Lorazepam is a benzodiazepine medication developed by DJ Richards. It went on the market in the United States in 1977. Lorazepam is commonly used as the sedative and anxiolytic of choice in the inpatient setting owing to its fast (1 to 3 minute) onset of action when administered intravenously.[1] Lorazepam is also one of the few sedative-hypnotics with a relatively clean side effect profile. Lorazepam is FDA approved for short-term (4 months) relief of anxiety symptoms related to anxiety disorders, anxiety-associated insomnia, anesthesia premedication in adults to relieve anxiety or to produce sedation/amnesia, and treatment of status epilepticus.[2] Off-label (non-FDA-approved) uses for Lorazepam include rapid tranquilization of the agitated patient, alcohol withdrawal delirium, alcohol withdrawal syndrome, insomnia, panic disorder, delirium, chemotherapy-associated anticipatory nausea and vomiting (adjunct or breakthrough), as well as psychogenic catatonia.[3]

Individuals with chronic health conditions persist in smoking despite the presence of smoking-related illness. The aim of this study was to examine whether chronic health conditions moderate response to reduced nicotine content cigarettes (0.4, 2.4, 5.2, 15.8 mg/g of tobacco). This is a secondary analysis of a controlled clinical laboratory study that examined the acute effects of cigarettes varying in nicotine content among individuals especially vulnerable to smoking and tobacco dependence. Participants in the present study were categorized as having 0, 1-2, or ≥3 smoking-related chronic health conditions (i.e., chronic condition severity, CCS). Repeated-measures analysis of variance was used to examine whether CCS moderated response to cigarettes across measures of addiction potential (i.e., concurrent choice testing between nicotine dose pairs, Cigarette Purchase Task (CPT) performance, positive subjective effects), tobacco withdrawal, cigarette craving, and smoking topography. No main effects of CCS or interactions of CCS and nicotine dose were observed for concurrent choice testing, positive subjective effects, tobacco withdrawal, or smoking topography. Main effects of CCS were noted on the CPT with greater CCS being associated with less persistent demand. There was an interaction of CCS and nicotine dose on Factor 1 of the Questionnaire on Smoking Urges with the effects of dose significant only among those with 1-2 chronic conditions. Overall, we see minimal evidence that chronic condition severity affects response to reduced nicotine content cigarettes. A policy that reduces the nicotine content of cigarettes to minimally addictive levels may benefit smokers already experiencing smoking-related chronic conditions.

: In this article, we describe a middle-aged woman with a history of addiction to opioid medications who eventually became dependent on kratom. Her kratom-related withdrawal symptoms responded to a trial of buprenorphine-naloxone. Subsequently, she was maintained on this medication.

Cessation from prolonged use of ∆9 -tetrahydrocannabinol (THC), the primary active compound responsible for the cannabimimetic effects of cannabis, results in a mild to moderate withdrawal syndrome in humans and laboratory animals. Whereas manipulations of the endogenous cannabinoid system (eg, cannabinoid receptors and endocannabinoid regulating enzymes) alter nicotine withdrawal, in this study we asked the reciprocal question. Do nicotinic acetylcholine receptors (nAChRs) modulate THC withdrawal? To assess the role of different nAChR subtypes in THC withdrawal, we used transgenic mouse, preclinical pharmacological, and human genetic correlation approaches. Our findings show that selective α3β4* nAChR antagonist, AuIB, and α3β4* nAChR partial agonist, AT-1001, dose-dependently attenuated somatic withdrawal signs in THC-dependent mice that were challenged with the cannabinoid-1 receptor antagonist rimonabant. Additionally, THC-dependent α5 and α6 nAChR knockout (KO) mice displayed decreased rimonabant precipitated somatic withdrawal signs compared with their wild-type counterparts. In contrast, β2 and α7 nAChR KO mice showed no alterations in THC withdrawal signs. Moreover, deletion of β2 nAChR did not alter the reduced expression of somatic signs by the preferred α6β4* antagonist, BulA [T5A;P60]. Finally, the human genetic association studies indicated that variations in the genes that code for the α5, α3, β4, and α6 nAChRs were associated with cannabis disorder phenotypes. Overall, these findings suggest that α3β4* and α6β4* nAChR subtypes represent viable targets for the development of medications to counteract THC dependence.

Orexin and its receptors were shown to be involved into mechanisms of pathological craving to alcohol. This paper demonstrates that the orexin receptor type 1 (OX1R) mRNA level significantly decreased in the prefrontal cortex of rats chronically (during 6 months) consuming ethanol compared with intact control. The same results were observed on day 1 and day 7 of alcohol withdrawal after chronic alcoholization. On the contrary, in the hippocampus, the OX1R mRNA level increased on day 1 and day 7 of alcohol withdrawal. In the ventral tegmental area, the OX1R mRNA level did not change on the day 1 and day 7 of alcohol withdrawal compared with the groups of chronic alcoholization and intact control. These findings point out involvement of the prefrontal cortex and hippocampus first of all in mechanisms mediating chronic alcohol intoxication. The ventral tegmental area is described as a typical dopaminergic structure providing the executive mechanism of emotion reactions connected with alcohol abuse in particular. It is possibe, that the modulating action of orexins on dopaminergic neurons in this structure does not provide a significant effect on control of emotion reactions in alcoholism.