Sedative

A sedative or tranquilliser[note 1] is a substance that induces sedation by reducing irritability[1] or excitement.[2] They are CNS depressants and interact with brain activity causing its deceleration. Various kinds of sedatives can be distinguished, but the majority of them affect the neurotransmitter gamma-aminobutyric acid (GABA), which are brain chemicals performing communication between brain cells. In spite of the fact that each sedative acts in its own way, they all produce beneficial relaxing effects by increasing GABA activity.[3]

Sedative
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Clinical data
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At higher doses, it may result in slurred speech, staggering gait, poor judgment, and slow, uncertain reflexes. Doses of sedatives such as benzodiazepines, when used as a hypnotic to induce sleep, tend to be higher than amounts used to relieve anxiety, whereas only low doses are needed to provide a peaceful effect.[4]

Sedatives can be misused to produce an overly-calming effect (alcohol being the classic and most common sedating drug). In the event of an overdose or if combined with another sedative, many of these drugs can cause deep unconsciousness (see hypnotic) and even death.

Terminology

There is some overlap between the terms "sedative" and "hypnotic".

Advances in pharmacology have permitted more specific targeting of receptors, and greater selectivity of agents, which necessitates greater precision when describing these agents and their effects:

The term "chemical cosh"

The term "chemical cosh" (a club) is sometimes used popularly for a strong sedative, particularly for:

Types of sedatives

Therapeutic use

Doctors often administer sedatives to patients in order to dull the patient's anxiety related to painful or anxiety-provoking procedures. Although sedatives do not relieve pain in themselves, they can be a useful adjunct to analgesics in preparing patients for surgery, and are commonly given to patients before they are anaesthetized, or before other highly uncomfortable and invasive procedures like cardiac catheterization, colonoscopy or MRI.

Risks

Sedative dependence

Some sedatives can cause psychological and physical dependence when taken regularly over a period of time, even at therapeutic doses.[6][7][8][9] Dependent users may get withdrawal symptoms ranging from restlessness and insomnia to convulsions and death. When users become psychologically dependent, they feel as if they need the drug to function, although physical dependence does not necessarily occur, particularly with a short course of use. In both types of dependences, finding and using the sedative becomes the focus in life. Both physical and psychological dependence can be treated with therapy.

Misuse
Main article: Drug overdose
Further information: Combined drug intoxication
See also: Benzodiazepine overdose and Barbiturate overdose

Many sedatives can be misused, but barbiturates and benzodiazepines are responsible for most of the problems with sedative use due to their widespread recreational or non-medical use. People who have difficulty dealing with stress, anxiety or sleeplessness may overuse or become dependent on sedatives. Some heroin users may take them either to supplement their drug or to substitute for it. Stimulant users may take sedatives to calm excessive jitteriness. Others take sedatives recreationally to relax and forget their worries. Barbiturate overdose is a factor in nearly one-third of all reported drug-related deaths. These include suicides and accidental drug poisonings. Accidental deaths sometimes occur when a drowsy, confused user repeats doses, or when sedatives are taken with alcohol.

A study from the United States found that in 2011, sedatives and hypnotics were a leading source of adverse drug events (ADEs) seen in the hospital setting: Approximately 2.8% of all ADEs present on admission and 4.4% of ADEs that originated during a hospital stay were caused by a sedative or hypnotic drug.[10] A second study noted that a total of 70,982 sedative exposures were reported to U.S. poison control centers in 1998, of which 2310 (3.2%) resulted in major toxicity and 89 (0.1%) resulted in death. About half of all the people admitted to emergency rooms in the U.S. as a result of nonmedical use of sedatives have a legitimate prescription for the drug, but have taken an excessive dose or combined it with alcohol or other drugs.[11]

There are also serious paradoxical reactions that may occur in conjunction with the use of sedatives that lead to unexpected results in some individuals. Malcolm Lader at the Institute of Psychiatry in London estimates the incidence of these adverse reactions at about 5%, even in short-term use of the drugs. The paradoxical reactions may consist of depression, with or without suicidal tendencies, phobias, aggressiveness, violent behavior and symptoms sometimes misdiagnosed as psychosis.[12]

Dangers of combining sedatives and alcohol

Sedatives and alcohol are sometimes combined recreationally or carelessly. Since alcohol is a strong depressant that slows brain function and depresses respiration, the two substances compound each other's actions and this combination can prove fatal.

Worsening of psychiatric symptoms

The long-term use of benzodiazepines may have a similar effect on the brain as alcohol, and are also implicated in depression, anxiety, posttraumatic stress disorder (PTSD), mania, psychosis, sleep disorders, sexual dysfunction, delirium, and neurocognitive disorders (including benzodiazepine-induced persisting dementia which persists even after the medications are stopped).[13] As with alcohol, the effects of benzodiazepine on neurochemistry, such as decreased levels of serotonin and norepinephrine, are believed to be responsible for their effects on mood and anxiety.[14][15][16][17][18][19] Additionally, benzodiazepines can indirectly cause or worsen other psychiatric symptoms (e.g., mood, anxiety, psychosis, irritability) by worsening sleep (i.e., benzodiazepine-induced sleep disorder). Like alcohol, benzodiazepines are commonly used to treat insomnia in the short-term (both prescribed and self-medicated), but worsen sleep in the long-term. While benzodiazepines can put people to sleep but, while asleep, the drugs disrupt sleep architecture: decreasing sleep time, delaying time to REM sleep, and decreasing deep slow-wave sleep (the most restorative part of sleep for both energy and mood).[20][21][22]

Dementia

Sedatives and hypnotics should be avoided in people with dementia, according to the medication appropriateness tool for co‐morbid health conditions in dementia criteria.[23] The use of these medications can further impede cognitive function for people with dementia, who are also more sensitive to side effects of medications.

Amnesia

Sedatives can sometimes leave the patient with long-term or short-term amnesia. Lorazepam is one such pharmacological agent that can cause anterograde amnesia. Intensive care unit patients who receive higher doses over longer periods, typically via IV drip, are more likely to experience such side effects. Additionally, the prolonged use of tranquilizers increases the risk of obsessive and compulsive disorder, where the person becomes unaware whether he has performed a scheduled activity or not, he may also repetitively perform tasks and still re-performs the same task trying to make-up for coutinous doubts. Remembering names that were earlier known becomes an issue such that the memory loss becomes apparent.

Disinhibition and crime

Sedatives — most commonly alcohol[24] but also GHB, Flunitrazepam (Rohypnol), and to a lesser extent, temazepam (Restoril), and midazolam (Versed)[25] — have been reported for their use as date rape drugs (also called a Mickey) and being administered to unsuspecting patrons in bars or guests at parties to reduce the intended victims' defenses. These drugs are also used for robbing people.

Statistical overviews suggest that the use of sedative-spiked drinks for robbing people is actually much more common than their use for rape.[26] Cases of criminals taking rohypnol themselves before they commit crimes have also been reported, as the loss of inhibitions from the drug may increase their confidence to commit the offence, and the amnesia produced by the drug makes it difficult for police to interrogate them if they are caught.

gollark: In threeish weeks.
gollark: Sadly, LyricLy removed all FUN roles a while ago.
gollark: Can this be weaponized?
gollark: Hmm, I just watched a video and I now dislike tumbleweed.
gollark: It's just `/kill`.

See also

Notes
  1. Also spelled tranquillizer (Oxford spelling) and tranquilizer (US spelling); see spelling differences

References
  1. "Johns Hopkins Colon Cancer Center - Glossary S".
  2. "sedative" at Dorland's Medical Dictionary
  3. "Sedatives | Psychology Today". Psychology Today. Retrieved 2017-11-20.
  4. Montenegro M, Veiga H, Deslandes A, Cagy M, McDowell K, Pompeu F, Piedade R, Ribeiro P (June 2005). "[Neuromodulatory effects of caffeine and bromazepam on visual event-related potential (P300): a comparative study]". Arquivos de Neuro-Psiquiatria. 63 (2B): 410–5. doi:10.1590/S0004-282X2005000300009. PMID 16059590.
  5. Smith, Rebecca (25 October 2010). "'Chemical cosh' will be cut for dementia sufferers". Telegraph.co.uk. Retrieved 12 September 2015.
  6. Yi PL, Tsai CH, Chen YC, Chang FC (March 2007). "Gamma-aminobutyric acid (GABA) receptor mediates suanzaorentang, a traditional Chinese herb remedy, -induced sleep alteration". Journal of Biomedical Science. 14 (2): 285–97. doi:10.1007/s11373-006-9137-z. PMID 17151826.
  7. Ebert B, Wafford KA, Deacon S (December 2006). "Treating insomnia: Current and investigational pharmacological approaches". Pharmacology & Therapeutics. 112 (3): 612–29. doi:10.1016/j.pharmthera.2005.04.014. PMID 16876255.
  8. Sarrecchia C, Sordillo P, Conte G, Rocchi G (1998). "[Barbiturate withdrawal syndrome: a case associated with the abuse of a headache medication]". Annali Italiani di Medicina Interna (in Italian). 13 (4): 237–9. PMID 10349206.
  9. Proudfoot H, Teesson M (October 2002). "Who seeks treatment for alcohol dependence? Findings from the Australian National Survey of Mental Health and Wellbeing". Social Psychiatry and Psychiatric Epidemiology. 37 (10): 451–6. doi:10.1007/s00127-002-0576-1. PMID 12242622.
  10. Weiss AJ, Elixhauser A. Origin of Adverse Drug Events in U.S. Hospitals, 2011. HCUP Statistical Brief #158. Agency for Healthcare Research and Quality, Rockville, MD. July 2013.
  11. Professor Jeffrey S Cooper (10 December 2007). "Toxicity, Sedatives". USA: eemedicine. Retrieved 18 December 2008.
  12. "benzo.org.uk - Benzodiazepines: Paradoxical Reactions and Long-Term Side-Effects". Retrieved 12 September 2015.
  13. American Psychiatric Association (2013). Diagnostic and statistical manual of mental disorders, fifth edition. Arlington, VA: American Psychiatric Association.
  14. Collier, Judith; Longmore, Murray (2003). "4". In Scally, Peter (ed.). Oxford Handbook of Clinical Specialties (6 ed.). Oxford University Press. p. 366. ISBN 978-0-19-852518-9.
  15. Professor Heather Ashton (2002). "Benzodiazepines: How They Work and How to Withdraw".
  16. Lydiard RB, Laraia MT, Ballenger JC, Howell EF (May 1987). "Emergence of depressive symptoms in patients receiving alprazolam for panic disorder". The American Journal of Psychiatry. 144 (5): 664–5. doi:10.1176/ajp.144.5.664. PMID 3578580.CS1 maint: ref=harv (link)
  17. Nathan RG, Robinson D, Cherek DR, Davison S, Sebastian S, Hack M (January 1985). "Long-term benzodiazepine use and depression". The American Journal of Psychiatry. American Journal of Psychiatry. 142 (1): 144–5. doi:10.1176/ajp.142.1.144-b. PMID 2857068.CS1 maint: ref=harv (link)
  18. Longo LP, Johnson B (April 2000). "Addiction: Part I. Benzodiazepines--side effects, abuse risk and alternatives". American Family Physician. 61 (7): 2121–8. PMID 10779253.
  19. Tasman A, Kay J, Lieberman JA (2008). Psychiatry, third edition. Chichester, England: John Wiley & Sons. pp. 2603–2615.
  20. Ashton H (May 2005). "The diagnosis and management of benzodiazepine dependence". Current Opinion in Psychiatry. 18 (3): 249–55. doi:10.1097/01.yco.0000165594.60434.84. PMID 16639148.
  21. Morin CM, Bélanger L, Bastien C, Vallières A (January 2005). "Long-term outcome after discontinuation of benzodiazepines for insomnia: a survival analysis of relapse". Behaviour Research and Therapy. 43 (1): 1–14. doi:10.1016/j.brat.2003.12.002. PMID 15531349.
  22. Poyares D, Guilleminault C, Ohayon MM, Tufik S (2004-06-01). "Chronic benzodiazepine usage and withdrawal in insomnia patients". Journal of Psychiatric Research. 38 (3): 327–34. doi:10.1016/j.jpsychires.2003.10.003. PMID 15003439.
  23. Page AT, Potter K, Clifford R, McLachlan AJ, Etherton-Beer C (October 2016). "Medication appropriateness tool for co-morbid health conditions in dementia: consensus recommendations from a multidisciplinary expert panel". Internal Medicine Journal. 46 (10): 1189–1197. doi:10.1111/imj.13215. PMC 5129475. PMID 27527376.
  24. Weir E (July 2001). "Drug-facilitated date rape". CMAJ. 165 (1): 80. PMC 81265. PMID 11468961.
  25. Negrusz A, Gaensslen RE (August 2003). "Analytical developments in toxicological investigation of drug-facilitated sexual assault". Analytical and Bioanalytical Chemistry. 376 (8): 1192–7. doi:10.1007/s00216-003-1896-z. PMID 12682705.
  26. Thompson, Tony (19 December 2004). "'Rape drug' used to rob thousands". The Observer. Retrieved 2008-05-08.

Further reading
  • Tone, Andrea. The Age of Anxiety: A History of America's Turbulent Affair with Tranquilizers (Basic Books, 2009) 288 pp.; ISBN 978-0-465-08658-0 excerpty and text search
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