Brain Changes Associated With Long-Term Ketamine Abuse, A Systematic Review PMC

ketamine abuse effects

Where possible, the support of friends and family is also fundamental when recovering from ketamine addiction. The World Health Organization (WHO) estimates that, when injected, drug and alcohol rehab in laguna beach lethal doses of ketamine begin around 11 mg/kg of body weight. Ketamine has a relatively short half-life (the time required for active substances in the body to reduce by half).

ketamine abuse effects

A magnetic resonance cholangiopancreatography showed mild dilatation of the proximal common bile duct with narrowing of the common hepatic duct without cholelithiasis. All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article, or claim that may be made by its manufacturer, is not guaranteed or endorsed by the publisher. The original contributions presented in the study are included in the article/supplementary material, further inquiries can be directed to the corresponding author/s.

How is Ketamine Abused?

It is sometimes used off-label for pain relief and can provide sedative effects. In addition, the FDA now recognizes the antidepressant benefits of ketamine when it is combined with oral depressants. Widely known for its medicinal properties, ketamine’s effects have made it a popular addition to the party scene. It has also joined the ranks of GHB (gamma hydroxybutyrate) and Rohypnol (Flunitrazepam) as a date rape drug. John C. Umhau, MD, MPH, CPE is board-certified in addiction medicine and preventative medicine.

ketamine abuse effects

Using diffusion-weighted MRI scans, fractional anisotropy (FA) can be used for estimating white matter fiber density, myelination and axonal diameter. FA reductions were found in bilateral frontal and left temporoparietal white matter in 41 ketamine users with a mean use of 2 grams/day for 3.4 years, in comparison with 44 drug-free controls (Liao et al., 2010). FA in the left and right frontal white matter was negatively correlated with the total lifetime consumption of ketamine.

Ketamine can disrupt the senses, judgment, and motor function for up to 24 hours after use. These effects have seen a growing and worrying use of this drug for date rape. Coupled with its ability to produce an out-of-body experience, this drug can cause visual and auditory perceptual changes. As a Schedule III drug, ketamine is available for medicinal use with a prescription.

Also, the ventral striatum (VS) showed lower connectivity with the right superior temporal sulcus (STS) and the left superior frontal gyrus (SFG) which was mediated by higher scores on the Barratt Impulsiveness Scale (BIS-11) (Hung et al., 2020b). Ketamine is a general anesthetic agent commonly used in pediatric patients, especially for neurosurgery and for surgeries requiring cardiopulmonary bypass (1). Ketamine can produce a dissociative state and hallucinations and therefore is not commonly used in adult anesthetic practice. Because of the hallucinatory effects of the drug, recreational ketamine abuse has been increasingly reported in recent years.

Ketamine Slang Terms

Overall, no difference in sgACC connectivity was found between groups, but in ketamine users higher depression scores correlated with lower sgACC connectivity to the right lateral and bilateral medial OFC. Further analysis revealed functional connectivity changes, with male and female ketamine users showing higher sgACC connectivity than controls to the bilateral superior temporal gyrus or dorsomedial prefrontal cortex (dmPFC), respectively (Li et al., 2017). Also, they found a correlation between higher sgACC connectivity with the dmPFC and higher depression scores in women, but not in men. Although ketamine has strong short-term antidepressant effects, the current data would suggest that chronic ketamine use may actually induce depression via sex-specific dysregulation of brain networks for positive and negative emotions. It remains unclear whether the altered connectivity patterns found in this study could be a direct result of ketamine. Being under the influence of ketamine was not an exclusion criterion for participation in this study.

People who have used this drug report harsh flashbacks even weeks after the drug has been cleared from the body. This drug has been linked to conditions like depression, hysteria, memory loss, and high blood pressure in regular users. There are different ways to identify a person the signs of a potential ketamine addiction. We’ll be examining the symptoms to look out for, and factors that can increase the risk of developing a dependence or addiction to ketamine. This article will also look into trusted treatments that can help overcome ketamine misuse. The search concept combination can be displayed as ketamine AND (chronic OR long term OR abuse OR dependence OR known long term use effects OR induced adverse effects).

Therefore, the different functional connectivity patterns could in part be caused or influenced by the direct, short term effects of ketamine. The drug can produce a dissociative state and hallucinations, making ketamine a favorite recreational agent among drug addicts. Chronic drug addiction substance use disorder diagnosis and treatment ketamine abuse can damage many organs, including the brain, heart, liver, gastrointestinal tract, and genitourinary system. Ketamine is a phencyclidine derivative that is licensed for anesthetic use in humans and in veterinary medicine, especially in developing countries.

Theoretically, this may be a concern in people who have consumed energy drinks, often done at nightclubs where ketamine may be abused. This agent is a lipid soluble compound, has an initial rapid distribution and large volume of distribution, with a half-life of 10 to 15 minutes. Secondarily, the drug distributes into peripheral tissues with a slower elimination half-life of up to 3 hours, undergoes hepatic metabolism and is excreted in the urine.

  1. Because of these heterogenous results, we could not perform a quantitative bias analysis.
  2. Subsequently we excluded articles that were only about brain function and not about neuro-anatomical outcomes (e.g., performance on cognitive tests).
  3. Theoretically, this may be a concern in people who have consumed energy drinks, often done at nightclubs where ketamine may be abused.

It is also used with an oral antidepressant for treatment-resistant depression (TRD) in adults. It is used under strict medical supervision and is not used by patients at home. For ketamine to be helpful in addiction treatment, it must be used under the close care of medical professionals. Ketamine triggers activity of a neurotransmitter called glutamate in the frontal cortex of your brain.

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At higher doses, ketamine produces a dreamlike state, hallucinations, distorted visual perceptions, a sensation of a near-death experience, amnesia, and delirium, making it a favorite recreational agent of drug abuse (3). “Special K,” “Vitamin K,” “K,” “kit-kat,” “keets,” “super acid,” “super K,” “cat valiums,” and “jet” are the terms used by drug abusers for recreational ketamine. Acute toxic effects of ketamine include tachycardia, abdominal pain, hypertension, raised intracranial pressure, muscle rigidity, cognitive dysfunction, and sometimes death (2, 5). The results were subdivided into structural differences in gray and white matter, functional differences and effects on neurotransmission. Given the limited number of included studies and diversity of outcome measures in the studies, the data was deemed not suitable for meta-analysis. Therefore, we performed a conceptual synthesis of these heterogenous results.

New Study Maps Ketamine’s Effects on Brain

An overdose of ketamine can cause unconsciousness or slowed breathing, which is very dangerous. Different amounts of ketamine will give different “highs.” A medicinal dose is usually around 1 to 2 milligrams for each kilogram of body weight. Addiction to substances such as ketamine is characterized by an inability to stop despite addiction relapse negative consequences, preoccupation with the substance, and disruptions that interfere with important aspects of life. When people try to stop using ketamine, they may also experience symptoms of withdrawal. A ketamine overdose can occur when the substances is taken in large amounts or when combined with other substances.

Ketamine was first used in medical procedures for anesthesia in the 1960s. It has also been implicated for the treatment of psychotic symptoms in schizophrenia, treatment of depression, and treatment of addiction—although ketamine itself is a commonly misused drug. Cholestasis related to chronic ketamine abuse has been described recently (10, 11). Biliary dyskinesia resulting from the direct effect of the drug on the smooth muscles or through the vagus nerve may be the cause of cholestasis. Full recovery from the hepatobiliary disease over time has been observed with complete abstinence from ketamine abuse (10, 11).

One study investigated how long-term ketamine use affected neurotransmitter systems (Narendran et al., 2005). D1 receptor availability was significantly upregulated in the dorsolateral prefrontal cortex of ketamine users compared to controls, which could result from increased receptor density or affinity. D1 binding potential correlated with the total amount of ketamine consumption (Narendran et al., 2005). In a pilot that studied white matter connectivity, chronic ketamine users showed higher connectivity between caudate nuclei and the dorsal anterior cingulate cortex (dACC). Ketamine users also showed a higher connectivity between the pallidum and the bilateral cerebellum. Furthermore, in ketamine users, the putamen showed higher connectivity to the OFC, which correlated with duration of ketamine use.

Because of these heterogenous results, we could not perform a quantitative bias analysis. Bias could play a role, since the 5 studies by Liao et al. (2010, 2011, 2012, 2016, 2018) were based on the same sample. For that reason, we compared the results if four of these five studies were left out of the analysis, to the situation in which all five studies were included. The former finding, that ketamine decreases dopamine in the midbrain, may indicate why long-term abuse of ketamine could cause users to exhibit similar symptoms to people with schizophrenia, a mood disorder. The latter finding, that ketamine increases dopamine in the parts of the brain that regulate metabolism, on the other hand, may help explain why it shows promise in treating eating disorders.

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