|Systematic (IUPAC) name|
|Licence data||US FDA:|
|IV, IM, Insufflated, oral, topical|
|Metabolism||Hepatic, primarily by CYP3A4|
|Biological half-life||2.5–3 hours|
|CAS Registry Number|
|Molecular mass||237.725 g/mol|
|Melting point||262 °C (504 °F)|
|(what is this?)|
Ketamine (INN) is a medication used mainly for starting and maintaining anesthesia. Other uses include sedation in intensive care, as a pain killer, as treatment of bronchospasm, as a treatment for complex regional pain syndrome and as an antidepressant. It induces a trance-like state while providing pain relief, sedation, and memory loss. Heart function, breathing, and airway reflexes generally remain functional.
Common side effects include psychological reactions as the medication wears off. These reactions may include agitation, confusion, or psychosis. Elevated blood pressure and muscle tremors are relatively common, while low blood pressure and a decrease in breathing is less so. Spasms of the larynx may rarely occur.
Pharmacologically, ketamine is classified as an NMDA receptor antagonist, but it also acts at numerous other sites (including opioid receptors and monoamine transporters). Like other drugs of the arylcyclohexylamine class, such as phencyclidine (PCP), ketamine is classified as a dissociative agent.
Ketamine was first developed in 1962. It is on the World Health Organization's List of Essential Medicines, the most important medication needed in a basic health system. It is legally sold under a very wide variety of brand names, including Ketalar. Ketamine's use as a recreational drug has been implicated in a number of annual deaths.
- 1 Use
- 2 Side effects
- 3 Pharmacology
- 4 Chemistry
- 5 History
- 6 Legal status
- 7 International brand names
- 8 Research
- 9 Veterinary medicine
- 10 See also
- 11 References
- 12 External links
Uses as an anaesthetic:
- Anesthesia in children, as the sole anesthetic for minor procedures or as an induction agent followed by muscle relaxant and tracheal intubation
- Asthmatics or people with chronic obstructive airway disease
- As a sedative for physically painful procedures in emergency departments
- Emergency surgery in field conditions in war zones
- To supplement spinal or epidural anesthesia/analgesia using low doses
Since it suppresses breathing much less than most other available anaesthetics, ketamine is used in medicine as an anesthetic; however, due to the hallucinations it may cause, it is not typically used as a primary anesthetic, although it is the anaesthetic of choice when reliable ventilation equipment is not available.
Ketamine is frequently used in severely injured people and appears to be safe in this group. A 2011 clinical practice guideline supports the use of ketamine as a dissociative sedative in emergency medicine. It is the drug of choice for people in traumatic shock who are at risk of hypotension. Low blood pressure is harmful in people with severe head injury and ketamine is least likely to cause low blood pressure, often even able to prevent it.
The effect of ketamine on the respiratory and circulatory systems is different from that of other anesthetics. When used at anesthetic doses, it will usually stimulate rather than depress the circulatory system. It is sometimes possible to perform ketamine anesthesia without protective measures to the airways. Ketamine is considered relatively safe because protective airway reflexes are preserved.
Ketamine may be used for postoperative pain management. Low doses of ketamine reduce morphine use and nausea and vomiting after surgery. High quality evidence in acute pain is insufficient to determine if ketamine is useful in this situation.
It may also be used as an intravenous analgesic with opiates to manage otherwise intractable pain, particularly if this pain is neuropathic. It has the added benefit of counteracting spinal sensitization or wind-up phenomena experienced with chronic pain. At these doses, the psychotropic side effects are less apparent and well managed with benzodiazepines. Ketamine is an analgesic that is most effective when used alongside a low-dose opioid; as while it does have analgesic effects by itself, the doses required for adequate pain relief when it is used as the sole analgesic agent are considerably higher and far more likely to produce disorienting side effects. A review article in 2013 concluded, "despite limitations in the breadth and depth of data available, there is evidence that ketamine may be a viable option for treatment-refractory cancer pain".
Low-dose ketamine is sometimes used in the treatment of complex regional pain syndrome (CRPS). A 2013 systematic review found only low-quality evidence to support the use of ketamine for CRPS.
Ketamine has been tested in treatment-resistant bipolar depression, major depressive disorder, and people in a suicidal crisis in emergency rooms. Benefit is often of a short duration. The quality of the evidence supporting benefit, however, is generally low.
The drug is given by a single intravenous infusion at doses less than those used in anesthesia, and preliminary data indicate it produces a rapid (within 2 hours) and relatively sustained (about 1–2 weeks long) reduction in symptoms in some people. Initial studies have resulted in interest due to its rapid onset, and because it appears to work by blocking NMDA receptors for glutamate, a different mechanism from most modern antidepressants that operate on other targets.
Ketamine use as a recreational drug has been implicated in deaths, globally with more than 90 deaths in England and Wales in the years of 2005-2013. They include from accidental poisonings, drownings, and traffic accidents, as well as further suicides. The majority of deaths were among young people. This has led to increased regulation (e.g., upgrading ketamine from a Class C to a Class B banned substance in the U.K.).
Unlike the other well-known dissociatives Phencyclidine (PCP) and dextromethorphan (DXM), ketamine is very short-acting. It takes effect within about 10 minutes, while its hallucinogenic effects last 60 minutes when insufflated or injected and up to two hours when ingested orally.
At subanesthetic doses, ketamine produces a dissociative state, characterised by a sense of detachment from one's physical body and the external world which is known as depersonalization and derealization. At sufficiently high doses, users may experience what is called the "K-hole", a state of extreme dissociation with visual and auditory hallucinations. John C. Lilly, Marcia Moore and D. M. Turner (amongst others) have written extensively about their own entheogenic use of, and psychonautic experiences with ketamine. Both Moore and Turner died prematurely (due to hypothermia and drowning respectively) during presumed unsupervised ketamine use.
Ketamine is generally safe for those critically ill, when administered by trained medical professionals. Even in these cases, there are known side effects that include one or more of the following:
- Cardiovascular: abnormal heart rhythms, slow heart rate or fast heart rate, high blood pressure or low blood pressure
- Central nervous system: Ketamine is traditionally avoided in people with or at risk of intracranial hypertension (ICP) due to concerns about ketamine causing increased intracranial pressure. It does not increase ICP more than opioids.
- Dermatologic: Transient erythema, transient morbilliform rash
- Gastrointestinal: Anorexia, nausea, increased salivation, vomiting
- Local: Pain or exanthema of the injection site
- Neuromuscular and skeletal: Increased skeletal muscle tone (tonic-clonic movements)
- Ocular: Double vision, increased intraocular pressure, nystagmus
- Respiratory: Airway obstruction, apnea, increased bronchial secretions, respiratory depression, laryngospasm
- Other: Anaphylaxis, dependence, emergence reaction
In 10-20% of patients at anesthetic doses experience adverse reactions that occur during emergence from anesthesia, reactions that can manifest as seriously as hallucinations and delirium. These reactions may be less common in some patients subpopulations, and when administered intramuscularly, and can occur up to 24 hours postoperatively; the chance of this occurring can be reduced by minimizing stimulation to the patient during recovery and pretreating with a benzodiazepine, alongside a lower dose of ketamine. Patients who experience severe reactions may require treatment with a small dose of a short- or ultrashort-acting barbiturate.
In 1989, psychiatry professor John Olney reported ketamine caused irreversible changes in two small areas of the rat brain, which, however, has significant differences in metabolism from the human brain, so may not occur in humans.
The first large-scale, longitudinal study of ketamine users found current frequent (averaging 20 days/month) ketamine users had increased depression and impaired memory by several measures, including verbal, short-term memory, and visual memory. Current infrequent (averaging 3.25 days/month) ketamine users and former ketamine users were not found to differ from controls in memory, attention, and psychological well-being tests. This suggests the infrequent use of ketamine does not cause cognitive deficits, and that any deficits that might occur may be reversible when ketamine use is discontinued. However, abstinent, frequent, and infrequent users all scored higher than controls on a test of delusional symptoms.
Short-term exposure of cultures of GABAergic neurons to ketamine at high concentrations led to a significant loss of differentiated cells in one study, and noncell-death-inducing concentrations of ketamine (10 μg/ml) may still initiate long-term alterations of dendritic arbor in differentiated neurons. The same study also demonstrated chronic (>24 h) administration of ketamine at concentrations as low as 0.01 μg/ml can interfere with the maintenance of dendritic arbor architecture. These results raise the possibility that chronic exposure to low, subanesthetic concentrations of ketamine, while not affecting cell survival, could still impair neuronal maintenance and development.
More recent studies of ketamine-induced neurotoxicity have focused on primates in an attempt to use a more accurate model than rodents. One such study administered daily ketamine doses consistent with typical recreational doses (1 mg/kg IV) to adolescent cynomolgus monkeys for varying periods of time. Decreased locomotor activity and indicators of increased cell death in the prefrontal cortex were detected in monkeys given daily injections for six months, but not those given daily injections for one month. A study conducted on rhesus monkeys found a 24-hour intravenous infusion of ketamine caused signs of brain damage in five-day-old but not 35-day-old animals. Some neonatal experts do not recommend the use of ketamine as an anesthetic agent in human neonates because of the potential adverse effects it may have on the developing brain. These neurodegenerative changes in early development have been seen with other drugs that share the same mechanism of action of NMDA receptor antagonism as ketamine.
The acute effects of ketamine cause cognitive impairment, including reductions in vigilance, verbal fluency, short-term memory, and executive function, as well as schizophrenia-like perceptual changes.
Urinary tract effects
A 2011 systematic review examined 110 reports of irritative urinary tract symptoms from ketamine abuse. Urinary tract symptoms have been collectively referred as "ketamine-induced ulcerative cystitis" or "ketamine-induced vesicopathy", and they include urge incontinence, decreased bladder compliance, decreased bladder volume, detrusor overactivity, and painful haematuria (blood in urine). Bilateral hydronephrosis and renal papillary necrosis have also been reported in some cases. The pathogenesis of papillary necrosis has been investigated in mice, and mononuclear inflammatory infiltration in the renal papilla resulting from ketamine dependence has been suggested as a possible mechanism.
The time of onset of lower urinary tract symptoms varies depending, in part, on the severity and chronicity of ketamine use; however, it is unclear whether the severity and chronicity of ketamine use corresponds linearly to the presentation of these symptoms. All reported cases where the user consumed greater than 5 g/day reported symptoms of the lower urinary tract. Urinary tract symptoms appear to be most common in daily ketamine abusers who have abused the drug for an extended period of time. These symptoms have presented in only one case of medical use of ketamine. However, following dose reduction, the symptoms remitted.
Management of these symptoms primarily involves ketamine cessation, for which compliance is low. Other treatments have been used, including antibiotics, NSAIDs, steroids, anticholinergics, and cystodistension. Both hyaluronic acid instillation and combined pentosan polysulfate and ketamine cessation have been shown to provide relief in some patients, but in the latter case, it is unclear whether relief resulted from ketamine cessation, administration of pentosan polysulfate, or both. Further follow-up is required to fully assess the efficacy of these treatments.
In case reports of three patients treated with esketamine for relief of chronic pain, liver enzyme abnormalities occurred following repeat treatment with ketamine infusions, with the liver enzyme values returning below the upper reference limit of normal range on cessation of the drug. The result suggests liver enzymes must be monitored during such treatment.
Other drugs which increase blood pressure may interact with ketamine in having an additive effect on blood pressure including: stimulants, SNRI antidepressants, and MAOIs. Increase blood pressure and heart rate, palpitations, and arrhythmias may be potential effects.
- Oral ketamine is easily broken down by bile acids, thus has a low bioavailability (about 20%). Often, lozenges or "gummies" for sublingual or buccal absorption prepared by a compounding pharmacy are used to combat this issue.
- Some specialists stop the subcutaneous infusion when the first dose of oral ketamine is given. Others gradually reduce the infusion dose as the oral dose is increased.
Ketamine is also used as an ingredient in creams, gels, and liquids (only available from compounding pharmacies, as it is not a branded product, specific formulation and ratios are specified by the prescribing physician) for topical application in cases of refractory nerve pain. Other ingredients found useful by pain specialists and their patients, as well as the compounding pharmacists who make the topical mixtures, include amitriptyline, cyclobenzaprine, clonidine, tramadol, gabapentin, baclofen, and mepivacaine and other longer-acting local anaesthetics (e.g. tetracaine, procaine).
Ketamine acts primarily as an antagonist of the NMDA receptor, and this action accounts for most of its effects. However, the complete pharmacology of ketamine is more complex, and it is known to directly interact with a variety of other sites to varying degrees. Known actions of ketamine include:
- Non-competitive antagonist of the NMDA receptor (NMDAR)
- Negative allosteric modulator of the nACh receptor
- Weak agonist of the μ-opioid and κ-opioid receptors (10- and 20-fold less affinity relative to NMDAR, respectively), and very weak agonist of the δ-opioid receptor
- Agonist of the sigma receptor and D2 receptor
- Weak mACh receptor antagonist (10- to 20-fold less affinity relative to NMDAR)
- Inhibitor of the reuptake of serotonin, dopamine, and norepinephrine
- Voltage-gated sodium channel and L-type calcium channel blocker, and HCN1 cation channel blocker
- Inhibitor of nitric oxide synthase
Ketamine appears to inhibit the NMDAR by binding both in the open channel and at an allosteric site. The S(+) and R(-) stereoisomers bind with different affinities: Ki = 3200 and 1100 nM, respectively.
The significance of these additional mechanisms in the therapeutic effects of ketamine is poorly understood due to its relatively complex pharmacological profile.
Effects in central nervous system
NMDAR antagonism is responsible for the anesthetic, amnesic, dissociative, and hallucinogenic effects of ketamine, although activation of κ-opioid receptors and possibly sigma and mACh receptors may also contribute to its psychotomimetic properties. Dopamine reuptake inhibition is likely to underlie the euphoria the drug produces, although an additional involvement of μ-opioid receptor activation cannot be excluded. The mechanism of actions for the possible antidepressant effects of ketamine at lower doses have yet to be elucidated.
NMDAR antagonism results in analgesia by preventing central sensitization in dorsal horn neurons; in other words, ketamine's actions interfere with pain transmission in the spinal cord. Inhibition of nitric oxide synthase lowers the production of nitric oxide – a neurotransmitter involved in pain perception, hence further contributing to analgesia. The action of ketamine at sigma and μ-opioid receptors is relatively weak, and evidence is mixed as to whether the latter is of significance to its analgesic effects.
Ketamine also interacts with a host of other targets to cause analgesia. In particular, it blocks voltage-dependent calcium channels and sodium channels, attenuating hyperalgesia; it alters cholinergic neurotransmission, which is implicated in pain mechanisms; and it inhibits the reuptake of serotonin and norepinephrine, which are involved in descending antinociceptive pathways.
Effects in peripheral systems
- Cardiovascular: Ketamine inhibits the reuptake of catecholamines, stimulating the sympathetic nervous system, resulting in cardiovascular symptoms.
- Gastrointestinal: Serotonin reuptake inhibition is thought to underlie nausea and vomiting.
- Respiratory: Catecholamine elevation and stimulation of β2 adrenergic receptors probably causes bronchodilation, although other processes may also be involved. The exact mechanism is not fully understood.
Ketamine is absorbable by intravenous, intramuscular, oral, and topical routes due to both its water and lipid solubilities. When administered orally, it undergoes first-pass metabolism, where it is biotransformed in the liver by CYP3A4 (major), CYP2B6 (minor), and CYP2C9 (minor) isoenzymes into norketamine (through N-demethylation) and finally dehydronorketamine. Intermediate in the biotransformation of norketamine into dehydronorketamine is the hydroxylation of norketamine into hydroxynorketamine by CYP2B6 and CYP2A6. Dehydronorketamine, followed by norketamine, is the most prevalent metabolite detected in urine. As the major metabolite of ketamine, norketamine is one-third to one-fifth as potent anesthetically, and plasma levels of this metabolite are three times higher than ketamine following oral administration. Bioavailability through the oral route reaches 17–20%; bioavailability through other routes are: 93% intramuscularly, 25–50% intranasally, 30% sublingually, and 30% rectally. Peak plasma concentrations are reached within a minute intravenously, 5–15 min intramuscularly, and 30 min orally. Ketamine's duration of action in a clinical setting is 30 min to 2 h intramuscularly and 4–6 h orally.
In chemical structure, ketamine is an arylcyclohexylamine derivative. Ketamine is a chiral compound. Most pharmaceutical preparations of ketamine are racemic; however, some brands reportedly have (mostly undocumented) differences in their enantiomeric proportions. The more active enantiomer, esketamine (S(+)-ketamine), is also available for medical use under the brand name Ketanest S, while the less active enantiomer, arketamine (R(–)-ketamine), has never been marketed as an enantiopure drug for clinical use.
Ketamine was first synthesized in 1962 by Calvin Stevens, a professor of Chemistry in Wayne State University and a Parke Davis consultant conducting research on alpha-hydroxyimine rearrangements. After promising preclinical research in animals, ketamine was introduced to testing in human prisoners in 1964. These investigations demonstrated ketamine's short duration of action and reduced behavioral toxicity made it a favorable choice over phencyclidine(PCP) as a dissociative anesthetic. Following FDA approval in 1970, ketamine anesthesia was first given to American soldiers during the Vietnam War.
See the foregoing discussion and citations regarding the increasing stringency of governmental regulation that has resulted from a significant number of deaths of youth and young adults by overdose, accident, and suicide in which nonmedical/recreational ketamine use is implicated (in the Recreational use section, above).
Nonmedical use of ketamine began on the West Coast of the United States in the early 1970s. Early use was documented in underground literature such as The Fabulous Furry Freak Brothers. It was used in psychiatric and other academic research through the 1970s, culminating in 1978 with the publishing of psychonaut John Lilly's The Scientist, and Marcia Moore and Howard Alltounian's Journeys into the Bright World, which documented the unusual phenomenology of ketamine intoxication. The incidence of nonmedical ketamine use increased through the end of the century, especially in the context of raves and other parties. However, its emergence as a club drug differs from other club drugs (e.g. MDMA) due to its anesthetic properties (e.g., slurred speech, immobilization) at higher doses; in addition, there are reports of ketamine being sold as "ecstasy". The use of ketamine as part of a "postclubbing experience" has also been documented. Ketamine's rise in the dance culture was rapid in Hong Kong by the end of the 1990s. Before becoming a federally controlled substance in the United States in 1999, ketamine was available as diverted pharmaceutical preparations and as a pure powder sold in bulk quantities from domestic chemical supply companies. Much of the current ketamine diverted for nonmedical use originates in China and India.
In addition to its ability to cause confusion and amnesia, and the significant number of cases to lead to overdose, accidents, and suicidal feelings, ketamine can leave users vulnerable to date rape (i.e., because of the associated confusion and amnesia).
In the United Kingdom, it became labeled a Class C drug on 1 January 2006. On 10 December 2013 the UK Advisory Council on the Misuse of Drugs (ACMD) recommended that the government reclassify ketamine to become a Class B drug, and on 12 February 2014 the Home Office announced they would follow this advice "in light of the evidence of chronic harms associated with ketamine use, including chronic bladder and other urinary tract damage".
The UK Minister of State for Crime Prevention, Norman Baker, responding to the ACMD's advice, said the issue of its recheduling for medical and veterinary would be addressed "separately to allow for a period of consultation."
In Canada, ketamine is classified as a Schedule I narcotic, since 2005. In Hong Kong, as of 2000, ketamine is regulated under Schedule 1 of Hong Kong Chapter 134 Dangerous Drugs Ordinance. It can only be used legally by health professionals, for university research purposes, or with a physician's prescription. By 2002, ketamine was classified as class III in Taiwan; given the recent rise in prevalence in East Asia, however, rescheduling into class I or II is being considered.
In December 2013, the government of India, in response to rising abuse and the use of ketamine as a date rape drug, has added it to Schedule X of the Drug and Cosmetics Act requiring a special license for sale and maintenance of records of all sales for two years.
International brand names
Brand names for ketamine vary internationally:
- Anesject (ID)
- Brevinaze (ZA)
- Calypsol (AE, BB, BG, BH, BM, BS, BZ, CY, CZ, EG, GY, HU, IL, IQ, IR, JM, JO, KW, LB, LY, OM, PK, PL, PR, QA, RU, SA, SR, SY, TH, TT, YE)
- Ivanes (ID)
- Kanox (MY)
- Keiran (VE)
- Ketacor (PH)
- Ketalar (AE, AR, AT, AU, BB, BE, BH, BM, BR, BS, BZ, CH, CY, DK, EG, ES, FI, FR, GB, GR, GY, HK, HN, ID, IE, IL, IN, IQ, IR, IT, JM, JO, KW, LB, LU, LY, MY, NL, NO, OM, PE, PT, QA, SA, SE, SR, SY, TR, TT, TW, US, UY, YE, ZA)
- Ketalin (MX)
- Ketamax (PH)
- Ketamin-S (+) (PY)
- Ketanest (NL, HR, PL, DE, AT)
- Ketashort (CO)
- Ketava (MY)
- Ketazol (PH)
- Ketmin (IN)
- Ketalor (ES)
- Narkamon (DE, PL)
- Paard (BE)
- Soon-Soon (TW)
- Tekam (AE, BH, CY, EG, IL, IQ, IR, JO, KW, LB, LY, OM, QA, SA, SY, YE)
- Velonarcon (PL)
Treatment of addiction
Russian doctor Evgeny Krupitsky has claimed to have encouraging results by using ketamine as part of a treatment for alcohol addiction which combines psychedelic and aversive techniques. Krupitsky and Kolp summarized their work to date in 2007.
In veterinary anesthesia, ketamine is often used for its anesthetic and analgesic effects on cats, dogs, rabbits, rats, and other small animals. It is an important part of the "rodent cocktail", a mixture of drugs used for anesthetizing rodents. Veterinarians often use ketamine with sedative drugs to produce balanced anesthesia and analgesia, and as a constant-rate infusion to help prevent pain wind-up. Ketamine is used to manage pain among large animals, though it has less effect on bovines. It is the primary intravenous anesthetic agent used in equine surgery, often in conjunction with detomidine and thiopental, or sometimes guaifenesin.
- Nitrous oxide
- Malenka RC, Nestler EJ, Hyman SE (2009). "Chapter 15: Reinforcement and Addictive Disorders". In Sydor A, Brown RY. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 374–375. ISBN 9780071481274.
Phencyclidine (PCP or angel dust) and ketamine (also known as special K) are structurally related drugs that are classified as dissociative anesthetics. These drugs are distinguished from other psychotomimetic agents, such as hallucinogens, by their distinct spectrum of pharmacologic effects, including their reinforcing properties and risks related to compulsive abuse ... The reinforcing properties of PCP and ketamine are mediated by the binding of these drugs to specific sites in the channel of the NMDA glutamate receptor, where they act as noncompetitive antagonists. PCP is self-administered directly into the NAc, where its reinforcing effects are believed to result from the blockade of excitatory glutamatergic input to the same medium spiny NAc neurons inhibited by opioids and dopamine
- Hijazi, Y; Boulieu, R (July 2002). "Contribution of CYP3A4, CYP2B6, and CYP2C9 isoforms to N-demethylation of ketamine in human liver microsomes". Drug Metabolism and Disposition 30 (7): 853–8. doi:10.1124/dmd.30.7.853. PMID 12065445.
- Green, SM; Roback, MG; Kennedy, RM; Krauss, B (2011). "Clinical Practice Guideline for Emergency Department Ketamine Dissociative Sedation: 2011 Update". Annals of Emergency Medicine 57 (5): 449–61. doi:10.1016/j.annemergmed.2010.11.030. PMID 21256625.
- "Ketamine Injection Prescribing Information as of February 2013.". drugs.com. Retrieved 1 December 2014.
- "Ketamine Side Effects". drugs.com. Retrieved 1 December 2014.
- Kohrs, R; Durieux, ME (November 1998). "Ketamine: Teaching an old drug new tricks". Anesthesia & Analgesia 87 (5): 1186–93. doi:10.1213/00000539-199811000-00039. PMID 9806706.
- Bergman, SA (1999). "Ketamine: Review of its pharmacology and its use in pediatric anesthesia". Anesthesia Progress 46 (1): 10–20. PMC 2148883. PMID 10551055.
- "Ketamine - CESAR". Center for substance abuse research. University of Maryland. Retrieved 26 September 2014.
- "WHO Model List of EssentialMedicines" (PDF). World Health Organization. October 2013. Retrieved 22 April 2014.
- See Max Daly, 2014, "The Sad Demise of Nancy Lee, One of Britain's Ketamine Casualties," at Vice (online), July 23, 2014, see , accessed 7 June 2015.
- Hayley Dixon, 2014, "Ketamine death of public schoolgirl an 'act of stupidity which destroyed family'," at The Telegraph (online), February 12, 2014, see , accessed 7 Jume 2015.
- The Crown, 2013, "Drug related deaths involving ketamine in England and Wales," a report of the Mortality team, Life Events and Population Sources Division, Office for National Statistics, the Crown (U.K.), see  and , accessed 7 Jume 2015.
- Heshmati, F; Zeinali, MB; Noroozinia, H; Abbacivash, R; et al. (December 2003). "Use of ketamine in severe status asthmaticus in intensive care unit". Iranian Journal of Allergy, Asthma, and Immunology 2 (4): 175–80. PMID 17301376.
- Cohen, L; Athaide, V; Wickham, ME; Doyle-Waters, MM; Rose, NG; Hohl, CM (Jul 16, 2014). "The Effect of Ketamine on Intracranial and Cerebral Perfusion Pressure and Health Outcomes: A Systematic Review.". Annals of Emergency Medicine 65: 43–51.e2. doi:10.1016/j.annemergmed.2014.06.018. PMID 25064742.
- Nickson, Chris (7 August 2013). "Intubation, Hypotension and Shock". Life in the Fastlane (blog). Critical Care Compendium. Retrieved 10 April 2014.[unreliable medical source?]
- Manley, G; Knudson, MM; Morabito, D; Damron, S; et al. (2001). "Hypotension, hypoxia, and head injury: Frequency, duration, and consequences". Archives of Surgery 136 (10): 1118–23. doi:10.1001/archsurg.136.10.1118. PMID 11585502.
- Hemmingsen, C; Nielsen, JE (1991). "Intravenous ketamine for prevention of severe hypotension during spinal anaesthesia". Acta Anaesthesiologica Scandinavica 35 (8): 755–7. doi:10.1111/j.1399-6576.1991.tb03385.x. PMID 1763596.
- Wong, DHW; Jenkins, LC (1975). "The cardiovascular effects of ketamine in hypotensive states" (PDF). Canadian Anaesthetists' Society Journal 22 (3): 339–48. doi:10.1007/BF03004843. PMID 1139377.
- Adams, HA (December 1997). "S-(+)-ketamin kreislaufinteraktionen bei totaler intravenöser anästhesie und analgosedierung" [S-(+)-ketamine. Circulatory interactions during total intravenous anesthesia and analgesia-sedation]. Der Anaesthesist (in German) 46 (12): 1081–7. doi:10.1007/s001010050510. PMID 9451493.
- Wong, JJM; Lee, JH; Turner, DA; Rehder, KJ (2014). "A review of the use of adjunctive therapies in severe acute asthma exacerbation in critically ill children". Expert Review of Respiratory Medicine 8 (4): 423–41. doi:10.1586/17476348.2014.915752. PMID 24993063.
- Goyal, S; Agrawal, A (May 2013). "Ketamine in status asthmaticus: A review". Indian Journal of Critical Care Medicine 17 (3): 154–61. doi:10.4103/0972-5229.117048. PMC 3777369. PMID 24082612.
- Jat, KR; Chawla, D (November 2012). "Ketamine for management of acute exacerbations of asthma in children". Airways Group. Cochrane Database of Systematic Reviews 11 (11): Art. No. CD009293. doi:10.1002/14651858.CD009293.pub2. PMID 23152273.
- Bell, RF; Dahl, JB; Moore, RA; Kalso, EA (25 January 2006). "Perioperative ketamine for acute postoperative pain". Pain, Palliative and Supportive Care Group. Cochrane Database of Systematic Reviews (1): CD004603. doi:10.1002/14651858.CD004603.pub2. PMID 16437490.
- Sin, B; Ternas, T; Motov, SM (March 2015). "The Use of Subdissociative-dose Ketamine for Acute Pain in the Emergency Department.". Academic emergency medicine : official journal of the Society for Academic Emergency Medicine 22 (3): 251–7. doi:10.1111/acem.12604. PMID 25716117.
- Elia, N; Tramèr, MR (January 2005). "Ketamine and postoperative pain: A quantitative systematic review of randomised trials". Pain 113 (1): 61–70. doi:10.1016/j.pain.2004.09.036. PMID 15621365.
- Bredlau, AL; Thakur, R; Korones, DN; Dworkin, RH (October 2013). "Ketamine for pain in adults and children with cancer: A systematic review and synthesis of the literature". Pain Medicine 14 (10): 1505–17. doi:10.1111/pme.12182. PMID 23915253.
- Correll, GE; Maleki, J; Gracely, EJ; Muir, JJ; Harbut, RE (September 2004). "Subanesthetic ketamine infusion therapy: A retrospective analysis of a novel therapeutic approach to complex regional pain syndrome". Pain Medicine 5 (3): 263–75. doi:10.1111/j.1526-4637.2004.04043.x. PMID 15367304.
- O'Connell, NE; Wand, BM; McAuley, J; Marston, L; et al. (2013). "Interventions for treating pain and disability in adults with complex regional pain syndrome". Pain, Palliative and Supportive Care Group. Cochrane Database of Systematic Reviews 4 (4): Art. No. CD009416. doi:10.1002/14651858.CD009416.pub2. PMID 23633371.
- Tondo, L; Vázquez, GH; Baldessarini, RJ (February 2014). "Options for pharmacological treatment of refractory bipolar depression.". Current psychiatry reports 16 (2): 431. doi:10.1007/s11920-013-0431-y. PMID 24425269.
- Caddy, C; Giaroli, G; White, TP; Shergill, SS; Tracy, DK (April 2014). "Ketamine as the prototype glutamatergic antidepressant: pharmacodynamic actions, and a systematic review and meta-analysis of efficacy.". Therapeutic advances in psychopharmacology 4 (2): 75–99. doi:10.1177/2045125313507739. PMID 24688759.
- ECRI Institute, under contract to AHRQ. December 2013 AHRQ Healthcare Horizon Scanning System – Potential High-Impact Interventions Report. Priority Area 05: Depression and Other Mental Health Disorders
- National Institute of Mental Health (7 August 2006). "Experimental Medication Kicks Depression in Hours Instead of Weeks". NIH News (Press release). National Institutes of Health; Dept. of Health and Human Services; United States.
National Institute of Mental Health director Thomas Insel said, "To my knowledge, this is the first report of any medication or other treatment that results in such a pronounced, rapid, prolonged response with a single dose. These were very treatment-resistant patients."
- Naughton, M; Clarke, G; O'Leary, OF; Cryan, JF; Dinan, TG (Mar 2014). "A review of ketamine in affective disorders: current evidence of clinical efficacy, limitations of use and pre-clinical evidence on proposed mechanisms of action.". Journal of Affective Disorders 156: 24–35. doi:10.1016/j.jad.2013.11.014. PMID 24388038.
- "Do you know... Ketamine". Knowledge Exchange. Toronto: Centre for Addiction and Mental Health. 2003. Archived from the original on 2014-04-07. Retrieved 27 July 2014.
- Giannini, AJ; Loiselle, RH; Giannini, MC; Price, WA (1985). "Phencyclidine and the dissociatives". Psychiatric Medicine 3 (3): 197–217. PMID 2893430.
- Giannini, AJ; Underwood, NA; Condon, M (November 2000). "Acute ketamine intoxication treated by haloperidol: A preliminary study". American Journal of Therapeutics 7 (6): 389–91. doi:10.1097/00045391-200007060-00008. PMID 11304647.
- Giannini, AJ (1999). Drug Abuse. Los Angeles: Health Information Press. p. 104. ISBN 1885987110.
- References for recreational use in literature:
- Lilly, John Cunningham (1997). The Scientist: A Metaphysical Autobiography. Berkeley, CA: Ronin. pp. 144–. ISBN 0914171720.
- Kelly, Kit (2001). The Little Book of Ketamine. Ronin. pp. 23, 40–45, 46–51, ibid. ISBN 9781579511210.
- Alltounian, Howard Sunny; Moore, Marcia (1978). Journeys Into the Bright World. Rockport, MA: Para Research. ISBN 9780914918127.
- Palmer, Cynthia; Horowitz, Michael (2000). Sisters of the Extreme: Women Writing on the Drug Experience. Inner Traditions. pp. 254–8, ibid. ISBN 9780892817573.
- Turner, D.M. (1994). The Essential Psychedelic Guide. San Francisco: Panther Press. ISBN 0964263610.
- Jansen, Karl (2001). Ketamine: Dreams and Realities. Multidisciplinary Association for Psychedelic Studies. pp. 50, 89. ISBN 0966001931.
- Cohen, L; Athaide, V; Wickham, ME; Doyle-Waters, MM; Rose, NG; Hohl, CM (January 2015). "The effect of ketamine on intracranial and cerebral perfusion pressure and health outcomes: a systematic review.". Annals of Emergency Medicine 65 (1): 43–51.e2. doi:10.1016/j.annemergmed.2014.06.018. PMID 25064742.
- Merck Manual; Drug Information Provided by Lexi-Comp. Last full review/revision May 2014 Ketamine
- Wang, Xin; Ding, Xibing; Tong, Yao; Zong, Jiaying; Zhao, Xiang; Ren, Hao; Li, Quan (24 May 2014). "Ketamine does not increase intracranial pressure compared with opioids: meta-analysis of randomized controlled trials". Journal of Anesthesia 28: 7. doi:10.1007/s00540-014-1845-3.
- Strayer, RJ; Nelson, LS (2008). "Adverse events associated with ketamine for procedural sedation in adults". American Journal of Emergency Medicine 26 (9): 985–1028. doi:10.1016/j.ajem.2007.12.005. PMID 19091264.
- Quibell, R; Prommer, EE; Mihalyo, M; Twycross, R; et al. (March 2011). "Ketamine*". Journal of Pain and Symptom Management (Therapeutic Review) 41 (3): 640–9. doi:10.1016/j.jpainsymman.2011.01.001. PMID 21419322.
- Neurological effects of ketamine introduction references:
- Olney, JW; Labruyere, J; Price, MT (June 1989). "Pathological changes induced in cerebrocortical neurons by phencyclidine and related drugs". Science 244 (4910): 1360–2. doi:10.1126/science.2660263. PMID 2660263.
- Anderson, Cliff (June 2003). "The Bad News Isn't In: A Look at Evidence for Specific Mechanisms of Dissociative-Induced Brain Damage and Cognitive Impairment". Erowid.[unreliable medical source?]
- Tryba, M; Gehling, M (October 2002). "Clonidine - A potent analgesic adjuvant". Current Opinion in Anaesthesiology 15 (5): 511–7. doi:10.1097/00001503-200210000-00007. PMID 17019247.
- Dong, C; Anand, KJS (June 2013). "Developmental neurotoxicity of ketamine in pediatric clinical use". Toxicology Letters 220 (1): 53–60. doi:10.1016/j.toxlet.2013.03.030. PMID 23566897.
- Morgan, CJA; Muetzelfeldt, L; Curran, HV (2009). "Consequences of chronic ketamine self-administration upon neurocognitive function and psychological wellbeing: A 1-year longitudinal study". Addiction 105 (1): 121–33. doi:10.1111/j.1360-0443.2009.02761.x. PMID 19919593.
- Vutskits, L; Gascon, E; Potter, G; Tassonyi, E; et al. (May 2007). "Low concentrations of ketamine initiate dendritic atrophy of differentiated GABAergic neurons in culture". Toxicology 234 (3): 216–26. doi:10.1016/j.tox.2007.03.004. PMID 17418473.
- Hargreaves, RJ; Hill, RG; Iversen, LL (1994). "Neuroprotective NMDA antagonists: the controversy over their potential for adverse effects on cortical neuronal morphology.". Acta neurochirurgica. Supplementum 60: 15–9. doi:10.1007/978-3-7091-9334-1_4. PMID 7976530.
- Sun, L; LI, Q; Li, Q; Zhang, Y; et al. (November 2012). "Chronic ketamine exposure induces permanent impairment of brain functions in adolescent cynomolgus monkeys". Addiction Biology 19: 185–94. doi:10.1111/adb.12004. PMID 23145560.
- Slikker, W; Zou, X; Hotchkiss, CE; Divine, RL; et al. (2007). "Ketamine-induced neuronal cell death in the perinatal rhesus monkey". Toxicological Sciences 98 (1): 145–58. doi:10.1093/toxsci/kfm084. PMID 17426105.
- Patel, P; Sun, L (April 2009). "Update on neonatal anesthetic neurotoxicity: Insight into molecular mechanisms and relevance to humans". Anesthesiology (commentary) 110 (4): 703–8. doi:10.1097/ALN.0b013e31819c42a4. PMC 2737718. PMID 19276968.
- Krystal, JH; Karper, LP; Seibyl, JP; Freeman, GK; et al. (March 1994). "Subanesthetic effects of the noncompetitive NMDA antagonist, ketamine, in humans. Psychotomimetic, perceptual, cognitive, and neuroendocrine responses". Archives of General Psychiatry 51 (3): 199–214. doi:10.1001/archpsyc.1994.03950030035004. PMID 8122957.
- Middela, S; Pearce, I (January 2011). "Ketamine-induced vesicopathy: A literature review". International Journal of Clinical Practice 65 (1): 27–30. doi:10.1111/j.1742-1241.2010.02502.x. PMID 21155941.
- Morgan, CJA; Curran, HV; Independent Scientific Committee on Drugs (ISCD) (January 2012). "Ketamine use: A review". Addiction 107 (1): 27–38. doi:10.1111/j.1360-0443.2011.03576.x. PMID 21777321.
- Yeung, LY; Rudd, JA; Lam, WP; Mak, YT; et al. (December 2009). "Mice are prone to kidney pathology after prolonged ketamine addiction". Toxicology Letters 191 (2–3): 275–8. doi:10.1016/j.toxlet.2009.09.006. PMID 19766175.
- Bell, RF (June 2012). "Ketamine for chronic noncancer pain: concerns regarding toxicity.". Current opinion in supportive and palliative care 6 (2): 183–7. doi:10.1097/SPC.0b013e328352812c. PMID 22436323.
- Hui, TW; Short, TG; Hong, W; Suen, T; et al. (March 1995). "Additive interactions between propofol and ketamine when used for anesthesia induction in female atients". Anesthesiology 82 (3): 641–8. doi:10.1097/00000542-199503000-00005. PMID 7879932.
- Hong, W; Short, TG; Hui, TW (December 1993). "Hypnotic and anesthetic interactions between ketamine and midazolam in female patients". Anesthesiology 79 (6): 1227–32. doi:10.1097/00000542-199312000-00013. PMID 8267198.
- Akhavanakbari, G; Mohamadian, A; Entezariasl, M (April 2014). "Evaluation the effects of adding ketamine to morphine in intravenous patient-controlled analgesia after orthopedic surgery". Perspectives in Clinical Research 5 (2): 85–7. doi:10.4103/2229-3485.128028. PMC 3980550. PMID 24741486.
- Eker, HE; Yalcin Cok, O; Aribogan, A; Arslan, G (October 2011). "Children on phenobarbital monotherapy requires more sedatives during MRI". Pediatric Anesthesia 21 (10): 998–1002. doi:10.1111/j.1460-9592.2011.03606.x. PMID 21564387.
- Lankenau, SE; Sanders, B; Bloom, JJ; Hathazi, D; et al. (March 2007). "First injection of ketamine among young injection drug users (IDUs) in three U.S. cities". Drug and Alcohol Dependence 87 (2–3): 183–93. doi:10.1016/j.drugalcdep.2006.08.015. PMC 1852477. PMID 16979848.
- "Ketamine in Palliative Care" (PDF). Palliative Care Guidelines. Edinburgh: NHS Lothian, NHS Scotland, Health and Social Care Directorates, Scotland. August 2013 [August 2010]. Archived (PDF) from the original on 2013-10-29.
- Harrison, NL; Simmonds, MA (February 1985). "Quantitative studies on some antagonists of N-methyl D-aspartate in slices of rat cerebral cortex". British Journal of Pharmacology 84 (2): 381–91. doi:10.1111/j.1476-5381.1985.tb12922.x. PMC 1987274. PMID 2858237.
- Narita, M; Yoshizawa, K; Aoki, K; Takagi, M; et al. (September 2001). "A putative sigma1 receptor antagonist NE-100 attenuates the discriminative stimulus effects of ketamine in rats". Addiction Biology 6 (4): 373–6. doi:10.1080/13556210020077091. PMID 11900615.
- Seeman, P; Guan, HC; Hirbec, H (August 2009). "Dopamine D2High receptors stimulated by phencyclidines, lysergic acid diethylamide, salvinorin A, and modafinil". Synapse 63 (8): 698–704. doi:10.1002/syn.20647. PMID 19391150.
- Pharmaceutical Society of Australia; The Royal Australian College of General Practitioners; Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists (2011). "2.1.1 IV General Anaesthetics". Australian Medicines Handbook 2011 (12th ed.). Adelaide: Australian Medicines Handbook Pty Ltd. p. 13. ISBN 9780980579048.
- Chen, X; Shu, S; Bayliss, DA (2009). "HCN1 channel subunits are a molecular substrate for hypnotic actions of ketamine". Journal of Neuroscience 29 (3): 600–9. doi:10.1523/JNEUROSCI.3481-08.2009. PMC 2744993. PMID 19158287.
- Orser, BA; Pennefather, PS; MacDonald, JF (1997). "Multiple mechanisms of ketamine blockade of N-methyl-D-aspartate receptors". Anesthesiology 86 (4): 903–17. doi:10.1097/00000542-199704000-00021. PMID 9105235.
- Hirota, K; Lambert, DG (October 1996). "Ketamine: Its mechanism(s) of action and unusual clinical uses". British Journal of Anaesthesia 77 (4): 441–4. doi:10.1093/bja/77.4.441. PMID 8942324.
- Browne, CA; Lucki, I (2013). "Antidepressant effects of ketamine: mechanisms underlying fast-acting novel antidepressants". Frontiers in Pharmacology 4: 161. doi:10.3389/fphar.2013.00161. PMC 3873522. PMID 24409146.
- Aroni, F; Iacovidou, N; Dontas, I; Pourzitaki, C; et al. (August 2009). "Pharmacological aspects and potential new clinical applications of ketamine: Reevaluation of an old drug". Journal of Clinical Pharmacology 49 (8): 957–64. doi:10.1177/0091270009337941. PMID 19546251.
- Rowland, LM (July 2005). "Subanesthetic ketamine: How it alters physiology and behavior in humans". Aviation, Space, and Environmental Medicine 76 (Suppl 7): C52–8. PMID 16018330.
- Meller, ST (December 1996). "Ketamine: Relief from chronic pain through actions at the NMDA receptor?". Pain (correspondence) 68 (2–3): 435–6. doi:10.1016/S0304-3959(96)03167-3. PMID 9121834.
- Sinner, B; Graf, BM (2008). "Ketamine". In Schüttler, J; Schwilden, H. Modern Anesthetics. Handbook of Experimental Pharmacology 182. pp. 313–33. ISBN 9783540728139. doi:10.1007/978-3-540-74806-9_15. PMID 18175098.
- Li, JH; Vicknasingam, B; Cheung, YW; Zhou, W; et al. (2011). "To use or not to use: An update on licit and illicit ketamine use". Substance Abuse and Rehabilitation 2 (1): 11–20. doi:10.2147/SAR.S15458. PMC 3846302. PMID 24474851.
- Haas, DA; Harper, DG (1992). "Ketamine: A review of its pharmacologic properties and use in ambulatory anesthesia". Anesthesia Progress 39 (3): 61–8. PMC 2148758. PMID 1308374.
- Krüger, AD (1998). "[Current aspects of using ketamine in childhood]". Anaesthesiologie und Reanimation (in German) 23 (3): 64–71. PMID 9707751.
- Clark, Michael R. (2011). Chronic Pain and Addiction. Basel, Zwitzerland: Karger AG. pp. 166–. ISBN 3805597258.
- Morris, H; Wallach, J (July 2014). "From PCP to MXE: A comprehensive review of the non-medical use of dissociative drugs". Drug Testing and Analysis 6 (7-8): 614–32. doi:10.1002/dta.1620. PMID 24678061.
- Domino, EF (September 2010). "Taming the ketamine tiger". Anesthesiology 113 (3): 678–84. doi:10.1097/ALN.0b013e3181ed09a2. PMID 20693870.
- Corssen, G; Domino, EF (January–February 1966). "Dissociative anesthesia: Further pharmacologic studies and first clinical experience with the phencyclidine derivative CI-581". Anesthesia & Analgesia 45 (1): 29–40. doi:10.1213/00000539-196601000-00007. PMID 5325977.
- "Ketamine". Center for Substance Abuse Research (CESAR); University of Maryland, College Park. 29 October 2013. Archived from the original on 2013-11-12. Retrieved 27 July 2014.
- History of non-medical use in literature references:
- Increased non-medical use references:
- Awuonda, M (13 July 1996). "Swedes alarmed at ketamine misuse". The Lancet 348 (9020): 122. doi:10.1016/S0140-6736(05)64628-4.
- Curran, HV; Morgan, C (April 2000). "Cognitive, dissociative and psychotogenic effects of ketamine in recreational users on the night of drug use and 3 days later". Addiction 95 (4): 575–90. doi:10.1046/j.1360-0443.2000.9545759.x. PMID 10829333.
- Gahlinger, PM (1 June 2004). "Club drugs: MDMA, gamma-hydroxybutyrate (GHB), Rohypnol, and ketamine". American Family Physician 69 (11): 2619–26. PMID 15202696.
- Jansen, KL (6 March 1993). "Non-medical use of ketamine". BMJ 306 (6878): 601–2. doi:10.1136/bmj.306.6878.601. PMC 1676978. PMID 8461808.
- Joe-Laider & Hunt 2008
- Joe-Laidler, K; Hunt, G (1 June 2008). "Sit down to float: The cultural meaning of ketamine use in Hong Kong". Addiction Research & Theory 16 (3): 259–71. doi:10.1080/16066350801983673. PMC 2744071. PMID 19759834.
- Ketamine sold as "ecstasy" references:
- Tanner-Smith, EE (July 2006). "Pharmacological content of tablets sold as "ecstasy": Results from an online testing service" (PDF). Drug and Alcohol Dependence 83 (3): 247–54. doi:10.1016/j.drugalcdep.2005.11.016. PMID 16364567.
- Copeland, J; Dillon, P (2005). "The health and psycho-social consequences of ketamine use". International Journal of Drug Policy 16 (2): 122–31. doi:10.1016/j.drugpo.2004.12.003.
- Measham, Fiona; Parker, Howard; Aldridge, Judith (2001). Dancing on Drugs: Risk, Health and Hedonism in the British Club Scene. London: Free Association Books. ISBN 9781853435126.[verification needed][page needed]
- Moore, K; Measham, F (2006). "Ketamine use: Minimising problems and maximising pleasure". Drugs and Alcohol Today 6 (3): 29–32. doi:10.1108/17459265200600047.
- WHO Model List of Essential Medicines (PDF) (18th ed.). World Health Organization. October 2013 [April 2013]. p. 1 [p. 5 of pdf]. Retrieved 22 April 2014.
- Marshall, Donnie R.; (Deputy Administrator); Drug Enforcement Administration; Dept. of Justice (13 July 1999). "Schedules of Controlled Substances: Placement of Ketamine into Schedule III [21 CFR Part 1308. Final Rule 99-17803]" (PDF). Rules and Regulations. Federal Register 64 (133): 37673–5.
- "Club 'horse' drug to be outlawed". BBC News. 28 December 2005. Archived from the original on 2009-09-03. Retrieved 7 May 2010.
- Advisory Council on the Misuse of Drugs (ACMD); Baker, Norman (10 December 2013), Ketamine: A review of use and harm (PDF) (Policy paper), Crown copyright; Open Government Licence, retrieved 22 January 2014.
- Baker, Norman; (Minister for Crime Prevention); Home Office; United Kingdom (12 February 2014), Response to ACMD recommendation on ketamine (PDF) (Correspondence to Les Iverson [chair of]; Advisory Council on the Misuse of Drugs), Crown copyright; Open Government Licence, retrieved 21 February 2014.
- Dixon, Hayley (12 February 2014). "Party drug ketamine to be upgraded to Class B". The Daily Telegraph. Retrieved 2 August 2014.
- Legal status of ketamine in Canada references:
- "Statutes of Canada (S.C.)". Justice Laws Website. Government of Canada. 12 June 2014.
- "Order Amending Schedule I to the Controlled Drugs and Substances Act" (PDF). Canada Gazette Part II 139 (19). 21 September 2005. p. 2130. Retrieved 2 August 2014.
- "Status of ketamine under CDSA". Canadian Society of Customs Brokers. 2 May 2005. Retrieved 2 August 2014.
- "Statutes of Canada (S.C.)". Justice Laws Website. Government of Canada. 12 June 2014.
- "Government to tighten control on Ketamine", info.gov.hk (press release) (Government of the Hong Kong Special Administrative), 22 November 2000, archived from the original on 2013-06-26, retrieved 2 August 2014
- Ho Wai-kin, Victor (2011). Criminal Law in Hong Kong. Kluwer Law International. p. 33. ISBN 9789041133069.
- Chang, Rich (4 December 2012). "Ketamine to be made a class-two drug: Official". Taipei Times. p. 3.
- "Ketamine drug brought under 'Schedule X' to curb abuse". The Times of India. 7 January 2014. Retrieved 2 August 2014.
- Deb Roy, Sumitra (30 December 2013). "Govt makes notorious 'date rape' drug ketamine harder to buy or sell". The Times of India. Archived from the original on 2013-12-30.
- Krupitsky, EM; Grineko, AYa; Berkaliev, TN; Paley, AI; et al. (1992). "The combination of psychedelic and aversive approaches in alcoholism treatment". Alcoholism Treatment Quarterly 9 (1): 99–105. doi:10.1300/J020V09N01_09.
- Krupitsky, EM; Grinenko, AY (1997). "Ketamine psychedelic therapy (KPT): A review of the results of ten years of research". Journal of Psychoactive Drugs 29 (2): 165–83. doi:10.1080/02791072.1997.10400185. PMID 9250944.
- Krupitsky, Evgeny; Kolp, Eli. "Ch. 6: Ketamine Psychedelic Psychotherapy". In Winkelman, Michael J.; Roberts, Thomas B. Psychedelic Medicine: New Evidence for Hallucinogens as Treatments. Vol. 2. Westport, CT: Praeger. ISBN 9780275990237.
|Wikimedia Commons has media related to Ketamine.|