What Is Ketamine Addiction

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Ketamine addiction is defined by meeting ≥ 2 of the DSM-5 criteria for Ketamine Use Disorder within a 12-month period, including [37] :

Cravings for ketamine, irritability, and restlessness within 2 hours of last use [1]
Increased use due to tolerance (e.g. 1g per day to 4g hourly) despite knowledge of physical consequences (e.g. urge incontinence) [1]

Physical Indicators Of Ketamine Addiction

Tremors

Muscle rigidity tremors in up to 7% are physical indicators of compulsive ketamine use caused by [3]:

A 4% reduction (in mm) of cortical thickness in the frontal and parietal lobes after consuming 0.8g of ketamine ≥ 30 times a month for over 5 years [4]
Disruptions within the glutamatergic system (e.g. increased by 3.7% in the medial temporal cortex but reduced by 2.3% in the thalamus) after consuming ketamine 3 or more times a week for 12 months [5]
Severe brain damage after 4 – 12 years of consuming ≥ 1 gram of ketamine a day, including lesions in the grey and white matter of the prefrontal, parietal, occipital, limbic, brainstem, and corpus striatum regions [6]

Garg, Amit et al (2014) documented how a man who injected up to 4g of ketamine daily experienced tremors around 2 hours after his last dose due to abnormal neuromuscular activity (e.g. myoclonus, muscle rigidity) caused by the reversal of NMDA-receptor blockade [1].

Dissociation-Induced Body Freezing

Dissociation-induced body freezing is a physical indicator of an addiction to ketamine because NMDAR-mediated excitatory postsynaptic currents are inhibited by 35% for up to 6 hours after use, disrupting sensory-motor integration and resulting in [7]:

A ‘K-hole’ lasting between 10 - 60 minutes, including mind-body dissociation, a ‘floating’ sensation, or feeling paralysed in up to 71% after daily ketamine usage, typically appearing catatonic or zombie-like to a sober person watching [8]
Out of body experiences in 64%, including lying on the floor and “melting into surroundings”, feeling present in an alternative reality, and being unable to feel body parts after consuming 3.8g per session, 20 days a month, for up to 6 years [9]

Butler, Gavin (2017) reported how a 26-year-old fell into a ‘K-hole’ for 20 minutes after snorting 170mg of ketamine, claiming to fall through a mattress into another dimension whilst losing track of reality and time and being unable to move his body that felt like a ‘lifeless shell' [10].

Altered Speech Patterns

Altered speech patterns are physical indicators of compulsive ketamine use caused by a 60% reduction in dopamine and impaired thalamocortical connectivity in the prefrontal and motor cortices after 3 years of daily use, resulting in [11][12]:

Talking in ‘slow motion’ with a monotonous voice due to an 18% reduction in verbal fluency and a 60% increase in dissociation within 12 months of consuming 2 – 4 grams daily [13]
Slurred speech and ‘slowed thinking’ in up to 71% after consuming ketamine around 233 times, with up to 37% claiming to struggle with speaking and putting thoughts into words during and after being intoxicated [8]
Cognitive disorganisation and blunted affect in 6 – 10%, as some users claim, “It makes me feel emotionally void, I don’t have anything to say” after consuming ketamine 4 or more times per week for 5 – 6 years [9]

Fine Motor Skills Loss

Difficulty handling small objects (e.g. coins) is a physical indicator of ketamine use disorder because hyperintense degeneration in the cerebellum and disrupted neural signalling in motor pathways occur after 4 years of daily use, impairing balance, bimanual coordination, and motor precision abilities [6].

Taffe, Michael A. (2002) found that administering 1.78mg/kg ketamine twice weekly for 9 weeks impaired fine motor coordination and delayed retrieval latency by approximately 13 seconds in rhesus monkeys required to retrieve 15 raisins from holes to demonstrate bimanual dexterity [14].

Ketamine abuse contributes to 9% of fatal drug and alcohol-related vehicle crashes due to a loss of fine motor skills needed for precise, controlled, and coordinated movements between the hands and feet to steer, shift gears, or apply pressure to pedals whilst driving [15]:

Lucuta, L. et al (2024) documented how a 44-year-old male was found inside a car stopped in the middle of a traffic island with motoric agitation and trembling hands, claiming to have had a ‘black out’ after consuming ketamine 3.5 hours previously [16]
Lucuta, L. et al (2024) documented how a 33-year-old male was pulled over for dangerous driving and had trembling hands and quivering eyelids, an insecure turn during a walk-and-turn-test, and an insecure finger-finger-test after consuming ketamine before driving [16]

Psychological Indicators Of Ketamine Addiction

Ketamine Induced Psychosis

Ketamine-induced psychosis is a psychological indicator of ketamine misuse because chronic NMDA receptor blockade disrupts glutamate and dopamine transmission (e.g. up-regulated by 24%) in the dorsolateral prefrontal cortex, resulting in [17]:

Auditory, tactile, and visual hallucinations in up to 75% of regular users who spend over £60 a week on ketamine, with around 6.3% of cases developing into a psychotic disorder [8][18]
A 16% increase in delusional behaviour (e.g. convinced about having special powers) within 12 months amongst frequent users (3g consumed 20 times in 28 days) compared to infrequent users (1g consumed 3 times in 28 days) [12]

Liang, Hua Jun, et al (2015) found that 30.2% of ketamine users developed a psychotic disorder after 9 years of psychoactive substance abuse, although symptoms were exacerbated in 28% of patients who used 3 or more drugs (e.g. cocaine, ecstasy) alongside ketamine [19].

Lane, Hsien-Yuan, et al (2016) reported how a 26-year-old experienced manic and major depressive episodes with auditory hallucinations after consuming 10-15g of ketamine weekly for 12 months, although psychotic symptoms subsided and mood stabilised within 3 weeks of entering rehab and taking 10mg aripiprazole and 200mg sertraline daily [20].

Ketamine-Induced Amnesia

Ketamine-induced amnesia is a psychological indicator of ketamine abuse because glutamate signalling is disrupted, and regional grey matter volume is reduced by 6 - 10% in the left dorsolateral prefrontal cortex and medial orbitofrontal cortex after 5 years of misuse, resulting in [21]:

31% of users being “unable to remember things” due to a 9 - 23% decrease in visual and verbal working memory (e.g. remembering a phone number) function after using ketamine for around 15 days a month for 5 years [8][22]
An 18-23% reduction in episodic memory function (e.g. prose recall immediate and delayed) as neural firing is suppressed in the hippocampus after consuming 10.2g of ketamine per week for up to 10 years [23]

Memory loss occurs in 50% of ketamine consumers as a result of ‘blacking out’ and feeling out of control whilst high, as one user said, “I couldn’t remember if I had actually taken my K” after regaining consciousness following an ‘intense K-hole experience’ [9][10].

Sleep Paralysis And Sleepwalking

Sleep paralysis/sleepwalking is a psychological indicator of ketamine dependence caused by disruptions in glutamatergic neurotransmission (e.g. increased by 4% in the medial temporal cortex vs reduced by 2% in the thalamus), leading to [5]:

Irregular transitions between sleep stages, e.g., the number of REM cycles decreases by 61%, whereas the duration of NREM (in minutes) is extended by 46% after daily ketamine consumption [24]
Poor quality sleep (PSQI >5) in 82% of heavy users, including <5 hours of sleep per night, a >60-minute sleep latency, and sleep efficiency <65% after consuming around 1.37g of ketamine daily for almost 5 years [25]

Around 21% of chronic ketamine consumers (used up to 2000 times) experience night terrors/sleep paralysis, fragmentary sleep, and frightening dreams whilst claiming to feel “uncomfortably sleepy’ within 2 hours of drug-taking [1][8].

Long-Term Effects Of Ketamine Addiction

Ketamine Bladder Syndrome

Ketamine Bladder Syndrome typically occurs within 24 months of heavy use (e.g. up to 20g daily) because the urothelium is repeatedly irritated as the drug is excreted in the urine and passed through the bladder, leading to [2]:

Epithelial inflammation, diffuse bladder wall thickening, enhancement of the bladder mucosa, and inflammatory changes in the surrounding perivesical fat in 71 – 75% after 1-15 years of drug abuse [27][28]
Suprapubic pain, dysuria, abnormally frequent urination (e.g. every 15 – 90 minutes vs 5 – 6 times daily), and an overwhelming urge to urinate due to a reduced functional voiding capacity (e.g. 20–200 vs 400 - 700 ml) [27][29]
Secondary renal impairment (serum creatinine levels >120 μmol/L) in up to 51%, unilateral or bilateral hydronephrosis and papillary necrosis, requiring endoscopic insertion of JJ stents or a nephrostomy insertion for decompression of the upper tracts [27]

Gill, Paul, et al (2018) described the experiences of 12 ketamine addicts aged 20 – 43 who developed ketamine bladder syndrome after gradually consuming higher doses (up to 20g daily) over a 12-year period:

“I kept going to the toilet every half hour, and I still can’t use public transport because I have to get off after a five-minute journey.”
“I wasn’t passing much, and I had really bad burning and blood in my urine. Then just before my 18th birthday, I was admitted because I couldn’t go to the toilet anymore.”
“Within about six months, it was like nothing you’ve ever seen.... Every time I was weeing, it looked like a murder scene in my toilet.”
“I was in that much pain, I was screaming, I was in absolute agony, it was worse than childbirth... it felt like somebody was slicing me open.” [2]

Developing Complex Mental Health Disorders

Schizophrenia occurs in 2% of long-term (9 years) ketamine abusers because repeated NMDA receptor blockade increases the severity of abnormal thought content, perceptions, and speech production (e.g. delusions, hallucinations, thought-blocking) by 2-4-fold due to [5][19]:

Excessive glutamate release in the anterior cingulate and medial temporal cortex (e.g. increased by 2-4%) after consuming around 100g of ketamine each month [5]
Imbalances in dopamine transmission within the mesolimbic system, as D1 receptor availability is increased by 9 - 18% in the hippocampus, amygdala, and ventral striatum after chronic use (e.g. 2.8 vials per week for 4 years) [17]
Neuroanatomical changes, including white matter lesions, a 4% reduction of cortical thickness, and a 10% decrease in grey matter volume of the prefrontal cortex after 6 years of drug-taking [4][21]

Lahti, Adrienne C. et al (1995) found that schizophrenic individuals experienced a 25 – 50% increase in psychotic symptoms within 24 hours of taking ketamine, including the recurrence of delusions and auditory/visual hallucinations caused by further disruptions in glutamatergic signalling [29].

Permanent Depersonalisation Or Derealisation

Permanent depersonalisation/derealisation is a consequence of long-term ketamine dependence because:

The brain’s default mode network (DMN), responsible for self-referential thinking (e.g. identity, time, memory), becomes deactivated after repeatedly using high doses of a dissociative drug (e.g. 2 – 4g of ketamine per session for 7 years) [13]
Up to 6% of long-term users (9 years of use) have co-occurring schizophrenia, PTSD, or depressive disorders and typically have high levels of dissociation (DES score >30), increasing by 2-fold after frequent ketamine use (>4 times weekly) [13][19][30]

Morgan, Celia J. A. et al (2010) found that frequent users (20 uses per month) of ketamine had high levels of dissociation (DES score >30) at baseline and 12 months later, and ex-users (4+ weeks of abstinence after 7 years of use) still experienced depersonalisation after 1 year, as scores increased by 11% from baseline [13].

Who Is More Likely To Develop an Addiction To Ketamine?

More Likely To Develop A Ketamine Addiction	Self-Medication For Depression Developing Into Addiction	Illicit Use Developing Into Addiction	Prescribed Use Developing Into Addiction
Why?	17% consume up to 3.8g per session for ‘escapism’ [9] Users rely on the ‘numbing’ effect and re-dose to prolong emotional relief [1]	Used by up to 93% at parties with friends due to initial peer pressure or curiosity [9] Up to 73% frequently use (20 days per month) after seeing ‘friends doing it’ or to ‘feel excitement’ [8][9]	A doctor prescribes ketamine for ‘antidepressant benefits’ that last 4 - 5 days [31] Drug-taking occurs against prescribed advice due to noticeable mood improvements
Case Studies	“It takes the edge off everything; if I’m unhappy, it takes it away in a bubble” [9] “Ketamine was the only substance that helped my depression.” [31]	“It is a habit. If I stopped, I’d feel left out by my friends” “I’m doing it even when I’ve planned not to; It’s very addictive, but lots of my friends are ill.” [9]	“Mr. A reported using higher than prescribed doses of ketamine more frequently (10–12 times a day).” “Mr. A met criteria for ketamine dependence due to compulsive use and increased tolerance” [31]

How Do Different Routes Of Administration Change Ketamine Addiction?

	Pills	Powder	Injection
Onset Of High	20 - 60 mins	5 - 10 mins	10 - 30 secs (IV) vs 3 - 5 mins (IM)
Duration Of High	2 - 4 hrs	45 - 60 mins	30 - 60 mins (IV) vs 60 - 90 mins (IM)
How Does Addiction Develop?	Accidental use in 6%: “I realised they weren’t E, they were K.” I liked it, so I started using them together.” [9]	Cheaper than other powder-based ‘club’ drugs (e.g. £20 vs £40/g for MDMA) = allows regular use	Able to inject up to 4g hourly High/frequent doses = intense cravings within 2 hours [1]
Associated Health Risks	Hepatotoxicity due to being metabolised in the liver GERD, vomiting + abdominal pain	Contributes to 95% of ketamine-related hospital visits [3] Inflamed nasal passages/ sinus cavities + septum perforation	Contributes to 32.4% of ketamine-related deaths [32] 6% become HIV positive [33]

	Rectal Administration	Sublingual
Onset Of High	10 - 20 mins	15 - 30 mins
Duration Of High	1 - 2 hrs	1.5 - 2.5 hrs
How Does Addiction Develop?	Easy to hide heavy/frequent use due to no injection marks or smell	Typically prescribed for at-home use without medical supervision Hazardous drug-taking (e.g. microdosing) for self-medication
Associated Health Risks	Rectal bleeding, STIs, mucosal damage/tearing Exacerbates pre-existing anorectal conditions (e.g. Proctalgia Fugax)	Ulcers + sores in the mouth/under the tongue 9% of ketamine-related deaths occur after prescribed use [32]

Ketamine Classification In The UK

As of the 8th of January 2025, the UK government is seeking expert advice on reclassifying ketamine as a Class A substance (up to life in prison for supply/production + 7 years for possession) rather than a class B substance (up to 14 years in prison for supply/production + 5 years for possession) because:

In March 2023, an estimated 299,000 people aged 16-59 reported ketamine use in the previous 12 months, which is the largest number on record [34]
The number of users requiring ketamine addiction treatment is 8 times higher than in 2014-2015, including some school-aged children (13-16 years old) who report using ketamine as a party drug at least once a week [35][36]
Up to 10% of recreational users are admitted to the hospital due to self-harm/suicide attempts, falls/injuries, overdose, and tongue biting within 12 hours of drug-taking, and up to 59% of ketamine-induced deaths are accidental [1][32]
Irreversible damage to the bladder and urinary tract occurs in some cases because only 10% of symptomatic users seek medical help after experiencing ulcerations, fibrosis, bleeding, pain, and incontinence within 3 – 24 months of drug-taking [2]

References

[1] Garg, Amit, et al. “Use of Naltrexone in Ketamine Dependence.” Addictive Behaviours, vol. 39, no. 8, Aug. 2014, pp. 1215–16. Accessed 4 Apr. 2025.“Tremulousness, intense sweating, restlessness, within 2 h of last use of ketamine, ... he began injecting himself up to 4 g of ketamine per day, sometimes as often as hourly.”
[2] Gill, Paul, et al. “Participants’ Experiences of Ketamine Bladder Syndrome: A Qualitative Study.” International Journal of Urological Nursing, vol. 12, no. 2-3, July 2018, pp. 76–83. Accessed 9 Apr. 2025.“ Consequently, most participants developed noticeable KBS symptoms within around 6-24 months of this change in use”
[3] Raimondo Maria Pavarin, et al. “Ketamine Abusers Referring to Emergency Departments in Northern Italy: A Cross- Sectional Study.” PubMed, vol. 55, no. 4, National Institutes of Health, Dec. 2019, pp. 338–44. Accessed 4 Apr. 2025.“Table 2.”
[4] Tang, Jinsong, et al. “Widespread Reductions in Cortical Thickness Following Ketamine Abuse.” Journal of Psychiatry and Neuroscience, vol. 49, no. 3, Canadian Medical Association, May 2024, pp. 182–91. Accessed 4 Apr. 2025.“Table 2.”
[5] Stone, James M., et al. “Glutamate, N-Acetyl Aspartate and Psychotic Symptoms in Chronic Ketamine Users.” Psychopharmacology, vol. 231, no. 10, Nov. 2013, pp. 2107–16. Accessed 4 Apr. 2025.“Table 2.”
[6] Wang, Chunmei, et al. “Brain Damages in Ketamine Addicts as Revealed by Magnetic Resonance Imaging.” Frontiers in Neuroanatomy, vol. 7, July 2013. Accessed 4 Apr. 2025.“Majority dosage was 1 g a day, ... durations of drug addiction ranged from 0.5 to 12 years, ... brain regions affected were prefrontal, parietal, occipital, limbic, brainstem, and corpus striatum. The lesions affected both the gray and white matter.”
[7] Jin, Jianhui, et al. “The Blockade of NMDA Receptor Ion Channels by Ketamine Is Enhanced in Developing Rat Cortical Neurons.” Neuroscience Letters, vol. 539, Elsevier BV, Feb. 2013, pp. 11–15. Accessed 7 Apr. 2025.“At 6 h after washout, eEPSCs of adult neurons have completely recovered. However, eEPSCs were still remarkably inhibited in immature neurons (35.2±1.5% of control level, n=7).”
[8] Stirling, John, and Lauren McCoy. “Quantifying the Psychological Effects of Ketamine: From Euphoria to the K-Hole.” Substance Use & Misuse, vol. 45, no. 14, Oct. 2010, pp. 2428–43. Accessed 7 Apr. 2025.“As for k-hole experiences, a sense of floating (71%), confusion (79%), and disturbed speech (71%) were frequently reported, as was the sense of things being unexplainable (also 71%).”
[9] Muetzelfeldt, L., et al. “Journey through the K-Hole: Phenomenological Aspects of Ketamine Use.” Drug and Alcohol Dependence, vol. 95, no. 3, June 2008, pp. 219–29. Accessed 7 Apr. 2025.“The most appealing effects of the drug for roughly 66% of users were ‘melting into surroundings’, ‘visual hallucinations’, ‘out of body experience’, ... I was just lying on the floor not knowing what I was doing and it was like there was this different reality.”
[10] Butler, Gavin. We Asked People about the K-Holes That Changed Their Lives. 6 Nov. 2017. Accessed 7 Apr. 2025.“I was falling through my mattress into another dimension… I lost track of reality and time, ... I tried to move but my body seemed to just vibrate as the K kept disconnecting me from my body, ... After about 20 minutes I got my consciousness back.”
[11] Liao, Yanhui, et al. “Decreased Thalamocortical Connectivity in Chronic Ketamine Users.” PLOS ONE, edited by Emmanuel Andreas Stamatakis, vol. 11, no. 12, Dec. 2016. Accessed 7 Apr. 2025.“Ketamine user group showed significantly less connectivity between the thalamic nuclear groups and the cortical regions-of-interest, including the prefrontal cortex, the motor cortex /supplementary motor area, and the posterior parietal cortex.”
[12] Yu, Hao, et al. “Mapping the Central Effects of Chronic Ketamine Administration in an Adolescent Primate Model by Functional Magnetic Resonance Imaging (FMRI).” PubMed, vol. 33, no. 1, National Institutes of Health, Jan. 2012, pp. 70–77. Accessed 7 Apr. 2025."There was a significant reduction in the positively stained axon projections of dopaminergic neurons in the prefrontal cortex of chronically ketamine challenged monkeys (Fig. 4) (mean + SEM of TH+ cells/mm2 in ketamine group: 415.16).
[13] Morgan, Celia J. A., et al. “Consequences of Chronic Ketamine Self-Administration upon Neurocognitive Function and Psychological Wellbeing: A 1-Year Longitudinal Study.” Addiction, vol. 105, no. 1, Jan. 2010, pp. 121–33. Accessed 7 Apr. 2025.“Table 2 - 4.”
[14] Taffe, Michael A., et al. “Ketamine Impairs Multiple Cognitive Domains in Rhesus Monkeys.” Drug and Alcohol Dependence, vol. 68, no. 2, Oct. 2002, pp. 175–87. Accessed 8 Apr. 2025.“Figure 5.”
[15] Cheng, Jack Y. K., et al. “An Epidemiological Study on Alcohol/Drugs Related Fatal Traffic Crash Cases of Deceased Drivers in Hong Kong between 1996 and 2000.” Forensic Science International, vol. 153, no. 2-3, Oct. 2005, pp. 196–201. Accessed 8 Apr. 2025.“The most frequently detected drugs for SVC group (11 cases) were: 46% central nervous system (CNS) stimulants (including designer drugs like MDMA); 36% cannabis; 18% benzodiazepines and 9% ketamine.”
[16] Lucuta, L., et al. “Ketamine in DUID Cases in the Greater Cologne Area.” Forensic Science International, vol. 354, Jan. 2024, p. 111905. Accessed 8 Apr. 2025.“ The police described psychomotor impairments including motoric agitation, strong tension, trembling hands, and a lack of concentration, ... accused stated that he consumed ketamine powder 3.5 and 6.5 h prior to the incident.”
[17] Narendran, Rajesh, et al. “Altered Prefrontal Dopaminergic Function in Chronic Recreational Ketamine Users.” American Journal of Psychiatry, vol. 162, no. 12, Dec. 2005, pp. 2352–59. Accessed 8 Apr. 2025.“Dorsolateral prefrontal cortex D 1 receptor availability was significantly up-regulated in chronic ketamine users ([ 11C]NNC 112 binding potential: mean= 1.68 ml/g, SD=0.40) relative to comparison subjects (mean=1.35 ml/g, SD=0.35).”
[18] Ronald Y. L. Chen et al. A Study on the Cognitive Impairment and Other Harmful Effects Caused by Ketamine Abuse. Feb. 2025. Accessed 8 Apr. 2025.“Table 5.”
[19] Liang, Hua Jun, et al. “Ketamine Users Have High Rates of Psychosis And/or Depression.” Journal of Addictions Nursing, vol. 26, no. 1, Jan. 2015, pp. 8–13. Accessed 8 Apr. 2025.“Table 2 - 3.”
[20] Lane, Hsien-Yuan, et al. “Mania Following Ketamine Abuse.” Neuropsychiatric Disease and Treatment, Jan. 2016, p. 237. Accessed 8 Apr. 2025.“Initially, he took ketamine 5 g/wk for several weeks and then 10–15 g/wk for months (with a total duration of 12 months), ... After the manic-like period, his mood gradually shifted to a depressive state, he had experienced marked euphoria, labile mood, dissociation, and auditory hallucinations.”
[21] Hung, Chia-Chun, et al. “Effects of Early Ketamine Exposure on Cerebral Gray Matter Volume and Functional Connectivity.” Scientific Reports, vol. 10, no. 1, Sept. 2020, p. 15488. Accessed 8 Apr. 2025.“Table 3.”
[22] Liang, H. J., et al. “Cognitive Impairments in Poly-Drug Ketamine Users.” Addictive Behaviors, vol. 38, no. 11, Nov. 2013, pp. 2661–66. Accessed 8 Apr. 2025.“Table 4.”
[23] Morgan, Celia J. A., et al. “Long-Term Heavy Ketamine Use Is Associated with Spatial Memory Impairment and Altered Hippocampal Activation.” Frontiers in Psychiatry, vol. 5, Dec. 2014. Accessed 8 Apr. 2025.“Table 3.”
[24] Kantor, Sandor, et al. “Ketamine Supresses REM Sleep and Markedly Increases EEG Gamma Oscillations in the Wistar Kyoto Rat Model of Treatment-Resistant Depression.” Behavioural Brain Research, vol. 449, July 2023. Accessed 8 Apr. 2025.“Table 1.”
[25] Tang, Jinsong, et al. “Sleeping Problems in Chinese Illicit Drug Dependent Subjects.” BMC Psychiatry, vol. 15, no. 1, Feb. 2015. Accessed 8 Apr. 2025.“We found that the prevalence of sleep disturbance was 81.98% in ketamine users with PSQI >5), ... ketamine users used 1.37 ± 1.38 g ketamine powder and 1.53 ± 0.94 times per day.”
[26] Chu, Peggy Sau-Kwan, et al. “The Destruction of the Lower Urinary Tract by Ketamine Abuse: A New Syndrome?” BJU International, vol. 102, no. 11, Dec. 2008, pp. 1616–22. Accessed 9 Apr. 2025.“Forty-two (71%) patients had a cystoscopy that showed various degrees of epithelial inflammation, ... micturition frequency was every 15–90 min, while the functional voiding capacity was 20–200 mL only.”
[27] Mason, K., et al. “Ketamine-Associated Lower Urinary Tract Destruction: A New Radiological Challenge.” Clinical Radiology, vol. 65, no. 10, Oct. 2010, pp. 795–800. Accessed 9 Apr. 2025“Abnormal findings associated with ketamine use were identified in nine patients (75%) and included diffuse bladder wall thickening, enhancement of the bladder mucosa, and inflammatory change in the surrounding perivesical fat.”
[28] Wrenn, Keith. Dysuria, Frequency, and Urgency. Butterworths, 2012. Accessed 9 Apr. 2025.“The average adult bladder holds between 400 and 700 ml of urine. Normal patterns of urination may vary considerably; adults generally void 5 to 6 times daily but no more than once after retiring. The average 24-hour urinary output is 1200 to 1500 ml. Urinary frequency may occur because of either increased urine volume or decreased bladder capacity (i.e., less than 200 ml).”
[29] Lahti, Adrienne C., et al. “Subanesthetic Doses of Ketamine Stimulate Psychosis in Schizophrenia.” Neuropsychopharmacology, vol. 13, no. 1, Aug. 1995, pp. 9–19. Accessed 10 Apr. 2025.“Table 3.”
[30] Traumadissociation. Dissociative Experiences Scale - II. 2024. Accessed 10 Apr. 2025..“High levels of dissociation are indicated by scores of 30 or more, scores under 30 indicate low levels.”
[31] Schak, Kathryn M., et al. “Potential Risks of Poorly Monitored Ketamine Use in Depression Treatment.” American Journal of Psychiatry, vol. 173, no. 3, Mar. 2016, pp. 215–18. Accessed 10 Apr. 2025.“Mr. A” was a 52-year-old divorced man with a 30-year history of recurrent major depressive disorder. He received a single intravenous ketamine infusion, which he reported provided antidepressant benefit for 4–5 days. Because of his perceived mood improvement, he sought out a ketamine prescriber.".
[32] Darke, Shane, et al. “Characteristics and Circumstances of Death Related to the Self‐Administration of Ketamine.” Addiction, vol. 116, no. 2, July 2020, pp. 339–45. Accessed 10 Apr. 2025.“Death was attributed to toxicity in 82.3% of cases (accidental, 58.8%; deliberate, 23.5%), suicide by violent means (8.8%) and traumatic accident (8.8%), ... In 32.4% the final route of ketamine administration was by injection.”
[33] Lee, Tony Szu-Hsien, et al. “Clinical and Behavior Characteristics of Individuals Who Used Ketamine.” Scientific Reports, vol. 12, no. 1, Jan. 2022. Accessed 10 Apr. 2025.“Table 1.”
[34] Home Office. Home Office Requests Review of Ketamine Classification. 8 Jan. 2025. Accessed 10 Apr. 2025.“The prevalence of the drug in England and Wales has risen significantly in recent years. In the year ending March 2023, an estimated 299,000 people aged 16-59 had reported ketamine use in the last year – the largest number on record.”
[35] Office for Health Improvement & Disparities. Adult Substance Misuse Treatment Statistics 2023 to 2024: Report. 28 Nov. 2024. Accessed 10 Apr. 2025.“The number of ketamine users starting treatment (3,609) is now over 8 times higher than it was in 2014 to 2015, when the number was 426.”
[36] Greater Manchester: Testing and Research on Emergent and New Drugs. 2023-2024 Monitoring Cycle. Trend Focus: Ketamine. 2024. Accessed 10 Apr. 2025.”Two-fifths (42%) were school-aged (13 to 16), ... a similar percentage (62%, n=13) of females aged under-18 reported using ketamine at least once a week.”
[37] Fitzgerald, Nicole D., et al. “Test-Retest Reliability and Cross-Cultural Applicability of DSM-5 Adopted Diagnostic Criteria for Ketamine Use Disorders.” Drug and Alcohol Dependence, vol. 228, Nov. 2021. Accessed 30 May 2025.“With regard to the DSM-5, a ketamine use disorder included meeting two or more of 11 adopted criteria, with at least two being met in the same 12-month period, ... a craving criterion was added from an existing item that assessed craving for ketamine after several hours or days of not using ketamine, ... feeling anxious, restless, or irritable (15.1%) after not using ketamine.”

About the author

Mischa Ezekpo

Mischa Ezekpo has a Bachelors degree in Psychology from Northumbria
University, and a Masters degree in Childhood Development and
Wellbeing, from Manchester Metropolitan University. Since 2018, Mischa
has written and published work on Addiction, Mental Health, Depression, and Eating Disorders. Content reviewed by Laura Morris (Clinical Lead).

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Last Updated: July 18, 2025