Abstract
In severe depression thoughts of suicide can develop over weeks or months. Traditional pharmacologic or psychotherapeutic treatments take several weeks before they begin to improve symptoms. This gradual improvement is consistent with our everyday experience of the self. However, a new treatment, ketamine, can alter depressive symptoms within hours or even minutes. Ketamine can stop suicidal thoughts in as little as 20 minutes and is being developed to treat suicidal patients in the emergency room. Rapid changes in a belief as complex as suicide raise new questions about the self and identity. More complicated models of the self are required to understand how rapid changes in complex beliefs are possible without invoking unrealistic specificity in the brain (i.e. grandmother cells for belief). If the brain has multiple competing selves within modules then ketamine could work by either turning a self module on or off. This is consistent with a modified version of the global workspace theory of consciousness where a self module provides the context for the spotlight of attention.
Highlights
KetamineKetamine was first developed in 1962 as a general anesthetic.[11]. It is classified as a dissociative anesthetic and can produce a sense of detachment and often hallucinations at lower subanesthetic doses
While simple beliefs can change permanently in minutes or even seconds, complicated beliefs are closely tied to identity and are typically resistant to rapid change
Mr J’s story is not unique and many patients with depression often feel they have two selves: their depressed self and their normal self striving to return. When he presented to the emergency room Mr J clearly had one self that wanted to get rid of the bothersome depression and suicidal thoughts and get on with his day
Summary
Ketamine was first developed in 1962 as a general anesthetic.[11]. It is classified as a dissociative anesthetic and can produce a sense of detachment and often hallucinations at lower subanesthetic doses. The mechanism of action of ketamine is through the blockade of glutamine binding sites on NMDA receptors. Glutamine is the primary excitatory neurotransmitter in the brain and NMDA receptors are found throughout the brain and are responsible for synaptic plasticity and memory formation.[12] The action of ketamine is not specific to any brain region but appears to. Globally effect excitatory neurons.[12] Similar to the discovery of the original tricyclic class of antidepressants, the efficacy of ketamine for depression was discovered serendipitously. Ketamine improves symptoms, including suicidal thoughts, within hours or minutes.[7,8] To date there have been numerous open label trials of ketamine and it appears to be a promising treatment but large scale placebo controlled clinical trials are needed to determine if it can be used successfully to treat depression in standard clinical practice.[5,6,7,8,9,10,14] Depression often returns within a few days of the first ketamine treatment and the larger clinical trials will help determine how many consecutive doses are required to sustain remission
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