Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Sedatives and Hypnotics Drugs: Barbiturates01:20

Sedatives and Hypnotics Drugs: Barbiturates

Sedatives and hypnotics encompass a drug class that acts on the central nervous system (CNS) to alleviate anxiety, promote relaxation and induce sleep.These drugs function by amplifying the actions of the neurotransmitter γ-aminobutyric acid (GABA), resulting in reduced neuronal activity. Barbiturates, a subset of sedatives and hypnotics first synthesized in the late 1800s, are categorized into ultra-short, short, intermediate, and long-acting groups based on their duration of effect. A key...
CNS Depressants: Barbiturates and Benzodiazepines01:14

CNS Depressants: Barbiturates and Benzodiazepines

CNS depressants include drugs from the category of barbiturates and benzodiazepines. They are valuable medications for managing anxiety disorders and insomnia. Barbiturates, once used to induce and maintain sleep, have been replaced mainly by benzodiazepines due to barbiturate's toxicity, tolerance, and overdose risks. They interact with GABAA receptors, leading to sedation at low doses and potentially coma and death at higher doses. Phenobarbital, a long-acting barbiturate, possesses...
Traumatic Brain Injury l: Introduction01:28

Traumatic Brain Injury l: Introduction

DefinitionTraumatic brain injury, or TBI, is a disturbance of normal brain function induced by an external mechanical force, such as a direct blow to the head or a penetrating injury. It can affect both brain structure and function, producing a wide range of clinical outcomes. TBI is a heterogeneous condition, meaning its effects may differ based on the type, location, and severity of the injury.Basis of ClassificationTBI is classified based on severity, injury mechanism, or pathophysiology. In...
Parenteral Anesthetics: Overview01:24

Parenteral Anesthetics: Overview

Intravenous anesthetics are drugs administered parenterally to induce anesthesia or sedation. Propofol is a widely used agent formulated as a 1% emulsion in soybean oil, glycerol, and egg phosphatide. It induces rapid anesthesia primarily due to its rapid distribution from the bloodstream to target tissues and is metabolized in the liver. However, it can cause significant pain on injection and hypertriglyceridemia. Fospropofol, a water-based prodrug of propofol, lacks these adverse effects.
Antiepileptic Drugs: GABAergic Pathway Potentiators01:18

Antiepileptic Drugs: GABAergic Pathway Potentiators

γ-aminobutyric acid or GABA, plays a pivotal role as an inhibitory neurotransmitter in the brain. GABA pathway potentiators, also known as GABAergic drugs, are a class of pharmaceutical agents designed to enhance the functioning of the GABAergic system. These medications primarily treat epilepsy, a neurological disorder characterized by recurrent seizures.
The key GABA pathway potentiators used in epilepsy management are as follows.
Benzodiazepines are a well-known class of drugs used for their...
Sedatives and Hypnotics Drugs: Benzodiazepines01:19

Sedatives and Hypnotics Drugs: Benzodiazepines

Benzodiazepines have both sedative and hypnotic properties. They include compounds such as diazepam (Valium) and alprazolam (Xanax). Structurally, their cores are similar, consisting of the fusion of a benzene ring and a diazepine ring, but they share a common mechanism of action in the central nervous system (CNS).
Benzodiazepines work by enhancing the effects of the inhibitory neurotransmitter GABA. They bind to the GABAA receptor, increasing its affinity for GABA, which opens chloride...

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Heritable single-cell gene expression states shape functional variability in innate immune responses.

bioRxiv : the preprint server for biology·2026
Same author

Non-invasive assessment of coronary inflammation improves the diagnostic accuracy of coronary death in post-mortem CT angiography.

Journal of cardiovascular computed tomography·2026
Same author

TRACTION for Greater Surgical Use of Tranexamic Acid.

The New England journal of medicine·2026
Same author

Tranexamic acid for preventing severe bleeding in caesarean births.

BMJ (Clinical research ed.)·2026
Same author

Impact of a Research Integrity Assessment (RIA) of Randomized Controlled Trials Included in Interventional COVID-19 Systematic Reviews: A Meta-Epidemiological Study.

Cochrane evidence synthesis and methods·2026
Same author

Redefining Fibrinolytic Insufficiency in Sepsis-Associated DIC.

Seminars in thrombosis and hemostasis·2026

Related Experiment Video

Updated: May 16, 2026

Assessing Changes in Synaptic Plasticity Using an Awake Closed-Head Injury Model of Mild Traumatic Brain Injury
09:49

Assessing Changes in Synaptic Plasticity Using an Awake Closed-Head Injury Model of Mild Traumatic Brain Injury

Published on: January 20, 2023

Barbiturates for acute traumatic brain injury.

Ian Roberts1, Emma Sydenham

  • 1Cochrane Injuries Group, London School of Hygiene & Tropical Medicine, North Courtyard, KeppelStreet, London, WC1E 7HT, UK. Ian.Roberts@Lshtm.ac.uk.

The Cochrane Database of Systematic Reviews
|December 14, 2012
PubMed
Summary

Barbiturate therapy for severe traumatic brain injury does not improve survival or reduce disability. This treatment can cause hypotension in one in four patients, potentially worsening outcomes.

More Related Videos

Murine Model of Controlled Cortical Impact for the Induction of Traumatic Brain Injury
05:01

Murine Model of Controlled Cortical Impact for the Induction of Traumatic Brain Injury

Published on: August 16, 2019

Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury
10:33

Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury

Published on: August 14, 2019

Related Experiment Videos

Last Updated: May 16, 2026

Assessing Changes in Synaptic Plasticity Using an Awake Closed-Head Injury Model of Mild Traumatic Brain Injury
09:49

Assessing Changes in Synaptic Plasticity Using an Awake Closed-Head Injury Model of Mild Traumatic Brain Injury

Published on: January 20, 2023

Murine Model of Controlled Cortical Impact for the Induction of Traumatic Brain Injury
05:01

Murine Model of Controlled Cortical Impact for the Induction of Traumatic Brain Injury

Published on: August 16, 2019

Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury
10:33

Advanced Diffusion Imaging in The Hippocampus of Rats with Mild Traumatic Brain Injury

Published on: August 14, 2019

Area of Science:

  • Neuroscience
  • Critical Care Medicine
  • Pharmacology

Background:

  • Raised intracranial pressure (ICP) is a critical complication of severe brain injury, linked to high mortality.
  • Barbiturates are hypothesized to reduce ICP by suppressing cerebral metabolism and reducing cerebral blood volume.
  • However, barbiturates can also decrease blood pressure, potentially compromising cerebral perfusion pressure.

Purpose of the Study:

  • To evaluate the efficacy of barbiturates in reducing mortality, disability, and ICP in acute traumatic brain injury.
  • To quantify the incidence and severity of side effects associated with barbiturate use.

Main Methods:

  • A systematic review of randomized controlled trials (RCTs) was conducted.
  • Searches were performed across multiple electronic databases up to September 2012.
  • Data from seven trials involving 341 patients were analyzed for outcomes and adverse events.

Main Results:

  • Barbiturate use did not significantly alter mortality (RR 1.09) or death/disability (RR 1.15) compared to no barbiturate.
  • While ICP was reduced in some trials, barbiturate therapy significantly increased the occurrence of hypotension (RR 1.80), affecting one in four patients.
  • Comparisons with mannitol and thiopental showed no survival benefit, with pentobarbital being less effective than mannitol for ICP control.

Conclusions:

  • Current evidence does not support the use of barbiturates for improving outcomes in acute severe head injury.
  • The significant risk of hypotension associated with barbiturate therapy may counteract any potential benefits on ICP by impairing cerebral perfusion pressure.