Ketamine Treatment
The Evolution of Ketamine
Over the past 50 years, ketamine’s reputation has evolved from a powerful battlefield anesthetic to a leading alternative to antidepressants and other mainstream modalities in the treatment of pain and mental health disorders. Ketamine was approved by the FDA in 1970 and first used as a sedative for emergency surgeries on the frontlines of the Vietnam War. Ketamine was initially lauded for its effectiveness, safety, and mild side effects.
Over the last decade, ketamine has become an invaluable asset for various pain and mental health issues. It is recognized for its neuro-regenerative properties and potential to offer quick relief of symptoms. In fact, the World Health Organization named ketamine to its list of essential medicines.

Ketamine Treatment for Mood Disorders
Scientific research has highlighted ketamine’s unique ability to treat mood disorders like major depressive disorder (MDD), anxiety, post-traumatic stress disorder (PTSD), and obsessive-compulsive disorder (OCD).
Ketamine blocks the N-methyl-D- aspartate (NMDA) receptor from reabsorbing glutamate. This blockage causes the release of brain-derived neurotrophic factor (BDNF).
BDNF is an important brain chemical responsible for the maturation and maintenance of the neuronal dendrites and synapses that are necessary for normal brain connectivity. In conjunction with glutamate, BDNF helps restore and maintain and promote the healthy growth of new neuronal connections.
The neurons in various parts of your brain need to be able to connect to each other via their dendrites and their synaptic contact. Prolonged stress and anxiety diminish BDNF leading to visible changes in neuroanatomy and subsequent serious mood disorders such as depression, PTSD, OCD, and anxiety.
Ketamine Treatment for Chronic Pain
It is believed that one of the leading causes of chronic pain conditions is the overactivity of the NMDA receptor in the brain. Ketamine helps chronic pain by attaching to the NMDA receptor and inhibiting its activity, thereby muting chronic pain symptoms.
By connecting to those receptors, ketamine may be able to amplify the number of glutamate neurotransmitters in the empty space between neurons. Glutamate then interacts with the AMPA receptors.
While it also stimulates opiate receptors, its role as an NMDA receptor antagonist is much more important in the treatment of chronic pain. By blocking the receptor, pain signal transmission is interrupted, giving central pain centers a chance to reset. A series of low-dose ketamine infusions in awake patients can dramatically alter — or even eliminate — chronic pain.
