Author: Gary Jackson

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

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. Ketamine withdrawal treatment aims to help you get off the drug and stay off it. Some of the literature in the addiction treatment sphere mentions cases of reported anxiety and/or depression following cessation of ketamine use. However, for many ketamine abusers, withdrawal isn’t a major issue, as ketamine doesn’t produce a clinically significant withdrawal syndrome.

Central nervous system side effects such as agitation are less intense than those seen with PCP abuse.

Associated Data

Many experience hallucinations that can last longer than the anesthetic effects. Ketamine is typically injected or snorted, but it can be smoked or taken in pill form. The effects of smoking it or swallowing it tend to be less intense than those of directly injecting it. In some cases, it’s used as a date rape drug, as it’s odorless and colorless. Substitute drugs are not used as the Narconon program is a drug free program. Many users will attempt to take enough of the drug to experience a condition of complete dissociation from body or environment that they consider enjoyable.

• Both alcohol and ketamine are central nervous system depressants, so the combined effects are dangerous.
• Evidence shows that ketamine is safe for use in people within a wide age range when taken correctly.
• Axial diffusivity is thought to be a measure of axonal density and radial diffusivity is thought to be related to the degree of myelination (Liao et al., 2010).
• Intranasal dosing (which is currently under evaluation for the treatment of depression) could also widely expand the availability of ketamine treatment.

Perpetrators who use it in this manner may slip it into a beverage of the person they wish to victimize. Individuals who take ketamine recreationally report sensations, such as being separated from their body or a pleasant feeling of floating. Some people have an almost complete sensory detachment that they compare to a near-death experience. Refractory status epilepticus (RSE) is a form of status epilepticus that does not respond to standard antiseizure drugs. The FDA has approved ketamine for general anesthesia only, but the drug has some off-label uses.

Dangerous Ketamine Side Effects

The included studies followed a cross-sectional and retrospective design with considerable variability among studies in terms of subject age, ketamine type and dosage. It should be noted that in some studies, ketamine users had a mood disorder and for many of the studies it was unclear whether the ketamine users were diagnosed with another substance use disorder or another psychiatric illness. Part of the structural and functional neuroanatomical differences could therefore be attributed to these concomitant conditions. Finally, we were unable to receive a few records containing potentially relevant data. Collectively, these studies suggest that ketamine may improve the ability to establish and maintain abstinence in SUDs. Improvement in cravings, motivation to quit, and self-administration have been shown in cocaine use disorder (19, 20, 26).

• Three of these studies are focused on alcohol use disorder, and the other three are focused on cocaine, opioid, and cannabis use disorders.
• Addiction can negatively impact quality of life, physical health, mental well-being, and relationships.
• It should be noted that in some studies, ketamine users had a mood disorder and for many of the studies it was unclear whether the ketamine users were diagnosed with another substance use disorder or another psychiatric illness.
• Physiologic response to opioid withdrawal can also be severe, and includes nausea, emesis, diarrhea, myalgias, intractable lacrimation and rhinorrhea, fevers, dysphoria and insomnia.

In 2010, the global prevalence of alcohol and illicit drug use disorders were 9.6 and 10.9% respectively (1). Mortality rates have risen to epidemic proportions in some countries due to increasing prevalence of opioid use. For example, the United States, which accounts for 25% of global overdose mortality, has experienced an 88% increase in opioid overdose deaths each year from 2013 to 2016 (2, 3). Substance use disorders (SUDs) include cognitive, behavioral, and physiological symptoms.

How is Ketamine Abused?

Within the ketamine users group, adolescent onset users were compared to adult-onset users. Adolescent-onset users showed a significantly smaller left precuneus volume than the adult-onset group and the healthy control group. Lower functional connectivity was found between the thalamus and the motor-, posterior parietal- and prefrontal cortex. Functional connectivity between the posterior parietal cortex and right lateral dorsal nucleus was significantly correlated to individual ketamine craving scores (Liao et al., 2016).

For nearly 50 years, the Narconon network of rehab centers have been helping the addicted repair the guilt, stamp out the cravings and lift the depression that is so common to addicts. Without a thorough rehab program, these factors of addiction will keep a person trapped. It may be stolen from a vet clinic in the US or obtained from international sources and then trafficked into the US. It is easily obtained in Mexico and those wishing to abuse the drugs may cross the border and purchase it. Some people may cross the border to obtain either ketamine or the anti-anxiety drug Rohypnol for the purpose of rendering a person incapable of resisting a sexual assault. Either drug can cause amnesia so that the victim may not even remember the event.

A possible mechanism for the white matter changes identified in the reviewed recreational ketamine studies could be AMPA-receptor mediated excitotoxicity. In rats, ketamine was found to acutely elevate presynaptic glutamate in the prefrontal cortex at AMPA/kainite receptors (Moghaddam et al., 1997), and prolonged ketamine exposure may provoke cell death by regional glutamate-induced excitotoxicity. Excitation of AMPA receptors specifically induces axonal damage (Fowler et al., 2003), which could provide a potential mechanism for the prominent white matter changes observed after sustained ketamine exposure in three of the reviewed studies. Also, white matter changes in one of these studies preceded more widespread cortical atrophy with longer ketamine use, supporting that axonal cells are most vulnerable for glutamate-induced excitotoxicity by ketamine. However, these observations are still based on comparison between subjects rather than longitudinal data. One study investigated how long-term ketamine use affected neurotransmitter systems (Narendran et al., 2005).