Also, antiepileptic drugs can affect CFF, 42 whereas infusion of branched chain amino acids has no effect. 43 Thus, medication has to be considered in the interpretation of CFF data.…”

Section: Kircheis Et Al Hepatology February 2002mentioning

confidence: 99%

Critical flicker frequency for quantification of low-grade hepatic encephalopathy

Kircheis¹,

Wettstein²,

et al. 2002

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Subclinical hepatic encephalopathy (SHE) is currently diagnosed by psychometric tests or neurophysiologic techniques. In view of its sociomedical relevance, simple and reproducible tests for routine diagnosis are required. This study evaluates critical flicker-frequency thresholds for quantification of low-grade hepatic encephalopathy. A total of 115 patients (92 with cirrhosis, 23 controls) were analyzed for HE severity (mental state, computerized psychometric tests), and the threshold frequencies at which light pulses are perceived as fused (fusion frequency) or flickering light (critical flicker frequency [CFF]). CFF was a highly reproducible parameter with little age, day-time, and training dependency. CFFs in cirrhotic patients without HE (HE 0) were not different from those found in noncirrhotic controls. Significantly lower CFFs were found in cirrhotic patients with subclinical or manifest HE, and the various HE groups separated from each other at a high level of significance (P < .01). By using a CFF cut-off value of 39 Hz, a 100% separation of patients with manifest HE from noncirrhotic controls and HE 0 cirrhotic patients was obtained. SHE patients separated from HE 0 cirrhotic patients with high sensitivity (55%) and specificity (100%). The HE severity-dependent differences were found in both, alcoholic and posthepatitic cirrhosis. Statistically significant correlations (P < .01) were found between CFFs and individual psychometric tests. Aggravation of preexisting HE after transjugular intrahepatic portosystemic stent shunt (TIPS) implantation was accompanied by a corresponding decrease of CFF, whereas improvement of HE increased CFF. In conclusion, CFF is a sensitive, simple, and reliable parameter for quantification of low-grade HE severity in cirrhotic patients and may be useful for the detection and monitoring of SHE. H epatic encephalopathy (HE) is a frequent complication of cirrhosis and its appearance indicates poor prognosis. 1-4 HE is usually classified into 4 stages according to the presence and severity of neuropsychiatric symptoms on clinical evaluation. 5 However, a significant proportion of cirrhotic patients, who appear normal on clinical examination, exhibit various quantifiable neuropsychologic deficits and this condition has been termed subclinical hepatic encephalopathy (SHE). 6-10 Whereas detection of overt HE (grade I-IV) is made clinically and does not provide a major diagnostic challenge, diagnosis of SHE is problematic. Psychometric and electrophysiologic tests are currently used for detection of SHE. In addition, proton-magnetic resonance spectroscopy of the brain may bear a not yet fully elaborated diagnostic potential, 11 but is unsuitable for clinical routine. Electrophysiologic tests such as visual-evoked, somatosensory-evoked, or brain stem auditory-evoked potentials suffer from methodologic problems, require sophisticated equipment and analysis, and exhibit a lower sensitivity than psychometric tests. 7,12-14 Psychometric bedside tests, such as the number-connection test...

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“…In addition, residual morning sedation has not been detected with either drug at these doses when administered at bedtime, 25,26 or with zaleplon 10 mg when administered as little as 4 h before wake time (middle-of-the-night dosing). 27,28 Normal subjects were studied to avoid potential influence of the inherent sleep disruption of insomnia patients.…”

Section: Introductionmentioning

confidence: 99%

The Effect of Two Benzodiazepine Receptor Agonist Hypnotics on Sleep-Dependent Memory Consolidation

Hall-Porter

Schweitzer

Eisenstein

et al. 2014

Journal of Clinical Sleep Medicine

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Results: ANOVA revealed a signifi cant condition effect for the WPT (p = 0.025) and a trend for the FTT (p = 0.067), which was signifi cant when sex was added to the model (p = 0.014). Improvement in memory performance following sleep was lower with bedtime dosing of zolpidem-ER compared to placebo and middle-of-the-night dosing of zaleplon. There were no differences between placebo and zaleplon. Conclusions:The results suggest that in some circumstances hypnotics may have the potential to reduce the degree of sleep-dependent memory consolidation and that drug-free sleep early in the night may ameliorate this effect. S C I E N T I F I C I N V E S T I G A T I O N SA growing body of evidence demonstrates that sleep promotes memory consolidation in healthy individuals.1-3 Numerous studies using various designs and memory tasks have consistently found that memory consolidation (i.e., improvement on a given memory task from initial training/test to retest) is significantly greater after a period of sleep than a period of wake. This is commonly referred to as sleep-dependent memory consolidation (SDMC). 4 For example, improvements on a procedural memory fi nger-tapping task were observed after a night of sleep but not after 4-, 8-, or 12-hour daytime periods without sleep. 5,6 Studies examining declarative memory consolidation, such as with a word pair association task, also demonstrate improvements in performance after sleep.7 In addition to improvements in memory following overnight sleep, memory consolidation is also enhanced during naps as short as 45 minutes. Improvements in procedural 8,9 and declarative 10 memory occur with naps, but not following similar durations of wakefulness. These fi ndings suggest that memory consolidation that occurs during wakefulness is enhanced during sleep.Synaptic plasticity, which refers to structural or functional neural changes in response to stimuli, 2 is thought to be the cellular substrate underlying the processes of memory formation and consolidation.11 Sleep has been found to enhance plasticity in animals, 12 which is consistent with the idea that sleep enhances memory consolidation. In humans, fMRI studies have shown that sleep-dependent learning of a motor skill task is accompanied by changes in multiple brain areas, BRIEF SUMMARYCurrent Knowledge/Study Rationale: Few studies have investigated the impact of hypnotic medication on sleep-dependent memory consolidation. This study compared the effect of differing time of exposure to two hypnotics on the sleep-dependent consolidation of declarative and non-declarative memory. Study Impact: This study contributes to the research surrounding sleep-dependent memory and hypnotics, indicating that hypnotic exposure during most of the night may reduce sleep-dependent memory consolidation; whereas hypnotic exposure only during the second half of the night appears to have no effect.

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A comparison of the residual effects of zaleplon and zolpidem following administration 5 to 2 h before awakening

Cited by 106 publications

References 27 publications

Zolpidem Ingestion, Automatisms, and Sleep Driving: A Clinical and Legal Case Series

Zolpidem Ingestion, Automatisms, and Sleep Driving: A Clinical and Legal Case Series

Critical flicker frequency for quantification of low-grade hepatic encephalopathy

The Effect of Two Benzodiazepine Receptor Agonist Hypnotics on Sleep-Dependent Memory Consolidation

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