Severe Encephalatrophy and Related Disorders From Long-Term Ketamine Abuse: A Case Report and Literature Review

Furthermore, in ketamine users, the putamen showed higher connectivity to the OFC, which correlated with duration of ketamine use. 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). alcohol and menopause 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).

What Patients Need to Know About Ketamine

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. The emerging data with KET01 suggest that it is indeed possible to achieve rapid improvement in depression without the characteristic side effects of ketamine-based medications. This raises the potential for broader and safe use of a ketamine-based medication for depression, with an improved tolerability profile.

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But in addition to its anesthetic and antidepressant potency, the drug has “dissociative effects,” including hallucinations, that have led to recreational use. A fundamentally different approach is being pursued by Ketabon, where we are developing KET01, an oral prolonged-release form of ketamine administered as a tablet. The resulting low concentration of circulating ketamine is not sufficient to elicit characteristic side effects that are most likely mediated via the NMDA receptor, such as dissociation, sedation and blood pressure increase.

Ketamine Slang Terms

In contrast, they found higher functional connectivity in the left middle occipital gyrus. In a pilot that studied white matter connectivity, chronic ketamine users showed higher connectivity gallbladder and alcohol consumption between caudate nuclei and the dorsal anterior cingulate cortex (dACC). Ketamine users also showed a higher connectivity between the pallidum and the bilateral cerebellum.

However, this drug can be fatal because it is usually combined with other substances like alcohol (which also has sedative effects) or hallucinogens like LSD and PCP. While users report feeling complete bliss on ketamine, consuming high amounts of this drug can produce effects similar to a near-death experience. Coupled with its ability to produce an out-of-body experience, this drug can cause visual and auditory perceptual changes. The original contributions presented in the study are included in the article/supplementary material, further inquiries can be directed to the corresponding author/s. Although the ketamine high can be extremely pleasant, it can lead to serious dependence.

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

1. The dissociative effect alters the users perception of light and sound and produces feelings of detachment from self and surroundings.
2. 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.
3. Nevertheless, the introduction of Spravato represents a significant milestone in the treatment of depression.
4. In a study by Hung et al. (2020a), chronic ketamine users compared to healthy controls showed higher functional connectivity between the left DLPFC and the right inferior frontal/superior temporal gyrus and the left OFC and the right insula/inferior temporal gyrus.
5. No person with alcohol abuse disorder or alcohol intoxication should take ketamine, even in doctor-prescribed doses, as it can cause death.
6. Many depressed individuals do not respond adequately to current treatments, and about a third remain treatment-resistant after multiple treatment attempts.

Despite the fact that antidepressants can be immensely helpful for people, they don’t work for everyone. Ketamine and esketamine were approved for forms of depression that haven’t responded to traditional oral antidepresants (such as fluoxetine/Prozac, sertraline/Zoloft, etc.). In circumstances where insurance pays for treatment (more common with esketamine than ketamine), patients are often required to have tried at least two oral antidepressants before starting treatment with ketamine/esketmaine. (The exception would be when a patient is imminently suicidal, in which case the treatment would often be started while the patient is hospitalized.) What counts as “trying” an oral antidepressant?

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 barbiturates with other substances, such as cocaine, MDMA or amphetamines. One of the most significant advantages of ketamine is its ability to induce anesthesia rapidly and reliably, making it particularly well-suited for use in emergency settings or during procedures where rapid onset is essential.

Additionally, the patient did not have a long history of using some drugs except dexamethasone more than 3 months. However, dexamethasone was used after the patient was found to have severe brain atrophy. In a study by Hung et al. (2020a), chronic ketamine users compared to healthy controls showed higher functional connectivity between the left DLPFC and the right inferior frontal/superior temporal gyrus and the left OFC and the right insula/inferior temporal gyrus.

FA in the left and right frontal white matter was negatively correlated with the total lifetime consumption of ketamine. 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). In 16 ketamine users averaging 2.4 grams/day for 7.3 years, a lower level of axial diffusivity was found compared to 16 polydrug controls, especially in the frontal part of the right hemisphere (Edward Roberts et al., 2014). Axial diffusivity was significantly lower in eight white matter clusters in the right hemisphere in the ketamine group compared to the control group, the three largest being located in the frontal cortex (Edward Roberts et al., 2014).

The dissociative effect alters the users perception of light and sound and produces feelings of detachment from self and surroundings. Hallucinations, delirium and emergence phenomena can occur, particularly at higher doses or in susceptible individuals. Furthermore, concerns have been raised regarding its abuse potential and the development of tolerance and dependence with chronic use. By antagonizing this receptor, ketamine disrupted glutamatergic neurotransmission, leading to its characteristic dissociative and anesthetic effects. Substance abuse treatment for drug abuse must work holistically for it to have a lasting effect. In other words, it must treat the damaging effects of substance abuse on the body but then it must also help the addict learn how to build a new drug-free life, sometimes from the ground up, when addiction has destroyed everything.

As we are unsure when the abnormal live function and brain atrophy began, the brain atrophy may have been liver mediated. However, as the liver symptoms lasted a short time and were treated quickly, it is unlikely that such severe brain atrophy was caused by abnormal liver function. We infer that the severity of the brain atrophy may not be related to abnormal renal and liver function.