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The abuse of benzodiazepines by pregnant women can cause intoxication in the neonate. Benzodiazepines can diffuse readily across the placenta to the fetus because of their high lipid solubility. After the sixth month of pregnancy, the loss of the cytotrophoblasts from the placenta further facilitates the transport of benzodiazepines across the placenta. They may persist for at least a week in pharmacologically active concentrations after administration of high dosages to the mother. We report about a floppy, drowsy and pulmonary impaired newborn delivered in the 36th week of gestation. The mother was a regular user of clorazepate, a long-acting benzodiazepine during pregnancy.

Acute benzodiazepine intoxication produces severe impairment of neurocognitive skills related to driving. It is less clear whether such impairments also occur in patients who use benzodiazepines chronically. The current review evaluated neurocognitive skills of long-term benzodiazepine users and addressed 2 major questions: do long-term users develop tolerance for the impairing effects of benzodiazepines on neurocognitive performance, and if so, does tolerance warrant a change in driver fitness classification systems that currently deem users of benzodiazepines unfit to drive? Neurocognitive impairments were reported in patients who on average used benzodiazepines for 5–15 years. In addition, sensitivity to acute benzodiazepine impairment decreased in long-term users, suggesting (partial) tolerance. Definitions of clinical relevance of neurocognitive impairments in long-term users and how these were affected by duration of benzodiazepine use were generally lacking. Also, sensitivity of neurocognitive tasks to drug effects and their validity to predict fitness to drive were generally unknown. Because of these limitations, no firm conclusion can be drawn regarding a re-classification of long-term benzodiazepine effects on driver fitness.

Background Recently the number of new psychoactive substances have significantly increased, becoming popular among experienced users of designer drugs. A significant group includes benzodiazepine derivatives, which have not been introduced as medications but are abused by people experimenting with new and classical psychoactive substances. Case presentation The aim of this paper was to present the case of a clonazolam ingestion by a person who was not habituated to benzodiazepines. The intake caused only prolonged coma, decreased muscle tone, and deep tendon reflexes without any other concomitant toxicity and cardio-respiratory failure. Conclusions Clonazolam concentrations in patient’s blood, measured three times were 0.077 mg/L, 0.015 mg/L, 0.009 mg/L after 4, 8 and 12 h, respectively. Clonazolam’s human toxicity has not been well established, so any case of poisoning should be closely monitored.

Stupor is a diagnostic challenge at emergency department. Differential diagnosis includes idiopathic recurrent stupor, formerly attributed to “endozepine-4” accumulation. This condition has been recently questioned because many suspected cases resulted in exogenous benzodiazepine intake that eludes the conventional toxicological assay. In case of unexplained recurrent stupor, to extend the benzodiazepine search in nonconventional matrices can allow unmasking of hidden toxic behavior.

Benzodiazepines have been one of the most commonly prescribed medications since their introduction in the 1960s. They have long eclipsed the use of barbiturates, primarily because of their improved safety profile. Continued controversy exists regarding what role the benzodiazepines should have in the treatment of anxiety disorders, and whether there is potential long-term risk with the development of dementia. In addition to the beneficial therapeutic effects, there are inherent risks with use, including abuse, dependence, intoxication, and withdrawal, which every clinician needs to be able to recognize and manage.

Summary The efficacy and safety of flumazenil were assessed in comparison to placebo in a double-blind randomised study of 31 adults intoxicated with benzodiazepines. The criteria of efficacy were the degree of sedation, and orientation in time and space. Patients who received flumazenil awoke within minutes but central depression returned partly one hour later, which reflects the short elimination half-life of the drug. Side effects were few and the results indicate that flumazenil is effective in the primary management of benzodiazepine overdose and in states where benzodiazepines have been taken with other drugs.

Naloxone (0.8–1.6 mg i.v.) effectively counteracted the clinical signs associated with benzodiazepine intoxication in 9 out of 10 emergency room patients. Naloxone (0.8–2.8 mg i.v.) also favorably influenced the state of consciousness in 9 out of 9 alcohol-intoxicated patients. In cases of acute narcotic overdose, the action of naloxone is almost immediate. Since a longer time was required for naloxone to counteract benzodiazepine or alcohol intoxication, the mechanism of action may be different from that implied in narcotic overdose. In the present cases, naloxone may have acted directly on the respiratory or consciousness centres of the brain.