The effect of nalorphine on eliciting symptoms of either alcohol or narcotic withdrawal was studied. Five male alcoholics were challenged with nalorphine and saline, both while sober and during alcohol ingestion. After nalorphine, pulse rate decreased in patients when sober, but increased when they were ingesting alcohol. Nalorphine administration resulted, during alcohol ingestion, but not in the sober state, in lacrimation, a symptom of narcotic withdrawal, in one patient, and in the following symptoms of alcohol or narcotic withdrawal in one or more patients: weakness, anorexia, insomnia, disorientation, and tremor. These findings suggest that morphine-like alkaloids play a role in the mediation of alcohol withdrawal symptoms.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.3109/10826087809045256 | DOI Listing |
PLoS One
January 2025
Dept. of Psychiatry, Harvard Medical School, McLean Hospital, Belmont, Massachusetts, United States of America.
Opioid dependence is defined by an aversive withdrawal syndrome upon drug cessation that can motivate continued drug-taking, development of opioid use disorder, and precipitate relapse. An understudied but common opioid withdrawal symptom is disrupted sleep, reported as both insomnia and daytime sleepiness. Despite the prevalence and severity of sleep disturbances during opioid withdrawal, there is a gap in our understanding of their interactions.
View Article and Find Full Text PDFHarm Reduct J
January 2025
Turning Point, Eastern Health, Richmond, VIC, Australia.
Background: People in justice settings experience higher rates of psychiatric morbidity, including alcohol and drug use disorders, compared with the general population. However, our understanding of opioid-related harms in justice settings is limited. This study used ambulance data to examine opioid-related harms and experiences of care in New South Wales (NSW), Australia, during periods of incarceration or detention.
View Article and Find Full Text PDFGenes Brain Behav
February 2025
Laboratory of Addiction Genetics, Department of Pharmaceutical Sciences and Center for Drug Discovery, Northeastern University, Boston, Massachusetts, USA.
Opioid use disorder is heritable, yet its genetic etiology is largely unknown. C57BL/6J and C57BL/6NJ mouse substrains exhibit phenotypic diversity in the context of limited genetic diversity which together can facilitate genetic discovery. Here, we found C57BL/6NJ mice were less sensitive to oxycodone (OXY)-induced locomotor activation versus C57BL/6J mice in a conditioned place preference paradigm.
View Article and Find Full Text PDFSheng Li Xue Bao
December 2024
State Key Laboratory of Medical Neurobiology, MOE Frontiers Center for Brain Science, Institutes of Brain Science, Fudan University, Shanghai 200032, China.
At present, the problem of drug addiction treatment mainly lies in the high relapse rate of drug addicts. Addictive drugs will bring users a strong sense of euphoria and promote drug seeking. Once the drug is withdrawn, there will be withdrawal symptoms such as strong negative emotions and uncomfortable physical reactions.
View Article and Find Full Text PDFEur J Neurosci
January 2025
Department of Psychology, University of Georgia, Athens, Georgia, USA.
Resting-state functional connectivity analyses have been used to examine synchrony in neural networks in substance use disorders (SUDs), with the default mode network (DMN) one of the most studied. Prior research has generally found less DMN synchrony during use and greater synchrony during cessation, although little research has utilized this method with opioid use. This study examined resting brain activity in treatment-seeking persons who use opioids at two points-when using opioids and when opioid-free-to determine whether the DMN exhibits different levels of connectivity during opioid use and cessation and whether differences in connectivity predict subsequent relapse.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!