What Is Ketamine? A Clinician’s Complete Guide to the Anaesthetic, Antidepressant, Hallucinogen, and Substance of Abuse, From FDA-Approved Uses to Recreational Risks

What ketamine is in pharmacological terms, the FDA-approved uses including anaesthesia and treatment-resistant depression with esketamine (Spravato), how ketamine clinics deliver the medication for depression and PTSD, the recreational use patterns that have made ketamine one of the more concerning party drugs of recent decades, the medical risks including ketamine bladder syndrome and cognitive effects of long-term use, and the addiction potential that is becoming better understood.

Clinically reviewed by Dr. Ponlawat Pitsuwan, Physician and Addiction Medicine Specialist, Phuket Island Rehab.

Ketamine is a dissociative anaesthetic medication first synthesised in 1962 and approved by the FDA for use in human anaesthesia in 1970. The medication works primarily as a non-competitive antagonist at the NMDA glutamate receptor, with additional activity at opioid, monoaminergic, and other receptors that contribute to its complex clinical profile. The substance is used in medical settings for surgical anaesthesia (particularly in emergency settings and in low-resource environments), for procedural sedation, for chronic pain management, and increasingly for treatment-resistant depression through the FDA-approved esketamine nasal spray (Spravato) and through off-label intravenous ketamine infusion in ketamine clinics. Ketamine is also one of the more widely used recreational dissociatives, sold under street names including K, special K, vitamin K, ket, and cat valium, typically in powder form for snorting at doses of 50 to 200 milligrams. Recreational use produces a characteristic dissociative experience including detachment from body, altered time perception, and at high doses the K-hole of complete dissociation. Long-term heavy use produces a recognised medical syndrome of ketamine bladder pain and cystitis, cognitive impairment, and psychological dependence. The substance is Schedule III in the United States, reflecting its accepted medical use and meaningful but lower abuse potential compared with Schedule II controlled substances.

What ketamine actually is

Ketamine is a dissociative anaesthetic medication first synthesised in 1962 by Calvin Stevens at Parke-Davis Laboratories as a structural analogue of phencyclidine (PCP) with similar anaesthetic properties but a more favourable safety profile. The medication was approved by the FDA for human anaesthetic use in 1970 under the brand name Ketalar and became widely used in surgical, emergency, and veterinary medicine. The military used ketamine extensively during the Vietnam War for battlefield anaesthesia, and its safety profile in inexperienced hands and in low-resource settings made it the World Health Organization’s recommended anaesthetic for many global health contexts.

The medication is classified as a Schedule III controlled substance in the United States, reflecting accepted medical use combined with meaningful abuse potential. The schedule is less restrictive than Schedule II (which includes opioids, stimulants, and many other potent controlled substances) but more restrictive than Schedule IV (which includes benzodiazepines including Xanax). The classification recognises that ketamine has substantial medical value while having moderate abuse potential. Ketamine is also classified internationally under the United Nations Convention on Psychotropic Substances.

The chemical structure of ketamine exists as two enantiomers, the S-ketamine (esketamine) and R-ketamine (arketamine) forms. The racemic mixture containing equal amounts of both enantiomers is the standard form used for anaesthesia and is the form most commonly encountered in recreational use. S-ketamine alone is marketed as Spravato (esketamine nasal spray) for treatment-resistant depression. The two enantiomers have somewhat different pharmacological profiles, with S-ketamine being more potent at the NMDA receptor and producing more pronounced dissociative effects than R-ketamine. The clinical implications of the differences continue to be investigated, with R-ketamine showing promise as a potentially more selective antidepressant in research settings.

Multiple formulations and routes of administration are used. Intravenous ketamine is the standard for anaesthesia and for many of the depression treatment protocols. Intramuscular ketamine is widely used in emergency settings and in veterinary medicine. Oral ketamine has limited bioavailability and produces different subjective effects from parenteral routes. Intranasal ketamine, particularly the FDA-approved esketamine product, has become more important since 2019 for depression treatment. Recreational use is typically intranasal (snorting powder) or intramuscular, with intravenous use less common except in users with substantial experience.

How ketamine works in the brain

Ketamine acts primarily as a non-competitive antagonist at the N-methyl-D-aspartate (NMDA) glutamate receptor. The NMDA receptor is one of the main excitatory receptors in the brain, and its blockade produces wide-ranging effects including the dissociative state, reduced sensory processing, altered consciousness, and the antidepressant effects that have become the basis for ketamine’s expanded medical use. The non-competitive nature of the blockade means that ketamine binds to a site inside the open channel rather than competing with glutamate at its binding site, producing use-dependent blockade that becomes more pronounced when the receptor is more active.

Beyond the NMDA receptor, ketamine has activity at several other receptor systems that contribute to its complex profile. The medication has partial agonist activity at mu, delta, and kappa-opioid receptors, which contributes to its analgesic effects and may play a role in its antidepressant effects. It interacts with monoaminergic systems including dopamine and serotonin transport, contributing to mood effects. It has activity at sigma receptors, muscarinic acetylcholine receptors, and AMPA glutamate receptors, with the downstream activation of AMPA receptors thought to be central to the antidepressant mechanism through stimulation of synaptic plasticity and brain-derived neurotrophic factor (BDNF) release.

The clinical effects depend on dose. At anaesthetic doses (1 to 4 milligrams per kilogram intravenously) the medication produces full dissociative anaesthesia in which the patient cannot respond to surgical stimuli. At lower doses used for procedural sedation (0.5 to 1 milligram per kilogram) it produces sedation with maintained airway and some response. At antidepressant doses (0.5 milligrams per kilogram intravenously) it produces brief dissociation and a window of altered consciousness without full anaesthesia. At recreational doses (50 to 200 milligrams snorted or 30 to 100 milligrams intramuscularly) the user experiences varying depths of dissociation including the characteristic K-hole at higher doses.

The antidepressant effects of ketamine, which are now the basis for substantial clinical interest, are unusual in several ways. The effects develop rapidly, within hours of a single dose rather than the weeks required for SSRI antidepressants. The effects are substantial in many treatment-resistant patients who have not responded to standard medications. The effects often persist for days to weeks after a single dose, particularly when repeated doses are given over a course of treatment. The mechanism involves AMPA receptor activation, BDNF release, synaptic plasticity, and downstream changes that are still being characterised.

FDA-approved uses and medical applications

Anaesthesia is the original and longest-standing FDA-approved use. Ketamine is used as a primary anaesthetic for surgical procedures, particularly in emergency settings where its cardiovascular stability and maintained airway reflexes are valuable, in pediatric procedures, in patients with cardiovascular instability where other anaesthetics carry higher risk, in burn dressing changes and other painful procedures requiring deep sedation, and in low-resource settings where the simpler equipment requirements compared with other anaesthetics matter. The use of ketamine as a primary anaesthetic for routine elective surgery has declined as newer agents have come into use, but it remains important in specific clinical contexts.

Procedural sedation in emergency departments and other settings is a common application. The medication provides effective sedation and analgesia for short painful procedures including fracture reductions, abscess drainage, joint reductions, foreign body removal, and similar interventions. The maintained airway reflexes and cardiovascular stability make ketamine particularly suitable for these uses compared with propofol, which can produce respiratory depression that requires airway management. The combination of sedation, analgesia, and amnesia produced by ketamine matches the needs of procedural sedation well.

Treatment-resistant depression became an FDA-approved indication with the 2019 approval of esketamine nasal spray (Spravato) by Janssen Pharmaceuticals. The approval was a landmark for both ketamine specifically and depression treatment generally, as it was the first novel mechanism antidepressant in decades and provided rapid relief for patients who had failed multiple SSRI and SNRI trials. The medication is administered in certified treatment centres under medical supervision because of the dissociative effects and the requirement for monitoring after each dose. The treatment course typically involves twice-weekly dosing for the first four weeks followed by weekly or every-other-week maintenance dosing for additional months.

Off-label use of intravenous ketamine for depression has expanded substantially over the past decade through specialty ketamine clinics that provide the medication outside the formal Spravato pathway. The off-label protocols typically involve a series of six to eight infusions over two to three weeks at 0.5 milligrams per kilogram intravenously, with each infusion lasting 40 minutes and the patient monitored throughout. The off-label use has growing evidence support but is not covered by most insurance, with patients typically paying $400 to $800 per infusion out of pocket. The expansion of ketamine clinics has produced concerns about quality control, patient selection, and integration with broader mental health treatment.

Other off-label medical uses include chronic pain management (particularly for complex regional pain syndrome and neuropathic pain), end-of-life care for refractory symptoms, treatment-resistant obsessive-compulsive disorder, post-traumatic stress disorder in research settings, and acute suicidal ideation where the rapid antidepressant effect can stabilise patients in psychiatric emergency. The evidence base for these uses ranges from established (chronic pain) to emerging (PTSD, suicidality) and the regulatory environment for the off-label uses varies across jurisdictions.

Ketamine clinics: what they do and what to expect

Ketamine clinics have grown substantially in number since approximately 2015 in the United States and other countries. The clinics typically provide intravenous ketamine for treatment-resistant depression, anxiety, PTSD, OCD, and chronic pain conditions. The clinical model varies between clinics, with some operating as integrated mental health practices with psychiatric assessment and psychotherapy alongside the ketamine infusions, and others operating as more focused infusion centres that deliver the medication without integrated mental health care. The quality of the model substantially affects the outcomes patients can expect.

A typical course of ketamine infusion therapy involves initial assessment by a psychiatrist or other qualified physician, with attention to the diagnosis, treatment history, suitability for the treatment, and any contraindications. The induction phase typically involves six infusions delivered over two to three weeks, with each infusion at 0.5 milligrams per kilogram body weight delivered intravenously over 40 minutes. The patient is monitored throughout with vital signs and is allowed to rest in a quiet room for 30 to 60 minutes after each infusion before being discharged. The patient cannot drive after the infusion and needs to be accompanied or use ride-share for transportation.

The subjective experience during the infusion involves a developing dissociation that builds over the first 15 to 20 minutes, peaks during the middle of the infusion, and gradually fades over the subsequent 30 minutes. Patients describe the experience variably, with some finding it pleasant and meaningful, others finding it neutral or mildly uncomfortable, and a small minority finding it distressing or destabilising. The experience can include visual phenomena, altered sense of self, feelings of being connected to something larger than the self, and emotional content including grief and joy. The capacity to integrate these experiences with ongoing psychotherapy is one of the differences between clinics that produce sustained benefit and those that produce only short-term symptom relief.

Maintenance treatment after the induction phase varies by clinic and by patient. Some patients benefit from monthly or every-other-month booster infusions to maintain the antidepressant effect. Others discontinue treatment after the initial course and resume only if symptoms recur. The lack of clear consensus on long-term protocols is one of the unresolved questions in ketamine therapy and is the subject of ongoing research. Discontinuation typically does not produce a withdrawal syndrome, but recurrence of depression can be significant in patients who relied heavily on the treatment for symptom control.

Selecting a reputable ketamine clinic requires attention to several factors. The clinical credentials of the prescribing physician matter, with psychiatrists and addiction medicine specialists generally providing more thorough assessment than non-psychiatric physicians. The integration with broader mental health care matters, with clinics that coordinate with the patient’s existing psychiatrist or therapist providing better continuity than clinics that operate in isolation. The protocol used should be evidence-based, with the standard 0.5 mg/kg over 40 minutes being the most established. The screening for safety should include assessment for psychotic illness, bipolar disorder, substance use disorder, and other conditions that may be contraindications or that may need specific management.

Recreational use and the street drug ketamine

Ketamine has been used recreationally since the 1970s and has become one of the more widely used dissociative substances in current illicit markets. Street names include K, special K, vitamin K, ket, kit kat, cat valium, super C, super K, jet, and many others. The substance is typically diverted from veterinary, anaesthesia, or medical supply chains, with much of the illicit supply originating in India, China, and other countries with looser pharmaceutical controls. The powder form (after evaporation of injectable solution or extraction from veterinary preparations) is the most common street form, sold by weight in small bags.

Recreational dose ranges depend on the desired experience. Bumps of 30 to 60 milligrams snorted produce mild dissociation and the empathetic euphoria characteristic of ketamine intoxication. Stronger doses of 75 to 150 milligrams snorted produce more pronounced dissociation with substantial cognitive and perceptual changes. High doses of 200 milligrams or more snorted, or 100 milligrams or more intramuscularly, produce the K-hole experience of complete dissociation, often described as a near-death-like experience with loss of contact with the body and surroundings. K-holes typically last 15 to 30 minutes and are sought by some users for the intensity of the experience and avoided by others as too dissociative.

The acute experience varies with dose and route but typically includes a sense of detachment from body and environment, altered perception of time (often slowed dramatically), visual changes including geometric patterns and altered perception of objects, emotional intensification or flattening depending on dose and individual response, and at higher doses the full dissociative state with loss of contact with surroundings. Physical effects include nystagmus (rapid involuntary eye movements), modest cardiovascular activation, altered coordination, and at high doses the loss of motor function characteristic of K-hole.

Festival and party use has expanded substantially in the 2010s and 2020s. The substance fits the dance music and electronic music subcultures well because of its dissociative effects, the relatively short duration of the experience (1 to 2 hours for moderate doses), and the social compatibility with dancing and music. Combined use with MDMA (ecstasy), cocaine, alcohol, and cannabis is common at festivals. The combination patterns carry substantial risk including cardiovascular events, hyperthermia, hyponatremia, and the medical emergencies associated with polysubstance use in physically demanding environments.

Medical risks of long-term ketamine use

Ketamine bladder syndrome (also called ketamine-induced cystitis or ketamine bladder pain syndrome) is the most clinically distinctive long-term complication of heavy recreational use. The syndrome was first described in 2007 in heavy ketamine users and has since been characterised in detail. The presentation includes severe lower urinary tract symptoms (pain, frequency, urgency, blood in urine), inflammation and ulceration of the bladder wall, reduced bladder capacity, and in advanced cases the loss of bladder function requiring surgical intervention. The mechanism involves direct toxicity of ketamine or its metabolites on the urothelium combined with chronic inflammation.

The severity of bladder symptoms correlates with the dose and duration of use. Users taking small amounts occasionally do not typically develop the syndrome. Users taking moderate amounts weekly may develop mild symptoms over years. Users taking large amounts daily can develop severe symptoms within months. The syndrome may partially or fully reverse with cessation of ketamine use, particularly if caught early, but advanced cases can result in permanent bladder damage. Surgical interventions including bladder augmentation or cystectomy may be needed in severe cases.

Cognitive effects of long-term heavy ketamine use have been documented in research studies. The most consistent findings are deficits in working memory, episodic memory, and executive function in heavy users compared with controls. The deficits are partial and not consistent across all users, but appear to be more pronounced with longer duration of use, higher cumulative dose, and more frequent use patterns. Some recovery of cognitive function occurs with cessation, but persistent deficits may remain in heavy long-term users.

Other long-term effects include possible hepatotoxicity with very heavy use, with case reports of liver function abnormalities in heavy users. Cardiovascular effects are typically modest at recreational doses but can be more concerning in users with pre-existing cardiovascular disease. Psychological effects of long-term use can include persistent dissociation that extends beyond the acute experience, depression, anxiety, and the cognitive and motivational changes that often accompany chronic substance use of any kind. Concurrent substance use is common and complicates the clinical picture.

Addiction potential and dependence

The addiction potential of ketamine was historically considered low compared with opioids, stimulants, alcohol, and benzodiazepines, but more recent clinical experience and research suggest that the abuse liability is more meaningful than was previously appreciated. Hallucinogen use disorder including ketamine is a DSM-5 diagnostic category, and patterns of compulsive use, tolerance, and inability to control use are well-documented in heavy users. Several factors make ketamine dependence clinically meaningful even if the abuse liability does not match that of the major substances of abuse.

Tolerance develops with regular use, with the doses required to produce the same effect escalating over weeks to months of frequent use. The escalation can be substantial, with chronic users taking five to ten times the doses that produced effects in their early use. The escalation drives further use and contributes to the medical complications including bladder syndrome that emerge with high cumulative exposure. Psychological dependence is real, with users describing inability to enjoy life without ketamine, anxiety at running out of supplies, and the organisation of daily life around the substance that characterises addiction more broadly.

Withdrawal from chronic heavy ketamine use is less well-characterised than withdrawal from other substances and does not appear to include the severe physical syndromes of opioid, alcohol, or benzodiazepine withdrawal. The symptoms reported include depression (sometimes severe), anxiety, fatigue, sleep disturbance, irritability, and craving. The protracted nature of these symptoms can extend for weeks to months and is part of why discontinuation is difficult for heavy users.

Treatment for problematic ketamine use follows the general principles of substance use disorder treatment with some specific considerations. The bladder symptoms often provide motivation for treatment when other consequences have not. The treatment of any underlying depression, anxiety, or PTSD that may have driven the use is particularly important because untreated mood and anxiety conditions are powerful drivers of relapse. The integration with broader mental health care, ideally including evidence-based psychotherapy for any co-occurring conditions, produces better outcomes than treatment focused only on the substance use. Phuket Island Rehab provides residential addiction medicine treatment for international patients with hallucinogen use disorder including ketamine.

Ketamine in suicidality and acute psychiatric emergencies

One of the more striking findings about ketamine in recent years has been its effect on acute suicidal ideation. Multiple studies have demonstrated rapid reduction of suicidal ideation within hours of a ketamine dose, with the effect often persisting for days to weeks. This finding has substantial implications for psychiatric emergency care, where patients with acute suicidal ideation traditionally have had few options for rapid stabilisation and have often required hospitalisation. Ketamine offers the possibility of rapid relief that could prevent some hospitalisations and stabilise patients enough to engage with outpatient treatment.

The use of ketamine specifically for suicidality is currently more research than standard clinical practice, but the evidence is sufficient that some psychiatric emergency services and crisis stabilisation units have begun offering ketamine as an option for selected patients. The intramuscular or intranasal route allows administration outside of formal intravenous infusion settings. The benefits are weighed against the medical considerations including the dissociative experience, the need for monitoring after dosing, and the long-term considerations of starting a patient on a substance with abuse potential during a vulnerable period.

Patients with acute suicidal ideation in the context of treatment-resistant depression are among the most likely beneficiaries of ketamine treatment. The combination of rapid antidepressant effect and specific anti-suicidal effect addresses the most clinically urgent aspects of the presentation. The treatment is typically integrated with hospitalisation or with intensive outpatient follow-up to support the patient through the period of acute risk. The longer-term treatment plan addresses the underlying depression with whatever combination of medications and psychotherapy is appropriate.

Practical considerations for patients considering ketamine therapy

Patients considering ketamine therapy for treatment-resistant depression should approach the decision systematically. The first step is ensuring that conventional treatments have been adequately tried, including multiple SSRI or SNRI trials at adequate doses and durations, augmentation strategies, and evidence-based psychotherapy. Ketamine is typically considered for treatment-resistant depression, defined as failure to respond to at least two adequate trials of standard antidepressants, rather than as a first-line treatment.

The second step is choosing between FDA-approved esketamine (Spravato) and off-label intravenous ketamine. The two have similar mechanisms but different practical features. Spravato is FDA-approved with formal evidence base, is administered in certified centres, and may be covered by insurance under specific conditions. Off-label intravenous ketamine has growing evidence base, is delivered at specialty clinics, is typically not covered by insurance, and offers somewhat more flexibility in protocol. The choice depends on availability, insurance coverage, and clinician recommendation.

The third step is verifying the credentials and quality of the providing clinic. The questions to ask include the credentials of the prescribing physician, the protocol used, the screening procedures, the monitoring procedures during and after infusion, the integration with broader mental health care, the cost and insurance coverage, and the aftercare and maintenance planning. Reputable clinics provide clear information about all of these elements and integrate with the patient’s existing mental health care.

The fourth step is realistic expectation-setting. Ketamine therapy produces substantial benefit in many patients with treatment-resistant depression, but the response rate is not 100 percent and the duration of effect varies. Some patients experience dramatic improvement that persists for months. Others experience partial improvement. A minority experience minimal benefit. The maintenance phase requires ongoing engagement that may or may not be sustainable over time. Combining ketamine therapy with evidence-based psychotherapy and standard antidepressants typically produces better outcomes than ketamine alone.

When alcohol use coexists with ketamine use

Alcohol use disorder, the clinical term for what most people call alcoholism, frequently coexists with ketamine use in the festival and electronic music subcultures where both substances are common. The pattern of heavy weekend drinking combined with ketamine use can develop into a problematic pattern that the user does not see as either an alcohol problem or a ketamine problem because they associate their substance use with the cultural context rather than with addiction. The combination is concerning because both substances have central nervous system depressant effects and the combined risk includes accidents, dangerous physical environments, and acute medical events.

Treatment of alcohol use disorder co-occurring with ketamine use follows the general principles of integrated treatment. Medical detoxification under supervision is needed for the alcohol component when withdrawal is severe. Behavioural treatment addresses both substances and the festival and dance culture context that supports both. Treatment of any underlying anxiety, depression, or trauma that may drive the use is essential for long-term recovery. Phuket Island Rehab provides residential addiction medicine treatment for international patients with co-occurring alcohol use disorder and hallucinogen use including ketamine.

Summary

Ketamine is a dissociative anaesthetic medication with FDA-approved uses for human anaesthesia and, since 2019, for treatment-resistant depression through the esketamine nasal spray (Spravato). The medication acts primarily as a non-competitive NMDA glutamate receptor antagonist with additional activity at opioid, monoaminergic, and other receptors. Medical applications include anaesthesia, procedural sedation, chronic pain management, treatment-resistant depression, and emerging uses in suicidality, PTSD, and other conditions. Ketamine clinics provide off-label intravenous ketamine for depression and related conditions, with quality varying substantially across clinics. Recreational use is widespread, with street names including K, special K, and ket, typically taken intranasally at doses of 50 to 200 milligrams, producing the dissociative experience and at high doses the K-hole of complete dissociation. Long-term heavy use produces ketamine bladder syndrome, cognitive impairment, and psychological dependence. The addiction potential is more meaningful than was previously appreciated and warrants attention. As Dr. Ponlawat Pitsuwan summarises, “Ketamine is one of the more clinically interesting substances because it sits at the intersection of accepted medical practice, emerging psychiatric treatment, and substantial recreational use. Each of these contexts produces different patterns of risk and benefit, and the patient’s relationship with ketamine needs to be understood in context to be useful clinically.”

Frequently asked questions

What is ketamine used for?

Ketamine is FDA-approved for human anaesthesia and, since 2019, for treatment-resistant depression in the form of esketamine nasal spray (Spravato). Off-label uses include procedural sedation, chronic pain management, depression and PTSD treatment at specialty ketamine clinics, and emerging applications in acute suicidality. Recreational use of ketamine as a dissociative drug is widespread in festival and party contexts.

Is ketamine an antidepressant?

Ketamine has rapid antidepressant effects that develop within hours of a dose and can persist for days to weeks. The FDA-approved esketamine nasal spray (Spravato) is indicated specifically for treatment-resistant depression. Off-label intravenous ketamine is widely used for the same indication at specialty clinics. The mechanism involves NMDA receptor antagonism and downstream effects on synaptic plasticity, distinct from the SSRI and SNRI antidepressants that take weeks to produce effect.

Is ketamine addictive?

Ketamine carries meaningful abuse potential, though historically considered less than opioids, stimulants, or benzodiazepines. Tolerance develops with regular use, psychological dependence can emerge, and patterns of compulsive use are documented. Hallucinogen use disorder including ketamine is a DSM-5 diagnostic category. Heavy long-term use produces medical complications including ketamine bladder syndrome that can be permanent.

What is a K-hole?

A K-hole is the experience of complete dissociation that occurs at high doses of ketamine, typically 200 milligrams or more snorted or 100 milligrams or more intramuscularly. The experience involves loss of contact with the body and surroundings, often described as near-death-like, with profound altered perception of time, identity, and reality. K-holes typically last 15 to 30 minutes. Some users seek the experience for its intensity; others find it frightening and avoid it.

What is ketamine bladder syndrome?

Ketamine bladder syndrome (ketamine-induced cystitis) is a medical condition that develops in heavy ketamine users, with symptoms of bladder pain, urinary frequency and urgency, blood in urine, and reduced bladder capacity. The condition is caused by direct toxicity of ketamine on the bladder wall combined with chronic inflammation. Early cessation may allow recovery; advanced cases can produce permanent damage requiring surgical intervention. Any heavy ketamine user with urinary symptoms should stop the substance and consult a urologist.

How does ketamine therapy work?

Ketamine therapy for depression typically involves a series of intravenous infusions at 0.5 mg/kg over 40 minutes, or intranasal esketamine doses, delivered over two to three weeks for induction. The patient experiences dissociation during the infusion and is monitored for 30 to 60 minutes afterward. The antidepressant effect develops within hours of the first dose and is typically sustained or strengthened across the induction course. Maintenance treatment at less frequent intervals may continue for months. Integration with psychotherapy and standard antidepressant treatment generally produces the best outcomes.

Sources

• U.S. Food and Drug Administration (FDA). Spravato (esketamine) prescribing information. https://www.accessdata.fda.gov/drugsatfda_docs/label/2019/211243lbl.pdf
• Krystal JH, Charney DS, Duman RS. A new rapid-acting antidepressant. Cell. 2020;181(1):7. https://www.cell.com/cell/fulltext/S0092-8674(20)30215-9
• Berman RM, Cappiello A, Anand A, et al. Antidepressant effects of ketamine in depressed patients. Biological Psychiatry. 2000;47(4):351-354. https://www.biologicalpsychiatryjournal.com/article/S0006-3223(99)00230-9/abstract
• National Institute on Drug Abuse (NIDA). Hallucinogens. https://nida.nih.gov/research-topics/hallucinogens
• Shahani R, Streutker C, Dickson B, Stewart RJ. Ketamine-associated ulcerative cystitis: a new clinical entity. Urology. 2007;69(5):810-812.
• Morgan CJA, Curran HV. Ketamine use: a review. Addiction. 2012;107(1):27-38. https://onlinelibrary.wiley.com/doi/10.1111/j.1360-0443.2011.03576.x
• Substance Abuse and Mental Health Services Administration (SAMHSA). National Helpline. https://www.samhsa.gov/find-help/national-helpline

Ketamine, esketamine, arketamine, Spravato, Ketalar, dissociative anaesthetic, NMDA receptor, N-methyl-D-aspartate, glutamate, non-competitive antagonist, mu-opioid receptor, kappa-opioid receptor, dopamine, serotonin, AMPA receptor, BDNF, brain-derived neurotrophic factor, synaptic plasticity, Calvin Stevens, Parke-Davis, FDA, Janssen Pharmaceuticals, Schedule III controlled substance, DEA, World Health Organization, WHO, anaesthesia, procedural sedation, surgical anaesthesia, chronic pain, complex regional pain syndrome, neuropathic pain, treatment-resistant depression, major depressive disorder, post-traumatic stress disorder, PTSD, obsessive-compulsive disorder, OCD, suicidal ideation, K-hole, dissociation, dissociative experience, derealisation, depersonalisation, ketamine clinic, intravenous infusion, intranasal esketamine, intramuscular ketamine, oral ketamine, hallucinogen use disorder, DSM-5, tolerance, psychological dependence, withdrawal, ketamine bladder syndrome, ketamine-induced cystitis, lower urinary tract symptoms, urinary frequency, hematuria, bladder damage, cognitive impairment, working memory, episodic memory, executive function, MDMA, ecstasy, cocaine, alcohol use disorder, polysubstance use, SSRI, SNRI, sertraline, fluoxetine, venlafaxine, cognitive behavioural therapy, CBT, psychotherapy, NIDA, SAMHSA, NHS, residential rehab, Phuket Island Rehab, addiction medicine.