Ketamine Effects: After- & Short-Term Effects of Ketamine

The only known source of ketamine is via diversion of prescription products. Illicit production usually involves evaporating the liquid from the diverted injectable solution to produce understanding alcohol use disorder national institute a powder that is formed into tablets or sold as a powder for intranasal use. Central nervous system side effects such as agitation are less intense than those seen with PCP abuse.

  1. However, these observations are still based on comparison between subjects rather than longitudinal data.
  2. Examining the variability in individual behavioral and neural response to ketamine provides the potential to generate predictions of how people may respond to it, providing hope for the millions suffering from treatment-resistant depression.
  3. However, it has been shown that frequencies of cytochrome P450 variants responsible for ketamine metabolism do not vary significantly between people with Asian or Caucasian ancestry (Mizutani, 2003; Peltoniemi et al., 2016).
  4. The effectiveness, however, is varied with only some patients feeling the benefits.
  5. Ketamine is often used as what is called a date rape drug by individuals who want to sexually assault others.
  6. Ketamine is not a first line treatment for status epilepticus, and it is generally used when other treatments are contraindicated or when they have not effectively stopped a prolonged seizure.

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

When higher doses of ketamine are abused, or during emergence, it is reported to produce vivid dreams and an “out-of-body”, “K-hole” or “near-death” hallucinogenic experience, often reported as terrifying (similar to bad LSD trip). Ketamine is a noncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist, and it blocks HCN1 receptors. However, at higher doses it may also bind to the opioid mu and sigma giving up and divorcing your alcoholic husband receptors. Glutamate is involved with learning, memory, emotion, and pain recognition. It can exhibit sympathomimetic activity which can lead to rapid heart rate and elevated blood pressure. Ketamine was involved in 0.033% of the United States Emergency Department visits involving illicit drugs in 2005, with this proportion increasing slightly to 0.12% in 2011 (Drug Abuse Warning Network, 2011).

Treatment for Ketamine Addiction

Sensations the user may seek include floating, stimulation and visual effects. When abused, it is typically insufflated (“snorted” up the nose) in social situations. It is also injected, consumed orally as a liquid (mixed into drinks), or smoked in marijuana or tobacco. It is frequently abused in combination with other substances, such as cocaine, MDMA or amphetamines. In addition to its legal, medical uses, ketamine and synthesized analogs have become drugs of abuse with hallucinogenic properties. As mentioned previously, an overdose is a medical emergency, so it’s important to seek immediate medical attention and call 911 right away if you suspect an overdose.

K-Hole and the Effects of Ketamine

Allergic reactions – get emergency medical help if you have signs of an allergic reaction, including hives, difficulty breathing, and swelling of your face, lips, tongue, or throat. Ketamine became an FDA-approved medicine on February 19, 1970, as a general anesthetic to be used as the sole anesthetic agent for diagnostic and surgical procedures that do not require skeletal muscle relaxation. It is also used for the induction of anesthesia prior to the administration of other general anesthetic agents and as a supplement to other anesthetic agents.

Data Extraction

If this progresses to vomiting, it can be very dangerous, as those in the midst of a state of dissociated confusion frequently end up supine—presenting a serious choking hazard. If you do see someone on ketamine, take a moment to roll them on their side or into the recovery position if possible to prevent this from happening. The first feeling of the high that the user will get is an overwhelming feeling of relaxation, sometimes described as a full-body buzz. Some users feel like they’re floating and some even describe it as being out of their bodies.

Being oblivious to concussions, deep cuts, or broken bones, people using ketamine may ignore their wounds -leading to permanent damage, infection, or secondary injuries. Before Spravato was approved in 2019, ketamine was prescribed off-label for the treatment of depression. Other off-label uses of ketamine include 12 things that happen when you quit drinking treating bipolar disorder, post-traumatic stress disorder, as well as substance use disorder. Ketamine is also used as a recreational drug that can be abused for its dissociative sensations and hallucinogenic effects. Ketamine is an injectable anesthesia that has been used in humans and animals since 1970.

This drug may be contraindicated for you if your blood pressure is unstable. In conclusion, these animal studies may provide important clues for the potential neurotoxic effects of prolonged ketamine use. Prolonged ketamine may either up- or downregulate important regulatory neuronal proteins, potentially resulting in impaired neuronal functioning and cognitive performance. It must be noted that the reported changes were dependent on the dosage and duration of ketamine use which were substantially higher than for clinical use, so our findings cannot be translated to clinical ketamine use. Coordination impairment is another short-term consequence, making everyday activities challenging and increasing the likelihood of accidents and severe injuries. In addition, the intense hallucinations and altered perceptions experienced during a ketamine overdose can contribute to confusion and disorientation, creating a dangerous situation for the individual.

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. 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. To date, the safety of prolonged ketamine administration has sparsely been investigated in humans in a prospective manner.

In the same sample, the authors compared smoking chronic ketamine users with non-ketamine smokers and with non-ketamine, non-smokers by performing fMRI. They found a higher activation in the anterior cingulate cortex (ACC) in response to ketamine cues. Also, ketamine subjects showed lower activation in the cerebellum and the middle temporal cortex in response to natural rewarding (sexual) cues (Liao et al., 2018). Many of the observed changes were correlated with the amount and duration of ketamine consumption, suggesting a possible dose dependent effect of prolonged ketamine on brain structure and function. Although the identified lower gray and white matter volumes or integrity could suggest direct neurotoxic effects of ketamine, the observed higher structural and functional connectivity and dopamine binding may suggest indirect compensatory effects.

While the drug is largely eliminated from the body within 14 to 18 hours after the last dose, it can also have longer-term effects. 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.

We included 16 studies in our review, totaling 440 chronic ketamine users with a mean ketamine use of 2–9.7 years and 2.4 grams per day, compared to 259 drug-free controls and 44 poly-drug controls. Five studies were based on the same sample (Liao et al., 2010, 2011, 2012, 2016, 2018). The included studies described structural gray matter and white matter differences, differences in brain functionality and differences in neurotransmitter receptor binding. All retrieved studies were retrospective cohort studies, level IV on the Sackett scale or level 2b on the Oxford CEBM levels of evidence scale (Sackett, 1989; Howick et al., 2018). A possible mechanism for the white matter changes identified in the reviewed recreational ketamine studies could be AMPA-receptor mediated excitotoxicity.

Lorazepam is typically given 2 to 4 mg intravenously or intramuscularly, and diazepam dosing generally is 5 mg to 10 mg IV. Butyrophenones, including haloperidol, have been used to treat psychotic episodes and agitation.[8] Haloperidol is typically given in doses of 5 mg to 10 mg IM and can be administered every 10 to 15 minutes until adequate sedation is achieved. However, providers should exercise caution when using haloperidol, as lowered seizure thresholds, QT prolongation, and torsades de pointes correlate with the prolonged use of haloperidol.

Original studies about recreative ketamine use in which neuroanatomical measurements were performed, either structural or functional, were included. To obtain the articles meeting this inclusion criterion we first excluded all articles that were not about ketamine. Subsequently we excluded articles that were only about brain function and not about neuro-anatomical outcomes (e.g., performance on cognitive tests). Lastly, we excluded papers that were about animals or were no original investigations. Finally, we found our complete dataset consisting of 16 studies (see Figure 1) for the inclusion flowchart.

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